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April 1995 
Volume 40, Number 4 

ISSN 0020-1 324-RECACP 



Resuscitation in Acute Care Hospitals 

Part I 



Resuscitation in Acute Care 

Hospitals — Conference Summary 
Development of AHA Guidelines for 

Practice Guidelines for Resuscitation 
Pacemakers & Electrical Therapy 

during ACLS 
Compression Techniques & Blood 

Flow during CPR 
Practice Guidelines for Ainway Care 

during CPR 
ACLS Drugs during Resuscitation 
ACLS Systems & Training Programs 

41st Annual Convention and Exhibition 
December 2-5 • Orlando, Florida 


Clinically Speaking 

tt In Pressure 
Regulated Volume 
Control, as the 
patient's compliance 
changes, the Servo 
Ventilator 300 with its 
real-time control, adjusts 
to find the lowest 
possible pressure to 
deliver the guaranteed 
volume. 9§ 

P»frJ. PtpadtkoM, MD 
AtfndlnQ PhytlclM, SICU 

§§ Recently, a patient 
who had ARDS was 
placed on the ventilator 
in the PRVC mode. 
We were able to 
ventilate her with 
consistently low peak 
ainway pressures, 
and she improved at 
a more rapid pace than 
we anticipated, ff 

§i The flexibility of the 
Sen/o 300 is superior. 
With a simple turn of a 
dial, you can make 
ventilatory adjustments 
and move between 
different modes. 99 

§6 Just as the 
Servo 900C did when 
it was introduced, the 
gas delivery system of 
the Servo 300 has set 
a new standard. §9 

§$ In volume 
support, the Servo 
300 automatically 
fine-tunes the pressure 
support level breath- 
by-breath, and frees 
the therapist for 
other duties. It's 
much more 
efficient. 99 

Ronnto Raynolds, BHT 

66 Patients feel 
more comfortable on 
the Servo Ventilator 
300. And it can be 
used with neonates, 
pediatrics, and adults - 
one ventilator, 
versus many 
ventilators. 99 

Amndlna PhytlelBH, SICU 
Unlnnllf of 

Siemens can also bring you 
the very best in ventilator care 
For more Information on 
the Servo Ventilator 300® 
or to arrange a personal 
demonstration, contact your 
local Siemens representative. 
Or call toll-free. 

Siemens Medical Systems, Inc. 

Patient Care Systems Division 
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Danvers, MA 01923 
Toil-Free 1-800-333-8646 


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A Monthly Science Journal. Established l')5fi. Olt'icial Journal ot the American Association tor Respiratory Care. 


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Pal Brougher BA RRT 


Kaye Weber MS RRT 


Ray Masferrer BA RRT 


James K Sloller MD, Chairman 
Richard D Branson RRT 
Cryslal L Dunlevy EdD RRT 
Charles G Durbm Jr MD 
Thomas D Easi PhD 
Dean Hess PhD RRT 
Neil R Maclnlyre MD 
Shelley C Mishoe PhD RRT 
Joseph L Rau PhD RRT 


Frank E Biondo BS RRT 
Howard J Birenbaum MD 
Robert L Chatbum RRT 
Patricia Ann Doorley MS RRT 
Donald R Ellon MD 
Robert R Fluck Jr MS RRT 
Ronald B George MD 
James M Hurst MD 
Charles G Irvin PhD 
MS Jastremski MD 
Robert M Kacmarek PhD RRT 
Hugh S Malhewson MD 
Michael McPeck BS RRT 
David J Pierson MD 
John Shigeoka MD 
Jack Wanger MBA RPFT RRT 
Jeffrey J Ward MEd RRT 


Stephen M Ayres MD 
Reuben M Chemiack MD 
Donald F Egan MD 
Gareth B Gish MS RRT 
George Gregory MD 
Ake Grenvik MD 
H Frederick Helmholz Jr MD 
John E Hodgkin MD 
William F Miller MD 
Thomas L Petty MD 
Alan K Pierce MD 
Henning Pontoppidan MD 
John W Severinghaus MD 
Barry A Shapiro MD 


Linda Barcus Donna Knauf 
Steve Bowden Denise Ditzenberger 
Brian Keagy 


April 1995 
Volume 40, Number 4 



The Proceedings of a Conference 

held October 21-23, 1994 

in Cancun. Mexico 

Chairmen and Guest Editors 
Thomas A Barnes EdD RRT and Charles G Durbin Jr MD 


335 Resuscitation in Acute Care Hospitals — The Time for Change Is Now! 

hy Charles G Durbin Jr — Charlottesville, Virginia 
338 The Development of AHA Guidelines for Emergency Cardiac Care 

hv Arthur B Sanders — Tuscan. Arizona 
346 Clinical Practice Guidelines for Resuscitation in Acute Care Hospitals 

hv Thomas A Barnes — Boston, Massachusetts 
364 Pacemakers and Electrical Therapy during Advanced Cardiac 

Life Support 

by Tom P Aufderheide — Milwaukee, Wisconsin 
380 Compression Techniques and Blood Flow during 

Cardiopulmonary Resuscitation 

by Henry R Halperin, Nisha C Chandra, Howard R Levin, 

Bariy K Raybum, and Joshua E Tsitlik 
393 Practice Guidelines for Airway Care during Resuscitation 

by Michael J Bishop — Seattle, Washington 
404 ACLS Drugs Used during Resuscitation 

by Joseph L Rau Jr— Atlanta, Georgia 
iXll ACLS Systems and Training Programs— Do They Make a Difference? 

by Paul E Pepe — Houston, Texas 


438 Removal of a Closed-System, Directional-Tip Suction Catheter 

hy Robert A Milisch, David S Rho, and Sheila A Schell—LaCrosse, 

Respiratory Care (ISSN 0020-1324) is a monthly publicaiion of Daedalus Enterprises Inc for ihe Amencan Association for Respiratory Care. Copyright © 1994 by Daedalus 

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Respiratory Care • April '95 Vol 40 No 4 



H : Flow Meter 

In status 

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< 40% 

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REf ERENCES: 1 Pelers Jl.^ssfuctefi): C«trwt C 
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April 1995 
Volume 40, Number 4 



442 Respiratory Physiology, 3rd edition by Allen H Mines; edited 

by William F Ganong. 
reviewed by Tim Opt Holt — Mobile, Alabama 

442 Principles and Practice of Pulmonary Rehabilitation, edited 
by R Casaburi and TL Petty. 

reviewed by Gretchen Lawrence — Dallas. Texas 

443 Essentials of Anatomy and Physiology, 3rd edition 

by Valerie C Scanlon with Instructors Guide and Student Workbook. 
reviewed b\ Marilyn A Cairns — Boston, Massachusetts 


318 Summaries of Pertinent Articles from Other Journals 


445 1995 Call for Open Forum Abstracts 


447 Instructions for Authors and Typists 


453 Examination Dates, Notices, Prizes 


454 Meeting Dates, Locations. Themes 


456 Authors in This Issue 

456 Advertisers in This Issue 

324 Advertiser Help Lines 

Respiratory Care • April '95 Vol 40 No 4 



ot" Pertinent Articles in Other Journals 

Editorials and Commentaries To Note 

Asthma Deaths in New Zealand: Whodunnit? (commentary) — GJ Blauw, RGJ Westendorp. Lancet 
1995;345:2-3. (Pertains to the paper by Pearce et al abstracted on Page 322.) 

Current Concepts in Transcription, Translation, and the Regulation of Gene Expression: A Primer for 
the Clinician— AA Knowlton. Chest 1995;107( 1 ):241-248. 

Does the Clinical Examination Predict Airflow Limitation? — DR Hollenian, DL Simel. JAMA 

Sepsis, Sepsis Syndrome, and the Systemic Inflammatory Response Syndrome (SIRS): Gulliver in 
Laputa— RC Bone. JAMA 1995;273(2);155-156. (Penains to the paper by Rangel-Frausto et al abstracted 
on Page 328.) 

Aerolized Heparin— D Kohler. J Aerosol Med 1994;7(4):307-314. 

Cost and Outcome of Intensive Care for 
Patients with AIDS, Pneumocystis carinii 
Pneumonia, and Severe Respiratory 
Failure— RM Wachter, JM Luce, S Safrin, 
DC Berrios, E Charlebois, AA Scitovsky. 
JAMA 1995;273:230. 

OBJECTIVE: To determine the costs and out- 
comes associated with intensive care unit 
(ICU) admission for patients with acquired 
immunodeficiency syndrome (AIDS)-related 
Pneumocystis cannii pneumonia (PCP), and 
severe respiratory failure. DESIGN: Survival 
and cost-effectiveness analysis. SETTING: A 
large municipal teaching hospital serving an 
indigent population. PATIENTS: Consecutive 
patients intubated and mechanically ventilated 
for AIDS, PCP, and respiratory failure from 
1981 through 1991 (n =113). The cohort was 
separated into three groups for analysis: pa- 
tients admitted to the ICU in 1981 through 
1985 (era 1, n = 43). admitted in 1986 
through 1988 (era II, n = 33l, and those admit- 
ted in 1989 through 1991 (era III, n = 37). 
charges and survival time; cost per year of life 
saved, using a zero-cost, /.ero-life assumption. 
RESULTS: Twenty-eight (25'7o of the 113 
patients mechanically ventilated for PCP and 
respiratory failure survived to hospital dis- 
charge: six (1 4%) of 43 in era 1,13 (39%) of 33 
in era II. and nine (24%) of 37 in era III (P = 
0.04). Posl-ICU admission charges averaged 
$57,874 for the entire cohort, remaining rela- 
tively stable across the three eras. Cost of care 

for survivors was significantly more expensive 
than for those dying before discharge. The cost 
of ICU admission and subsequent hospitaliza- 
tion averaged $174,781 per year of life saved; 
$305,795 in era I, $94,528 in era II, and 
$215,233 in era III. Improved survival rates and 
shorter lengths of ICU stay led to the improved 
cost-effectiveness in era II, while the opposite 
trends resulted in worsening cost-effectiveness 
in recent years. The strongest predictors of hos- 
pital mortality in era III were low CD4 cell 
counts on hospital admission and the develop- 
ment of pneumothorax during mechanical ven- 
tilation. CONCLUSIONS: The cost-effective- 
ness of intensive care for patients with PCP and 
severe respiratory failure improved during the 
first 8 years of the AIDS epidemic but fell in re- 
cent years such that it is now below that of 
many accepted medical interventions. 

Measurement of Thoracic Gas Volume in 
Patients Born Prematurely: .Should 
Occlusion Be Made at Knd-lnspiration or 
End-Expiration? — B Yuksel and A 
Oreenough. Pediatr Pulmonol 1994;18:295. 

It has been suggested that in infants born al 
term thoracic gas volume (TGV) may be more 
accurately estimated in a plethysmograph if 
end-inspiratory (TGV|) rather than end-expira- 
tory (TGVp) occlusions are used. The aim of 
this study was to assess whether the timing of 
occlusion affected TGV results in patients born 
very prcinalurely. Fifteen children with a medi- 
an gestational age of 28 weeks (range 23-34) 

and postnatal age of 10 months (range 6-24) 
were studied. Measurements of TGV and air- 
way resistance (Ra„i were made in a whole 
body plethysmograph after sedation with chlo- 
ral hydrate. End-expiratory and end-inspirato- 
ry occlusions were performed randomly in 
each subject. Overall, TGVi was significantly 
lower than TGVe (median. TGV| 233 mL; 
range. 130-498. Median TGVe 250 mL; range. 
132-604; P < 0.05; 95% confidence intervals 
for the difference. 4-50 mL). In 13 infants. 
TGVi was lower than TGVe; the remaining 
two patients did not differ significantly from 
the rest of the group and neither had neonatal 
chronic lung In only five infants did 
TGV| lie below the 95% confidence intervals 
of TGVe. however, two-way analysis of vari- 
ance with replicated measurements showed a 
significant difference between TGVe and 
TGVi (P < 0.05). The median Raw was 55 cm 
H:0/L/s (range. 36-71). A significant positive 
correlation was found between Ra„ and TGVe- 
TGVi (r- = 0.5, P < 0.01 ). We conclude that in 
children born very prematurely and with high 
Raw occlusion at end-expiration rather than 
end-inspiration yields higher TGV results at 

A New Kadii>[;raphic Scoring .System for 
Bronchopulmonary Dysplasia — MR Wein- 
stein, ME Peters, M Sadek, M Palta. Pediatr 
Pulmonol 1994:18:284. 

OBJECTIVES: To develop a simple, clinically 
nicaninglul radiographic score for bronchopul- 



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monary dysplasia (BPD). To investigate its re- 
liability, validity, and usefulness and to com- 
pare it to the Edwards score. WORKING HY- 
POTHESIS: Our radiographic scoring of BPD 
is reliable, correlates with respiratory support, 
and provides a necessary standardization in 
comparing severity of respiratory disease be- 
tween hospitals. STUDY DESIGN: 
Prospective cohort study. PATIENT SELEC- 
TION: The study included all neonates (n = 
366) with birth weight below 1501g admitted 
to 7 neonatal intensive care units, who had 
chest radiographs taken at age 25-35 days. 
METHODOLOGY: A simple radiographic 
scoring system was developed. Scores ranging 
from to 6 were assigned based on standard 
radiographs and descriptors of degree of ab- 
normality. All radiographs taken between days 
25 and 35 of life (n = 1087) were graded by a 
radiologist and a neonatologist. Radiographs 
from a stratified random sample of 37 neonates 
(10%) were also scored by the method of 
Edwards fn= 128 radiographs). A respiratory 
support index was constructed for days 25-35 
and correlated with the radiographic score. 
RESULTS: Between-reader correlation was r 
= 0.87 for our score and r = 0.88 for the 
Edwards score. The two scores correlated with 
each other at r = 0.94. The respiratory support 
inde.x correlated with our radiographic score at 
r = 0.75 overall, and r = 0.56 to 0.88 withm 
hospitals. Higher postnatal corticosteroid use 
was found at the hospitals with the lower corre- 
lations. CONCLUSIONS: Our radiographic 
scoring is reliable, valid, and gives results sim- 
ilar to the Edwards score. Radiographs play a 
standardizing role in assessing severity of BPD 
between hospitals. 

Pulmonary Mechanics in Ventilated 
Preterm Infants with Respiratory Distress 
Syndrome after Exogenous Surfactant 
Administration: A Comparison between 
Two Surfactant Preparations — ML 
Choukroun. B Lianas, H Apere. M Fayon. RI 
Galperine. H Guenard, JL Demarquez. Pediatr 
Pulmonol 1994:18:273. 

The effects of two surfactant preparations on 
lung mechanics have been studied on 24 venti- 
lated premature infants with respiratory dis- 
tress syndrome (RDS): 13 were given artificial 
surfactant (Exosurf Neonatal, Burroughs- 
Wellcome) and 1 1 natural porcine surfactant 
(Curosurf, Laboratoirc Serono France). 
Measurements of respiratory system compli- 
ance (Cjy„. Cs) and resistance (R,J were per- 
formed immediately before surfactant adminis- 
tration and repealed 6, 18. 24. 48. and 72 hours 
later. With Exosurf treatment. 6 hours after 
surfactant administration inhaled O; concen- 
tration (F|o,) could be lowered from (0.72 ± 
0.20, to 0.62 ± 0.33; P < 0.05). whereas C,s did 

not change (0.37 mL/cm HjO/kg, -i- 0.14 vs. 
0.39 -I- 0. 12, NS). After 24 hours and during the 
following days a significant increase in Crs oc- 
curred (24 hours post-Exosurf : 0.5 1 -f 0. 1 8. P < 
0.05). With Curosurf treatment, the improve- 
ment in oxygenation was greater and Fio; 
could be lowered much more after 6 hours 
(from F,02 0.78 ± 0.23 to 0.34 ± O.U, P < 
0.01). This was associated with an increase in 
Crs (from 0.39 ± 0.09 to 0.59 ± 0. 17, P < 0.05). 
During the following days. C„ was significant- 
ly higher in the group treated with Curosurf. 
Resistance was not altered by the type of sur- 
factant preparation used except after 72 hours, 
when Rpj increased in the group treated with 
Exosurf. In conclusion. Curosurf appears to be 
more effective than Exosurf with regard to im- 
mediate pulmonary changes in ventilator treat- 
ed premature infants with RDS. A rapid in- 
crease in Crs after Curosurf treatment indicates 
that recruitment of new functional areas of the 
lung is likely, to be associated with a stabiliza- 
tion of small airways and alveolar units. 

Multisite Evaluation of a Continuous 
Intra-Arterial Blood Gas Monitoring 
System — CP Larson Jr. AJ Vender, A Seiver. 
Anesthesiology 1994:81:543. 

BACKGROUND: We compared the perfor- 
mance of a new. continuous intraarterial blood 
gas (CIABG) monitor with arterial values ob- 
tained periodically and analyzed by conven- 
tional equipment. METHODS: A CIABG 
monitoring system consisting of a sterile, dis- 
posable, fiberoptic sensor and a microproces- 
sor-controlled monitor with a self-contained 
calibration unit and detachable display panel 
was used. The sensor was inserted through a 
20G radial artery cannula. Light was transmit- 
ted from the monitor to the sensor tip where it 
reacted with fluorescent dyes sensitive to oxy- 
gen or hydrogen ions (analytes). The change in 
the intensity of the photoluminescent radiation 
caused by the analytes was measured every 
20 s and derived blood gas values were dis- 
played. Twenty-nine sensors were evaluated in 
29 surgical or intensive care unit patients at 
one of three institutions (Stanford University 
Hospital. Evanston Memorial Hospital, and the 
Palo Alto Veterans Administration Hospital). 
The duration of study averaged 6 h (5-8 h) in 
the operating room, and 46 h (7-121 h) in the 
intensive care unit. A total of 552 values were 
compared with those obtained at regular inter- 
vals and analyzed in the hospital blood gas lab- 
oratory. Average bias (mean difference be- 
tween lab value and CIABG), precision (SD of 
difference), and drift (change in the bias with 
lime) were determined. RESULTS: At arterial 
oxygen tension (Po;) values of 32-528 mm Hg, 
the average bias was - 1 % meaning that the av- 
erage CIABG monitor values were 1% lower 

than those obtained by conventional equip- 
ment. The precision was 15%. At arterial Pq: 
values of 32-99 mm Hg, average bias and pre- 
cision were -0.3 ± 8.9 mm Hg. At arterial car- 
bon dioxide tension (Pco;) values of 24-54 mm 
Hg. average bias and precision were 1.3 ± 3.3 
mm Hg, and at pHa values of 7.23 ±7.57, aver- 
age bias and precision were 0.01 ± 0.04. 
Observed drift per day was -1.2% for arterial 
Po:, 0.3 mm Hg for arterial Pco; and 0.01 for 
pH. Bias and precision for samples compared 
in two pairs of like-model in vitro blood gas 
analyzers were 0.4 ± 4.6% for arterial Pq; over 
the full range, and 0.4 + 3.7 mm Hg for values 
less than 100 mm Hg, 0.5 + 1.8 mm Hg for ar- 
terial Pco; and 0.01 ± 0.01 forpHa. Although 
the occasional marked discrepancies between 
one or more CIABG and in vitro values could 
sometimes be corrected by flushing the arterial 
catheter or repositioning the sensor, usually we 
could not determine the cause of the discrepan- 
cy or which values were the more accurate. 
CONCLUSIONS: Over the range of values 
and under the clinical conditions studied. 
CIABG monitoring provides immediate blood 
gas results and trend information with suffi- 
cient agreement with in vitro results to be reli- 
able for decision making in most clinical cir- 
cumstances. Generally, the differences in the 
values between the two methods of analysis 
were the result of the combination of the inher- 
ent errors of each method. Additional studies 
need to be undertaken to evaluate the perfor- 
mance of the CIABG monitor across wider 
ranges of blood gas values, especially for arte- 
rial Po: values less than 60 mm Hg and arterial 
Po; values greater than 50 mm Hg. 

Effect of Cooling on Oxygen Consumption 
in Febrile Critically III Patients — CA 

Manthous. JB Hall. D Olson. M Singh, W 
Chatila. A Pohlman. R Kushner. GA Schmidt. 
LDH Wood. Am J Respir Crit Care Med 

Hyperthermic critically ill patients are com- 
monly cooled to reduce their oxygen consump- 
tion (Vo;). However, no previous studies in 
febrile humans have measured Vq, during 
cooling. We cooled 12 febrile, critically ill, 
mechanically ventilated patients while measur- 
ing V(),and COi production (Vco.) by analysis 
of inspired and expired gases. All patients were 
mechanically ventilated for hypoxemic, hyper- 
capnic, or shock-related respiratory failure and 
had a mean APACHE II score of 22.4 + 7.7. As 
temperature was reduced from 39.4 ± 0.8 to 
37.0 ± 0.5" C, Vo; decreased from 359.0 ± 
65.0 to 295.1 ± 57.3 mL/min (p < O.OI) and 
Vco! decreased from 303.6 ± 43.6 to 243.5 ± 
37.3 mL/min (p < 0.01). The re.spiratory quo- 
tient (RQ) did not change significantly and cal- 
culated energy expenditure decreased from 





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Technology for life 

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2,481 ± 426 to 1,990 + 33 kcal/day (p < 0.01 1. 
In 7 patients with right heart catheters, cardiac- 
output decreased from 8.4 ± 3,2 to 6,5 ± 1.8 
L/min (p < 0.01 ) as the oxygen extraction frac- 
tion also tended to decrease from a mean of 
28.2 ± 6,8 to 23,4 ± 4.7% (p = 0.12) during 
cooling. Accordingly, cooling the febrile pa- 
tient unloads the cardiorespiratory system and, 
in situations of limited oxygen delivery or hy- 
poxemic respiratory failure, may thus facilitate 
resuscitation and minimize the potential for 
hypoxic tissue injury. 

Mandibular Advancement Splint: An 
Appliance To Treat Snoring and 
Obstructive Sleep Apnea — RA O'Sullivan, 
DR Hillman, R Mateljan, C Pantin and K 
Finucane, Am J Respir Crit Care Med 

Snoring and obstructive sleep apnea (OSA) are 
related to narrowing of the upper airway. A 
mandibular advancement splint (MAS) could 
improve both conditions by increasing oropha- 
ryngeal and hypopharyngeal dimensions. The 
effects of a MAS on snoring and OSA was 

evaluated 35 ± 21 (mean ± SD) mo after issue 
in 57 subjects with habitual loud snoring, 39 of 
whom had an apnea-hypopnea index (AHl) > 
10, Assessment was by questionnaire (all sub- 
jects) and polysomnography (51 subjects, 47 
male) including measurement of sound inten- 
sity. Use of the MAS was randomized to first 
or second half of study. Snores were scored 
where inspiratory noise was greater than 5 dB 
above background. Total sleep time, sleep effi- 
ciency, % REM sleep, and % sleep spent 
supine were similar (p > 0.05) with and with- 
out the MAS. Snores per sleep minute, correct- 
ed for time in apnea, and sound intensity of 
snores (% snores < 50 dB) decreased with the 
MAS from 1 1,0 ± 5.8 and 42,0 ± 25.0% to 9.0 
+ 6,0 (p < 0,01) and 26,2 ± 25.2% (p < 0,01), 
respectively. Using the MAS significantly im- 
proved OSA: AHl decreased from 32.2 ± 28.5 
to 17.5 ± 22.7 (p<0.01) and arousal index de- 
creased from 31.4 ± 20.6 to 19.0 ± 14.6 (p < 
0.01 ). AHl decreased to < 20 with the MAS in 
12 of 17 subjects where untreated AHl was be- 
tween 20 and 60, and in 2 of 9 subjects where 
untreated AHl was > 60. Forty-five patients 
continued to use the MAS regularly. We con- 



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elude that the MAS can be an acceptable and 
effective treatment of snoring and also of OSA, 
particularly where the AHl is < 60. 

End of the New Zealand Asthma Mortality 
Epidemic — N Pearce, R Beasley, J Crane, C 
Burgess, and Rodney Jackson. Lancet 1995: 

In 1989, a case-control study reported that in- 
haled fenoterol was associated with the epi- 
demic of asthma deaths that had affected New 
Zealand since 1976. The New Zealand 
Department of Health issued warnings about 
the safety of fenoterol and restricted its avail- 
ability. The associated time trends are consis- 
tent with the hypothesis that fenoterol was the 
main factor in the New Zealand asthma mortal- 
ity epidemic. The epidemic commenced when 
fenoterol was introduced in 1976, and the New 
Zealand death rate remained the highest in the 
world for more than a decade. After publica- 
tion of the case control study, the death rate fell 
by half and has now remained low for a further 
3 years (1990-92). Time-trend data do not sug- 
gest a class effect of inhaled beta-agonists in 
the epidemic: there was no association be- 
tween beta-agonist sales and the start of the 
epidemic, and total sales of inhaled beta-ago- 
nists actually increased slightly during 1989- 
90 when the epidemic came to an end. Time- 
trend data are also inconsistent with the hy- 
pothesis that the epidemic may have occurred 
because of underprescribing of inhaled corti- 
costeroids. Similarly, time-trend data is incon- 
sistent with hypotheses postulating a major 
role of social factors such as unemployment. 
Data on time trends should be assessed with 
caution, because time trends in asthma deaths 
can be affected by many factors. Nevertheless, 
the New Zealand time trends are consistent 
with fenoterol being the main cause of the New 
Zealand asthma mortality epidemic and are in- 
consistent with a significant role for other sug- 
gested causes. 

Changes in Dyspnea, Health Status, and 
Lung Function in Chronic Airway 
Disease — DA Mahler. D Tomlinson, EM 
Olmstead, ANA Tosteson, GT O'Conner. Am 
J Respir Crit Care Med 1995:151:61. 

The purpose of this study was to examine lon- 
gitudinal changes in clinical parameters in pa- 
tients with chronic obstructive pulmonary dis- 
ease (COPD). We postulated that progressive 
dyspnea and decline in lung function over time 
would inlluence or impact patient's health sta- 
tus. Clinical ratings of dyspnea, general health 
status, and physiologic lung function were 
measured every 6 mo over a 2-yr period in an 
original group of 1 10 male patients with stable 
hut symptomatic COPD and no significant co- 


RE.SPIRATORY CARH • APRIi;95 Vol. 40 No 4 

A Study of Chronic 
Ventilator Patients 
in tlie 

chronic ventilator-dependent 
patients are costing American 
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patients who depend on life- 
support systems; why, how, 
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first-rate program for school children on the hazards of smoking. 
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morbidity. At enrollment, age was 67 ± 8 yr 
(mean ± SD), forced expiratory volume in one 
second (FEV,) was 1.28 ± 0.59 (44 ± 17% of 
predicted), and forced vital capacity (FVC) 
was 2.84 ± 0.84 (68 ± 18% of predicted!. A 
total of 34 patients "dropped out" because of 
death (n = 20), relocation (n = 7), and other 
reasons (n = 7). Dyspnea was measured using 
the transition dyspnea index (TDI), which rep- 
resented changes from the baseline state; gen- 
eral health status was measured using the 
Medical Outcomes Study (MOS) 20-item 
shortform survey; physiologic lung function 
was assessed by spirometry (FVC and FEVi.) 
and inspiratory muscle strength (Pimax). 
Statistical analyses were performed using all 
available data for each patient, including re- 
sults until the time at which patients died or 
were lost to follow-up. Repeated measures 
analysis of covariance showed there were sig- 
nificant decreases in the TDI focal score (-0.7 
± 2.9; p = 0.041, Pimax (from 59.0 ± 25.0 to 55.6 
± 26.2 cm HiO; p < 0.001 ), and physical func- 
tioning score of the MOS survey (from 32.7 + 
26.4 to 25.7 ± 27.2; p < 0.001) over the 2-yr 
period. Although changes were also noted for 
FVC (p < 0.02) and FEV,, (p < 0.02), these 
measures did not increase or decrease consis- 
tently over time. The five other health compo- 
nents of the MOS showed no significant 
change over time. The changes in dyspnea 
were significantly related to changes in lung 
function. Regression analysis revealed that the 
TDI focal score was a significant predictor for 

all components of general health status, where- 
as FEV], was a significant predictor of five of 
the six components of health. We conclude that 
dyspnea, Pjmax. and physical functioning de- 
cline over 2 yr in a cohort of patients with 
symptomatic COPD. Both dyspnea ratings and 
lung function, particularly FEV,, were signifi- 
cant predictors of various components of gen- 
eral health status. It is possible that physical 
functioning is the initial health component to 
decline in patients with COPD. whereas a 
longer time period may be required to demon- 
strate changes in other components. 
Alternatively, patients with COPD may adapt 
to deterioration in dyspnea and physiologic 
function by adjusting their lifestyle to maintain 
role and social functioning, mental health, and 
health perceptions and minimize pain. 

Reversal of Sinus Arrest and Atrio- 
ventricular Conduction Block in Patients 
with Sleep Apnea during Nasal Continuous 
Positive Airway Pressure — H Becker, U 
Brandenburg, JH Peter. P Von Wichert. Am J 
Respir Crit Care Med 1995;15 1:215. 

Sinus arrest and atrioventricular (AV) block 
have been demonstrated in as much as 30% of 
patients with sleep apnea (SA). The reversal of 
heart block after tracheostomy has been 
shown. Nasal continuous positive airway pres- 
sure (nCPAP) now is widely used as the treat- 
ment of SA, but little data are available on the 
effect of nCPAP on heart block in patients with 

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SA. During a 17-mo period 239 patients were 
found to have SA in an ambulatory study. 
Heart block was identified in 17(16 male, one 
female) of these patients. Standard 
polysomnography and two channel long-term 
ECG before and during nCPAP therapy were 
performed in order to asess the effect of 
nCPAP on SA and heart block. Mean age of 
the 17 patients was 50.7 yr (range. 27 to 78 yr), 
mean respiratory disturbance index (RDl) was 
90/h (SD ± 36.1 ) before nCPAP and 6/h (SD ± 
6.2) on the second treatment night. The num- 
ber of episodes of heart block during sleep de- 
creased significantly (p < 0.001) from 1,575 
before therapy to 165 during nCPAP. In 12 pa- 
tients (70.6%) heart block was totally prevent- 
ed by nCPAP. In another three patients, there 
was a 71 to 97% reduction in the number of 
episodes of heart block on the second treat- 
ment night, and in two of them a complete re- 
versal occurred thereafter. Two patients exhib- 
ited an increase in block frequency during 
nCPAP, which was reversed after 4 wk of 
nCPAP in one but persisted in the other. 
Clusters of sinus arrest and second degree AV 
block, which were identified during daytime in 
two patients while they reported to have fallen 
asleep, were not present after the initiation of 
nCPAP. The reduction of heart block using 
nCPAP is comparable to that achieved by tra- 
cheostomy. However, long-term ECG should 
be reassessed during therapy, as significant 
blocks may persist despite a normalization of 
RDI. In our opinion a cardiac pacemaker 
should be implanted if heart block is not re- 
duced substantially during nCPAP or if there is 
poor nCPAP compliance. 

Selective Deposition of Inhaled Aerosols to 
Mechanically Ventilated Rabbits — M 

Dahlbiich, P Wollmer, B Jonson. J Aerosol 
Med 1994;7:4. 

We have studied selective deposition of tracer 
aerosols to specific sites in airways and periph- 
eral regions of the rabbit lung by varying 
droplet size and breathing pattern. The differ- 
ent breathing patterns were controlled by a 
Servo Ventilator 9()0C and different droplet 
sizes (polydisperse) were generated by an air 
jet nebulizer (MA2) using two types of im- 
pactor vessels (MMD 2.3 and 4.1 |im). Three 
tracer aerosols were evaluated; Evans blue dye, 
'"''"Tc-DTPA and monodisperse fiuorescent 
polylalex spheres (PLS). When we combined 
liu-gc droplets with "rapid-shallow" breathing 
(central deposition mode, CDM), 30% of the 
aerosol was deposited in the central airways. 
When small droplets were combined with 
"deep-slow" breathing (peripheral deposition 
mode, PDM ) 60% was deposited in the periph- 
eral part of the lung. The different detection 
techniques showed similar results but gave 
complementary information. Since detection 
of the radiolabelled aerosol was more sensitive 



For patients with asttima 


SEREVENTis indicated for maintenance treatment of 
asttima and prevention of bronchiospasm in patients 
12 years of age and older witti reversible obstructive 
airway disease, including patients with symptoms of 
nocturnal asttima, wtio require regular treatment with 
inhaled, short-acting B2-agonists. 

Dosing should be two puffs (42 ijg) ofSEREVENT 
Inhalation Aerosol, twice daily, morning and evening, 
approximately 12 hours apart. 


(salmeferol xinafoote) 

inholation Aerosol 

Morning and Evening Inhaiafion 
for Active Days and Restful Nigiits 



SEREVENT SHOULD NOT BE USED TO TREAT ACUTE SYMPTOMS. Patients must be provided with a short-acting, 
inhaled li2-ogonisl for treatment of acute symptoms. 


Please consult Brief Summary of Prescribing Information on adjacent pages. 

Twice-Daily %«^-^ 

(salmeferol xinafoate) 



(salmeterol xinafoate) 
Inhalation Aerosol 

Bronchodilator Aerosol 
For Oral Inhalation Only 

The following is a brief summary only Before prescribing, see complete prescribing Information in 
Serevent' Infialation Aerosol product labeling 

CONTRAINDICATIONS: Serevent* Inhalation Aerosol Is contraindicated in patients with a history of 
hypersensitivity to any of the components 


MAY BE A LIFE-THREATENING CONDITION. Serious acute respiratory events, including fatali- 
ties, have been reported, both in the US and worldwide, when Serevent Inhalation Aerosol 
has been initiated in ttiis situation. 

Although It is not possible from these reports to determine whether Serevent Inhalation 
Aerosol contributed to these adverse events or simply failed to relieve the deteriorating 
asthma, the use of Serevent Inhalation Aerosol in this setting is inappropriate. 

crucial to inform patients of this and prescribe a short-acting, inhaled beta2-agonist for this 
purpose as well as warn them that increasing inhaled beta^-agonist use is a signal of dete- 
riorating asthma. 

STEROIDS. Corticosteroids should not be stopped or reduced when Serevent Inhalation 
Aerosol is initiated. 

(See PRECAUTIONS: Information for Patients section of the full prescribing information 
and the separate PATIENT'S INSTRUCTIONS FOR USE leaflet.) 

1 Do Not Introduce Serevent Inhalation Aerosol as a Treatment for Acutely Deteri orating Asthma: 
Serevent Inhalation Aerosol is intended for the maintenance treatment of asthma (see INDICATIONS 
and USAGE section of the lull prescribing information) and should not be introduced in acutely dete- 
riorating asthma, which is a potentially life-threatening condition There are no data demonstrating 
that Serevent Inhalation Aerosol provides greater efficacy than or additional efficacy to short-acting, 
inhaled beta2-agonists in patients with worsening asthma. Serious acute respiratory events, includ- 
ing fatalities, have been reported, both in the US and worldwide, in patients receiving Serevent 
Inhalation Aerosol In most cases, these have occurred in patients with severe asthma |e.g , 
patients with a history of corticosteroid dependence, low pulmonary function, intubation, mechani- 
cal ventilation, frequent hospitalizations, or previous life-threatening acute asthma exacerbations) 
and/or in some patients in whom asthma has been acutely deteriorating (eg , unresponsive to 
usual medications, increasing need for inhaled short-acting beta^-agonlsts, increasing need for sys- 
temic corticosteroids, significant increase in symptoms, recent emergency room visits, sudden or 
progressive deterioration in pulmonary function) However, they have occurred in a few patients 
with less severe asthma as well It was not possible from these reports to determine whether 
Serevent Inhalation Aerosol contributed to these events or simply failed to relieve the deteriorating 

2. Do Not U se Serevent In halation A erosol to Treat Acute Symptoms: A short-acting, inhaled beta?- 
agonist, not Serevent Inhalation Aerosol, should be used to relieve acute asthma symptoms When 
prescribing Serevent Inhalation Aerosol, the physician must also provide the patient with a short- 
acting, inhaled bela2-agonist |e g,, albuterol) for treatment of symptoms that occur acutely, despite 
regular twice daily (morning and evening) use of Serevent Inhalation Aerosol 

When beginning treatment with Serevent Inhalation Aerosol, patients who have been taking short- 
acting, inhaled betaj-agonists on a regular basis (e g , q id.) should be instructed to discontinue the 
regular use of these drugs and use them only for symptomatic relief if they develop acute asthma 
symptoms while taking Serevent Inhalation Aerosol (see PRECAUTIONS Information tor Patients) 
3 Watch for Increasing Use of Short-Acling. Inhaled Belaj-Agonisls, Which Is a fiHarke; of 
Delsrioratlng Asthma Asthma may deteriorate acutely over a period of hours or chronically over 
several days or longer II the palienl's short-acting. Inhaled beta?agonlst becomes less effective or 
the patient needs more inhalations than usual, this may be a marker of destabllizalion of asthma In 
this setting, the patient requires immediate re-evaluation with reassessment of the treatment regi- 
men, giving special consideration to the possible need for corticosteroids. If the pabent uses four or 
more inhalations per day of a short-acting, inhaled betai-agonist for 2 or more consecutive days, or 

Serevent® (salmeterol xinafoate) Inhalation Aerosol 

if more than one canister (200 inhalations per canister) of short-acting, inhaled beta2-agonist Is used 
in an 8-week period in conjunction with Serevent Inhalation Aerosol, then the patient should consult 
the physician for re-evaluation Increasing tt)e daily dosage of Serevent Inhalation Aerosol in tliis 
situation is not appropriate, Serevent Inhalation Aerosol should not be used more frequently 
than twice daily (morning and evening) at tfie recommended dose of two inhalations. 

4, Do N ot Use Ser event Inhalation Aerosol as a Substitute for Oral or Inhaled Corticosteroids: There 
are no data demonstrating that Serevent Inhalation Aerosol has a clinical antl-inflammatory effect 
and could be expected to take the place of, or reduce the dose of corticosteroids. Patients who 
already require oral or inhaled corticosteroids tor treatment of asthma should be continued on this 
type of treatment even if they feel better as a result of initiating Serevent Inhalation Aerosol. Any 
change in corticosteroid dosage should be made ONLY after clinical evaluation (see PRECAUTIONS: 
Information for Patients). 

5, Do Not Exceed Recommende d Dosage: As with other inhaled beta2-adrenergic drugs, Serevent 
Inhalation Aerosol should not be used more often or at higher doses than recommended Fatalities 
have been reported in association with excessive use of inhaled sympathomimetic drugs. Large 
doses of inhaled or oral salmeterol (12 to 20 times the recommended dose) have been associated 
with clinically significant prolongation of the OT interval, which has the potential for producing ven- 
tricular arrhythmias, 

6, Paradoxical Bronchospasm: As with other inhaled asthma medication, paradoxical bron- 
chospasm (which can be life threatening) has been reported following the use of Serevent 
Inhalation Aerosol, If it occurs, treatment with Serevent Inhalation Aerosol should be disconfinued 
immediately and alternafive therapy instituted 

7, Immediate Hvpersensitivitv Reactions: Immediate hypersensitivity reactions may occur after 
administration of Serevent Inhalation Aerosol, as demonstrated by rare cases of urticaria, 
angioedema, rash, and bronchospasm. 

8, Upper Airway Symptoms: Symptoms of laryngeal spasm. Irritation, or swelling, such as stridor 
and choking, have been reported rarely in patients receiving Serevent Inhalation Aerosol. 

General: 1 . Use With Spacer or Other Devices: The safety and effectiveness of Serevent® Inhalation 
Aerosol when used with a spacer or other devices have not been adequately studied. 

2. Cardiovascular and Other Effects: No effect on the cardiovascular system is usually seen after 
the administration of inhaled salmeterol in recommended doses, but the cardiovascular and central 
nervous system effects seen with all sympathomimetic drugs (e.g., increased blood pressure, heart 
rate, excitement) can occur after use of Serevent Inhalation Aerosol and may require discontinuation 
of the drug. Salmeterol, like all sympathomimetic amines, should be used with caution In pahents 
with cardiovascular disorders, especially coronary insufficiency, cardiac arrhythmias, and hyperten- 
sion; In patients with convulsive disorders or thyrotoxicosis; and in patients who are unusually 
responsive to sympathomimetic amines. 

As has been described with other beta-adrenergic agonist bronchodilators, clinically significant 
changes in systolic and/or diastolic blood pressure, pulse rate, and electrocardiograms have been 
seen infrequently in individual patients in controlled clinical studies with salmeterol 

3, Metabolic Eff e cts: Doses of the related betaj-adrenoceptor agonist albuterol, when adminis- 
tered intravenously have been reported to aggravate pre-existing diabetes mellitus and ketoacido- 
sis. No effects on glucose have been seen with Serevent Inhalation Aerosol at recommended doses. 
Administration of beta2-adrenoceptor agonists may cause a decrease in serum potassium, possibly 
through Intracellular shunting, which has the potential to increase the likelihood of arrhythmias. The 
decrease is usually transient, not requiring supptementafion 

Clinically significant changes in blood glucose and/or serum potassium were seen rarely during 
clinical studies with long-term administration of Serevent Inhalation Aerosol at recommended doses. 

It is Important that patients understand how to use Serevent Inhalation Aerosol appropriately and 
how It should be used in relafion to other asthma medications they are taking. Patients should be 
given the following informahon: 

1 . Shake well before using. 

2. The recommended dosage (two inhalations twice daily morning and evening) should not be 

3. Serevent Inhalation Aerosol is not meant to relieve acute asthma symptoms and extra doses 
should not be used for that purpose Acute symptoms should be treated with a short-acting, 
inhaled beta2-agonist such as albuterol (the physician should provide the patent with such med- 
ication and instruct the patient In how it should be used) 

4. The physician should be notified immediately If any of the following situations occur, which may 
be a sign of seriously worsening asthma. 

• Decreasing effectiveness of short-acting, inhaled beta2-agonists 

• Need tor more inhalations than usual of short-acting. Inhaled beta2-agonlsts 

• Use of four or more inhalations per day of a short-acfing beta2-agonist for 2 or more days 

• Use of more than one canister of a short-acting, inhaled beta2-agonist in an 8-week period 
(I.e., canister with 200 inhalations) 

5- Serevent Inhalation Aerosol should not be used as a substitute for oral or inhaled corticosteroids. 
The dosage of these medications should not be changed and they should not be stopped without 
consulting the physician, even if the patient feels better after initiafing treatment with Serevent 
Inhalation Aerosol, 

6 Patients should be caufioned regarding potential adverse cardiovascular effects, such as palpita- 
tions or chest pain, related to the use of additional beta2-agonisl. 

7- In patients receiving Serevent Inhalation Aerosol, other Inhaled medications should be used only 
as directed by the physician. 

Drug Interactions: Shorl-Acting Beta-Agonists: In the two 3-monlh, repetitlve-dose clinical trials 
(n= 1 84), the mean daily need for additional bela2-agonisl use was 1 to 1 Vi inhalations per day, but 
some patients used more Eight percent of patients used at least eight inhalations per day at least 
on one occasion Six percent used 9 to 12 Inhalations at least once There were 15 patients (8%) 
who averaged over four inhalations per day. Four of these used an average of 8 to 1 1 inhalations 
per day In these 15 patients there was no observed increase In frequency of cardiovascular adverse 

Serevent" (salmeterol xinafoate) Inhalation Aerosol 

euents. The safety of concomitant use of more ttian eigtit inhalations per day of short-acting 
betaragonists with Serevent Inhalation Aerosol has not been established- In 1 5 patients who expe- 
nenced worsening of asthma while receiving Serevent Inhalation Aerosol, nebulized albuterol (one 
dose in most) led to improvement in forced expiratory volume in 1 second (FEV,) and no increase in 
occurrence of cardiovascular adverse events 

Monoamine Oxidase Inhibitors and Tricyclic Antidepressants: Salmeterol should be adminis- 
tered With extreme caution to patients being treated with monoamine oxidase inhibitors or tncyclic 
antidepressants because the action of salmeterol on the vascular system may be potentiated by 
these agents 

Corticosteroids and Cromoglycate: In clinical trials, inhaled corticosteroids and/or inhaled cro- 
molyn sodium did not alter the safety profile of Serevent Inhalation Aerosol when administered con- 

Metfiy/xantfi/nes.-The concurrent use of intravenously or orally administered methylxanthines 
(e,g,, aminophylline, theophylline) by patients receiving Serevent Inhalation Aerosol has not been 
completely evaluated In one clinical trial, 87 patients receiving Serevent Inhalation Aerosol 42 meg 
twice daily concurrently with a theophylline product had adverse event rates similar to those in 71 
patients receiving Serevent Inhalation Aerosol without theophylline Resting heart rates were slightly 
higher in the patients on theophylline but were little affected by Serevent Inhalation Aerosol therapy. 

Carcinogenesis, Mutagenesis, Impairment of Fertility: In an 18-month oral carcinogenicity study 
in CD-mice, salmeterol xinafoate caused a dose-related increase in the incidence of smooth muscle 
hyperplasia, cystic glandular hyperplasia, and leiomyomas of the uterus and a dose-related increase 
in the incidence of cysts in the ovaries A higher incidence of leiomyosarcomas was not statistically 
significant; tumor findings were observed at oral doses of 1 4 and 10 mg/kg, which gave 9 and 63 
times, respectively, the human exposure based on rodenthuman AUG compansons 

Salmeterol caused a dose-related increase in the incidence of mesovanan leiomyomas and ovar- 
ian cysts in Sprague Dawley rats in a 24-month inhalation/oral carcinogenicity study Tumors were 
observed in rats receiving doses ot 68 and 2 58 mgAg per day (about 55 and 21 5 times the rec- 
ommended clinical dose [mg/m]) These findings in rodents are similar to those reported previously 
for other beta-adrenergic agonist drugs The relevance of these findings to human use is unlcnown 

No significant effects occurred in mice at 0.2 mgAg (1 .3 times the recommended clinical dose 
based on comparisons of the AUCs) and in rats at 0,21 mgAg (15 times the recommended clinical 
dose on a mg/m-' basis) 

Salmeterol xinafoate produced no detectable or reproducible increases in microbial and mam- 
malian gene mutation m vitro. No blastogenic activity occurred in vitro in human lymphocytes or in 
vivo in a rat micronucleus test. No effects on fertility were identified in male and female rats treated 
orally with salmeterol xinafoate at doses up to 2 mg/kg orally (about 1 60 times the recommended 
clinical dose on a mg/m- basis). 

Pregnancy: Teratogenic Effects: Pregnancy Category C: No significant effects of maternal expo- 
sure to oral salmeterol xinafoate occurred in the rat at doses up to the equivalent of about 160 
times the recommended clinical dose on a mg/m- basis Dutch rabbit fetuses exposed to salmeterol 
xinafoate in utero exhibited effects characteristically resulting from beta-adrenoceptor stimulation; 
these included precocious eyelid openings, cleft palate, sternebral fusion, limb and paw flexures, 
and delayed ossification of the frontal cranial bones. No significant effects occun-ed at 6 mglkq 
given orally (12 times the recommended clinical dose based on companson of the AtJCs) 

New Zealand White rabbits were less sensitive since only delayed ossification of the frontal 
bones was seen at 10 mg/kg given orally (approximately 1 ,600 times the recommended clinical 
dose on a mg/m' basis) Extensive use of other beta-agonists has provided no evidence that these 
class effects in animals are relevant to use in humans. There are no adequate and well-controlled 
studies with Serevent Inhalation Aerosol in pregnant women. Serevent Inhalation Aerosol should be 
used during pregnancy only if the potential benefit justifies the potential nsk to the fetus 

Use in Labor and Delivery: There are no well-controlled human studies that have investigated 
effects of salmeterol on preterm labor or labor at term Because of the potential for beta-agonist 
interference with utenne contractility, use of Serevent Inhalation Aerosol during labor should be 
restricted to those patients in whom the benefits clearly outweigh the nsks 

Nursing Mothers: Plasma levels of salmeterol after inhaled therapeutic doses are very low (85 to 
200 pg/mL) in humans. In lactating rats dosed with radiolabeled salmeterol, levels of radioactivity 
were similar in plasma and milk In rats, concentrations of salmeterol in plasma and milk were sim- 
ilar The xinafoate moiety is also transferred to milk in rats at concentrations of about half the corre- 
sponding level in plasma However, since there is no expenence with use of Serevent Inhalation 
Aerosol by nursing mothers, a decision should be made whether to discontinue nursing or to dis- 
continue the drug, taking into account the importance of the drug to the mother Caution should be 
exercised when salmeterol xinafoate is administered to a nursing woman 

Pediatric Use: The safety and effectiveness of Serevent Inhalation Aerosol in children younger than 
12 years of age have not been established 

Geriatric Use: Of the total number of patients who received Serevent Inhalation Aerosol in all clini- 
cal studies, 241 were 65 years and older Geriatric patients (65 years and older) with reversible 
obstructive airway disease were evaluated in tour well-controlled studies of 3 weeks' to 3 months' 
duration. Two placebo-controlled, crossover studies evaluated twice-daily dosing with salmeterol for 
21 to 28 days in 45 patients An additional 75 genatric patients were treated with salmeterol (or 3 
months in two large parallel-group, mulbcenter studies These 1 20 patients experienced increases 
in AM and Pfi/I peak expiratory flow rate and decreases in diurnal variation in peak expiratory flow 
rate similar to responses seen in the total populations of the two latter studies The adverse event 
type and frequency in geriatric patients were not different from those of the total populations stud- 

No apparent differences in the efficacy and safety of Serevent Inhalation Aerosol were observed 
when geriatric patients were compared with younger patients in clinical trials. As with other 
beta^-agonists, however, special caution should be observed when using Serevent Inhalation 
Aerosol in elderly patients who have concomitant cardiovascular disease that could be adversely 
affected by this class of drug Based on available data, no adiustment of salmeterol dosage in geri- 
atric patients is warranted 

ADVERSE REACTIONS: Adverse reactions to salmeterol are similar in nature to reactions to other 
selective beta2-adrenoceptor agonists, i e., tachycardia; palpitations, immediate hypersensitivity 
reactions, including urticaria, angioedema, rash, bronchospasm (see WARNINGS); headache; tremor; 
nervousness, and paradoxical bronchospasm (see WARNIhJGS) 

Two multicenter, 12-week, controlled studies have evaluated twice-daily doses of Serevent® 
Inhalation Aerosol in pabents 12 years of age and older with asthma The following table reports the 
incidence of adverse events in these two studies. 

Serevent" (salmeterol xinafoate) Inhalation Aerosol 

Adverse Experience Incidence in Two t^rge 12-Week Clinical Trials* 

Adverse Event Type 

Percent of Patients | 





42 mcgb.i.d, n=184 

ISCmcgqid, n=l85 

Ear, nose, and throat 

Upper respiratory 

tract infection 







Disease of nasal 





Sinus headache 



















Lower respiratory 




■ The only adverse expenence classified as serious was one case of upper respiratory tract infection in a 

patient treated with albuterol 

The table above includes all events (whether considered drug related or nondrug related by the 
investigator) that occurted at a rate of over 3% in the Serevent Inhalation Aerosol treatment group 
and were more common in the Serevent Inhalation Aerosol group than in the placebo group. 

Pharyngitis, allergic rhinitis, dizziness/giddiness, and influenza occurred at 3% or more but were 
equally common on placebo Other events occurring in the Serevent Inhalation Aerosol treatment 
group at a frequency of 1 % to 3% were as follows: 

Cardiovascular Tachycardia, palpitations 

Ear, Nose, and Throat: Rhinitis, laryngitis 

Gastrointestinal: Nausea, viral gastroenteritis, nausea and vomiting, diarrhea, abdominal pain 

Hypersensitivity: Urticaria 

Mouth and Teeth: Dental pain 

Musculoskeletal: Pain in joint, back pain, muscle cramp/contraction, myalgia/myositis, muscular 

Neurological: Nervousness, malaise/fatigue 

Respiratory: Tracheitis/bronchitis 

Skin: Rash/skin eruption 

Urogenital: Dysmenorrhea 

In small dose-response studies, tremor, nervousness, and palpitations appeared to be dose related 
Postmarlieting Experience: In extensive US and worldwide postmarketing expenence, serious 
exacertiations of asthma, including some that have been fatal, have been reported In most cases, 
these have occurred in patients with severe asthma and/or in some patients in whom asthma has 
been acutely detenorating (see WARNINGS no 1 ), but they have occun-ed in a tew patients with 
less severe asthma as well It was not possible from these reports to determine whether Serevent 
Inhalation Aerosol contnbuted to these events or simply failed to relieve the deteriorating asthma. 

Postmarketing expenence includes rare reports of upper airway symptoms of laryngeal spasm, 
irritation, or swelling, such as stndor and choking 

OVERDOSAGE: Overdosage with salmeterol may be expected to result in exaggeration of the 
phamiacologic adverse effects associated with beta-adrenoceptor agonists, including tachycardia 
and/or arrhythmia, tremor, headache, and muscle cramps Overdosage with salmeterol can lead to 
clinically significant prolongation of the QTc interval, which can produce ventricular arrhythmias. 
Other signs of overdosage may include hypokalemia and hyperglycemia. 

In these cases, therapy with Serevenf"' Inhalation Aerosol and all beta-adrenergic-stimulant 
drugs should be stopped, supportive therapy provided, and judicious use of a beta-adrenergic 
blocking agent should be considered, bearing in mind the possibility that such agents can produce 
bronchospasm. Cardiac monitoring is recommended in cases of overdosage. 

As with all sympathomimetic pressurized aerosol medications, cardiac arrest and even death 
may be associated with abuse of Serevent Inhalation Aerosol 

Rats and dogs survived the maximum practicable inhalation doses of salmeterol of 2,9 and 
0,7 mg/kg, respectively. The maximum nonlethal oral doses in mice and rats were approximately 
150 mg/kg anij > 1.000 mg/kg. respectively 

Dialysis is not appropnate treatment for overdosage of Serevent Inhalaton Aerosol 

Allen &Hanburys 

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December 1994 

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than the other methods, less aerosol could be 
given allowing a more precise evaluation of 
the deposition, both from the macro autoradio- 
graphic images as well as from the well- 
counter measurements. In order to investigate 
how far into the lung periphery the aerosol 
could be detected, we used PSL microspheres. 
PLS could be detected in the alveolar region by 
a fluorescent light microscope. However, a 
complete selectivity can not be obtained by 
aerosol delivery. The different technique used 
to reach selective deposition, showed that it is 
only possible to deposit the aerosol either more 
to the central or more to the peripheral parts of 
the respiratory tract in small subjects. 

An In Vitro Method for Determining 
Regional Dosages Delivered by Jet 
Nebulizers— KW Stapleton, WH Finlay, P 
Zuberbuhler. J Aerosol Med I994;7:4. 

A methodology for determining the regional 
dosages delivered to the respiratory tract by a 
jet nebutizer is presented and applied to the 
DeVilbiss PulmoNeb* disposable nebulizer 
delivering a 2.5 ml nebule of Ventolin® ( 1 
mg/mL salbutamol sulphate). Results are ob- 
tained both with tapping of the nebulizer, 
which enhances nebulizer performance, and 
without tapping. The nebulizer output is char- 
acterized by measuring the total mass and the 
mass of solids leaving the nebulizer per 
minute, and performing a control volume anal- 
ysis of the nebulizer. Particle size distributions 
are determined by phased Doppler anemome- 
try. Deposition probabilities are calculated 
using a semi-empirical model for the deposi- 
tion of hygroscopic aerosol particles in healthy 
adult Caucasian males. Deposition probabili- 
ties are then converted to regional dosages 
using the measured nebulizer output character- 
istics. The regional dosages (% of initial dose 
in nebulizer) of Ventolin® delivered to the ex- 
trathoracic, bronchial, and alveolar regions of 
the respiratory tract are 0.248 ± 0.005 mg 
(9.9%), 0.034 ± 0.001 mg( 1.4%), and 0.071 + 
0.002 mg (2.8%) respectively when the nebu- 
lizer was lapped during operation, and 0.18 4 ± 
0.(X)5 mg (7.4%), 0.025 ± 0.001 mg (1.0%), 
and 0.052 ± 0.002 mg (2.1%) when tapping 
was not used. This methodology provides a 
well controlled and rapid means of comparing 
the effectiveness of different nebulizers for use 
in aerosol therapy. 

Nebulizer Therapy with Antibiotics in 
Chronic Suppurative l^ung Disease MA 
Tag El-Din, l.B Palmer, M Hl-Tayeb, I Khalil, 
MS Gabr. J Aerosol Med I994;7:4. 

Aerosolized antibiotics have been shown to be 
a useful modality of treatment in patients with 
cystic fibrosis. In this investigation, we exam- 
ined the utility of this treatment in patients 

with other chronic suppurative lung disorders. 
These included 40 patients, 30 men and 10 
women with chronic airway infection (27 with 
bronchiectasis, 6 with chronic abscess, and 7 
with chronic suppurative bronchitis). 
Pathogenic organisms were isolated from the 
affected part of the lung by a fiberoptic bron- 
choscopy using a sterile disposable bronchial 
microbiology brush. Cultures from these 
speciCultures from these specimens were used 
to determine the appropriate antibiotic. A sec- 
ond control group of 20 patients was treated 
with systemic antibiotics alone. Both systemic 
and aerosolized antibiotics were administered 
in 20 patients. A statistically significant im- 
provement in clinical, and ventilatory func- 
tions was recorded in the first group compared 
to the second. Nebulized antibiotics used as ad- 
junctive therapy in association with systemic 
antibiotics may offer a therapeutic advantage 
in chronic suppurative lung diseases. 

The Natural History of the Systemic 
Inflammatory Response Syndrome 

(SIRS)— MS Rangel-Frausto, D Pittet. M 
Costigan, T Hwang, CS Davis, RP Wenzel. 
JAMA 1995;273(2):117. 

OBJECTIVE: Define the epidemiology of the 
four recently classified syndromes describing 
the biologic response to infection: systemic in- 
flammatory response syndrome (SIRS), sepsis, 
severe sepsis, and septic shock. DESIGN: 
Prospective cohort study with a follow-up of 
28 days or until discharge if earlier. SETTING: 
Three intensive care units and three general 
wards in a tertiary health care institution. 
METHODS: Patients were included if they 
met at least two of the criteria for SIRS: fever 
or hypothermia, tachycardia, tachypnea, or ab- 
normal white blood cell count. MAIN OUT- 
COMES MEASURES: Development of any 
stage of the biologic response to infection: sep- 
sis, severe sepsis, septic shock, end-organ dys- 
function, and death. RESULTS: During the 
study period 3,708 patients were admitted to 
the survey units, and 2,527 (68%) met the cri- 
teria for SIRS. The incidence density rates for 
SIRS in the surgical, medical, and cardiovascu- 
lar intensive care units were 857, 804. and 542 
episodes per 1,000 patient-days, respectively, 
and 671, 495, and 320 per 1,000 patient-days 
for the medical, cardiothoracic, and general 
surgery wards, respectively. Among patients 
with SIRS, 649 (26%) developed sepsis, 467 
( 18% 1 developed severe sepsis, and 1 U) (4%) 
developed septic shock. The median interval 
from SIRS to sepsis was inversely correlated 
with the number of SIRS criteria (two, three, or 
all four) thai ihc patients met. As the popula- 
tion of patients progressed Irom SIRS to septic 
shock, increasing proportions had adult respi- 
ratory distress syndrome, disseminated in- 
travascular coagulation, acute renal failure. 

and shock. Positive blood cultures were found 
in 17% of patients with sepsis, in 25% with se- 
vere sepsis, and in 69% with septic shock. 
There were also stepwise increases in mortality 
rates in the hierarchy from SIRS, sepsis, severe 
sepsis, and septic shock: 7%, 16%, 20%, and 
46%, respectively. Of interest, we also ob- 
served equal numbers of patients who ap- 
peared to have sepsis, severe sepsis, and septic 
shock but who had negative cultures. They had 
been prescribed empirical antibiotics for a me- 
dian of 3 days. The cause of the systemic in- 
flammatory response in these culture-negative 
populations is unknown, but they had similar 
morbidity and mortality rates as the respective 
culture-positive populations. CONCLUSIONS: 
This prospective epidemiologic study of SIRS 
and related conditions provides, to our knowl- 
edge, the first evidence of a clinical progres- 
sion from SIRS to sepsis to severe sepsis and 
septic shock. 

Treatment of Bronchospasm by Metered- 
Dose Inhaler Albuterol in Mechanically 
Ventilated Patients— CA Manthous, W 
Chatila, GA Schmidt, JB Hall. Chest 

p-2 agonist bronchodilators delivered by me- 
tered-dose inhalers (MDI) are commonly used 
in the treatment of bronchospasm in both intu- 
bated and nonintubated patients. Substantial 
data support the effectiveness of MDI delivery 
systems in nonintubated patients. However, 
few studies have examined the effectiveness of 
MDIs in intubated, mechanically ventilated pa- 
tients. MDIs are often used in conjunction with 
a spacing device that may enhance delivery of 
drug to the airways, but few in vivo data have 
demonstrated efficacy of this delivery method 
in ventilated patients. We studied 10 critically 
ill patients who had a peak (Ppeak) to pause 
(Ppaust) gradient of more than 15 cm H^O dur- 
ing sedated, quiet breathing on assist control 
ventilation. We administered 5. 10, and 15 
puffs (90 yUg per puff) of MDI albuterol 
through a specific spacer (Aerovent) at 30-min 
intervals, while measuring resisstive pressure 
(defined as Pp^-^t - Ppause) before and after treat- 
ments. Resistive airway pressure after 5 puffs 
decreased in 9 of 10 patients, from 25.1 ± 7.2 
to 20.8 ±5.6 cm H:O(p<0.12). The addition 
of 10 more puffs further reduced resistive pres- 
sure in 9 of 9 patients from 20.8 ± 5.6 to 19.0 ± 
4.4 (p < 0.01). Fifteen more puffs (.30 cumula- 
tive puffs) did not result in further improve- 
inent (p > 0.5). A toxic reaction occurred in 
one patient (systolic blood pressure decreased 
20 mm Hg) after 5 puffs of albuterol. We con- 
clude that MDI administered through this spe- 
cific spacer is effective in mechanically venti- 
lated patients in doses up to 15 puffs, and that 
therapy should be titrated to effectiveness and 









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Beginning in 1981, and every year thereafter, the AARC's science 
journal, RESPmATORY Care, has held a state-of-the-art conference for the 
purpose of generating timely special issues on topics of interest to the AARC 
membership in particular, and to the entire pulmonary community in 
general.* The Conference proceedings issues are probably the most important 
ones we publish all year. They concentrate unique information in one place, 
some of which has never before been presented. The April and May 1995 
issues contain the Proceedings from the 1994 Journal Conference 
"Resuscitation in Acute Care Hospitals." We are proud to bring you these 
papers and discussions, designed for you to use in your daily practice. 

Presentation and publication of a conference like this requires 
considerable planning. The AARC and the Journal thank the speakers, the 
Editorial Board, Conference Co-Chairmen Tom Barnes and Charlie Durbin, 
Editor Pat Brougher, and Associate Editor Kaye Weber for planning, writing, 
and editing these special issues and for participating in the Conference and 
sharing this important information with us. Last, but certainly not least, we 
are extremely grateful to Allen &? Hanburys, Division of Glaxo Inc, for their 
generous grant to the Association, which made the presentation of the 
Conference and publication of its Proceedings possible. Allen &? Hanburys has 
supported the last seven Journal Conferences, and we are enormously 
indebted to them. 


Ray Masferrer RRT 

Managing Editor, Respiratory Care 

*19BS— Complications of Respiratory Therapy (AprO. Volume 27, Number 4) 
1983— The Management of Acute Respiratory Failure (May. Volume 28, Number 5) 
1984— Portoperatlve Respiratory Care ( May and June, Volume 29, Numbers 5 and 6) 
1 985— Monitoring of Critically m Patients (June and July, Volume 30, Numbers 6 and 7) 
1986 — Neonatal Respiratory Care (June and July, Volume 31, Numbers 6 and 7) 
1987 — Mechanical Ventilation (June and July. Volume 32, Numbers 6 and 7) 
1988— PEEP (June and July, Volume 33, Numbers 6 and 7) 

1989 — Pulmonary Function Testing (June and July, Volume 34. Numbers 6 and 7) 
1990— Noninvasive Monitoring in Respiratory Care (June and July, Volume 35, Numbers 6 and 7) 
1991 — Respiratory Care of Infants and Children (June and July. Volume 36. Numbers 6 and 7) 
1991— Consensus Conference on Aerosol Delivery (Septomber. Volume 36, Number 9) 
1992 — Emergency Respiratory Care (June and July, Volume 37, Numbers 6 and 7) 

1992 — Consensus Conference on the Essentials of Mechanical Ventilators (Septomber, Volume 37, Number 9) 
1993— Oxygenation in the Critically ni Patient (June and July. Volume 38. Numbers 6 and 7) 
1994 — Controversies in Home Respiratory Care (April and May. Volume 39. Numbers 4 and 5) 




Thomas A Barnes 


Tom P Aufderheide 


Dean R Hess 


Joseph L Rau Jr 


Mickey Mathews 


Ray Masferrer 

Richard D Branson 


Cynthia Malinowski 

Pat Brougher 


Henry R Halperin 


William Kaye 

Paul E Pepe 


Karen M Boudin 


Sam Giordano 


Tom P Aufderheide 


Richard D Branson 

Doug Mclntyre 


Gordon Rubenfeld 

Homer Rodriguez 


Michael J Bishop 


Robert R Pluck Jr 


Charles G Durbin Jr 


Arthur B Sanders 

1 '^ 




A Special Issue 

based on a conference 

held October 21-23, 1994 

in Cancun, Mexico 

sponsored by 

The American Association for Respiratory Care 

and its science journal Respiratory Care 

with the aid of an education grant 
from Allen & Hanburys, Div of Glaxo Inc 

Chairmen & Guest Editors: 

Thomas A Barnes EdD RRT and Charles G Durbin Jr MD 

Tom P Aufderheide MD 
Thomas A Barnes MD 
Michael J Bishop MD 
Karen M Boudin MA RRT 
Richard D Branson RRT 
Charles G Durbin Jr MD 
Robert R Fluck Jr MEd RRT 
Henry R Halperin MD 


Robin Hamill MD 

Dean R Hess PhD RRT 

William Kaye MD 

Cynthia Malinowski MA RRT 

Paul E Pepe MD 

Joseph L Rau Jr PhD RRT 

Gordon D Rubenfeld MD 

Arthur B Sanders MD 


The chairmen, the speakers, Sam P Giordano MBA RRT, 
Ray Masferrer RRT. Paul J Mathews MPA RRT. Mickey 
Mathews RN. David J Durand MD, Doug Mclntyre RRT, 
Homer L Rodrigue/ RRT 

Conference Proceedings 

Resuscitation in Acute Care Hospitals — 
The Time for Change Is Now! 

Charles G Duibin Jr MD 

These are exciting times for those interested in and in- 
volved with restoring life to patients who have suffered car- 
diac and respiratory arrest. Believed to be effective only in 
patients with isolated arrhythmias (ie, ventricular fibrilla- 
tion), cardiopulmonary resuscitation (CPR) — basic life sup- 
port (BLS) and advanced life support (ACLS) — seemed to 
offer little improvement in survival among hospitalized pa- 
tients.'- Major improvements in resuscitation equipment 
and techniques have increased the likelihood of survival in 
patients in and outside the hospital setting.' The philosophy 
of ACLS training has undergone important changes. 
Multispecialty participation as resuscitation-team members 
is actively encouraged. A renewed interest in the resuscita- 
tion of hospitalized patients has led to new avenues of re- 
search into novel CPR techniques, identification of patient 
factors associated with good (and poor) outcomes, the pro- 
cess of resuscitation, and the use of do-not-resuscitate 
(DNR) orders. The search for unique modalities that may 
have a special place in in-hospital resuscitation continues. 

The development of this year's Journal Conference was 
stimulated by these and other exciting events. The role of 
the respiratory care practitioner (RCP) in resuscitation is ex- 
panding. During this past year, the AARC published the 
Clinical Practice Guideline, "Resuscitation in Acute Care 
Hospitals.""* Defining the level of training and responsibili- 
ties for RCPs who provide care to hospitalized patients, the 
Guideline emphasizes the need for patient assessment and 
prevention of cardiorespiratory arrest in high-risk patients 
and the application of the techniques of BLS and ACLS. 

Dr Durbin is Professor of Anesthesiology and Surgery, 
University of Virginia Health Science Center, Charlottesville, 

A version of this paper was presented during the Journal 
Conference "Resuscitation in Acute Care Hospitals" held in 
Cancun, Quintana Roo, Mexico, October 1994. 

Reprints: Charles G Durbin Jr MD, Department of Anesthesiology, 
University of Virginia Health Science Center, Box 238, Charlottes- 
ville VA 22908. 

Previously identified as airway assistants, RCPs are now as- 
suming the role of provider of emergency airway manage- 
ment, including endotracheal intubation, in many hospital 
settings.' '^ To be respected by peer professions and to ensure 
job security, RCPs need to be more active in resuscitation. 
In his paper, Tom Barnes discusses the critical tasks that 
RCPs should perform in resuscitation attempts.' He also 
calls for the of standardized definitions for cardiopul- 
monary arrest and "good" outcome and encourages more 
data collection by RCPs. 

A natural next step for RCPs is to routinely administer 
resuscitation drugs through the endotracheal tube. Dean 
Hess presents and evaluates this technique in his Conference 
paper.* Effective doses are not well established for various 
drugs delivered endotracheally, and endotracheal drug ad- 
ministration is an important topic for RCPs and pharmacolo- 
gists to investigate collaboratively. It appears that almost 
any needed drug can be given by this route, although the ap- 
propriate dose and volume of diluent have not been estab- 
lished. Joe Rau discusses some old and new drugs used in 
resuscitation in his Conference paper.' 

The educational efforts of the respiratory care communi- 
ty are affected by recent changes in resuscitation education. 
ACLS courses were often difficult for RCPs because of the 
content emphasis on cardiology and nursing skills (ie, inter- 
preting a rhythm strip and giving intravenous medications). 
The new 'course -completion" philosophy and incorporation 
of adult education methods make participation less threaten- 
ing than previously and encourage RCPs and others to suc- 
cessfully complete the ACLS course. Further, the rigid 
structure of ACLS courses has been abandoned, and specific 
courses tailored to specialized audiences is encouraged. Art 
Sanders discusses how these important changes in the 
American Heart Association's recommendations came 
about and how they are likely to develop in the future.'" 

When a patient is in cardiac arrest, early defibrillation of 
ventricular fibrillation is more important than opening the 
airway or performing chest compressions. Even 1 -2 minutes 
delay can make a difference in outcome." RCPs can make 
an important contribution to patient outcomes of in-hospital 
resuscitation by attempting defibrillation on arrival at the 

Respiratory Care • April '95 Vol 40 No 4 


Conference Summary 

scene. Because RCPs are often the first to arrive at the scene 
of in-hospital ciirdiorespiratory arrests.'- they are Hkely the 
appropriate professional to arrive with a defibrillator in 
hand, prepared to administer countershock without delay. 
With the new automated defibrillators, this skill is easily 
taught. Pacemaker technology and the importance of early 
defibrillation for patients who experience cardiac arrest are 
the topics covered by Tom Aufderheide." 

New techniques in chest compression continue to be de- 
veloped. The importance of controlled trials and the difficul- 
ties in gaining patient consent for pailicipation in emergen- 
cy device trials are evident from Henry Halperin's presenta- 
tion.''' A critical review of available airway-management 
guidelines and the processes by which they were developed 
and used are found in the paper by Mike Bishop.''" 
Emergency ventilation techniques and concerns during re- 
suscitation are discussed by Rich Branson."" 

Does ACLS make a difference? Paul Pepe creates a straw 
man to answer this question." The belief is that ACLS pro- 
vided to victims in a timely fashion is an important determi- 
nant of survival. Administrators concerned with in-hospital 
response to patients in cardiac arrest should carefully consid- 
er these data. Initially thought to be dismal, patient survival 
from in-hospital cardiorespiratory arrest is improved by rapid 
response of skilled resuscitation teams and by appropriate 
patient selection. Figure 1 shows the yearly initial survival 
and survival-to-discharge of patients undergoing CPR at the 
University of Virginia Hospital. These quality improvement 
data compare favorably to data obtained from out-of-hospital 
bystander-initiated resuscitation. Analysis of these data re- 
veals that patient selection and the use of DNR orders can 
improve the rate of survival for patients who undergo CPR. '** 
When to stop resuscitation efforts is discussed by Robin 
Hamill.''' Gordon Rubenfeld explores the problems with use 
and understanding of DNR orders.-" 

If RCPs are to have a prominent role as ACLS evolves, 
they must obtain appropriate training in all resuscitation 
techniques, and this training must begin with students of res- 
piratory care. Bob Fluck outlines this process.-' Techniques 
of maintaining performance after course completion is dis- 
cussed by Bill Kaye.-- Reliance on case-based teaching and 
refreshing manual skills are important advances in the 
teaching methods of ACLS. The experience of several respi- 
ratory care depailments in resuscitation-skills maintenance 
is shared in the paper by Karen Boudin.-' She discusses 
practical and inexpensive ways to promote and ensure 
ACLS expertise. 

The final paper from the Conference describes the differ- 
ences between adults and infants and children with respect 
to causes, treatment programs, and outcomes from acute 
emergencies.-'' Cindy Malinowski emphasizes the impor- 
tance of the airway in these patients. Temperature regula- 
tion, glucose, and prenatal events are profoundly important 
in attempts to resuscitate neonates. 

The catalyst for this conference was a growing sense 
among members of the respiratory care community that 
RCPs can play a pivotal role in hospital-based resuscitation 
programs. However, identifying and correcting knowledge 
and skills deficits are essential before widespread assump- 
tion of this critical role is possible. The Conference repre- 
sents a unique perspective from the literature on cardiopul- 
monary resuscitation, focusing entirely on the hospitalized 
patient. It is in this group of "victims' that the impact of im- 
proved RCP skills can be greatest. RCPs, as first responders, 
can lead the hospital-based team with initial defibrillation. 
An expanded role in airway management, drug delivery, 
data collection, and team leadership should naturally follow. 
My hope is that the papers from this outstanding Conference 
inspire the work that is needed to attain this goal, both na- 
tionally and at the local level. 



1988 1989 

n% Initial Survival 

1990 1991 1992 

■°o Survival to Discharge 

Fig. 1. These data are from the University of Virginia Medical 
Center's quality-improvement program showing the percentage of 
patients requiring cardiopulmonary resuscitation who survive ini- 
tially (mH) and those who survive to hospital discharge (1^). 


1 . Bedell SE, Delbanco TL, Cook EF, Epstein FH. Survival after 
cardiopulmonary resuscitation in the hospital. N Engl J Med 
1983; 309:.S69-576. 

2. Taffetl GE. In-hospital CPR. JAMA 1988; 260:2069-2072. 

3. Ballew KA. Philbrick JT, Craven DE. Schorling JB. Predictors of 
survival following in-hospital cardiopulmonary resuscitation. 
Arch Intern Med 1994; 154:2426-2432. 

4. American Association for Respiratory Care. Clinical practice 
guideline: resuscitation in acute care Hospitals. Respir Care 1993; 
38(1 1): 1 1 79- II 88. 

fi. Thalman JJ, Rinaldo-Gallo S, Maclnlyre NR. Analysis of an en- 
dotracheal intubation service provided by respiratory care practi- 
tioners. Respir Care l993;38(5):469-473. 

6. /.yla EL, Carlson J. RCPs as secondary pro\ idcrs ol ciidotiachcal in- 
tubation: one hospital's experience. Respir Caic 1 994;39( I ):30-33. 

7. Barnes TA. Clinical practice guidelines for in-hospital cardiopul- 
monary resuscilalion, Respir Care 1 99.S;4()(4 1:346-363. 


Ri;sPiRATC)KV Carf. • April "95 Vol 40 No 4 

Conference Summary 

8. Hess D. Methods of emergency drug administration. Respir Care 
1995:40(5):in press. 

9. Rau J. ACLS drugs used for cardiac arrest. Respir Care 1995: 

10. Sanders A. Development of AHA guidelines for emergency car- 
diac care. Respir Care 1995;40(4):338-345. 

11. Hargarten KM, Stueven HA. Waite EM, Olson DW, Mateer JR, 
Aufderheide TP, Darin JC. Prehospital experience with defibrilla- 
tion of coarse ventricular fibrillation: a ten-year review. Ann Emerg 
Med 1990:19:157-162. 

12. Palmisano JM. Akingbola OA, Moler FW, Custer JR. Simulated 
pediatric cardiopulmonary resuscitation: Initial events and re- 
sponse times of a hospital arrest team. Respir Care 1994:39(7): 

13. Aufderheide T. Pacemakers and electrical therapy during ad- 
vanced cardiac life support. Respir Care 1995:40(4):364-379. 

14. Halperin H. Compression techniques and blood flow during car- 
diopulmonary resuscitation. Respir Care 1995:40(4):38O-392. 

15. Bishop MJ. Airway management and clinical guidelines for use 
during resuscitation. Respir Care 1995;49(4):393-403. 

Branson RD. Techniques of emergency ventilation. Respir Care 
1995:40(5):in press. 

Pepe P. ACLS systems and training programs: do they make a 
difference? Respir Care 1995:40(4):427-436. 
Schwenzer KJ, Smith WA, Durbin CG: Selective application of 
cardiopulmonary resuscitation improves survival rates, Anesth 
Analg 1993:76:478-484. 

Hamill R. When is enough, enough? Respir Care 1995:40(5):in 

Rubenfeld GM. Do not resuscitate orders: a critical review of the 
literature. Respir Care 1995:40(5):in press. 
Fluck R. The first ACLS course: resuscitation training for stu- 
dents. Respir Care 1995:40(5):in press. 

Kaye W. Research in advanced cardiac life support training: 
which methods improve skill and knowledge retention? Respir 
Care 1995:40(5):in press. 

Boudin KM. Strategies for maintaining ACLS skills in hospitals. 
RespirCare 1995:40(5l:in press. 

Malinowski C. Pediatric advanced life support and neonatal re- 
suscitation program. Respir Care 1995;40(5):in press. 



The Development of AHA Guidelines for Emergency Cardiac Care 

Arthur B Sanders MD 

I. Introduction 

II. Historical Overview 

III. ECC Guidelines Development— 1992 

IV. The Transformation of Guidelines into 

Educational Material 

V. Dissemination & Implementation 

VI. The ECC Cycle 

VII. In Summary 


In 1992 the American Heart Association (AHA) 
Emergency Cardiac Care Guidelines for Basic Life Support 
(BLS), Advanced Cardiac Life Support (ACLS) and 
Pediatric Advance Life Support (PALS) were published in 
the Journal of the American Medical Association (JAMA).' 
These were followed by textbooks, handbt)oks, and instruc- 
tor's manuals published in 1994 to disseminate these 
Guidelines through the Emergency Cardiac Care (ECC) 
network of the AHA.-"* Although many clinical guidelines 
have been published by many institutions and specialty so- 
cieties, the ECC Program developed by the American Heart 
Association in collaboration with other organizations has 
probably been the most successful and widely accepted. 
The reasons for this wide acceptance are related to many 
factors. The ECC Guidelines are among the oldest in the 
medical community and maintain an established tradition 
of over 20 years. '''* Guidelines for the treatment of cardiac 
arrest fulfill an important need. All health care profession- 
als and, indeed, many citizens may be faced with the need 
to treat a patient in cardiac arrest. When faced with this cri- 
sis, one has no time to consult textbooks, colleagues, or 

Dr Sanders is Professor of F.niergency Medicine, University of Arizona 
Health Science Center. Tucson. Arizona. 

A version of this paper was presented by Dr Sanders during the 
RESHtRATORY Carr Journal Conference "Resuscitation in Acute Care 
Hospitals," held in Cancun. Mexico. October 21-2.1. 1994. 

journal articles. The treatment of a cardiac arrest patient is 
the ultimate emergency. If appropriate treatment is prompt- 
ly given, the patient has a good chance for resuscitation and 
long-term survival. However, if appropriate treatment is 
not rendered within minutes the patient will die. Thus, the 
ECC program addresses a crucial need for health-care pro- 
fessionals, as well as many citizens, to have the knowledge 
and skills to appropriately treat patients in cardiac arrest. 

The ECC program has grown remarkably in the past 30 
years. Perhaps the major factor in the success of the pro- 
gram has been its implementation through a network of 
volunteers through local and state affiliates of the AHA. 
The acceptance and importance of these Guidelines to the 
medical community have given rise to what has been 
termed the "ACLS industrial complex."-'"" This wide ac- 
ceptance of the Guidelines has also led to their implemen- 
tation at almost every hospital and community throughout 
the United States. 

In the few studies that have assessed the outcome fol- 
lowing ACLS training, the institution of ACLS programs 
has been associated with improved resuscitation from car- 
diac arrest. Lowenstein et al " found that successful in-hos- 
pital resuscitation increased from 32% in the 6-month peri- 
od before to 60% in the 6-month period after mandatory 
ACLS courses for medical house officers were instituted. 
Similarly, our group found that the institution of an ACLS 
Provider Course in a small rural hospital was associated 
with improveiTient in initial resuscitation for patients with 
ventricular fibrillation and out of-hospital arrest, '- 

In this paper I review the historical development of the 
AHA Emergency Cardiac Care Program, and then detail 


Rhspiratory Cark • April "95 Vol 40 No 4 

AHA Guidelines Development 

the process of Guidelines development in 1992. Following 
Guidelines completion, the ECC Committee developed a 
new educational philosophy for translating the Guidelines 
into sound teaching material. Finally, I review the ECC 
cycle and demonstrate the continuous and dynamic guide- 
lines process. 

Historical Overview 

The modem era of cardiopulmonary resuscitation (CPR) 
in emergency cardiac care was ushered in by the paper enti- 
tled "Closed Chest Cardiac Massage" by Kouwenhoven, 
Jude, and Knickerbocker in JAMA in I960." This article 
coupled the elements of closed-chest cardiac massage, arti- 
ficial ventilation, and electrical defibrillation for resuscita- 
tion of patients in cardiac arrest. In 1966, a report from the 
National Academy of Sciences/ National Research Council 
(NAS/NRC) recommended training health care profession- 
als in cardiac resuscitation techniques.' The AHA devel- 
oped its network of training materials in the late 1 960s and 
extended the program to lay persons in the early 1970s.'^ In 
1973, the National Conference To Establish Standards for 
CPR and ECC was sponsored by the AHA and the NAS/ 
NRC. This resulted in the first formal publication of guide- 
lines in 1974.'' The Conference strongly recommended CPR 
training programs for the lay public and also established 
training programs for basic and advanced life support for 
health care professionals. Finally, it recommended integrat- 
ing programs with Emergency Medical Service (EMS) sys- 
tems that were developing in many communities throughout 
the United States.'''''* It was recognized that although the 
training of health-care professionals can have an impact on 
in-hospital cardiac arrests, most arrests occur outside of the 
hospitals. These arrests could only be addressed effectively 
through a competent communitywide EMS system involv- 
ing education of citizens in CPR.' * '"* The second National 
Conference was held in 1979 and resulted in the publication 
of Guidelines in 1980.' Subsequent conferences were held 
in 1985 and 1992.' ** Each conference evaluated the existing 
protocols in light of the new scientific developments and re- 
sulted in consensus recommendations for ECC Guidelines 
and future programs. 

ECC Guidelines Development— 1992 

One key element in the development of the 1992 
Guidelines was an internal administrative shift within the 
AHA. In 1991, the AHA moved the ECC program from 
the Office of Education and Community Programs to man- 
agement under the Office of Scientific Affairs. This repo- 
sitioning within the AHA was highly important to setting 
the tone for the approach to the ECC Guideline develop- 
ment process. Previously, ECC had been operated under 

the auspices of the AHA Office of Education and Com- 
munity Programs along with other initiatives such as the 
work-site and school-site programs that are designed pri- 
marily to educate the public regarding heart-healthy life 
styles. These were generally community-oriented educa- 
tional efforts and did not undergo the same scientific 
scrutiny and rigor as the programs under the Office of 
Scientific Affairs. This shift in program administration 
was a recognition that cardiac resuscitation is an important 
.scientific discipline that deserves the same scrutiny and 
rigor as other scientific issues in the AHA. 

Consistent with this shift in philosophy, the leadership 
of the ECC Committee, Drs Kerber. Paraskos, Omato, 
Cummins, Chandra, and others determined to tighten up 
the scientific rigor in the consensus process for the 1992 
Guidelines. Criteria were developed for evaluating scien- 
tific data. Particular attention was paid to evaluating the 
quality of the research and the presence of studies from 
multiple groups of investigators. A system for evaluating 
research was developed for all reviewers and experts on 
the consensus panels.' ''*"' Reviewers asked critical ques- 
tions: Were studies available in experimental laboratory 
models? What evidence was available in humans? Were 
there prospective, randomized, multicentered, placebo- 
controlled, double-blinded studies with large sample 
sizes? Did negative studies have large enough sample size 
to minimize error? Were the findings clinically important? 
Were proposals feasible in the health care system? Were 
the studies conducted in an ethical manner? Were outcome 
studies available to demonstrate the effectiveness of CPR 
for long-term survival and neurologic outcome? 

The next step was the utilization of a system for classi- 
fying therapeutic recommendations. '^ Recommendations 
were to be used based on the strength of the supporting sci- 
entific evidence as evaluated by the scientific template. 
Recommendations were classified as follows:'" 

Class I: All evidence supports the usefulness and ef- 
fectiveness of the therapy, and its application 
is indicated. 

Class Ila: The weight of evidence is in favor of the use- 
fulness and efficacy of the therapy. 

Class lib: The therapy is not well established by scientif- 
ic evidence but may be helpful and probably is 
not harmful. 

Class III: The therapy is inappropriate, without scientific 
evidence, and may be harmful. 

The consensus process in 1992 was developed as a multi- 
stage procedure. "■ First, a conference planning committee 
was formulated under the leadership of the ECC Committee. 
Collaboration and sponsors were recruited from organiza- 
tions in medicine including the American Academy of 

Respiratory Care • April '95 Vol 40 No 4 


AHA Guidelines Development 

Pediatrics. American College of Cardiology. American Red 
Cross, European Resuscitation Council. Heart and Stroke 
Foundation of Canada, and The National Heart, Lung and 
Blood Institute.' In addition, cooperating agencies support- 
ing the Consensus Conference included 67 societies and 
specialty organizations from all over the world including the 
American Association for Respiratory Care. As in the past, 
the Planning Committee used the 1986 Guidelines as the 
prototype by which to evaluate changes.' '■*"' This technique 
thus requires that a modification to the Guidelines have a 
reasonable amount of scientific evidence that it is 'better' 
than the earlier recommendations. The shortcoming of this 
approach is the fact that some studies may demonstrate no 
overall difference in outcome between the older and the 
newer therapy. The Committee would thus favor the use of 
the older, previously used therapy . 

Next the Planning Committee identified key issues to 
be used for panel discussions.'^ These issues were general- 
ly controversial topics or those about which new scientific 
evidence had been published. A preliminary fact-finding 
conference was held in September 1991 to begin the con- 
sensus development process, with approximately 200 ex- 
perts invited to attend. The experts generally participated 
in one panel discussion and then rotated through other pan- 
els to react and contribute. The experts were asked to re- 
view all the evidence according to the scientific guidelines 
outlined," and each panel was to discuss and come to con- 
clusions about specific questions posed. For example, the 
panel on adrenergic agents was asked to recommend the 
agent of choice and the dosing schedule for adrenergic 
agents in the ACLS protocols. 

In the September 1991 meetings, the panels reviewed the 
scientific literature for three different audiences. The audi- 
ences, who were themselves experts in ECC. reacted to the 
analysis and gave their opinions. The panel thus heard a 
wide variety of reactions and opinions. In addition, each of 
the conference attendees was given the opportunity to an- 
swer a questionnaire on the specific issues posed to the pan- 
els. Thus, following the meeting, the panel had not only the 
benefit of the oral comments but written comments and the 
results of the attendees "voting" on the specific questions 

Following this preliminary fact-finding conference, 
panels were then instructed to write up their recommenda- 
tions for the National Consensus Meeting in February 
1992. This preliminary fact-finding panel system was well 
received by attendees and useful to the panelists. The audi- 
ence believed that they had had adequate opportunity to 
comment on important issues, and the panel members be- 
lieved that the comments were important to developing an 
rnrrrt// recommendation for the National Conference.'^ "' 

The National Guidelines Conference was held in 
February 1992. Presentations were riiade as state-of-the-art 

lectures by experts in the field. Panel discussions were 
held for the more controversial issues. Examples of state- 
of-the-art presentations included Adult Airway Manage- 
ment, Issues in the Maintenance of Defibrillators, and 
Antiarrhythmics during Cardiac Arrest. Examples of panel 
discussions included Acid-Base Management, Adrenergic 
Agonists, Education in ACLS Training Programs, and 
Ethical Issues in Resuscitation.' Once again, input was 
sought from all attendees and spirited discussions ensued 
in many sessions. 

The experts were then charged with writing up the final 
review and recommendations for publication in JAMA and 
the ACLS textbook. Each section of written material then 
underwent review at several levels. For ACLS materials, 
reviews were done first by the ACLS Subcommittee, then 
by the ECC Committee, and finally the Scientific Affairs 
Committee of the AHA. Following these reviews and 
modifications, the manuscripts were sent to JAMA where 
they were again reviewed by independent reviewers. Each 
step was guided by the ACLS Subcommittee Chair, 
Richard Cummins, and the AHA publication staff. The 
Guidelines were published in October 1992 in a dedicated 
issue of JAMA' The ACLS Textbook and ACLS Drug and 
Algorithm Handbook were published in 1994 by the 
American Heart Association.- ■* 

The Transformation of Guidelines into 
Educational Material 

The next important step was the conversion of the .sci- 
entific guidelines into educationally sound presentations 
for teaching in ACLS, PALS, and BLS courses. My dis- 
cussion focuses on the ACLS process. Two important de- 
cisions were made based on extensive discussions at the 
Fact Finding and National ECC Conferences. The purpose 
of ACLS education was clearly defined by Dr Billi et al"" 

The purpose of ACLS programs is the education of health 
professionals whose jobs include the management of pa- 
tients in cardiac arrest or near The goal of each 
ACLS course is to have each participant succeed in acquir- 
ing the skills and knowledge required for resuscitation. 

Using this clear educational objective, it soon became obvi- 
ous that the implementation of ACLS in many communities 
distorted the AHA's intent. Even though it had never been 
the intent of the AHA, the goal of many courses became 
certification. Many problems were associated with this cer- 
tification mentality. Participants soon learn that their goal is 
passing the written exam and testing stations to get their 
ACLS cards. Recertification becomes reduced to passing 
these tests again so that cards can be renewed, rather than 
focusing on improving knowledge and skills.'-''"' 


Respiratory Care • April '95 Vol 40 No 4 

AHA Guidelines Development 

The emphasis on certification is not bad in itself. Certifi- 
cation is an important process that can provide assurances 
that health care professionals have attained the appropriate 
knowledge and skills to practice. For example, the Ameri- 
can Board of Emergency Medicine certifies physician com- 
petency in emergency medicine. Applicants must complete 
a rigorous 3-year training program at an approved emer- 
gency medicine residency program, then achieve a passing 
grade in a criterion-referenced written exam, and, finally, 
pass an oral examination based on emergency department 
cases. Successful candidates must recertify after 10 years 
by again passing a written or oral exam. Each of these ex- 
aminations has been carefully standardized and tested for 
reliability and validity. Certification in medicine carries 
with it a great deal of responsibility for the health and safe- 
ty of the public. 

ACLS was never designed to be a certifying program. In 
fact, the 1987 ACLS textbook clearly stated that ACLS 
course completion "in no way warrants performance, nor 
does it, per se, qualify or authorize a person to perfonn any 
procedures, and is in no way related to licensure, which is a 
function of the appropriate legislative, health and education- 
al authorities."* In addition, ACLS participants are all given 
a question on their written exam reaffirming this point. ''^ 

Despite this stated position, ACLS is often used by in- 
stitutions to certify competency. Hospitals may require 
physicians to be ACLS certified and to produce a current 
card in order to work in their emergency departments or 
critical care units. EMS agencies may require a similar cer- 
tification for their prehospital care professionals. 
Insurance companies have been known to offer discounts 
on their malpractice policies to physicians in some special- 
ties who are ACLS certified. 

It is this distortion of purpose that has created a problem 
for both ACLS students and instructors. The ACLS course 
had not been designed for the purpose for which it was 
being used. The course has much variability especially 
with regard to evaluation techniques. The evaluation pro- 
cedures had never undergone rigorous reliability and va- 
lidity testing, and little standardization exists across the 
various sites. Therefore, the AHA decided to focus on the 
defined goals for the ACLS program. ACLS now provides 
an educational experience for participants and leaves the 
issue of certification and competency testing to other agen- 
cies such as state medical boards and other specialty 

Furthermore, the atmosphere of a certification experi- 
ence is often filled with anxieties and fears.*"" Such anxi- 
eties and fears regarding passing the certification examina- 
tion can actually interfere with the educational goals of the 
ACLS programs. The ECC Committee believes that when 
students are stressed, they tend to retreat for protection 
rather than opening themselves up to new concepts, and. 

therefore, the ECC Committee made the decision to elimi- 
nate the concept of certification and focus on sound educa- 
tional principles. With this new educational paradigm, 
evaluation becomes an educational tool for improving the 
skills and knowledge regarding resuscitation,'"'- and the 
course becomes flexible to meet the needs of the partici- 
pants. The Committee believes that because there is less 
anxiety and stress associated with the course, the partici- 
pants are better able to learn the material. The written 
ACLS test can be used in creative ways.-* Some course di- 
rectors allow participants to grade the exams themselves 
and then go over the questions. There is no definitive pass 
or fail grade that the student must achieve.' The student 
must, however, go through the required nine case scenar- 
ios and the CPR defibrillation station in order to success- 
fully complete the course. 

Required knowledge and skills are defined for each 
case scenario. At the end of the course, participants receive 
a record based on their evaluations by the instructor. The 
final record will include one of the following classifica- 
tions: Complete-IP — superior performance with instructor 
potential; Complete Provider Level — satisfactory perfor- 
mance in all core cases; NYC, or not yet complete — un- 
able to satisfactorily complete the nine required cases, may 
return for a reasonable amount of remediation. 

The second educational concept that characterized the 
transition from guidelines development to educational 
course is the emphasis on active learning through the use 
of clinical scenarios.' About half of previous ACLS cours- 
es was devoted to a series of canned lectures in basic topics 
such as pharmacology, dysrhythmia recognition, and acid- 
base balance. These lectures mirrored the textbook chap- 
ters on similar topics that cried out for clinical relevance. 
The lectures from which the participants absorbed facts 
were an example of passive learning. They did not encour- 
age the higher levels of learning like analysis and synthesis 
in which participants put the facts together in the setting of 
clinical practice. Course evaluations consistently demon- 
strated that the lecture series was the weakest part of the 
course. In contrast, the interactive clinical scenarios, such 
as in the megacode teaching stations, were rated highly 
both by students and instructors. This change in education- 
al direction is consistent with progress in medical educa- 
tion. Many medical schools are realizing the significant 
limitations of lectures and are promoting problem-based 
interactive learning to set up lifelong patterns of learning 
in medicine. Many medical schools have revised their en- 
tire curriculum to reflect problem-based learning. 

The ACLS Instructor's Manual defines the core knowl- 
edge and skills that must be covered and evaluated in all 
nine core cases. The material, however, is structured in a 
clinically relevant way. For example, instructors must still 
teach participants about the pharmacology of ACLS drugs. 

Respiratory Care • April "95 Vol 40 No 4 


AHA Guidelines Development 

However, the information is presented in the context of 
clinical cases in which the drugs are used — atropine in 
asystole and epinephrine in ventricular fibrillation are ex- 
amples.' A matrix in the Instructor's Manual lists each di- 
dactic topic and where it is covered in the case scenarios. - 
My experience has been that when the new course was 
pilot tested at several institutions, participants gave it 
'rave' reviews. The Committee is confident that within a 
few years, as instructors become comfortable with the 
course and use their creativity, the new methods of teach- 
ing will become much superior to the old ACLS course. 
Instructors will wonder why we waited so long to change. 
Thus, educationally speaking, 1994 marked a new era 
in ACLS training. The paradigm has shifted from the certi- 
fication model to the education model. The ECC Com- 
mittee believes that no matter how knowledgeable and 
skillful health-care professionals are, they can still im- 
prove their ACLS knowledge and skills when challenged 
with the appropriate material. The new case-based interac- 
tive teaching material may at first be more difficult for 
some instructors. There are no canned lectures. Instructors 
must carefully think about their material and their audi- 
ence and choose from a variety of options. Creativity is 
highly encouraged. I have heard teachers report exciting 
ways of presenting ACLS material including role playing 
and ACLS and Jeopardy-like games. 

Dissemination & Implementation 

A key element in dissemination is the ECC network de- 
veloped by the AHA. This network encompasses state af- 
filiates and regional divisions. The ECC Committee devel- 
ops overall policies and guidelines that often are imple- 
mented through subcommittees of BLS, ACLS, and PALS 
and then disseminated through the States and a network of 
National Faculty. Each affiliate has at least one National 
Faculty in BLS, ACLS, and PALS. National Faculty then 
disseminate the materials to Affiliate Faculty in each State. 
Affiliate Faculty disseminate the materials to ACLS in- 
structors and assure that courses are being taught with up- 
to-date materials and guidelines. The ACLS instructors 
implement it in the provider courses. The Committee be- 
lieves that the maintenance of this dissemination ECC net- 
work is a key element in the success of the ECC programs. 

The ECC Cycle 

The ECC program takes on its most public posture in 
the development of the Guidelines and educational materi- 
al. The work of the ECC Committees, however, is based 
on a cycle of approximately 7 years. Throughout the cycle, 
the Committee remains active and constantly re-evaluates 
the science in relation to the Guidelines. The ECC cycle 

includes: assessment of research, guideline development, 
production of written material, education development, 
production of educational material, implementation, and 
program evaluation.'^ The 3 years past was a period of in- 
tense application during which the science was critically 
evaluated, guidelines revised, and new educational materi- 
al developed. The Guidelines probably will not need major 
revisions until the end of the decade. 

What occupies the ECC Committees during the rest of 
the cycle? What if new developments occur in the manage- 
ment of cardiac arrest patients? Will the recommendations 
in 1996 be outdated and based on 1992 scientific litera- 

The ECC process is structured as a dynamic ongoing 
process. In 1994-95, the ECC program has entered a phase 
of re-evaluation and long-range planning. ECC is looking 
at its various roles including administration, research, edu- 
cation, and public policy. New subcommittees on public 
policy and program administration have been formulated, 
and planning is underway for new initiatives to stimulate 
research and evaluate our educational programs. 

The ECC network is continually reassessing the Guide- 
lines and making appropriate changes to ensure that the 
recommendations are consistent with optimal care. The 
Handbook of Drugs and Algorithms is being updated for 
1995. We anticipate minor changes and new information 
about drug protocols and options. If there is a need for 
major revision, the ACLS Committee re-evaluates the data 
and, if necessary, uses outside expertise to come to a con- 
sensus. In the past cycle, a number of such issues and con- 
troversies were brought to the ACLS Committee, with ap- 
propriate actions taken. For example, the efficacy of auto- 
matic external defibrillators (AED) and the "chain of 
survival" concept came to light years before the 1992 con- 
sensus conference.-" -- The Committee decided that these 
issues were important enough and their science rigorous 
enough that new guidelines could be developed and new 
teaching modules incorporated into the ACLS course. -- 
These were promptly disseminated through the ECC net- 
work. By 1992, the application of AEDs was an estab- 
lished, required module of the ACLS course and necessi- 
tated little discussion and update in the review process. 

Another example was the controversy surrounding the 
appropriate dose of epinephrine for patients in cardiac ar- 
rest. In the late 1980s and early 1990s, studies in animal 
models demonstrated that larger doses of epinephrine pro- 
vided more effective perfusion pressures and myocardial 
blood How during CPR.-' In addition, human anecdotal 
studies appeared to confirm these observations.''' However, 
prospective randomized clinical trials had not been done. 
Nevertheless, many clinicians started to use 
epinephrine to treat patients in cardiac airest and much 
pressure was exerted by the medical community on the 


Respiratory Care • April '95 Vol 40 No 4 

AHA Guidelines Development 

ACLS Committee to modify the Guidelines and recom- 
mend higher doses of epinephrine. The Committee inten- 
sively followed the discussions and concluded, with the use 
of the scientific template, that not enough evidence existed 
to change the Guidelines.--'' When clinical trials were done 
in 1992. the data showed no overall survival benefit ac- 
crued from the use of high-dose epinephrine.-*"-^ These 
studies, however, were useful for changing some of the rec- 
ommendations in the 1992 Guidelines. There was evidence 
that epinephrine should be used at lesser time intervals. 
Thus, the time interval was changed from 5 minutes be- 
tween doses to 3 minutes.' In addition, evidence showed 
that certain subgroups, such as pediatric patients or patients 
with pulseless electrical activity, may benefit from the use 
of higher doses of epinephrine. Therefore, the Guidelines 
were modified so that clinicians can judge the individual 
situation and, after the first dose of epinephrine, give higher 
doses of epinephrine if they believe this is indicated. ' Thus, 
the Committee, using rigorous scientific criteria, has been 
able to respond to new developments and to keep the 
Guidelines current. 

In Summary 

In summary, the value of the ECC training programs is 
improving the outcome for patients in cardiac arrest. It is 
believed that, by giving clinicians overall guidelines to use 
for this emergency situation, better decisions will be made. 
The Guidelines are in a dynamic state of re-evaluation, and 
the development process for guidelines is imperfect. 
However, every effort has been made to look at all sides of 
any controversy and make decisions based on scientific 
evidence. In addition, recommendations are now based on 
the relative strength of the scientific data. The process will 
continue even in the absence of National Consensus meet- 
ings. Finally, the importance of transmitting the Guide- 
lines to participants in an educationally sound program has 
received a great deal of emphasis. The ACLS course is 
now interactive and based on clinical scenarios. The em- 
phasis is on improving the knowledge and skills of the par- 
ticipants who take the course rather than on certification or 
evaluation. The effect of these changes will be evaluated 
over the next several years. 


1. American Heart Association, Emergency Cardiac Care Com- 
mittee and Subcommittees. Guidelines for cardiopulmonary re- 
suscitation and emergency cardiac care. JAMA I992;268:217I- 

2. American Heart Association. Textbook of advanced cardiac life 
support. Dallas, Texas: American Heart Association. 1994. 

3. American Heart Association. Instructor's manual for advanced car- 
diac life support. Dallas, Texas: American Heart Association, 1994. 

4. American Heart Association. Advanced cardiac life support algo- 
rithms and drugs 1993 handbook. Dallas, Texas: American Heart 
Association, 1994. 

5. Ad hoc Committee on Cardiopulmonary Resuscitation. National 
Academy of Sciences, National Research Council. Cardio- 
pulmonary resuscitation. JAMA 1966;198:138-145. 

6. American Heart Association. Standards for cardiopulmonary re- 
suscitation (CPR) and emergency cardiac care (ECC). JAMA 

7. American Heart Association. Standards and guidelines for car- 
diopulmonary resuscitation (CPR) and emergency cardiac care 
(ECC). JAMA 1980;244:453-509. 

8. American Heart Association. Standards and guidelines for car- 
diopulmonary resuscitation (CPR) and emergency cardiac care 
(ECC). JAMA 1986;255:2905-2989. 

9. Billi JE. The educational direction of the ACLS training program. 
Ann Emerg Med 1993;(Part 2):484-488. 

10. Billi J. Membrino G. Education in adult advanced cardiac life 
support training programs: changing the paradigm. Ann Emerg 
Med 1993;22(Part2):475-483. 

1 1 . Lowenstem SR. Sabyan EM, Lassen CF, Kern DC. Benefits of 
training physicians in advanced cardiac life support. Chest 1986; 

12. Sanders AB, Berg RA, Burtess M, Genova RT, Kern KB, Ewy 
GA. The efficacy of an ACLS training program for resuscitation 
from cardiac artest in a rural community. Ann Emerg Med 1994; 

13. Kouwenhoven WB, Jude JR, Knickerbocker GG. Closed-chest 
cardiac massage. JAMA 1960;173:1064-1067. 

14. Paraskos J. History of CPR and the role of the National Confer- 
ence. Ann Emerg Med 1993;22(Part 2):275-280. 

15. American Heart Association. National Conference on Cardiopul- 
monary Resuscitation and Emergency Cardiac Care. Dallas, 
Texas: American Heart Association, 1992. 

16. Cummins RO, Chamberlain D. Consensus development in resus- 
citation: the growing movement towards international ECC 
guidelines. In: Paradis N, Nowak R, Halperin H: Cardiac arrest: 
the pathophysiology and therapy of sudden death. Baltimore; 
Williams & Wilkins Inc. (in press). 

17. Gunnar R. Bourdillon P. Dixon D, Fuster V, Karp RB, Kennedy 
JW, et al. ACC/AHA Guidelines for the early management of pa- 
tients with acute myocardial infarction. Circulation 1990:82:664- 

18. American Heart Association. Textbook of advanced cardiac life 
support. Dallas, Texas: American Heart Association, 1987. 

19. American Heart Association. Instructor's manual for advanced 
cardiac life support. Dallas Texas: American Heart Association, 

20. Cummins RO, Oraato JP, Thies WH, Pepe PE. Improving survival 
from sudden cardiac death: The "chain of survival" concept. Circu- 
lation 1991;83:1832-1847. 

21. Cummins RO, Thies W, Paraskos J, Kerber RE, Billi JE. Seidel J. 
et al. Encouraging early defibrillation: the American Heart 
Association and automated external defibrillators. Ann Emerg 
Med 1990;19:1245-1248. 

22. American Heart Association. Instructor's manual for advanced 
cardiac life support supplement (early defibrillation). Dallas, 
Texas: American Heart Association, 1990. 

23. Brown C, Werman H, Davis E. Hobson J, Hamlin R. The effects 
of graded doses of epinephrine on regional myocardial blood flow 
during cardiopulmonary resuscitation in swine. Circulation 1987; 

24. Koscove E. Paradis N. Successful resuscitation from cardiac ar- 

Respiratory Care • April "95 Vol 40 No 4 


AHA Guidelines Development 

rest using high-dose epinephrine therapy: report of two cases. 

JAMA 1988;259:3031-3034. 

Omato JP. High-dose epinephrine during resuscitation: a work of 

caution (editorial ). JAM A 1 99 1 ;265: 1 1 60- 1 1 6 1 . 

Brown C, Martin D. Pepe P. Stueven H, Cummins RO, Gonzalez E, 

et al. A comparison of standard-dose and high-dose epinephrine in 
cardiac arrest outside the hospital. N Engl J Med 1992:327: 151-155. 
27. Stiell 1. Herbert P, Weitzman B. Wells GA, Raman S. Slark RM, 
et al. High-dose epinephrine in adult cardiac arrest. N Engl J Med 

Sanders Discussion 

Durbin: You mentioned that ACLS 
cards were no longer expected to be a 
standard for job opportunities or crite- 
ria for employment: however, at local 
and state levels this is common prac- 
tice, and even in the minds of 
providers, it's an important compo- 
nent — the recognition for having 
achieved something. My institution is 
still requiring 'the card,' although the 
card doesn't say certification any- 
more. It says course completion. I 
don't think that's going to change. My 
guess is people are going to be re- 
quired to complete the ACLS course, 
and we'll have the same concerns 
about satisfactory versus unsatisfacto- 
ry pert'ormance. My state hasn't yet 
decided what to do with the ACLS 
written test. We don't know whether 
to use it as an evaluative tool or a 
teaching tool. Opinion is quite mixed 
on that. Do you see anything else re- 
placing the ACLS card as an indicator 
of job performance? 

Sanders: 1 don't think it is necessarily 
bad — for an institution to say "We 
want you to take a continuing medical 
education (CME) course." ACLS is a 
CME course, and the AHA will give a 
card attesting to course completion. A 
hospital can ask its staff to maintain 
and update knowledge and skills by 
taking specific CME courses. The 
problem is that some institutions con- 
fuse ACLS as a certit'ication for ihc 
treatment of patients in cardiac arrest. 
It was never designed to be a certifica- 
tion course; it is a CME course. If a 
hospital or training institution wants to 
use the material in ACLS to test its 

staff or students, it is free to do so. It is 
the hospital that should decide what 
are the minimum standards necessary 
for that institution and how often the 
course should be taken. For example, 
a physician training program may re- 
quire successful completion of all 
elective as well as required case sce- 
narios and advanced airway manage- 
ment skills. 

Pepe: One of the interesting things 
that evolves whenever you develop 
consensus guidelines like these (which 
are generally useful because then ev- 
erybody on a clinical resuscitation 
team knows what the general clinical 
plan is) is that oftentimes they are used 
in courts of law. At least one journalist 
has written that doctors' own guide- 
lines hurt them in court.' I can see a 
scenario in which someone didn't fol- 
low the ACLS guidelines,-"* and there 
might be a need for defense where 
they might come back to the Heart 
Association and say, "What's your 
feeling about this?" Specifically, Art 
(Sanders), are doctors allowed to prac- 
tice within a wider range than we've 
allowed here? Or do you think the 
Guidelines are broad enough that they 
still allow them to have a lot of leeway 
in those areas? 

1. Felsenthal E. Doctors' own guidelines 
hurt them in court. (Legal Beat) Wall 
Street Journal October 19, 1994. 

2. American Heart Association, Emer- 
gency Cardiac Care Committee and 
Subcommittees. Guidelines for cardio- 
pulmonary resuscitation and emergency 
cardiac care. Part Llnlroduclion. JAM.A. 

3. American Heart Association. Textbook 
of Advanced Cardiac Life Support. Dal- 
las. 1 987: 1 -248 and 1994: 1-1 to UvlO. 

4. American Heart Association. Emer- 
gency Cardiac Care Committee and sub- 
committees. Guidelines for cardiopul- 
monary resuscitation and emergency 
cardiac care. Part III: Adult advanced 
cardiac life support. JAMA. 1992:268: 

Sanders: Well, the guidelines are ex- 
actly that — they're guidelines not clin- 
ical practice standards. The recom- 
mendations are graded based on their 
scientific efficiency, and there is room 
for flexibility in most of the algo- 
rithms. For example, early defibrilla- 
tion is a Class-I recommendation. If it 
is not used, that is bad medical prac- 
tice. On the other hand, there is a great 
deal of flexibility for the use of bicar- 
bonate in patients in cardiac arrest. 
Overall, there are very few recommen- 
dations that cairy the highest recom- 
mendation, Class-I. 

Barnes: At some of the ACLS cours- 
es that I've attended, I've noticed that 
at the airway station you don't really 
have to demonstrate competency in in- 
tubating the trachea, you just have to 
be able to bag-valve the patient ade- 
quately. Yet, some of us believe that 
tracheal intubation early in the effort is 
important. What are your thoughts 
about requiring everyone who suc- 
cessfully completes the course to be 
able to intubate the trachea? Do you 
think that's a good idea? Or should 
just specialized groups be so trained? 

Sanders: Again, taking it out of the 
certification model and using the edu- 
cation model — if I had a group of 
medical students or anesthesia resi- 
dents or emergency medicine resi- 
dents, 1 would want to teach and 
allow ihcm to practice endotracheal 


Ri;spiRAr{)R">' Carl • April '^5 Vol 40 No 4 

Sanders Discussion 

intubation. As medical director I can 
make that decision based on what will 
be the best learning material for my 
audience. If I have a group of nurses 
who never intubate, then I would 
teach other methods of airway con- 
trol. So, again, the new ACLS format 
allows you to tailor your course to 
your audience. 

Barnes: 1 have just one follow-up 
question. Do you think the Heart 
Association ought to provide any 
guidance then in terms of which 
members of the resuscitation team 
should be able to intubate? You me- 
ntioned that nurses should not. 
Should anesthesiologists and resi- 

Bishop: That issue is covered by my 
talk. According to the American Heart 
Association — the key determinant of 
who should manage the airway during 
resuscitation is that it be someone with 
ongoing training and practice. I think 
the fact that someone successfully 
puts a tube into a mannequin on a one- 
time basis is probably irrelevant. 

41st Annual Convention and Exhibition 
December 2-5 • Orlando, Florida 

Respiratory Care • April "95 Vol 40 No 4 


Clinical Practice Guidelines for Resuscitation 
in Acute Care Hospitals 

Thomas A Barnes EdD RRT 




Goals of Resuscitation 

A. Survival 

B. Quality of Life 

C. Years of Useful Life 
Cost Analysis 
Characteristics of Hospitalized 

Patients & CPR Outcome 

A. Disease Categories 

B. Age-Related CPR Outcome 

C. Outcomes of CPR in Children 
Guidelines for Resuscitation in 

Acute Care Hospitals 

A. Origin 

B. Differences between AARC and 
AHA Resuscitation Guidelines 

C. Applications of RACH Guideline 

by RCPs 

D. Application of Guidelines in Community Hospitals 


The AARC Clinical Practice Guideline (CPG), Resus- 
citation in Acute Care Hospitals (RACH) "... encompass- 
es all care necessary to deal with sudden and often life- 
threatening events affecting the cardiopulmonary system, 
and involves the identification, assessment, and treatment 
of patients in danger of or in frank arrest in the acute-care 

Dr Bamcs is Director ol ItiL' RcspiralDry Therapy Program, Department of 
Cardiopulmonary Sciences. Northeastern University. Boston. Mas.sachu- 

A version of this paper was presented by Dr Barnes during the iyy4 
Journal Conference entitled, "Resuscitation in Acute Care Hospitals" 
held in Cancun, Quintana Roo, Mexico, Octoher. 1994. 

Reprints: Thomas A Barnes EdfJ RRT. Department of Cardiopulmonary 
Sciences. Northeastern University. 100 Dockser Hall. .^60 Huntington 
Avenue, Boston MA 021 K5. 

hospital, including the high-risk-delivery patient. This in- 
cludes ( 1 ) alerting the resuscitation team and the managing 
physician; (2) using adjunctive equipment and special 
techniques for establishing, maintaining, and monitoring 
effective ventilation and circulation; (3) monitoring the 
electrocardiograph (ECG) and recognizing dysrhythmias; 
(4) using defibrillators and mechanical ventilators; (5) ad- 
ministering oxygen and drugs, including instillation of 
drugs via the endotracheal tube; and (6) stabilizing such 
patients in the postarrest period."' Like all AARC CPGs, it 
underwent extensive review before publication, but it is a 
fluid document that is periodically revised and serves as a 
stimulus for further research on resuscitation. 

Over the last three decades, practitioners have sought to 
identify the goals of cardiopulmonary resuscitation (CPR) 
in terms of survival, quality of life, and years of useful life 
following a resuscitative attempt.-' In a paper that first de- 
scribed closed-chest cardiac massage, Kouwenhoven et al 
reported a long-term survival rale of 70%. ■* Reviews of 


Rhspiratory Care • April "95 Vol 40 No 4 

Resuscitation Guidelines 

CPR during the last 30 years report a significantly lower 
survival-to-hospital discharge rate, with a limited number 
of studies addressing long-term survival after CPR.-' The 
high cost of CPR and futility of aggressive care of termi- 
nally ill patients has raised questions regarding who should 
have do-not-resuscitate (DNR) orders placed in their chart 
and how to reach that decision. The differences among 
hospitalized patients affect outcome-' and raise the issue 
of whether the results of outcome studies should be ap- 
plied broadly.''-^ 

The RACH Guideline is an attempt to improve CPR 
outcomes in hospitalized patients by fostering a high level 
of performance on resuscitation teams by respiratory care 
practitioners (RCPs). In the quest to improve outcome, the 
use of the RACH Guideline and more research should doc- 
ument not only the initial result of CPR but also identify 
longer-term success such as survival to discharge, years of 
survival, and quality of life following discharge from the 
hospital.'-' The unique contributions of RCPs in applica- 
tion of equipment and monitoring may improve long-term 
survival and the quality of life following CPR.** 

The differences in how CPR is administered in hospi- 
tals of various sizes and types need to be studied further. 
The RACH Guideline needs to be applied according to the 
level of advanced life support training of RCPs in each in- 
stitution and the ability of other resuscitation-team mem- 
bers to respond rapidly to respiratory and/or cardiac ar- 

Goals of Resuscitation 


Since closed-chest CPR was first described 34 years 
ago, it has become a commonly performed procedure in 
hospitals and has sparked the development of rapid-re- 
sponse CPR teams.* The goals of CPR have always been 
reported in terms of the patients' survival but recently 
there has been an interest in defining their long-term func- 
tional status. Many studies of in-hospital survival, includ- 
ing one review of 75 such papers describing 19,190 pa- 
tients, report that 35% were resuscitated, with survival to 
hospital discharge of 15%.- The increased interest in uti- 
lization of resources has lead to studies on long-term CPR 
outcomes. Robinson and Hess' reviewed 31 studies by uni- 
versity or Veterans Affairs (VA) hospitals and reported a 
survival to hospital discharge that ranged from 5 to 35% 
with most studies showing CPR survival to hospital dis- 
charge of 11-20%. Another review of 19,955 patients 
pooled from 98 studies of in-hospital CPR survival to hos- 
pital discharge between 1960 and 1990 found that the suc- 
cess of CPR had not changed in 30 years (15% survival to 
hospital discharge).' This study also reported that commu- 

nity hospitals had higher CPR success than teaching hospi- 
tals (19% versus 14%). However, other factors related to 
patient mix may have influenced outcomes. Urberg and 
Ways'" reported only an 11% CPR survival to hospital dis- 
charge after an in-hospital cardiac arrest in a community 
hospital but mention that patients who were living inde- 
pendently prior to hospitalization had a higher survival 
rate (19%) than homebound (3%) or nursing-home (3%) 
patients. Another report from a 600-bed community hospi- 
tal found that of 272 patients receiving CPR in 1984 only 
1 1% survived to hospital discharge." This study also com- 
pared these data with those from 129 patients admitted to 
their critical-care units in 1982 and 1983 in whom CPR 
was withheld, based on their poor response to therapy. 
There was an 1 1% survival rate for patients who had re- 
ceived CPR compared to a 16% survival rate for the DNR 
group. Kyff et al" suggested that the criteria for adminis- 
tering CPR to hospitalized patients should be improved. 

Several factors have been reported to affect CPR out- 
come (initial resuscitation, survival to hospital discharge, 
quality of life after CPR, and long-term survival). These 
factors are age (Table 1), underlying disease,'" initial car- 
diac rhythm,'-"'*"*-"-'-""-"-"-'* initial pH,'"^ speed at 
which CPR was initiated,"-' patient's location in the hos- 
pital,''''-"' time of day,'" use of DNR orders, "> witnessed 
arrests,''--" duration of CPR," living independently prior 
to hospitalization,'" initiating CPR before 4 minutes had 
elapsed,'" average end-tidal CO2 (Petco:) < 10 torr,'*''** 
serum creatinine > 220 mmol/L,*" homebound life- 
style,'"'*' increasing APACHE (Acute Physiology and 
Chronic Health Evaluation) II score," and active compres- 
sion-decompression CPR.'** '''' 

Many papers in the literature report that age is not a pre- 
dictor of CPR outcome (Table 1 ). Factors related to age such 
as being homebound or unable to live independently prior to 
admission appear to affect the survival rate more strong- 
ly. -'■■*' Most papers that report age as a predictor of survival 
have failed to control other intervening variables such as type 
of dysrhythmia,'-'*-*-" the presence of coma and shock,'*'" 
underlying disease category,'*'*-* whether the arrest was 
witnessed,-' duration of CPR,-'-" or the patient's location in 
the hospital.-' O'Keeffe et al''* reported that age was an im- 
portant independent determinant of survival after CPR and 
that ". . . the best results were obtained with witnessed arrests, 
ventricular dysrhythmias, and resuscitation lasting less than 
5 minutes: however, elderly patients were less likely to be re- 
suscitated in all circumstances." TTiese investigators did con- 
trol for severity of illness by considering the number of diag- 
noses and a multifactorial morbidity index, but they did not 
control for whether the patients were living independently 
prior to hospitalization, which Urberg and Ways'" found to 
be an important factor for survival after CPR. Schneider et 
al' found that survival to discharge after CPR was 16.2% for 

Respiratory Care • April '95 Vol 40 No 4 


Resuscitation Guidelines 

Summary of the Literature Reporting the Effect of Age on 
Survival-to-Hospital-Discharge after CPR for Adult In-Hospital 
Cardiac Arrest 

Source — First 
Author. Year 

in Study 

Survival to 
Survivors Discharge 

of Age 

Smith.'- 1965 




Survival more common 
in those < 50 years of 

Ho,'-' 1967 




Age not a factor 





Age not a factor 

Jung." 1968 




Age not a factor 

Saphir,"" 1968 




Age of 40-59 years asso- 
ciated with survival 





Age not a factor 





Middle age associated 
with survival 

Dykema." 1973 




Age not a factor 

Scott,-" 1981 




Age not a factor 

Bedell.^' 1983 




Age not a factor 

Scaff,^ 1984 




Age not a factor 





Age not a factor 

Kvale.^' 1987 




Only 7% of cohort aged 

> 75 years were alive 

I year after discharge; 
none of the patients aged 

> 85 years survived 
initial CPR. 

Rozenbaum.--' 1988 




Age not a factor 

Taffet,^ 1988 




Success related to 
age < 70 years 





Age not a factor 

Bums,-' 1989 




Age 40-70 years associ- 
ated with better outcome. 





Poorer outcome in 
patients aged > 70 years 





Age < 70 years associated 
with improved outcome. 

George." 1989 




Mortality greater in 
patients aged > 65 years 

Tonolani." 1990 




Age < 68 years associ- 
ated with survival. 

Thomas," 1990 




Age not a factor 

Peterson." 1991 




Age not a factor 





Survival to discharge 
was significantly poorer 
in patients aged > 70 

Landry." 1992 




Age not a factor 

.Schneider." 1993 19.955 


Age not a factor 
Patients aged < 70 years 
had a success rate of 
16%, and those aged 
>7() years had a 1 29f 
success rate. 





Age not a factor 





Age not a factor 

Robinson,' 1994 




Age not a factor 

patients < 70 years of age and 1 2.4% for those 70 years of 
age or older. In spite of the .statistically significant difference 
(p < 0.001 ) between age groups, Schneider identified other 
intervening factors and concluded, "The increasing pes- 
simism about the value of CPR, specifically its futility in the 
elderly patient, is not supported by this review." 

Cardiopulmonary Resuscitation (CPR) Outcomes Factors That 
Relate to Respiratory Care Practitioners' (RCPs") Perfomiance on 
Resuscitation Teams 

CPR Outcome 

Expected RCP 



Initial rhythm 

Recognizes and 

Responding RCP's must 

Witnessed airest 

defibrillates VF 
pulseless VT 


have current ACLS or 

Speed at which 

Responds to 


ELS response should be 

CPR is 

patients in 

< 3 min and ACLS < 8 min. 


arrest in < 4 

Requires adequate staffing 

Time of day 

minutes at all 
times, on all 

and that responding RCPs 
have current ACLS [raining. 

the hospital 

Duration of CPR Is capable of 
and other 
ACLS skills 

RCPs must be capable of 
serving as primary members 
of the resuscitation team and 
as team leader and be skilled 
in the use of all equipment 
and techniques for 


Is skilled in the 


RCPs must know how to 

use of all 

operate manual or automated 

equipment and 



decomprcssion dc\ ices. 

Initial pH 


RCPs must be able to inler- 

PeO). < 10 ton- 



intciprcl hlcxxj-gas values. 


vital si'jns. and level of 

existing arrest 

consciousness as signs of 
impending or existing arrest. 

•RACH. resuscitation in acule-carc hospii.iK, \( I 
pediatric advanced life support; NRP. iicpii,ii,il ir 
port: RCC emergency eardiae care; Vh, \cmi 
dia; .ACD. active compression-dcconiprfssion 

.cd CMihM \\k suppiirl; PALS. 
sii.i il.ilinii program; HI.S. hasic lil'c sup- 
1,11 rihiill.uiMii; vr. NcnlriciiUirlachvear. 

Factors reported lo affect outcomes after CPR, men- 
tioned previously, may be related to RCP performance as a 
resuscitation-team member. Bach of these outcome factors 
are opportunities for RCPs on the code team to improve the 
success of the resuscitation and are addressed in the RACH 
Guideline (Table 2). RCPs should be keenly aware of the 
initial cardiac rhythm during resuscitation because ventric- 
ukir fibrilkition ( VF) and tachyairhythmias appear to be im- 


Ri:si'iR..\r()R'»- Carl; • April '95 Voi, 40 No 4 

Resuscitation Guidelines 

I — Jt- \^ — Jl/-— V- 

Early CPR 

Very early defib. I^P^I 

Early ACLS 



I X^ Jj/ Jt- J^A j^A \^ j|^ 





Fig. 1 . Survival rates are estimates of the probability of survival to hospital discharge for patients with w/itnessed collapse and with ventricular fib- 
rillation as initial rhythm. Estimates are based on a large number of published studies. (Repnnted, with permission, from Reference 54.) 

portant determinants of CPR outcome.""''""''' They must be 
prepared to recognize VF and pulseless ventricular tachy- 
cardia (VT) quickly and treat both with defibrillation to in- 
crease the chances of restoring a spontaneous cardiac 
rhythm. A simple rationale supports defibrillation of VF as 
early as possible.'''* 

• The most frequent initial rhythm in sudden car- 
diac arrest is VF. 

• The only effective treatment for VF is electrical 

• The probability of successful defibrillation di- 
minishes rapidly over time. 

• VF tends to convert to asystole within a few min- 
utes (approximately 50% are in asystole within 4- 
8 minutes). 

High survival rates from cardiac arrest with VF can be 
achieved if the event is witnessed and treated with defibril- 
lation within minutes. In 4 studies of cardiac arrest in su- 
pervised cardiac rehabilitation programs, 90 of 101 victims 
(89%) were successfully resuscitated.-^" ■''-' A study by 
Palmisano et al^ demonstrated, with 37 simulated cardiac 
arrests, that RCPs are among the first members of code 
teams to respond (median response time 3.2 minutes). 
Based on their data, all RCPs carrying the code beeper 
should be trained as ACLS providers and retrained at fre- 
quent intervals. This level of training would allow RCPs, 
as first responders, to defibrillate patients in VF and pulse- 

less VT when they are the best trained respondents to car- 
diac-arrest calls. 

Duration of the resuscitation effort impacts CPR out- 
come — ie, shorter codes have a better record of long-term 
survival.-^' Successful defibrillation depends on the 
metabolic state of the myocardium — longer duration of VF 
leads to greater myocardial deterioration. Consequently, 
with the passing of time, defibrillation is less likely to con- 
vert VF to a spontaneous rhythm (Fig. 1 j.''"" Also, early 
intubation of the trachea immediately following defibrilla- 
tion has been identified by American Hospital Association 
Guidelines for CPR and Emergency Cardiac Care as the 
next important step." The study by RCPs at Duke 
University Medical Center has shown that a specially 
trained group of RCPs can perform emergency tracheal in- 
tubations with a 95% success rate.''' The intubation success 
of RCPs in hospitals compares favorably with that of 
paramedics in the field.''" The early placement of an endo- 
tracheal tube during CPR improves ventilation and oxy- 
genation, and provides a route for administering cardiac 
drugs when IV access cannot be established quickly.''* All 
respiratory therapy students are taught to perform tracheal 
intubation before they are allowed to graduate and many 
respiratory therapy schools require students to successfully 
complete an ACLS-provider course prior to graduation. 
Another factor to consider is that some larger respiratory 
care departments require that 2 RCPs, who are likely to be 

Respiratory Care • April '95 Vol 40 No 4 


Resuscitation Guidelines 

among the first to arrive at the scene of a cardiac arrest, carry 
code beepers. These early arriving RCPs may very well be 
the best qualified practitioners to defibrillate VF and pulse- 
less VT and to intubate the trachea. Although time-of-day 
has not been a reliable predictor of CPR success, the staffing 
of the night and weekend shifts may result in fewer qualified 
respondents arriving at resuscitations and response time may 
be longer for some members of the team. RCPs, by the na- 
ture of their responsibilities with ventilator patients who are 
monitored continuously on all shifts, are always available, 
and their participation on the code teams should help to re- 
move time-of-day as predictor of CPR success. It is impor- 
tant for directors of respiratory care departments to assure 
that all RCPs who carry the code beeper have current training 
in ACLS. 

Certain locations in the hospital, eg, operating rooms and 
cardiac catheterization laboratories, have been reported to 
have a better CPR outcome than general patient-care units. ^ 
Hospital areas that have poorer success with CPR are radiol- 
ogy and outpatient departments.^ RCPs can play a role in im- 
proving outcomes in such areas by annving at these locations 
with defibrillators, intubation and airway equipment, and 
other ACLS equipment similar to the way paramedics re- 
spond to caidiac aijests outside the hospital. The studies 
comparing active compression-decompression (ACD) CPR 
with standard techniques report improved survival when 
ACDs aie used (Fig. 2).-'*'*'' RCPs are well qualified to use 
these new devices because they routinely deal with high- 
technology equipment. The monitoring of Petco: as an indi- 
cator of adequate chest compressions has proved to be a way 
of determining when the person doing chest compressions 
needs to be relieved."*-*' RCPs are taught capnography in res- 
piratory therapy schools and have occasion as practitioners to 
monitor Peico: '" selected patients who are mechanically 
ventilated. A Petco: < 10 torr has been identified as a predic- 
tor of poor CPR outcome.'*''* RCPs have the experience and 



Fig. 2. End-tidal Pco. (Mean (SD)] of 9 resuscitated patients [15 (4)] 
and 26 nonresuscitated patients [7 (5)]. (Reprinted, with permission, 
from Reference 45.) 

training to conduct or participate in clinical research using 
capnography to evaluate ACD devices. Last, but not least, 
initial pH has been reported to affect CPR outcome.''^ 
However, successful resuscitation from severe acute hyper- 
capnia has been reported to be possible as long as tissue 
anoxia and ischemia are prevented.''- The RCP has a impor- 
tant role in assuring that patients do not slip into respiratory 
acidosis with severe hypoxemia. Experience in monitoring 
patients on mechanical ventilators and arterial-blood sam- 
pling and analysis qualifies the RCP to monitor acid-base 
balance and oxygenation during resuscitations. 

Quality of Life 

Schwenzer et al' recently reported that they found no con- 
venient categories of absolute nonsurvival or absolute futility 
and concluded: 

Physicians are under no obligation to provide, and patients 
have no right to obtain medical therapies that are futile, in- 
cluding CPR. The question remains, 'When is CPR fu- 
tile?' We conclude from our study that the outcome from 
CPR is matter of probability, not certainty, and that the de- 
cision to withhold CPR should be made in individual pa- 
tients rather than by their diagnostic classification or age; 
and recommend that patients' perceptions of their quality 
of life before and after CPR should guide their and our de- 

Quality of life can be subjectively described and still 
provide useful information about the success and appropri- 
ateness of CPR efforts. Robinson and Hess' found 24 of 83 
patients (29%) survived in-hospital CPR and were dis- 
charged. Follow-up of these 24 patients showed that 13 pa- 
tients (54%) were alive a mean of 3 1 months after hospital 
discharge, and 10 of the 13 (77%) were living indepen- 
dently. They asked continuing care physicians to choose 
from 4 levels of functioning based on their subjective 
knowledge of resuscitated patients and not on objective 
findings. The 10 patients who were living independently 
were described by primary physicians as "alive and well" 
and functioning "normally" without limitations. Two of 
these 10 returned to their pre-hospitalization employment. 
Three patients were described as having health limitations 
that did not require institutionalization — angina in two pa- 
tients and chronic renal failure in one patient. The high de- 
gree of functional status that Robinson and Hess' found in 
long-term survivors of in-hospital CPR at one community 
teaching hospital tended to be related to good health with- 
out chronic illnesses, prior to requiring CPR. 

Morris ct al''' studied the possible neurologic sequelae 
of 2.'^ children, 2 to 13 years of age. following successful 
CPR for cardiac arrest. They found that a majority of these 
children exhibited low-average to low levels of perfor- 


Ri;SI'IKAT()RY CAR!-: • Al'Rii, '9.3 VoL 40 No 4 

Resuscitation Guidelines 

mance on neuropsychologic, achievement, and adaptive 
behavior measures. Morris concluded that duration of car- 
diac arrest and medical-risk score significantly correlated 
with decreased functioning in children following cardiac 

Years of Useful Life 

Chan et al*^ reported long-term survival after hospital 
discharge following CPR due to primary VF in the acute 
phase of transmural myocardial infarction for 75 consecu- 
tive patients between October 1971 and May 1981. The 
cumulative survival rates at 1, 2, 5, and 10 years were 
84%, 77%, 67% and 40.5%, respectively, with a median 
survival time of 8.7 years. These investigators made no at- 
tempt to determine the years of useful life or to determine 
whether the survivors were living independently. Tresch 
and colleagues-"' studied CPR outcome in 196 nursing- 
home patients and found that 37 (19%) were successfully 
resuscitated and 10 (5%) survived to discharge. However, 
27% of patients who demonstrated VF at the time of arrest 
and whose arrests were witnessed survived. In contrast, 
only 2.3% of all other nursing home patients who received 
CPR survived. Most importantly, among those who sur- 
vived to hospital discharge, the functional status of the ma- 
jority (80%) of the survivors was similar to their prearrest 
status, and 40% of the survivors lived for more than 12 
months. Tresch et al concluded, "CPR should be initiated 
only in nursing-home patients whose cardiac arrest is wit- 
nessed and should be continued in patients whose initial 
documented cardiac rhythm is ventricular fibrillation or 
ventricular tachycardia." 

Age and years of useful life are interrelated — the older 
the patient, the fewer years of life remain and the greater 
likelihood that chronic illness is present. Some re- 
searchers, concerned about quality of life and the cost of 
medical care, have questioned the wisdom of resuscitation 
of the elderly. Kvale and D'Elia-' explored the role of age 
in resuscitation outcome of all patients age 75 years and 
older in a community hospital during a 1-year period. 
After retrospectively reviewing the records of 86 such pa- 
tients, they found that 41% survived the initial resuscita- 
tion effort but only 23% regained conscious functioning, 
12% left the hospital, and 7% survived to be discharged 
from the hospital and were alive 1 year later. None of the 
26 patients over the age of 85 years survived resuscitation. 
However, factors existing prior to hospitalization (such as 
living independently, being homebound, or residing in a 
nursing home) appear to be more important than age. 

CPR outcome may be dismal for patients in medical 
and surgical intensive care units where patients often have 
acute illness superimposed on chronic underlying condi- 
tions. A study by Landry et al'"' of 1 14 patients undergoing 

CPR in medical and surgical intensive care units during a 
2-year period found that of 50 patients (44%) who were 
initially successfully resuscitated, only 6 (5%) survived to 
hospital discharge. Only 1 of 29 patients with malignancy 
and 1 of 39 septic patients survived. Age, sex, and 
APACHE II scores were similar among survivors and non- 
survivors. Of the 6 survivors, 4 died within 1 year of dis- 
charge, and the other 2 survivors had severe disabilities. 
The primary underlying diseases that led to this poor CPR 
outcome was malignancy in 29 (25%), vascular disease in 
20 (18%), chronic liver disease in 8 (7%), end-stage renal 
disease in 6 (5%), chronic obstructive lung disease in 5 
(5%), and other conditions in 46 (40%) patients. 

Cost Analysis 

Ebell and Kruse'"' developed a cost model for CPR that 
includes a series of decision points, each with an associat- 
ed survival rate and cost. They report that the cost per pa- 
tient surviving increases exponentially as the rate of sur- 
vival to discharge decreases — the cost was $1 17,000 for a 
rate of survival-to-discharge of 10%, $248,271 for a rate of 
1%, and $544,521 for a rate of 0.2%. These authors sug- 
gest that health-care costs could be reduced most by de- 
creasing the length of hospital stay and charges for patients 
who survive the initial resuscitation event, by increases in 
the overall survival rate, and by stratification of hospital- 
ized patients according to their anticipated response to re- 
suscitation efforts. 

Certain unproved CPR techniques, such as the use of 
open-chest CPR (OC-CPR) in cardiac arrest of children, 
may be futile and expensive. Sheikh and Brogan*'' retro- 
spectively reviewed the records of 27 children who were 
brought to the emergency department undergoing CPR 
after blunt trauma. They found that CPR was successful 
with restoration of spontaneous circulation after closed- 
chest CPR (CC-CPR) in 17% of the children, whereas 20% 
of the children had restoration of spontaneous circulation 
after OC-CPR. Although this difference was statistically 
significant, none of these children regained consciousness 
or survived to discharge. The hospital charges for the chil- 
dren who underwent OC-CPR were significantly higher. 
Less than 30% of the hospital charges for both groups were 
reimbursed. Advocates for OC-CPR in adults claim that 
the circumstances of refractory cardiac arrest make it un- 
likely that well-controlled human studies in selected pa- 
tients can demonstrate that OC-CPR is superior to CC- 

CPR performed in patients who are unlikely to survive 
is expensive.-^''* Costs rise when physicians overestimate 
the efficacy of CPR and thus misrepresent the potential 
utility of the intervention for patients and their families. A 
survey of 451 physicians at a tertiary care hospital was 

Respiratory Care • April '95 Vol 40 No 4 


Resuscitation Guidelines 

conducted to determine the following: ( 1 ) the factors they 
consider when recommending in-hospital CPR, (2) the 
conditions under which they discuss CPR with patients, (3) 
their recent participation in CPR attempts, (4) their percep- 
tions of its effectiveness, (5) their personal wishes regard- 
ing their own resuscitation, and (6) their personal and pro- 
fessional demographic characteristics.*''* The survey results 
indicated that the physicians overestimated the likelihood 
of survival to hospital discharge after in-hospital CPR by 
as much as 300% for some clinical situations and predicted 
an overall success rate of 30%. Ebell" has found that 
groups of patients have been identified with negligible 
rates of survival to discharge following CPR. He claims 
that physicians should use such prediagnostic information 
to provide patients with good information when discussing 
consent for DNR orders. Several investigators believe that 
physicians should make a special effort to address the 
DNR status of patients falling into one of the negligible- 
survival groups identified by research on CPR out- 

Characteristics of Hospitalized Patients 
& CPR Outcome 

Disease Categories 

The disease category of hospitalized patients may effect 
CPR outcome (Table 3). Schwen.ser et al'' found that CPR 
was used more frequently in the acute disease, burn, and 
procedure-related groups. They also found a tendency to 
use CPR more with patients who had multiple medical 
problems. The procedure-related category raises the im- 
portant issue regarding suspension of DNR orders for pa- 
tients who experience cardiac arrest in the operating room 
or cardiac-catheterization laboratory. Several investigators 
have recommended suspending DNR orders during certain 
procedures because survival to hospital discharge follow- 
ing procedure-related CPR is more likely than following 
CPR in other circumstances. '■■*"■'-''■* Although children 
with congenital disease have a high-survival-to-hospital- 
discharge rate after CPR (Table 3), a number of these pa- 
tients sustain severe neurodevelopmental disabilities.'"''' 
Some patients who undergo procedures such as renal dial- 
ysis have a dismal long-term survival rate after CPR. Moss 
et al,"' after studying an 8-year experience with CPR pa- 
tients at a university dialysis program, concluded that CPR 
is a procedure that rarely results in extended survival for 
dialysis patients. He found that only 8% survived until 
hospital discharge compared to a control group with a 1 2% 
survival rate. At 6 months after CPR, 3% of 74 dialysis pa- 
tients were still alive compared with 9%' of 247 controls. 
Twenty-one (78%) of successfully resuscitated dialysis pa- 
tients died an average of 4.4 days later: 9.59! were on me- 

chanical ventilation in an intensive care unit at the time of 
their death. 

Outcome from Cardiopulmonary Resuscitation (CPR) by 
Disease Category^ 



Alive at 

Disease Category 







Multiple medical problems 




Acute disease without trauma 



41 (27.3) 





Congenital disease 



21 (50.0) 





Metastatic neoplasm 



3 (20.0) 











1 (33.3) 






Age-Related CPR Outcome 

Patients 70 years of age and older are less likely to re- 
ceive CPR than younger than 70 years.' However, a 
majority of the studies in the literature have concluded 
that, up to some limit, older patients are just as likely to 
survive to hospital discharge following CPR as younger 
patients (Table 1 ). A more important factor than advanced 
age is the number of chronic medical conditions of patients 
undergoing CPR. 

Outcomes of CPR in Children 

A study of CPR for children in pediatric intensive care 
units (PICUs) found that arrests are seldom unanticipated, 
were commonly nonrespiratory in nature, and generally 
occurred in spite of aggressive support.^' A 30-month 
study of 121 episodes of CPR in a PICU found that 48% 
were associated with at least a 24-hour survival, and 31% 
with discharge from the PICU. In this pediatric population. 
29% were noncomatose survivors 24 hours after 30 min- 
utes of resuscitation. Of 1 18 PICU deaths during the study 
period, 45 (38%) were associated with CPR. In the 73 re- 
maining PICU deaths. CPR had been withheld because of 
DNR orders. According to Von Seggern,'"' CNS status may 
be the most important prearrest factor influencing the out- 
come of pediatric CPR. Another study of 69 children 
(mean |SD| age 2.5 10.4] years), who were pulseless and 
apiieic prior to CPR and treated in the PICU following 
CPR, found that outcome was positively influenced by ( 1 ) 
CPR duration — when < 5 minutes, 54% were long-term 
survivors compared to 5% of patients resuscitated > 5 min- 
utes (p < 0.001); (2) number of epinephrine doses — 38% 
of 24 patients receiving 1 dose became long-term sur- 
vivors versus 0% of 26 receiving > 1 dose (p < 0.001 ): and 


Respiratory Carf. • April '95 Vol 40 No 4 

Resuscitation Guidelines 

(3) location of arrest — 50% of patients resuscitated in the 
operating room or cardiac-catheterization laboratory sur- 
vived to discharge compared to only 8% resuscitated in the 
PICU (p < 0.03).-*" A study of 47 pediatric patients after 
cardiopulmonary arrest found 18 (38%) were long-term 
survivors and discharged from the hospital without gross 
neurologic deficit.'* Favorable outcome was associated 
with in- vs out-of-hospital arrest; extreme bradycardia as a 
presenting factor; successful resuscitation using only ven- 
tilation, oxygen and closed-chest massage; and duration of 
CPR < 15 minutes. Another retrospective review of 42 pe- 
diatric cardiopulmonary arrests found overall that 6-month 
survival was 17%; however, only 9% of cardiac arrest pa- 
tients survived.'' Pure respiratory arrest had a markedly 
better outcome than cardiac arrest, and predictors of non- 
survival were duration of arrest > 15 minutes and the ad- 
ministration of < 1 one intravenous bolus of epinephrine. 
In a review of 96 pediatric patients who experienced car- 
diac arrest on medical and surgical units, Ludwig et al'* 
found that in 27%, airway and breathing techniques alone 
were life saving. The necessity for resuscitation was most 
commonly associated with pulmonary disease. These find- 
ings reflect the differences between pediatric CPR and 
adult CPR, and suggest limitations in applying adult stan- 
dards to infants and children. 

Davis'** retrospectively reviewed the charts of all ba- 
bies bom at the Ottawa General Hospital who weighed 
1,000 g or less at birth and were bom between June 1989 
and May 1992. There were 156 births of neonates weigh- 
ing less than 1,000 g during this 3-year period. Fifteen of 
25 neonates who weighed less than 500 g did not have ac- 
tive intervention at birth. Only 4 neonates who weighed 
501 to 750 g did not have active intervention in the deliv- 
ery room, including 2 neonates (525 g and 588 g) in whom 
intubation was attempted but impossible because of airway 
size. Another was a 510 g second-born twin of a mother 
with spinal muscular atrophy; this newborn showed even 
less vigor at birth than his larger brother who had failed to 
respond to 30 minutes of resuscitation. The final neonate 
of this nonintervention group had a known severe thora- 
columbar myelomeningocele and a "no resuscitation" de- 
cision had been made before birth. Resuscitation was at- 
tempted in 10 neonates who weighed 500 g or less. Eight 
of these received only intubation and ventilation in the de- 
livery room, 1 of these did not respond and died at 2 hours 
of age, while the other 7 survived for varying lengths of 
time (23 hours to 8 months). The remaining 2 of the 10 re- 
ceived cardiac compressions, epinephrine, and bicarbon- 
ate, and both died when resuscitative efforts were discon- 
tinued. Babies bom weighing 500 g or less at birth, who 
were actively resuscitated, had a neonatal survival rate (to 
28 days) of 10% and a survival-to-discharge rate of 0%. 

Twenty-five of 58 neonates with birth weights of 501 - 
750 g survived to discharge. Characteristics associated 
with failure to survive to discharge were no response to in- 
tubation and ventilation, the need for cardiac compres- 
sions, and administration of at least one dose of 
epinephrine (Fig. 3). Resuscitation was attempted in 69 in- 
fants who weighted 751-1,000 g at birth (Fig. 4). All 10 
who did not require intubation in the delivery room sur- 
vived. Babies that only required intubation and ventilation 
had a survival-to-discharge rate of 88%. Three neonates in 
this weight group who received cardiac compressions (but 
did not require epinephrine) all survived to discharge. Four 
of the 7 who received epinephrine survived to discharge. 
Overall survival-to-discharge rates for babies in whom re- 
suscitation was attempted were 43% for babies weighing 
501-750 g and 86% for those weighing 751-1,000 g. 

62 Babies with Birthweight 501-750 g 



AirwayA/ent Plus Plus Meds 

n = 50 Compressions n = 6 

I n = 2 

No Response Response 
n = 6 n = 44 

Survival to Discharge 

Fig. 3. Decision/outcome pathways for liveborn babies who weighed 
501 to 750 g at birth. "Airway/venf indicates that the neonate was in- 
tubated and ventilated as necessary. "No response" indicates that re- 
suscitative efforts were discontinued after the neonate failed to re- 
spond to intubation and ventilation alone. "Meds" indicates that the 
neonate received at least one dose of epinephrine. (Reprinted, with 
permission, from Reference 79.) 

Davis" also examined Apgar scores of the low-birth- 
weight neonates to determine whether they were reliable 
measures of to resuscitative efforts (Table 4). A 
5-minute Apgar score of < 5 was associated with a signifi- 
cantly poorer outcome in babies that weighted 501-750 g 
at birth. Those neonates with 5-minute Apgar scores of > 6 
had a 75% survival-to-discharge rate. In neonates weigh- 
ing 751-1 ,000 g, a 5-minute Apgar score of < 5 was associ- 
ated with a 63% survival-to-discharge rate. 

Respiratory Care • April '95 Vol 40 No 4 


Resuscitation Guidelines 

62 Babies with Birthweight 751-1 ,000 g 


and updating. The RACH Guideline is intended to provide a 
broad context within which specific departmental proce- 
dures, policies, and protocols can be developed*"' and should 
be instrumental in improving the level of respiratory care ad- 
ministered during CPR. 

Initial AirwayA/ent Plus Plus 

Steps n = 49 Compressions Meds 

n=10 n = 3 n = 7 


to n = 10 


Fig. 4. Decision/outcome pathways for liveborn babies who weighed 
751 to 1,000 g at birth. "Initial Steps" indicates that the neonate re- 
quired only drying, warming, suctioning, and/or free-flow oxygen for 
resuscitation. "Ainway/vent' indicates that the neonate was intubated 
and ventilated as necessary. "Meds" indicates that the neonate re- 
ceived at least one dose of epinephrine. {Reprinted, with permission, 
from Reference 79.) 

Guidelines for Resuscitation in 
Acute Care Hospitals 


The AARC published the RACH Guideline in November 
1993.' When the first CPG was published in 1991, it was de- 
scribed as: "... a systematically developed statement to help 
the practitioner deliver appropriate respiratory care in specif- 
ic clinical circumstances."**" The initial draft of the RACH 
Guideline was developed by the CPR Focus Group, re- 
viewed by consultants, the Clinical Practice Steering 
Committee, and 650 practitioners and finally published in 
Respiratory Care. Although guidelines are extensively 
reviewed prior to publication, they require periodic revision 

Table 4. Survival in Relation to .S-Minule Apgar Score 

Binh Weight 
Apgar Score 

n/N (%) 

501 -750 g 

Apgar 6-10 

24«2 (75) 

Apgar 4-5 

1/5 (20) 

Apgar 0-.^ 

0/21 (0) 


Apgar 6- 10 

48/51 (94) 

Apgar 4-5 

9/11 (82) 

Apgar 0-3 

3/8 (38) 

Reprinted, with permission from Reference 79. 

Differences between AARC and AHA 
Resuscitation Guidelines 

The AARC RACH Guideline is not a treatment proto- 
col, does not spell out institution procedures, and, conse- 
quently, does not include treatment algorithms.*" The AHA 
Guidelines For CPR and ECC use 10 algorithms and are 
designed to be educational tools.''' They illustrate and sum- 
marize information and serve as a memory aid (Fig. 5). 
The algorithms are designed to be used to treat a broad 
range of patients and are, by nature, oversimplified. 
Accordingly, the AHA Emergency Cardiac Care Com- 
mittee suggests that they be used wisely, viz, with flexibil- 
ity when clinically appropriate.'''* Several clinical recom- 
mendations from the AHA Guidelines apply to most treat- 
ment algorithms.'* 

• First, treat the patient not the monitor. 

• Algorithms for cardiac arrest presume that the 
condition under discussion continually persists, 
that the patient remains in cardiac arrest, and that 
CPR is always performed. 

• Apply different interventions whenever appropri- 
ate indications exist. 

• The flow diagrams present mostly Class I (ac- 
ceptable, definitely effective) recommendations. 
The footnotes present Class Ila (acceptable, prob- 
ably effective). Class lib (acceptable, possible ef- 
fective), and Class III (not indicated, may be 
harmful) recommendations. 

• Adequate airway management, ventilation, oxy- 
genation, chest compressions, and defibrillation 
are more important than administration of medi- 
cations and take precedence over initiating an in- 
travenous line or injecting pharmacologic agents. 

• Several medications (epinephrine, lidocaine, and 
atropine) can be administered via an endotracheal 
tube, but clinicians must use 2 to 2.5 times the in- 
travenous dose. 

• With a few exceptions, intravenous medications 
should be rapidly administrated by bolus. 

• After each intravenous medication, give a 20- to 
30-mL bolus of intravenous fluid and immediate- 
ly elevate the extremity. This will enhance the de- 
livery of the drug bolus to the central circulation: 
may take 1-2 minutes. 

• Last, treat the patient not the monitor. 


Ri;Sl'!RA TORY Carh • APRIL "95 VOL 40 No 4 

Resuscitation Guidelines 


•Perform CPR until defibrillator attacheda 

'VFWT present on defibrillator 


Deflbrillate up to 3 times if needed for 
persistent VFA/T (200 J, 200-300 J, 360 J) 


Rhythm after the first 3 shocl<s?b 

Persistent or 

Return of 



Go to Fig. 3 

Go to Fig. 4 

•Continue CPR 
•Intubate at once 
•Obtain I.V. access 

•Epinephrine 1 mg 
I.V. pushc.d repeat 
every 3-5 nnin 

•Assess vital signs 
•Support alrviiay 
•Support breathing 
•Provide medications 
appropriate for blood 
pressure, heart rate, 
and rhythm 

•Deflbrillate 360 J 
within 30-60 se 

•Administer medi- 
cations of probable 
benefit (Class lla) 
In persistant or 
recurrent VFA/Tf.g 

•Deflbrillate 360 J, 
30-60 s after each 
dose of medicatione 

'Pattern should be 
drug-shocl<, drug- 

Class I Delinilely helplul Class lib acceptable, 

possibly helplul 
Class lla acceptable, probably Class III not indicated, may 
helplul be harmlul 

a Precordial thump is a Class lib action in witnessed arrest. 

no pulse, and no delibrillator immediately available 
b Hypothermic cardiac arrest is treated diherenlly after this 

point See hypothermia algonlhm 
c The recommended dose of epinephrine is Img IV push 
every 3-5 mm II this approach fails, several Class lib 
dosing regimens can be considered 
•Intemiediate epinephnne 2-5 mg IV push, every 3-5 mm 
•Escalalmg epinephrine 1 mg-3mg-5mg IV push, 3 mm 

•High epinephrine 1 mg/kg IV push, every 3-5 mm 
d Sodium bicarbonate ImEq/kg is Class I it patient has 

known preexisting hyperkalemia 
e f^ultipie sequeced shocks are acceptable here (Class I}, 

especially when medications are delayed 
( f^edication sequence 

•Lidocame 1 0-1 5 mg/kg IV push Consider repeat m 3-5 
min to maximum dose of 3 mg^g A single dose of 1 5 
mg/kg in cardiac arrest is acceptable 
■Bretylium 5 mg/kg IV push Repeal in 5 mm al 10 mg/kg 
•Magnesium sulfate 1 -2 g IV in torsades de poinles or 
suspected hypomagnesemic state or refractory VF 
•Procainamide 30 mg/min in refractory VF (maximum total 

g Sodium bicarbonate 1 mEq/kg IV 
Class lla 

•If known preexislmg bicarbonate-responsive acidosis 
•If overdose with tricyclic antidepressants 
•To alkalinize the unne in drug overdoses 
Class lib 

•If intubated and continued long arrest interval 
•Upon return of spontaneous circulation alter long arrest 
Class III 
•Hypoxic lactic acidosis 

Fig. 5. Ventricular fibrillation/pulseless ventricular tachycardia 
(VFA/T) algorithm. ABC, ainway, breathing, circulation; CPR, car- 
diopulmonary resuscitation; PEA, pulseless electrical activity; Fig. 3 
refers to an algorithm for PEA and Fig. 4 refers to an algorithm tor 
asystole. (Rephnted. with permission, from Reference 54.) 

The RACH Guideline addresses the role of all creden- 
tialed practitioners on hospital resuscitation teams and de- 
fines them as Level I and Level II personnel according to 
responsibility and the training required for those respond- 
ing to the scene of the arrest. It also delineates specific 
standards for equipment resources such as ventilation, air- 

way management, and circulation devices; and the proper 
application of monitoring and electrical therapy devices. 

The current AHA Guideline was revised based on the 
fifth national conference on CPR and ECC, which was 
convened in February, 1992. The objectives were to "(1) to 
review and revise past conference recommendations in 
light of recent scientific and clinical data; (2) provide rec- 
ommendations for all CPR-ECC programs; (3) review and 
recommend changes in methods of education and evalua- 
tion; (4) provide guidelines for evaluating the efficacy of 
CPR-ECC programs, including their effectiveness in 
reaching and teaching the target populations; and (5) pro- 
viding ethical guidelines for withholding or withdrawing 
CPR or ACLS in appropriate circumstances."*" 

AHA and AARC Guidelines are both based on scientif- 
ic evidence. The AARC reviewed reports in the literature 
only from primary sources. The AHA also used primary 
sources and identified criteria for evaluating scientific data 
such as study design and method, source of the study, 
ethics of the study, and the feasibility of the proposed rec- 
ommendation.*^' The AHA developed a new system for 
classifying recommendations based on the strength of the 
supporting scientific evidence (shown in the paper by 
Aruthur B Sanders'*- also in this issue). 

RACH Guideline is an evolving document, limited in 
length and content to follow the AARC CPG format and is 
not intended to be used extensively as a specific training 
tool in the same way as the AHA CPR/ECC Guideline. 
The RACH Guideline is written specifically for inhospital 
resuscitation of sick people with health-care providers 
nearby. The AHA Guideline with algorithms and illustra- 
tions is designed to serve as a cornerstone for development 
of provider and instructor courses and training manuals for 
Basic Life Support (BLS), ACLS. Pediatric Advanced Life 
Support (PALS), and Neonatal Resuscitation Program 

Application of RACH Guideline by RCPs 

The RACH Guideline is profession-oriented document 
that speaks directly to the cunent role of RCPs and what it 
might be in the future with appropriate training. There are 
some critical recommendations that should be implement- 
ed immediately and others that deserve serious considera- 
tion for development in the near future. Particularly impor- 
tant is the training, evaluation by performance, and retrain- 
ing of Level I personnel in BLS and Level II personnel in 
ECC and ACLS or PALS and NRP as appropriate at < 1- 
year intervals.' ■*' A study by Batenhorst et al*^ evaluated 
516 CPR attempts and found no correlation between time 
of day and arrest incidence. Based on these data, I believe 
that 24-hour staffing for resuscitation teams is critical. 
Adequate staffing of resuscitation teams means that respi- 

Respiratory Care • April "95 Vol 40 No 4 


Resuscitation Guidelines 

ratory care departments should have a Level II RCP avail- 
able continuously (24 hours/day, 7 days/week) to respond 
to emergencies. It is my opinion that RCPs should assume 
5 critical tasks when they are the best trained responders at 
the scene: 

• emergency airway management — manual venti- 
lation, oxygen administration, and tracheal intu- 

• defibrillation of VF or pulseless VT with manual 
or semiautomatic defibrillators; 

• chest compressions; 

• tracheal instillation of cardiac drugs (ie, epi- 
nephrine, lidocaine, and atropine) if vascular ac- 
cess is not established; and 

• arterial blood gas and pH determinations. 

ACLS or PALS training can improve performance on re- 
suscitation teams and prepare RCPs to assume the tasks list- 
ed above. ^■' The evidence that early defibrillation to reverse 
ventricular fibrillation ( VF) and pulseless ventricular tachy- 
cardia (VT) improves outcome has resulted in an American 
Heart Association recommendation that three consecutive 
countershocks without CPR be delivered at the beginning of 
resuscitation before other measures are undertaken.'** The 
next critical step in the VF-pulseless VT algorithm is endo- 
tracheal intubation. The need for these critical early inter- 
ventions, underscores the utility of cross training the resus- 
citation-team members through ACLS courses. RCPs with 
current ACLS provider cards have demonstrated appropri- 
ate techniques for VFA'T defibrillation, advanced airway 
management, emergency tracheal intubation, and tracheal 
instillation of cardiac drugs. The study by Palmisano et a^ 
reports that RCPs in his facility had a median response time 
(from activation of simulated cardiac arrests) of 3.2 minutes; 
yet, endotracheal intubation was not accomplished until 6.0 
minutes had passed. Thalman and co-workers'"'' from the 
Respiratory Care Department at Duke University Medical 
center have demonstrated that RCPs can pertorm emergen- 
cy endotracheal intubations with a success rate comparable 
to that of paramedics. The AARC RACH Guideline lists en- 
dotracheal intubation and many other advanced tasks as the 
responsibilities of Level II personnel (RRTs, MDs, RNs). 

Caring for critically ill patients is part of the daily respon- 
sibility of RCPs who continuously monitor patienls who are 
mechanically ventilated. Failure to conect initial pH < 7.2 
by the time the second blood gas is drawn has been associat- 
ed with poor CPR outcome."' These patients are also con- 
nected to invasive and noninvasive monitoring devices, and 
the RCP is often the first to be called to setup, adjust, or in- 
terpret the data from these monitors. Capnography is con- 
sidered by some practitioners to be a valuable tool in the 
management of cardiac arrest, because PdCO: correlates well 
with cardiac output anti there are no other suitable noninva- 

sive ways to measure this important variable during resusci- 
tation.'*''"' An initial Petco: of ^ '5 torr has been reported to 
correctly predict eventual return of a pulse^' and, in another 
study, Peico: ^ 10 torr was associated with survival.''^ 
Improved ventilatory management with improved Pao^ and 
optimization of Paco: has been reported to improve out- 
come of CPR.**' Accordingly, the RACH Guideline ac- 
knowledges this expertise by including in the list of RCP 
Level I and II responsibilities the following monitoring re- 

• attaching ECG and automatic defibrillator elec- 

• attaching pulse oximeter and capnograph; 

• collecting arterial blood for analysis; 

• perfomiing advanced ECG monitoring and dys- 
rhythmia recognition; 

• interpretation of hemodynamic data; and 

• evaluation of oxygenation, ventilation, and acid- 
base balance. 

The RACH Guideline describes some skills for which 
many RCPs, responding to resuscitations, have limited re- 
sponsibility and training. RCPs must develop these skills 
and special training programs are offered by the AARC and 
its affiliates on the use of defibrillators, preparation and ad- 
ministration of caidiac drugs, and vascular access for early 
fiuid administration. However, the best way to receive train- 
ing in these skills may be through ACLS or PALS courses, a 
graduation requirement for students in many respiratory 
care programs. 

The AARC CPGs do not mandate staffing or salary lev- 
els, but hospitals both large and small need to review the 
RACH Guideline to deterinine what level of personnel 
they can send to resuscitations. Some respiratory care de- 
partments have set goals that require all staff members to 
maintain cuirent documentation of ACLS or PALS course 
completion. When it is not possible to train every practi- 
tioner in a department in ACLS, some respiratory care de- 
partments have required that the staff who respond to car- 
diac arrests retrain periodically in ACLS and/or PALS. In 
some instances, monetary inducements are paid to those 
individuals who document maintenance of resuscitation 

The large number of nurses, house officers, RCPs, and 
others who typically respond to resuscitations in large hos- 
pitals is not always desirable. A study by Sullivan et al'*-' 
used simulated cardiac arrests to monitor quality of in-hos- 
pilal resuscitations in a 6()0-bed academic hospital with a 
full complement of junior and senior house staff on all 
major services except pediatrics. More than half of the 
house staff had completed the university's ACLS training 
program. Sullivan reports thai the exercise revealed many 
unsuspected deficiencies:'*'' 


Ri si'iRA KiRV Cari; • April '95 Vol 40 No 4 

Resuscitation Guidelines 

Nurses did not apply mouth-to-mask breathing, use the 
defibrillator, or give supplementary oxygen while awaiting 
the arrival of the resuscitation team; the availability of dif- 
ferent models of defibrillators led to confusion and delay in 
defibrillation; and suction equipment generated inadequate 
vacuum pressure to evacuate aspirated material from an air- 
way. The first minutes of the resuscitation teams arrival 
were often chaotic as members tried to sort out who was 
going to take charge. There were seven different models of 
defibrillators in the hospital. In several instances the team 
members were unable to operate the synchronization mode 
of the defibrillator. 

Sullivan concluded that a quality application of the AHA 
Guidelines for CPR and ECC could not be assumed but re- 
quired an evaluation of performance to expose and correct 
the deficiencies. 

Application of Guidelines in Community Hospitals 

The RACH Guideline should be adopted by respiratory 
care departments of not only large urban teaching hospitals 
but also by those in smaller hospitals. A study of five small 
community hospitals by Birnbaum et al**^ attempted to de- 
fine the effectiveness of training personnel in ACLS and 
the changes that result in the process and quality of care to 
patients with ischemic heart disease that can be attributed 
to team members" participation in an ACLS course. 
Training in ACLS was accomplished for physicians, nurs- 
es and respiratory therapists using twelve 3-hr sessions in 
an interdisciplinary format and taught by a multidisci- 
plinary faculty. Successful completion of the course was 
accomplished by 58 of 69 physicians (84%), 197 of 250 
registered nurses (79%), and 6 of 9 respiratory therapists 
(67%). No statistically significant deterioration in didactic 
knowledge base could be detected during randomized skill 
checks over a period of 1 to 2 years after completion of the 
ACLS course. Slight deterioration in intubation and defib- 
rillation skills occurred in < 3 months after completion of 
the course. After ACLS training had been given, overall 
mortality rate decreased from 17.4% to 13.4% (p < 0.05). 
Birnbaum concluded that ACLS training in the community 
hospital favorably affects the survival rate of patients with 
ischemic heart disease.*^ Small hospitals are similar to 
large hospitals in that they have an ongoing need for RCPs 
to response to patients in cardiac arrest. They are more 
likely to have a smaller number of RCPs on duty at any 
given time, and there is a greater likelihood that fewer 
physicians and registered nunses will respond to resuscita- 
tions. Therefore, the RCP, responding to a resuscitation, is 
more likely to have to serve as team leader, defibrillate VF 
or VT, and intubate the trachea during the critical first 5 
minutes following cardiopulmonary anest. This level of 
responsibility requires that practitioners have ACLS train- 

ing that is usually only found in AHA courses where per- 
formance on mega-code stations demands leadership skills 
and detailed knowledge of ACLS treatment algorithms. 


The development of the AHA Guidelines for CPR and 
ECC and the AARC RACH Clinical Practice Guideline 
should both be instrumental in improving the performance 
of RCPs on in-hospital resuscitation teams. The AARC 
and AHA are assuming important leadership roles in this 
movement by publishing CPGs for CPR and ECC. RCPs 
with ACLS training are in a prime position to assume more 
responsibility on resuscitation teams within acute care fa- 
cilities. They should be prominent members of the resusci- 
tation team — committed to the entire team's perfor- 
mance — and be actively involved in ACLS training. The 
first step in that process is to study the current levels of 
RCP competence in ACLS. Further, RCPs and health-care 
providers should define the goals of resuscitation in terms 
of long-term survival, quality of life, and years of useful 
life after CPR. The cost of inadequate attention to which 
patients should have DNR orders is a drain on the entire 
health-care system. Research on the impact of disease cat- 
egories on CPR outcome should be used to educate physi- 
cians, nurses, and RCPs so they can help patients better un- 
derstand their chances of regaining their pre-CPR quality 
of life. Successful CPR outcome should be carefully de- 
fined using the patient's disease category. Each patient 
should be individually evaluated for DNR orders. As sug- 
gested by Schwenzer,'' "Patients' perception of their quali- 
ty of life before and after CPR should guide their and our 
decisions." However, we must all accept the responsibility 
for defining the limitations of medical technology and try 
to determine when CPR is futile. 


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Barnes Discussion 

Aufderheide: There are a number of 
analogies in emergency medicine tiiat 

support respiratory therapists intubat- 
ing and defibrillating. One analogy is 
the well-accepted concept of early 
defibrillation for first responders. 

Who defibrillates is less important to 
patient outcome than how quickly ap- 
propriate therapy is administered. 
And there's a second analogy — emer- 

Respiratory Care • April '95 Vol 40 No 4 


Barnes Discussion 

gency physicians in some institutions 
(because of administrative barriers) are 
not allowed to administer thrombol- 
ytics to patients with acute myocar- 
dial infarction who are straightfor- 
ward candidates and accurately diag- 
nosed. The National Heart Attack Alert 
Program has now issued a consensus 
opinion essentially stating that the 
first competent physician who accu- 
rately makes the diagnosis should be 
the person who initiates treatment.' 
Again, who intervenes is less impor- 
tant to patient outcome than how 
quickly appropriate therapy is admin- 

1. National Heart Attack Alert Program 
Coordinating Committee 60-Minutes- 
To-Treatment Working Group. Emer- 
gency Department: Rapid identification 
and treatment of patients with acute 
myocardial infarction. U.S. Department 
of Health and Human Services, NIH 
Publication No. 93-3278, September 
1993: 20. 

Mathews: I have two quick things, 
Tom. One is your idea of carrying the 
code box around. Houston Anderson 
has been doing that with his folks 
down at Duke for years, and I think 
they have a lot of data there.' My un- 
derstanding is that that's been an ex- 
tremely productive program and pro- 
vided the impetus for their intubation 
team. They assign a code box, which 
includes intubation materials and 
bag-mask-valve combinations, to the 
lead therapist. The lead therapist car- 
ries this box on rounds. 

I . Thalman JJ. Rinaldo-Callo S. Madntyrc 
NR. Analysis of an endotracheal intuba- 
tion service provided by respiratory care 
practitioners. RespirCare 19'J3;3X(.5):469- 


Barnes: It's pretty obvious to mc that 
the person carrying the code beeper 
should be an ACL.S provider and re- 
trained on a regular basis. But when 
we asked the AARC to come otii with 
a national position statcttient on this. 

the questions of cost arose. Can de- 
partments afford to have people car- 
rying code beepers trained in ACLS? 
Can they take the time away from 
their normal assignments, and if they 
have to send them to outside courses, 
can they pay the registration fees? 

Mathews: I think a better question is: 
Can the patients afford not to have 
that done? 

Barnes: I think that's true. There are 
places like the Mayo Clinic where 
they pay a differential as an incentive 
to the ACLS provider to carry the 
code beeper. 

Mathews: The second thing I want 
to address is. Are there data on sur- 
vival rates in medical centers with 
house staff versus medical centers 
without house staff and the implica- 
tions of that? 

Barnes: Interestingly enough, the 
community hospitals have a better 
survival rate than the teaching hospi- 

1. Bimbaum Ml.. Kuska BM. Stone HL. 
Robinson NE. Need for advanced car- 
diac life support training in rural, com- 
munity hospitals, Crit Care Med 1994; 

Mathews: I think that's an important 
thing to stress. 

Barnes: You have to be careful in 
making broad sweeping statements 
because the patient population has a 
lot to do with what the survival rate 
is. If you have a lot of people admit- 
ted to your institution from nursing 
homes who are not living indepen- 
dently, you're not going to have a 
very good survival rate. 

Ilamill: Two things. One wotikl be 
the comment about the community 
hospital versus private hospital. 1 siis 
pcct that the acuity is higher in (he 
university hospitals, and I think thai 

private hospitals and community hos- 
pitals, are probably better at address- 
ing code status proactively. Both of 
these may alter outcome. The other 
comment that I would like to make is 
regarding the Schwenzer study.' I 
think the beauty of that study is that 
the author really did identify patient 
groups that were likely to respond 
well to CPR and identified some 
groups that were not likely to re- 
spond. The original intent of the de- 
velopment of CPR by Jude et al- was 
to treat cardiac arrest in the face of 
acute problems and procedure-related 
events. These were the groups that 
Schwenzer et al found had the best 
outcome after CPR.' 

1. Schuenzer KJ. Smith WT. Durbin CO 
Jr. Selective application of cadiopul- 
monary resuscitation improves survival 
rates. Anesth Analg 1993;76(3):478- 

2. Judc J. Kouwenhoven W. Knicker- 
bocker G. Cardiac arrest: report of ap- 
plication of external cardiac mas.sage 
on 118 patienLs. JAMA 1961:178:1063- 

Barnes: I think the whole question 
comes down to if you have a low sur- 
vival rate in a certain disease category, 
do you automatically not resuscitate 
someone in that category? What I got 
from Schwenzer' s study was that you 
really shouldn't do that. You should 
deal with each patient as an individual. 
A lower proportion of people in that 
category may be resuscitated, but you 
don't close the door completely on cer- 
tain disease categories. 

Hamill: 1 would like to suggest that we 
need to take patients who are in high- 
risk groups or patients who would have 
a low probability of survival and, per- 
haps, offer those people informed con- 
sent for the process proactively and let 
them make their own decisions — as 
well as factoring in the multiple pre- 
cliclive factors such as disease process 
ami inevious life style. 


Ri:si'iKA lOK'i' Cari: • April "94 Vol .^9 No 4 

Barnes Discussion 

Barnes: The only problem with that 
is. Can the medical economy support 
the decision of letting a patient decide 
that he's going to be resuscitated 
when he has such a low probability of 
surviving to discharge and living in- 
dependently afterwards? Can the 
medical system afford that? 

Hamill: My personal experience is that 
when you seek informed consent from 
patients who have a low likelihood of 
surviving, the majority of them choose 
not to be resuscitated in the event of an 
arrest. I think we just don't ask often 
enough. Part of that is giving them the 
reality of the process and the outcome 
numbers. Most people, particularly 
when they're older, are going to tend to 
choose not to have it. 

Rubenfeld: You present a lot of inter- 
esting information. I just want to make 
one comment that's already been 
made, and I know Robin (Hamill) is 
going to deal with this on Saturday. 
Dealing broadly with these outcome 
studies about CPR, one has to be very 
cautious. The definitions of what con- 
stitutes CPR in the different studies 
frequently changes, whether they in- 
cluded ER resuscitations or sometimes 
ongoing resuscitation on patients as 
they came into the ER. I know these 
were all considered in your slides, but 
I just wanted to restress this point. 
This is perhaps the most important se- 
lection bias that occurs in the do not 
resusciate (DNR) issue. When you 
eliminate patients who are going to 
have particularly poor outcomes after 
CPR, your outcomes for CPR may 
look very good. There are good data to 
support that there is considerable vari- 
ation in the proportion of patients in 
various hospitals and various intensive 
care units who have DNR orders.' 
You have to be very careful about 
using broad interpretations of CPR 
outcome issues. 

I . Jayes RL, Zimmerman JE. Wagner DP. 
Draper EA, Knaus WA. Do-not-resus- 

citate orders in intensive care units: 
current practices and recent changes. 
JAMA 1993;270(18):2213-2217. 

Barnes: One of the things I noticed 
about the study done at the University 
of Virginia at Charlottesville' was 
that they had a high initial success 
rate for resuscitation and also sur- 
vival to discharge was good. I think 
it's because they have a well-devel- 
oped advanced DNR review and ad- 
vanced prerogative review. 

1. Schwenzer KJ, Smith WT. Durbin CG 
Jr. Selective apphcation of cadiopul- 
monary resuscitation improves survival 
rates. Anesth Analg 1993;76C3):478- 

Halperin: I would like to relate some 
data from our hospital's cardiac arrest 
team.' We looked at 550 patients over 
the last 4 or 5 years. The dichotomy be- 
tween chronically ill patients and those 
who were not chronically ill may have 
been a little bigger than at some other 
institutions because in witnessed ar- 
rests in patients who didn't have chron- 
ic illness, the survival to hospital dis- 
charge was 20-25%. However, if you 
looked at patients who had chronic 
renal failure, chronic liver failure, pa- 
tients in the ICU who had end-stage 
disease, the survival was actually less 
than 1%. Two thirds of the patients 
were in those latter categories and 
about one third of the patients were in 
the former category. It would make the 
cost-benefit analysis enormously dif- 
ferent because a lot of those chronical- 
ly ill patients ran up extraordinarily 
large hospital bills before they died. So, 
there's a move at our institution to use 
those kinds of data, in order to more 
agressively implement DNR orders. 

1. Thieman D, Bass E. Powe N, Halperin 
H, Steinberg E. Pre-arrest comorbidity, 
outcome, and cost in inpatient CPR. 
Circulation 1994;96(4, Part II):I-250. 

Sanders: I just wanted to comment 
about the issue of futility, which I 
think will be addressed in other pre- 

sentations but is so important. In my 
opinion, making the decision that re- 
suscitation of a patient in cardiac ar- 
rest is futile, without the patient's 
having provided an advance directive, 
is fraught with danger. Tremendous in- 
dividual biases exist. I agree com- 
pletely with your analysis of age and 
resuscitation outcome from cardiac 
arrest. In my review of the topic, age 
is not as important a factor as others 
such as comorbid diseases.'"' Even in 
the medical literature, the language 
itself suggests bias against older per- 
sons. An editorial in the Annals of In- 
ternal Medicine was entitled, "Resus- 
citation in the Elderly: A blessing or a 
curse?"'' Another article asks, "Should 
the elderly be resuscitated following 
out of hospital cardiac arrest?"' 
Again, these individual biases may be 
transmitted to other vulnerable popu- 
lations. Should AIDS patients be re- 
suscitated? We must be careful that 
individual biases do not influence 
discussions regarding futility. Futility 
needs to undergo a real consensus 
process and standardization through a 
societal network. We must all agree 
that the clinical studies provide 
definitive evidence that it is futile to 
resuscitate a patient with a specific 
condition. I think that, in light of pre- 
sent knowledge, making these deci- 
sions on an individual patient basis is 
just fraught with danger. 

1. Van Hoeyweghen RJ, Bossaert LL, 
MuUie A, Martens P, Delooz HH, 
Buylaert WA, et al. Survival after out- 
of-hospital cardiac arrest in elderly pa- 
tients. Ann Emerg Med 1992;21:1 179- 

2. Longstreth WT, Cobb LA, Fahrenbruch 
CE. Copass MK. Does age affect out- 
comes of out-of-hospital cardiopul- 
monary resuscitation?(editoriall JAMA 

3. Bedell SE, Delbanco TL. Cook EF. 
Epstein FH. Survival after cardiopul- 
monary resuscitation in the hospital. N 
Engl J Med 1983:309:569-576. 

4. Podrid PJ. Resuscitation in the elderly: 
a blessing or a curse? (editorial) Ann 
Intern Med 1989:111(31:119-195. 

5. Tresch DD, Thakur RK. Hoffman RG, 

Respiratory Care • April '94 'Vol 39 No 4 


Barnes Discussion 

Olson D. Brooks HL: Should the elder- 
ly be resuscitated following out-of- 
hospital cardiac arrest? Am J Med 

Barnes: I think that you have to 
make sure that the individual coun- 
seling is done by a physician who re- 
ally understands the probability of 
survival after resuscitation. If he sits 
down with a renal dialysis patient and 
tells that patient that he has a 15% 
chance of survival, then the patient's 
choice may be a lot different than if 
he were given the correct informa- 
tion. So, it's really important for 
physicians to know the biases in these 
studies and to understand the actual 
probability data very well. It's not 
easily done, because some studies re- 
strict different groups from the data. 
They keep cardiac-care-unit patients 
from the cohort and tailor the studies 
for a particular interest in their facili- 
ty. If you just lump all the studies to- 
gether, it's a big mistake. 

Bishop: In terms of the futility ques- 
tion I would like to describe two 
cases in which I was involved, either 
as chair of our Code-99 committee or 
as the physician, and point out that 
there may be substantial costs for in- 
appropriate CPR. I think there are 
some patients for whom it clearly is 
futile and not medically appropriate 
to proceed. One patient had terminal 
liver disease with repeated hemateme- 
sis from varices and whose blood was 
positive for several viral vectors. 
Despite the family's wishes that we 
do everything, it just didn't seem 
practical. There was no way we were 
going to successfully resuscitate this 
guy when his inevitable demise 
came. I instructed the physician who 
was on call each night to terminate 
any CPR, as soon as he got there. 
The second case was a patient who 
was flown by helicopter to us, a 1 (S- 
year-old girl with meningococccrtiia 
and Die (disseminated intravascular 

coagulation). She underwent a 45- 
minute attempt at resuscitation while 
bleeding out of every orifice, and 
clearly, there was no question that it 
wasn't going to be successful. As a 
result, we had many providers ex- 
posed to meningococcus. In both 
cases there was real hazard to the 
staff; it was clearly a futile situation, 
and I think the appropriate thing 
would have been not to initiate CPR. 
So, I'll throw that in as a bit of a chal- 
lenge to what Art (Sanders) just said. 

Fluck: Just to change the direction a 
little bit, Tom, you mentioned that 
therapists should be involved in mon- 
itoring patients on mechanical venti- 
lation before the arrest and also after 
the arrest. What about during the ar- 
rest? Because the Heart Association 
suggests that, in somebody who's in- 
tubated, ventilation can be asyn- 
chronous with compressions and be- 
cause the ventilator measures the oxygen 
concentration, exhaled tidal volume, and 
airway pressures, wouldn't that be use- 
ful also? 

Barnes: Yes, I think that needs to be 
looked at a little closer. You can al- 
ways manually trigger a ventilator. 
Certainly you're going to control the 
tidal volume and oxygen concentra- 
tion more accurately if you use a ven- 
tilator in that way. I'm not convinced 
that if you do a chest compression on 
top of ventilation, you're really going 
to cause that much harm. I think you're 

Pepe: One of the main themes of 
your talk was to address the issue of 
clinical empowerment. Should respi- 
ratory therapists be allowed to defib- 
rillate, to intubate, and so on? As far 
as I'm concerned, it's the same gen- 
eral principle as for paramedics, fire 
fighters, first responders — whomev- 
er. It is a medical fact that delegating 
care is not only feasible but effica- 
cious as long as the doctors, who are 
delegating the care are expert men- 

tors who basically know the subject 
at hand thoroughly and are able to 
train those people to such an extent 
that they'd say "I'd let them take care 
of my family member."'-' It doesn't 
matter who you are — nurse, doctor, 
respiratory therapist — if the setting is 
right, if the personnel are well- 
trained, if the expert mentor provid- 
ing the training will personally take 
responsibility and continue to moni- 
tor the care that is rendered, I think 
it's absolutely appropriate. But if you 
can't meet those conditions, that's 
where the problem comes in. If you 
just sort of say, "Well, let's let respi- 
ratory therapists do ACLS or let's let 
firefighters do ACLS or whatever." then 
you get into trouble. That constant 
monitoring is key, and Bill (Kaye) 
knows more about this than anybody 

1. Pepe PE, Bonnin MJ, Mattox KL. 
Regulating the scope of EMS services. 
Prehosp Disaster Med 1990:5:59-63. 

2. Pepe PE, Mattox KL, Duke JH, Fisher 
PB. Prentice FD. The effect of fulltime 
specialized physician supervision on 
the success of a large urban emergency 
medical services system. Crit Care 
Med 1993;21:1279-1286. 

3. Falk JL. Medical direction of emergen- 
cy medical service systems: a full-lime 
commitment whose time has come, (edi- 
torial )Crit Care Med 1993;21:1259-1260. 

Barnes: That's an area where the pre- 
hospital medical director, physicians 
working with paramedics, may do a 
better job than physicians in hospitals. 
We may not be doing as good a job as 
we can, identifying the nonphysicians 
within hospitals who can master cer- 
tain skills. That's why I think it's im- 
portant that the code beeper not be 
passed casually from one person to the 
next. There should be RCPs who iue 
specially trained, who have skills rec- 
ognized by the medical director of the 
department, and in whom the medical 
committee of the hospital has confi- 
dence that they can do what they were 
trained to do. 


Respiratory Carh • April '94 Vol 39 No 4 

Barnes Discussion 

Kaye: I think that we have to be very 
careful when we use the rubric 
ACLS. We need to talk about which 
of those critical actions have been 
shown to improve survival to hospital 
discharge. I agree totally that respira- 
tory care practitioners should be al- 
lowed to intubate, defibrillate, give 
drugs, even I.V. drugs. That's going 
to require, I would imagine, some 
change in state law, and why not? 
But, I think we need to identify the 
critical actions. As the first action in- 
hospital, is early CPR appropriate? I 
don't think so. But, early defibrilla- 
tion, as the first step is appropriate 
using automated external defibrilla- 
tors, not conventional defibrillators. 
Airway management clearly is need- 
ed — RCPs should be able to manage 
the airway. They should also be able 
to administer drugs, especially 
epinephrine and others via the endo- 
tracheal route. But I think we have to 
look at ACLS in its entirety. We have 
to stop being naive and start looking 
at the critical actions that have been 
shown to improve survival. We need 

to make sure that all of our providers 
are trained in those if that's part of 
their job responsibility. 

Barnes: That's a point well taken. I 
think the education of therapists is 
critical. We need to develop a more 
uniform standard. It's good to have 
standards, but if a standard applies 
only to a very select, elite group, then 
it's not as strong as if you have a 
common standard — every registered 
respiratory therapist will have these 
skills in their bag of competencies. Of 
course, the initial education and train- 
ing, and then the retraining are essen- 
tial. For some of these skills, like in- 
tubation and defibrillation, every 3 
months may not be too often to retrain. 

Malinowski: Tom, I just wanted to 
address another concern about intuba- 
tion that goes along with what we've 
talked about — the education that 
RCPs should have, but also their abili- 
ty to keep those skills and their experi- 
ence up-to-date. Intubation is a skill 
that, to be retained, has to be practiced 

on a regular basis. In your example of 
the code where the anesthesiologist 
comes 3 minutes later than the respira- 
tory care practitioner, I don't think that 
3 minutes, if there's good airway con- 
trol and ventilation, is going to make 
that big a difference in outcome, if that 
therapist does not have the skills or 
has not continued to practice intuba- 
tion. Each individual facility is going 
to have to examine their ability to pro- 
vide the therapists with ongoing prac- 
tice. Some hospitals will be able to 
have a training program and to pro- 
vide ongoing experience for the thera- 
pists, and some will not. The analogy 
regarding EMS personnel was inter- 
esting, but one of the things about 
paramedics is that they intubate regu- 
larly, if they are approved to do that. 
I'm not sure that in the RCP's realm, 
in some hospitals, they have that same 
opportunity as the paramedic. It will 
be the respiratory care manager's re- 
sponsibility to ensure that after good 
education and skills training during 
school, continuing reinforcement of 
these skills is facilitated. 

41st Annual Convention and Exhibition 
December 2-5 • Orlando, Florida 

Respiratory Care • April '94 Vol 39 No 4 


Pacemakers and Electrical Therapy during 
Advanced Cardiac Life Support 

Tom P Aufderheide MD 

I. Introduction 
II. Early Defibrillation 

III. Energy Requirements for Defibrillation 

A. Transthoracic Impedance 

B. Current-Based Defibrillation 

C. Electrode Position 

D. Electrode Size 

E. Synchronized Cardioversion 

F. Energy Requirements for Defibrillation 

G. Pediatric Energy Requirements 
H. Blind Defibrillation 

I. Asystole 

J. Defibrillator Checklists 

IV. Recommended Sequences for Defibrillation 

A. Adult Defibrillation 

B. Pediatric Defibrillation 

V. Automated External Defibrillation (AED) 

A. Use of AEDs during Resuscitation Attempts 

B. Advantages of AEDs 

VI. Transcutaneous Cardiac Pacing 
VII. In Conclusion 


Each year approximately 400,000 lives are lost in the 
United States alone due to sudden cardiac arrest. It is the 
leading cause of death in men between 20 and 65 years of 
age. In the majority of cases, cardiac arrest is caused by the 
sudden onset of ventricular fibrillation and usually repre- 
sents a primary electrical event not associated with a new 
myocardial infarction. If treated promptly, ventricular fib- 

Dr Aufderheide is Associate Professor, Department of Emergency 
Medicine. Medical College of Wisconsin. Milwaukee. Wisconsin. 

A version of this paper was presented by Dr Aufderheide during the 
Respiratory Care Journal Conference "Resuscitation in Acute Care 
Hospitals" held in Cancun, Mexico, October 2 1 -23. 1 994. 

Reprints: Tom P Aufderheide MD, Emergency Medicine Department, 
Medical College of Wisconsin. 8700 West Wisconsin Avenue, DH 204, 
Milwaukee WI 5.1226. 

rillation is reversible and in most instances can be fol- 
lowed by many years of productive life.' - 

Studies performed nearly a decade ago have shown that 
the most important factors associated with neurologically 
intact survival following cardiac arrest include the pres- 
ence of witnesses, ventricular fibrillation as the presenting 
rhythm, prompt initiation of bystander cardiopulmonary 
resuscitation (CPR), and the rapid provision of advanced 
life support care.'"" Subsequent studies have established a 
direct relationship between neurologically intact survival 
and the speed with which defibrillation is performed.^' 
This relationship is an important factor in the rationale for 
intensive and immediate care units in hospitals. Applica- 
tion of this concept to care of victims of cardiac arrest out- 
side the hospital has been implemented more slowly. 
Previous impediments to more rapid on-site defibrillation 
have been ( 1 ) medical concerns about the need for highly 
trained medical personnel to make precise diagnoses of 
rhythm and administer therapy; (2) legal concerns about 


Ri:,spiRAroRY Care • April "95 Vol 40 No 4 

Pacemakers & Electrical Therapy 

the liability of emergency personnel: and (3) the logistic, 
technical, and economic problems associated with safe and 
early defibrillation of victims of cardiac arrest. 

Newer concepts and technology have now shifted the 
paradigm toward early defibrillation as the standard of 
care for patients experiencing either prehospital or in-hos- 
pital cardiac arrest.* One widely accepted concept is that 
all first-responding personnel must be trained to operate, 
be equipped with, and be permitted to operate a defibrilla- 
tor if in their professional activities they are expected to re- 
spond to people in cardiac arrest.' ''' The availability and 
proven efficacy of automatic external defibrillators 
(AEDs) is a significant technologic advance that has al- 
lowed extension of defibrillation capability to lesser 
trained medical personnel.'-^"" The presence of transcuta- 
neous pacing capability on most modem defibrillators ad- 
ditionally makes this the initial pacing method of choice in 
emergency cardiac care because of the speed with which it 
can be instituted, ease of operation, and widespread avail- 
ability. "•'* 

Table I. 'Saves' per Shock and Cumulative 'Save Rate' for Counter- 
shocks Delivered during Resuscitation 


n= 1.497 

Saves Per 


Save Rate 
n = 372('7r) 
























343 (92.2) 




352 (94.6) 













*'Saves' = Patients discliarged from the hospital alive: save rates and cumulative 
save rates are recorded for patients grouped according to the number of counter- 
shocks they received during their entire resuscitation. These percentages were 
based on number of patients delivered each countershock (second column) for 
save rates and 372 total sur\ivors for the cumulative save rate. (From Reference 5. 
with permission.) 

This article will review the concepts of early defibrilla- 
tion, energy requirements for defibrillation, recommended 
sequence of defibrillation, automatic external defibrilla- 
tion, and transcutaneous pacing. 

Early Deflbrillation 

A high percentage of persons with nontraumatic cardiac 
arrest are in ventricular fibrillation within the first few 
minutes after their collapse.'''-" A number of studies have 
now demonstrated that rapid defibrillation is the major de- 
terminant of survival in cardiac arrest due to ventricular 
fibrillation.'-' -- 

A 10-year retrospective study in Milwaukee analyzed 
prehospital experience with defibrillation for 1,497 adult 
patients whose initial arrest rhythm was coarse ventricular 
fibrillation to determine the relationship between rapid de- 
livery of first countershock and survival and to determine 
whether a relationship existed between the number of 
countershocks delivered and the 'save rate' (defined as the 
number of patients discharged from the hospital alive). 
The number of saves, save rates, and cumulative save rates 
were recorded for patients grouped according to the num- 
ber of countershocks they received during their resuscita- 
tion (Table 1 ). More than 75% of saves occurred within the 
first three countershocks. The time to delivery of first 
countershock and the success in obtaining a perfusing 
rhythm were also analyzed. There was a dramatic decrease 
in the frequency of successful countershock to a perfusing 
rhythm with each 1 -minute delay in electrical counter- 
shock through 3 minutes. A plateau effect was evident be- 
yond this time period (Fig. 1 ).' 

Scattergram Presentation 

J Pulsatile after 1st Defibrillation 

vs Time of Delivery 


Time (min) 
o Paramedic Witness a Nonparamedic Witness 

Fig. 1. From a 10-year retrospective study of prehospital experi- 
ence vi/ith defibrillation for 1,497 adult patients. Percentage pul- 
satile after first countershock versus time of delivery. Percentage 
of patients converted to a pulsatile rhythm wras graphed against 
time. Only 3.4% of non-paramedic-viritnessed patients responded 
to countershock within 2 minutes of arrest; therefore, the slope 
does not differ from zero. (From Reference 5, with permission.) 

Respiratory Care • April "95 Vol 40 No 4 


Pacemakers & Electrical Therapy 



S 30 

§ 20 



1 1 17 16 



123456789 10 11 
Number of Countershocks/Patient 

Fig. 2. Relationship between the number of countershocks deliv- 
ered per patient (up to a maximum of 1 1 ) and the save rate of the 
total population. The number above each bar is the % save rate. 
(From Reference 5, with permission.) 

The relationship between the number of countershocks 
delivered per patient (up to a maximum of 1 1 ) and the save 
rate of the total population was also reviewed (Fig. 2). A lin- 
ear drop in save rate was present with each defibrillation at- 
tempt to a total of five countershocks but reached a plateau 
between the sixth and ninth countershock. The actual num- 
ber of saves and the relationship to the number of counter- 
shocks administered was also reviewed (Fig. 3). The number 
of saves diminished rapidly with each countershock. 
Delivery of more than 9 countershocks during resuscitation 
efforts yielded a save rate of only 0.5% (8 of 1.497).-'^ These 
data supported the early and timely delivery of electrical 
countershock after cardiac arrest on all patients presenting 
with coarse ventricular fibrillation.' 

2 3 4 5 6 7 8 9 10 11 12 13 14 1516 
Number of Countershocks 

Fig. 3. Actual number of saves versus number of countershocks 
delivered for defibrillation of coarse venticular fibrillation during 
prehospital management. (Adapted from Reference 5, with per- 

To improve survival rate, Hisenbcrg et al.^ in 1^80. 
trained emergency medical technicians to recogni/.e and 

treat out-of-hospital ventricular fibrillation with up to three 
defibrillatory shocks without the use of medications or spe- 
cial airway protection. Outcomes from cardiac arrest due to 
underlying heart disease were determined during two peri- 
ods: 2 years with standard care by emergency medical tech- 
nicians and I year with defibrillator-trained technicians. 
During the period with standard care, 4 of 100 patients with 
cardiac arrest were resuscitated and discharged alive from 
the hospital, as compared with 10 of 54 patients during the 
period with defibrillator-trained technicians (p < 0.01, Fig. 
4). Enhanced survival after cardiac arrest by providing 
early defibrillation established its importance as the major 
determinant of survival following cardiac arrest due to ven- 
tricular fibrillation.'-' 

All Patients Patients with Ventricular 


Fig. 4. Percentages of patients admitted and discharged after out- 
of-hospital cardiac arrest due to heart disease. During the stan- 
dard-technician period, care was provided by emergency medical 
technicians. During the defibrillator-technician period, care was 
provided by defibrillator-trained emergency medical technicians. 
(From Reference 7, with permission.) 

The importance of early defibrillation to successful out- 
come has resulted in a de-emphasis by the American Heart 
Association of the sole benefit of cardiopulmonary resus- 
citation and a recognition that successful resuscitation re- 
quires the systematic linking of a number of elements 
termed the chain-of-survival concept.-- -' It is now under- 
stood that a specific cascade of events must transpire to 
achieve satisfactory survival rates from cardiac arrest. 
These events include recognition of a cardiac arrest, rapid 
access to the emergency system, rapid call-processing by 
emergency medical dispatchers, quick times by 
emergency personnel, early initiation of CPR, early defib- 
rillation, and quick support from advanced cardiac life 
support (ACLS) teains. The phrase "chain of survival", 
contains these events — early access, eariy CPR. early de- 
fibrillation, and early ACLS. 


Respiratory Care • April "95 Vol 40 No 4 

Pacemakers & Electrical Therapy 

Energy Requirements for Deflbrillation 

Successful defibrillation requires selecting appropriate 
energy to generate an adequate transmyocardial current 
flow. If energy and current are too low, the shock is inef- 
fective. If energy and current are too high, myocardial 
damage may result.-''-^ Transthoracic impedance is a 
major determinant of defibrillation and cardioversion ener- 
gy requirements.-** 

Transthoracic Impedance 

Sufficient electrical current (amperes) must pass through 
the heart for successful defibrillation. Current flow is deter- 
mined by the energy chosen (joules, or J) and the transtho- 
racic impedance (ohms) or resistance to cunent flow. 
Factors influencing thoracic impedance include energy se- 
lected, electrode size, paddle-skin coupling material, num- 
ber of previous shocks, time interval between shocks, phase 
of ventilation, distance between electrodes (size of the 
chest), and paddle electrode pressure.-"" If transthoracic 
impedance is high, a low energy shock (< 100 J) may fail to 
generate enough current to achieve successful defibril- 
lation.-'-^""- Transthoracic impedance can be reduced by al- 
ways pressing firmly on handheld electrode paddles and 
using using a gel, paste, or saline-soaked gauze pads be- 
tween handheld electrode paddles and the chest. Alcohol 
pads can cause serious bums and should never be used. Not 
using a coupling material between electrodes and the chest 
wall results in very high transthoracic impedance.'" 

Current-Based Defibrillation 

Studies-''--^' have shown that transthoracic impedance 
is a major determinant of the energy requirements for de- 
fibrillation and that it is possible to accurately predict 
transthoracic impedance in advance of actual defibrillating 
shocks with specially equipped commercially available de- 
fibrillators. A promising alternative approach would be to 
select electric current (amperes) instead of energy (J). This 
approach has the potential to avoid inappropriately low en- 
ergy selection in the face of high impedance resulting in too 
low a current flow and consequent failure to defibrillate. -'•-'* 
The optimal current for ventricular defibrillation appears to 
be 30 to 40 amperes.-'-^--^-*-" 

Electrode Position 

Electrode position is designed to maximize current flow 
across the myocardium. The standard placement is one 
electrode just to the left of the upper part of the sternum 
below the clavicle and the other to the left of the nipple, 
with the center of the electrode in the mid-axillary line. An 

alternative is to place one paddle anteriorly over the left 
precordium and the other paddle posteriorly behind the 
heart in the right infrascapular location. Another approach 
is to place the anterior paddle over the left apex with the 
posterior paddle placed in the right infrascapular loca- 
tion. '*'■" Self-adhesive monitor-defibrillator electrode pads 
or handheld electrode paddles may be used in any of these 

Care should be taken so that paste or gel is not smeared 
between the paddles, which may result in superficial arc- 
ing of the current along the chest wall. Care also should be 
taken to avoid placing defibrillator electrodes near the 
pacemaker in patients with permanent pacemakers. This 
can cause pacemaker malfunction. The pacing threshold 
should be checked after defibrillation of patients with per- 
manent pacemakers.'' 

Electrode Size 

For adult defibrillation, self-adhesive pad electrodes 
and handheld paddle electrodes are generally 8 to 12 cm in 
diameter."* The smaller pediatric paddles should be used in 
infants weighing less than 10 kg (usually < 1 year of age). 
The larger adult paddles are recommended for children 
weighing more than 10 kg."*" 

Synclironized Cardioversion 

Synchronization of delivered energy reduces the possibili- 
ty of inducing ventricular fibrillation, which can occur when a 
shock impinges on the relative refractory period of the elec- 
trocardiographic complex.'^ Synchronization is recommend- 
ed for supraventricular tachycardia, atrial fibrillation, atrial 
flutter, and ventricular tachycardia in patients who are con- 
scious and have pulses. Patients with ventricular tachycardia 
who are pulseless, unconscious, hypotensive, or in pulmonary 
edema should received unsynchronized shocks to avoid the 
delay associated with attempts to synchronize. 

Energy Requirements for Defibrillation 

The recommended energy level for the first fibrillation 
attempt is 200 J.*' Second shocks should be delivered at 
200 to 300 J. A range of energy levels for repeated shocks 
is suggested because the probability that repeated shocks 
may be successful is additive. Furthermore, thoracic 
impedance may be reduced with repeated shocks, and 
transthoracic impedance is highly variable from patient to 
patient. If the first two shocks fail to defibrillate, a third 
shock of 360 J should be delivered immediately. If ventric- 
ular fibrillation is initially terminated by a shock but then 
recurs during the arrest sequence, shocks should be reiniti- 
ated at the energy level that previously resulted in success- 

Respiratory Care • April "95 Vol 40 No 4 


Pacemakers & Electrical Therapy 

ful defibrillation. Shock energy should be increased only if 
the shock fails to terminate ventricular fibrillation. 

Because early defibrillation is the major determinant for 
survival, shock should be administered as soon as the de- 
tlbrillator arrives.'-' If three rapidly administered shocks 
fail to defibrillate. CPR should be continued, intravenous 
access established, epinephrine administered, ventilation 
established or continued, and then shocks repeated. 

The recommended initial energy for cardioversion of 
atrial fibrillation is 100 J. The recommended initial energy 
for atrial flutter and paroxysmal supraventricular tachycar- 
dia is 50 J, with stepwise increases in energy if initial 
shocks fail to terminate the dysrhythmia.-' 

Cardioversion energy for ventricular tachycardia de- 
pends on the morphologic characteristics of the dysrhyth- 
mia. Ventricular tachycardia that is regular in form and 
rate (ie, monomorphic ventricular tachycardia) with or 
without a pulse responds well to the relatively lower ener- 
gy of 100 J. Ventricular tachycardia that is irregular in 
form and rate (ie, polymorphic ventricular tachycardia) be- 
haves like ventricular fibrillation and has a higher likeli- 
hood of successful conversion with a relatively higher ini- 
tial energy of 200 J. Stepwise increases in defibrillation 
energy should be implemented if the first shock fails to 
convert the dysrhythmia.^' 

Pediatric Energy Requirements 

The recommended energy for pediatric defibrillation 
for ventricular fibrillation is an initial dose of 2 J/kg.^-'" If 
the initial shock is unsuccessful, the energy dose should be 
doubled and repeated. If still unsuccessful, the victim 
should be defibrillated again at 4 J/kg. The initial energy 
dose for synchronized cardioversion is generally 0.5 J/kg. 
If necessary, this dose may be increased during subsequent 

Blind Defibrillation 

Performing defibrillation in the absence of diagnosis by 
an electrocardiographic (ECG) rhythm is potentially dan- 
gerous and rarely necessary because of the almost univer- 
sal availability of monitoring capabilities on modern man- 
ually operated defibrillators and diagnostic algorithms on 
automatic external defibrillators (AEDs). 


There is no evidence that defibrillation of asystole is 
beneficial. In some circumstances, however, ventricular 
fibrillation may mimic asystole in some ECG leads. 
Therefore, more than one ECG lead should be reviewed 
before concluding that the patient's rhythm is asystole. •'■' 

Defibrillator Checklists 

Reported malfunctions of defibrillators can be traced to 
improper maintenance and battery depletion. For these rea- 
sons, checklists have been developed to aid in reducing de- 
fibrillator malfunctions. Points of emphasis regarding the 
use of defibrillator checklists in the American Heart 
Association's Guidelines for Cardiopulmonary Resuscita- 
tion and Emergency Cardiac Care are: 

1 . Users must be trained in the proper use of checklists if 
they are to fulfill their intended function. 

2. Those who actually use the defibrillators being assessed 
must perform the check. 

3. If practical, checklists should be used with every shift 
change, however frequent. 

4. Use of checklists is intended to be supplementary to, 
and not in any way a replacement for, regularly sched- 
uled, more detailed maintenance checks recommended 
by the manufacturer. 

5. In manual defibrillators in which the remote defibrilla- 
tion option with adhesive pads is used instead of pad- 
dles, a charge-discharge cycle with a simulator can be 

The nationwide implementation of early defibrillation in a 
wide variety of settings with diverse frequencies of use 
would seem to confer an urgent need for preventive main- 
tenance wherever defibrillators are used. "''^ 

Recommended Sequences for Defibrillation 

Adult Defibrillation 

Ventricular fibrillation and ventricular tachycardia are 
the most important dysrhythmias to recognize during adult 
resuscitation because the majority of survivors will regain 
a pulse during interventions for these dysrhythmias. The 
adult algorithm for ventricular fibrillation and pulseless 
ventricular tachycardia is shown in Figure 5. 

The purpose of defibrillation is to completely depolar- 
ize the myocardium and provide an opportunity for the 
natural pacemakers of the heart to resume normal activi- 
ty .^^ Early defibrillation is critical but must be taken within 
the context of the chain-of-survival concept."" The initial 
three shocks should be delivered in sequence without in- 
terruption for CPR or medication administration. Research 
has shown that delays between the initial three shocks are 

If the patients has a nitroglycerin patch on his or her 
chest, it should be removed prior to defibrillation. The alu- 
minized backing on some transdermal delivery systems 
can result in electric arcing during defibrillation, with ex- 


Respiratory Care • April "95 Vol 40 No 4 

Pacemakers & Electrical Therapy 

plosive noises, smoice, visible arcing, patient burns, and 
impaired transmission of current. "'^- 


•Perform CPR until defibrillator attacheda 

'VFA/T present on defibrillator 

Defibrillate up to 3 times if needed for 
persistent VFA/T (200 J, 200-300 J, 360 J) 


Rhythm after the first 3 shocks?b 

Persistent or 

Return of 




Go to Fig. 3 

Go to Fig. 4 

•Continue CPR 
•Intubate at once 
•Obtain I.V. access 

•Epinephrine 1 mg 
I.V. push.c.d repeat 
every 3-5 min 

•Assess vital signs 
•Support airway 
•Support breathing 
•Provide medications 
appropriate for blood 
pressure, heart rate, 
and rhythm 

•Defibrillate 360 J 
within 30-60 se 

■Administer medi- 
cations of probable 
benefit (Class I la) 
in persistant or 
recurrent VFA/Tf.g 

•Defibrillate 360 J, 
30-60 s after each 
dose of medicatione 

•Pattern should be 
drug-shock, drug- 

Class I: Definitely helpful Class lib: acceptable. 

possibly helplul 
Class lla acceptable, probably Class III: not indicated, may 
helplul be harmlul 

a Precordial thump is a Class lib aclion in witnessed arrest, 

no pulse, and no defibrillator immediately available 
b Hypothermic cardiac arrest is treated ditterently after this 

point See hypothermia algonthm 
c The recommended dose of epinephnne is tmg IV push 
every 3-5 mm II this approach tails, several Class lib 
dosing regimens can be considered 
•Intemiediate epinephnne 2-5 mg IV push, every 3-5 mm 
•Escalating epinephnne 1 mg-3mg-5mg IV push, 3 mm 

•High epinephnne 1 mg/kg IV push, every 3-5 mm 
d Sodium bicarbonate 1 mEg/kg is Class I if patient has 

known preexisting hyperkalemia 
e fvlultiple sequeced shocks are acceptable here (Class I), 

especially when medications are delayed 
t Medication sequence 

•Lidocaine 1 0-15 mg/kg IV push Consider repeal in 3-5 
mm to maximum dose of 3 mg/kg A single dose ol 1 5 
mg/kg in cardiac arrest is acceptable 
•Bretylium 5 mg/kg IV push Repeat in 5 mm at 10 mg/kg 
•Magnesium sulfate 1-2 g IV in torsades de pointes or 
suspected hypomagnesemic state or refractory VF 
•Procainamide 30 mg/min in reffactorv VF (maximum total 
17 mg/kg) 
g Sodium bicarbonate 1 mEg/kg IV 
Class lla 

•If known preexisting bicarbonale-responsive acidosis 
•It overdose with tricyclic antidepressants 
•To alkalinize the unne in dmg overdoses 
Class lib 

•If intubated and continued long arrest interval 
•Upon return of spontaneous circulation after long arrest 
Class III 
•Hypoxic lactic acidosis 

Fig. 5. aha algorithm for ventricular fibrillation and pulseless ven- 
tricular tachycardia (VFA/T). (From Reference 45. with permis- 

The person performing defibrillation must always an- 
nounce the impending shock before it is administered.'-* 
The person who controls the defibrillator should state 
firmly and forcefully before each shock something like "I 
am going to shock on Three. One, I am clear. Two, you are 
clear. Three, everybody is clear." The person then makes a 

visual check to ensure that no one else has contact with the 
patient or stretcher prior to defibrillation. The person oper- 
ating the defibrillator need not use the exact wording given 
but should use wording that is similar. 

If the first three defibrillation shocks are unsuccessful, 
rescuers should intubate, hyperventilate, start an intra- 
venous line, and give 1 mg of I.V. epinephrine. If ventricu- 
lar fibrillation or ventricular tachycardia persists, 30 to 60 
seconds after the delivery of epinephrine, another counter- 
shock at 360 J should be administered. If this shock is un- 
successful, additional medication should be administered 
as outlined in Figure 5, with countershocks at 360 J admin- 
istered 30 to 60 seconds after each dose of medication in 
an alternating pattern of Drug-Shock, Drug-Shock. 

Pediatric Defibrillation 

Ventricular tachycardia and fibrillation are uncommon 
in children. Cardiopulmonary arrest is often the end result 
of progressive deterioration in respiratory function. In a 
study of terminal rhythms in infants and children, Walsh 
and Krongrad found that only 6% demonstrated ventricu- 
lar fibrillation and not a single episode occurred in a child 
without congenital heart disease.'''* 

Because respiratory arrest is the primary cause for car- 
diac arrest in children, pulseless ventricular tachycardia 
and ventricular fibrillation in children is managed first by 
stabilization of the airway and hyperventilation with 100% 
oxygen. Following airway stabilization and hyperventila- 
tion, three defibrillation attempts should occur in rapid 
succession (2 J/kg, 4 J/kg, and 4 J/kg). If these defibrilla- 
tion attempts are unsuccessful, epinephrine and lidocaine 
should be administered. Repeated defibrillations (4 J/kg) 
should be administered 30 to 60 seconds after medication. 
The pediatric pulseless arrest decision tree is shown in 
Figure 6. 

Automated External Defibrillation 

Automatic external defibrillators (AEDs) eliminate the 
need for training in rhythm recognition, make early defib- 
rillation by minimally trained personnel practical and 
achievable, and have sparked the extension of defibrilla- 
tion capability.""''** Providers of both in-hospital and pre- 
hospital ACLS should be familiar with AEDs and know 
how to interact with emergency personnel equipped with 
these devices. 

Improved survival rates for patients who have sustained 
cardiac arrest have been reported from communities that 
had no prehospital ACLS services but added early defibril- 
lation programs. In King County, Washington, survival 
rates of patients with ventricular fibrillation improved 
from 7 to 26% (Fig. 4)', and in rural Iowa the survival rate 

Respiratory Care • April '95 Vol 40 No 4 


Pacemakers & Electrical Therapy 

•Determine pulselessness and begin CPR 
•Confirm cardiac rhythm in more than one lead 

Ventricular fibrillation/ 
pulseless ventricular 



•Continue CPR 
•Secure airway 

•Hyperventilate with 100% oxygen 
•Obtain IV or 10 access but do 
not delay defibrillation 

•Defibrillate up to 3 times if 
needed. 2 J/kg, 4 J/kg. 4 J/kg 


Electromechanical dissociation 
Pulseless electrical activity 


identify and treat causes 
•Severe hypoxemia 
•Severe acidosis 
•Severe hypovolemia 
•Tension pneumothorax 
•Cardiac tamponade 
•Profound hypothermia 

•Epinephrine, first dose 
•IV/lO:0.01 mg/kg (1:10000) 
•ET:0,1 mg/kg (1:1000) 

•Lidocaine 1 mg/kg IV or 10 


•Continue CPR 
•Secure airway 

•Hyperventilate with 100% oxygen 
•Obtain IV or 10 access 


•Defibrillate 4 J/kg 30-60 s after 


•Epinephrine, first dose 
•IV/IO:0,01 mg/kg (1:10000) 
•ET: 0,1 mg/kg (1:1000) 


•Epinephrine, second and 
subsequent doses 
•IV/IO/ET: 0.1 mg/kg (1:1000) 
(doses up to 2 mg/kg of 
1:1000 may be effective) 
•Repeat every 3-5 min 
•Lidocaine 1 mg/kg 
•Consider bretylium 5 mg/kg first 
dose. 10 mg/kg second dose IV 

•Epinephrine, second and 
subsequent doses 

•IV/IO:0.01 mg/kg (1:10000) 
(doses up to 0.2 mg/kg of 
1:1000 may be effective 

•Repeat every 3-5 min 

•Defibrillate 4 J/kg 30-60 s after 

Fig. 6. AHA pediatric pulseless-arrest decision tree. (From 
Reference 45, with permission.) 

for ventricular fibrillation rose from 3 to 19%.-' South- 
eastern Minnesota,'''' Northeastern Minnesota.*'" and Wis- 
consin^' have also reported improved survival with the use 
of early defibrillation programs utilizing AEDs (Table 2). 

Table 2. Effectiveness of Early Defibrillation Programs 

a e c 1 Af. c 1 Odds Ratio 

, , Before Early Alter Ear y ,■ , , 

I.ocatKin „ ,_, .,, , - „ ,_, .,, _/ lor Improved 


Dctihrillation Defibrillation 

King County. Washington 7* 
Iowa 3(1/31) 

Southeast Minnesota 4(1/27) 

Northeast Minnesota 2 ( 3/ 1 1 K ) 

Wisconsin 4(32/893) 









11 (3.3/.304) 


•Values arc perccnl sur\'iving and. in parentheses, the number of patients in ventric- 
ular fibri nation. (From Reference 63. with permission.) 

AEDs are attached to the patient by two adhesive pads*- 
and connecting cables that function to record the rhythm 
and deliver the electric shock (Fig. 7*''). Semiautomated or 
shock-advisory devices require operator action, including 
pressing an Analyze button to initiate rhythm analysis and 
pressing a Shock button to deliver the shock. The operator 
presses the Shock button when the device identifies ven- 
tricular fibrillation and advises the operator accordingly. 

Fig. 7. Drawing of automated external defibrillator and its attacfi- 
ments to patient. (From Reference 63, with permission.) 

A fully automated defibrillator requires only that the 
operator attach the defibrillatory pad and turn on the de- 
vice. The device then analyzes the rhythm. If ventricular 
fibrillation (or ventricular tachycardia above a preset rate) 
is present, the device charges its capacitors and delivers a 

The AEDs available in 1995 are highly sophisticated 
microprocessor-based devices that analyze multiple fea- 
tures on the surface ECG signal, including frequency, am- 
plitude, and some integration of frequency and amplitude 
such as slope or wave morphology. A variety of filters 
check for QRS-like signals, radio transmission, and 60- 
cycle interference, and for loose electrodes and poor elec- 
trode contact. Some devices are programmed to detect 
spontaneous patient movements, continued heart beat and 
blood tlow. and movement of the patient by others. 

Two field studies have compared the rhythm detection 
ability of AEDs with that of emergency personnel. ''^■'''^ 
Although AEDs have not achieved 100%- accuracy in 
rhythm detection, they perform as well as emergency med- 
ical technicians (HMTs) who use conventional defihrilla- 


Re.spiratory Care • April '95 Vol 40 No 4 

Pacemakers & Electrical Therapy 

(Qj-g 63,64 jjjg Qpjy n;jajor errors reported in clinical trials 
have been occasional failures to deliver shocks to rhythms 
that may benefit from electrical therapy, such as extremely 
fine or coarse ventricular fibrillation. 

Although the occurrence of inappropriate shocks during 
patient movement has not been reported, AEDs should be 
placed in the analysis mode only when all movement has 
ceased, particularly movement associated with patient 
transport. If a patient requires rhythm analysis and treat- 
ment during transport, the vehicle must be brought to a 
complete stop before proceeding. 

Emergency personnel must not touch the patient while 
the AED analyzes the rhythm, charges the capacitors, and 
delivers the shocks. Chest compression and ventilation 
must cease while the device is operating. This permits ac- 
curate analysis of the cardiac rhythm and prevents acci- 
dental shocks to the rescuers. Movements induced by CPR 
can also lead the AED to stop its analysis. 

AEDs are not recommended for use in pediatric cardiac 
arrest. AEDs now have a minimum energy level of 200 J, 
which is high for patients weighing less than 50 kg (110 
pounds). The American Heart Association recommends 
(1994) that AEDs be attached only to patients in cardiac 
arrest who are more than 1 2 years old or weigh more than 
90 pounds.*'-' 

Use of AEDs during Resuscitation Attempts 

All AEDs can be operated in five simple steps: 

1 . Turn on the power. 

2. Attach the device. 

3. Initiate analysis of the rhythm. 

4. Assure that no one is touching the patient or bed. 

5. Deliver the shock if indicated. 

Most in-hospital or out-of-hospital response teams con- 
sist of at least two persons. One team member should 
begin basic life support, attending to airway management, 
ventilation, and chest compression. The other rescuer 
should place the AED close to the supine patient's left ear 
and perform the defibrillation protocols from the patient's 
left side. This position provides better access to the defib- 
rillator controls and easier placement of the defibrillator 
pads and allows the other rescuer room to perform CPR. 
The AED is turned on by pressing a power switch or by 
lifting the monitor screen to the up position. The adhesive 
defibrillator pads are opened quickly and attached first to 
the defibrillator cables and then to the patient's chest. The 
pads are placed in a modified Lead-II position (Fig. 7). 
When the pads are attached, CPR should be stopped, and 
the analysis button should be pressed. Assessment of the 
rhythm takes from 5 to 15 seconds. The interruption of 

CPR that occurs with the use of AEDs is a recognized ex- 
ception to the American Heart Association Guidelines that 
recommend that CPR not be stopped for more than 5 sec- 
onds. If ventricular fibrillation is present, the device will 
announce that a shock is indicated. The rescuer should as- 
sure that no one is touching the patient or the patient's bed 
in a fashion similar to that outlined for adult, two-rescuer 
CPR. After the first shock is delivered, CPR is not restart- 
ed. Instead, the Analyze control is pressed immediately to 
start another rhythm-analysis cycle. If ventricular fibrilla- 
tion persists, the device indicates this, and the sequence is 
repeated for the second and third shocks. The AED treat- 
ment algorithm is shown in Figure 8.*-' 

•ABCs if no pulses 

•Perform CPR until defibrillator attached' 

•Press "analyze" 

Defibrillate up to 3 times if needed for persistent 
VF/VT (200J, 200-300 J, 360 JjDc 

Pulse present 

( Check pulse" ) 


No pulse 

Return of spontaneous 

•Assess vital signs 
•Support ainvay 
•Support breathing 
•Provide medications 
appropriate for blood 
pressure, heart rate, 
and rhythm 

Check pulse, if absent 

•Press "analyze" 
•Defibrillate up to 360 J 
•Repeat 3 times 

• Healtii professionals with a duty to respond to 
a person in cardiac arrest stiould tiave a defibnl- 
iator available immediately or within 1-2 mm 

a The single rescuer with an AED should venfy 
unresponsiveness, open the airway (A), give two 
respirations (B), and check the pulse (C). if a fuii 
cardiac arrest is confirmed, the rescuer should 
attach Ihe AED and proceed with the algorithm 

b Pulse checlts not requried after shoclts 1, 2, 4, 
and 5 unless 'no shocit indicated" message is 

c li no shock is indicated, check pulse, repeal 1 min 
of CPR, check pulse again, and then reanalyze 
After three "no shock indicated' messages, repeat 
"analyze" penod every 1 -2 mm 

d For hypothermic patients limit shocks to 3 See 
hypothermia algorithm 

e. If VF persists after 9 shocks, repeat sets of three 
stacl<ed shocks with 1 min of CPR between each 
set until no "shock indicated" message is received. 
Shock until VF is no longer present or the patient 
converts 10 a periusing rhythm 

CPR for 1 min 

Check pulse, if absent 

Repeat sets of three stacked 
shocks with up to 360 Je 

Fig. 8, AHA automated external defibrillation (AED) treatment algo- 
rithm. Emergency cardiac care pending arrival of ACLS personnel, 
(From Reference 63, witfi permission,) 

If the initial three shocks fail to convert ventricular fib- 
rillation to a pulsatile rhythm and ACLS is not immediate- 
ly available, the rescuers should not press the Analyze but- 
ton but should instead resume CPR for 60 seconds. During 
CPR, the patient's carotid pulse should be checked. If ven- 

Respiratory Care • April '95 Vol 40 No 4 


Pacemakers & Electrical Therapy 

tricular fibrillation continues, the operator should then de- 
liver an additional round of three sequential defibrillatory 
shocks after the appropriate analysis. AEDs now available 
( 1995) return to a sequence of 200-joule-. 200-joule-, and 
360-joule shocks at this point. This entire sequence should 
be repeated if ventricular fibrillation persists, before pa- 
tient transport is considered (Fig. 8). 

In some situations, a single rescuer equipped with an 
AED might respond to a person in cardiac arrest. Under such 
circumstances, the need for rapid defibrillation and its imme- 
diate availability take precedence over contacting the EMS 
system. Consequently, the single-rescuer sequence becomes 

Verify unresponsiveness. 
Open the airway. 
Give two breaths. 
Check the pulse. 

If there is no pulse, attach the AED and proceed with 
the algorithm for ventricular fibrillation and pulseless 
ventricular tachycardia (Fig. 8). 

medical director and the enabling administrative codes of the 
state. Licensure and certification for use of AEDs is a func- 
tion of the appropriate state legislative or local health or EMS 
authority. *"' 

Transcutaneous Cardiac Pacing 

Transcutaneous cardiac pacing is the initial pacing 
method of choice because of the speed with which it can be 
instituted and because it is the least invasive pacing method 
available. Many of the newer defibrillators include a built-in 
transcutaneous pacemaker that increases the ready availabil- 
ity of pacing. 

The indications for standby and emergency pacing are 
shown in Table 3. Standby pacing may be used for patients 
who are clinically stable but who are at risk for becoming 
unstable. If a transcutaneous pacemaker is to be used in the 
standby mode, a brief trial of pacing should be attempted to 
determine whether capture (myocardial contraction in re- 
sponse to electrical pacing stimulation) can be achieved and 
whether the patient can tolerate pacing." 

It should be noted that no pulse check is recommended 
between the sequential shocks — that is, after Shocks I, 2, 
4, and 5. The AED automatically assesses the patient's 
rhythm and, therefore, pulse checks at this point are not in- 
dicated. Pulse checks between shocks for AEDs delay 
rapid identification of persistent ventricular fibrillation, in- 
terfere with the assessment capabilities of the devices, and 
increase the possibility of operator error.*' 

Advantages of AEDs 

Learning to use and operate an AED is easier than 
learning to perform CPR.'''' Many of the advantages of 
AEDs stem from the program of brief convenient training 
.sessions and continuing education.*' In systems in which 
compensation must be provided for the initial training time 
and skills review classes, the use of AEDs offer consider- 
able financial savings. ''•* In systems in which the anticipat- 
ed number of cardiac arrests is low, skill maintenance can 
be maintained with less continuing education.*''"" In clini- 
cal trials, emergency personnel using AEDs deliver the 
first shock an average of 1 minute sooner than personnel 
using conventional defibrillators.''''''^ The accuracy of 
rhythm detection by AEDs is at least as good as detection 
by EMTs using conventional defibrillators."""''' 

According to state laws, health providers can perform 
some medical procedures only with the medical authoriza- 
tion of a physician. The authorizing physician assumes med- 
ical control and takes legal responsibility for the performance 
of emergcncy-carc providers, The emergency rescuer always 
must operate under the authority of the medical license of the 

Table 3. Indications for Emergency and Standby Pacing 

Emergency pacing 

Hemodynamically compromising bradycardias* 

(BP < 80 mm Hg systolic, change in mental status, myocardial 
ischemia, pulmonary edema) 
Bradycardia with malignant escape rhythms 
(unresponsive to pharmacologic therapy) 
Overdrive pacing of refractory tachycardia 

Supraventricular or ventricular (currently indicated only in special 
situations refractory to pharmacologic therapy or cardioversion) 
Bradyasystolic cardiac arrest 

Pacing not routinely recommended in such patients. If used at all, 
pacing should be used as early as possible after onset of arrest. 
Standby pacing 

Stable bradycardias 

(BP> 80 mm Hg, no evidence of hemodynamic compromise, or 
hemodynamic compromise responsive to initial drug therapy) 
Prophylactic pacing in acute myocardial infarction 
Symptomatic sinus node dysfunction 
Mobilz II second-degree heart block 
Third-degree heart block 

Newly acquired: left bundle-branch block, right bundle-branch 
block, alternating bundle-branch block, or bifa.scicular block 

♦Include complete heart block, symptomatic .second-degree heart block, symptomatic 
sick sinus syndrome, drug-induced bradycardias (ie. digoxin, p-blcKkers. calcium 
channel blockers, or procainamide), permanent pacemaker failure, idioventricular 
bradycardias, symptomatic atrial fibrillation with slow ventricular response, refrac- 
tory bradycardia during resuscitation of hypovolemic shock, and hradyarrhythmias 
with malignant ventricular escape niech;inisnis, ( MtKiitlcd Irom Reference 4.'>, with 

Emergency pacing is required in patients with hemody- 
namically unstable bradycardia, defined as hypotension 



Pacemakers & Electrical Therapy 

(systolic blood pressure < 80 mm Hg), change in mental sta- 
tus, myocardial ischemia, or pulmonary edema. Because in- 
travenous atropine may speed the heart rate and produce in- 
creased myocardial ischemia, it should be used with caution 
in patients with acute myocardial infarction. Pacing should 
not be delayed in such patients if intravenous access is diffi- 
cult. It may be appropriate to initiate intravenous atropine 
therapy and pacing simultaneously to stabilize the patient as 
rapidly as possible.'** 

Transcutaneous pacing is a Class-I intervention for all 
symptomatic bradycardias (ie, a therapeutic option that is 
usually indicated, always acceptable, and considered useful 
and effective). Clinicians should remember that transcuta- 
neous pacing is always appropriate, although not as readily 
available as atropine. If the bradycardia is severe and the 
clinical condition is unstable, transcutaneous pacing should 
be implemented immediately. The bradycardia algorithm 
for the patient not in cardiac arrest is given in Figure 9. 

•Assess ABCs 

•Assess vital signs 

•Secure airway 

•Review history 

•Administer oxygen 

•Perform physical examination 

•Attach monitor, pulse oximeter, 

•Order 12-lead ECG 

and automatic sptiygmomano- 

•Order portable chest 



Too slow (< 60 beats/mi 



Either absolute (< 60 beats/min) or relative 

Serious signs or symptoms?*t 

No ^ 


Type II second-degree AV 
heart block? or 
Third-degree AV heart 


•Prepare for 
transvenous pacer 
•Use TCP as a bridge 

Intervention sequence 
•Atropine 0.5-1,0 mg 4:§ 

(I & Ma) 
•TCP, If available (1) 
•Dopamine 5-20 >fl/kg per 

•Epinephrine 2-10 fvg per 


'Serious signs or symptoms must be related lo the slow rate 

Clinical maniiestations include 

symptoms (ciiesl pain, shortness ot breath, decreased level ot consciousness) and 

signs (low BP, shock, pulmonafy congestion, CHF, acute Ml) 
tDo not delay TCP while awaiting IV access or for atropine lo take effect if patient is 

tDenen/ated transplanted hearts will not respond lo atropine Go at once to pacing, 

catecholamine infusion, or both 
§Atropme should be given in repeal doses in 3-5 mm up lo lota! of 04 mg/kg Consider 

shorter dosing intervals in severe clinical conditions It has been suggested that atropine 

should be used with caution in alnovenlncular (AV) block al the His-Purkinje level (type II 

AV block and new third-degree block with wide QRS complexes) (Class lib) 
i'Never treat third-degree heart block plus ventncular escape beats with lidocaine 
ijlsoproterenol should be used, if al all, with extreme caution Al low doses il is Class lib 

(possibly helpful); at higher doses it is Class III (harmful) 
#Vehfy patient tolerance and mechanical capture Use analgesia and sedation as needed 

pharmacologic therapy. Increasing the intrinsic heart rate 
with pacing may eliminate escape rhythms when standard 
antiarrhythmic medications fail. 

Overdrive pacing can also be used to terminate malignant 
atrial or ventricular tachycardias.^-^ This technique has shown 
promise in the treatment of supraventricular tachycardia and 
ventricular tachycardia; however, drug therapy remains the 
treatment of choice in stable patients and cardioversion the 
intervention of choice in unstable patients. ^-^■* 

Temporary pacing is most helpful in patients with se- 
vere bradycardia and a palpable pulse or with high-grade 
heart block in which the conducted beat results in a palpa- 
ble pulse. With complete cardiac arrest (asystole or elec- 
tromechanical dissociation), pacing is usually ineffec- 
(JYg 17.75.76 xhese rhythms usually indicate that a consider- 
able time has elapsed since the onset of cardiac arrest. If 
emergency pacing is to be used in these circumstances, it 
should be begun as early as possible.^' " 

Transcutaneous pacing can be used effectively by pre- 
hospital personnel, nurses, respiratory therapists, and other 
nonphysician providers, who have been trained appropri- 
ately. Newer defibrillators and multifunctional electrodes 
have been developed that allow defibrillation, pacing, and 
cardiographic monitoring through a single pair of anterior- 
posterior chest-wall electrodes. 

Experience with transcutaneous pacing in children is 
limited.''* It is reserved for children with profound symp- 
tomatic bradycardia refractory to basic and advanced life 
support and represents a Class-IIb recommendation (ie, a 
therapeutic option that is not well established by evidence 
but may be helpful and probably is not harmful). If the 
child weighs less than 15 kilograms, pediatric (small or 
medium) electrodes are recommended. ■'-''•^'* 

Failure to capture may be related to electrode placement 
or patient size. Electrode placement is similar to placement 
for defibrillation. Patients with barrel-shaped chests and 
large amounts of intrathoracic air conduct electricity poor- 
ly, have high thoracic impedance, and may be refractory to 
capture. In a similar way, the presence of a large pericar- 
dial effusions or tamponade increases the current required 
for capture.^' 

The muscle contraction caused by transcutaneous pac- 
ing may result in patient discomfort for those who are con- 
scious or who regain consciousness during resuscitative 
efforts.*"*' Analgesia with a narcotic or sedation with a 
benzodiazapine may allow patient tolerance until transve- 
nous pacing can be instituted. 

Fig. 9. AHA braidycardia algorithm (with the patient not in cardiac 
arrest). (From Reference 45, with permission.) 

Another indication for emergency pacing is bradycardia 
with malignant ventricular escape rhythms unresponsive to 

In Conclusion 

Early defibrillation may be the single greatest determi- 
nant of survival for patients with either prehospital or in- 
hospital cardiac arrest. The presence of transcutaneous 

Respiratory Care • April "95 Vol 40 No 4 


Pacemakers & Electrical Therapy 

pacing capability on most modem defibrillators additional- 
ly make this the initial pacing method of choice for emer- 
gency cardiac care. Empowering more appropriately 
trained first responders in electrical therapy should reduce 
the time to defibrillation and pacing, potentially improving 
survival for victims of cardiac arrest. 


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Aufderheide Discussion 

Halperin: Are there any real data in 
patients that show that patients are 
damaged by using too high an energy 
level for defibrillation? Because the 
implication is that maybe we should 
just use the highest energy and reduce 
the number of shocks that are deliv- 

Aufderheide: Defibrillation depends 
on selecting appropriate energy to 
generate an adequate transmyocardial 
current flow. If energy and current 
are too low, the shock will not termi- 
nate the dysrhythmia; if energy and 
current are too high, functional and 
morphologic damage may result.' - 
Transcutaneous pacing studies show 
that following a 60-minute transcuta- 
neous pacing period there is diffuse, 
superficial myocardial necrosis in- 
volving less than 1% of the epicardi- 
um.' The minor pathologic and enzy- 
matic changes apparently have no 
significant clinically adverse effects.'^' 
Nonetheless, to minimize myocardial 
damage, the accepted approach has 
been to use the lowest energy level 
possible to successfully convert the 

1. Dahl CF. Ewy GA, Warner ED. 
Thomas ED. Myocardial necrosis from 
direct current countershiK-k. Circulation 

2. Kcrber RE. Martins JB, Kienzle MCI. 
Constantin L. Olshansky B, Hopson R. 
Charbonnier F. Energy, current, and suc- 
cess in defibrillation and cardioversion: 
clinical studies using an automated im- 
pedance-based method of energy ad- 
justment. Circulation 1 988;77: 1 OiH- 1 046. 

3. Hedges JR. Syverud SA. Dalsey WC, 
Simko LA. van der Bel Khan J. Gabel 
M. Thomson DP. Threshold, enzymatic, 
and pathologic changes assix;iated with 
prolonged transcutaneous pacing in a 

chronic heart block model. J Emerg Med 

4. Syverud SA. Dalsey WC. Hedges JR. 
KickJighter E. Barsan WG. Joyce SM, et 
al. Transcutaneous cardiac pacing; deter- 
mination of myocardial injury in a canine 
model. Ann Emerg Med 1983;12:745-748. 

5. Kicklighter EJ, Syverud SA, Dalsey 
WC. Hedges JR. Van der Bel Khan JM. 
Pathological aspects of transcutaneous 
cardiac pacing. Am J Emerg Med 1985; 

Halperin: Could you comment on the 
conference coming up on public-ac- 
cess defibrillation — because I thought 
the thrust of that was to make auto- 
matic defibrillators much more wide- 
ly available. 

Aufderheide: There is a conference 
titled "Public Access Defibrillation: 
A New Strategy to Prevent Sudden 
Death," meeting in Washington DC 
on December 8-10, 1994. It has been 
designed to provide a forum for dis- 
cussion of medical, social, and legal 
issues surrounding increased public 
access to automatic defibrillators for 
use in bystander-witnessed cardiac 
arrests. Although early defibrillation 
is the major determinant for survival 
following cardiac arrest, the risk-ben- 
efit ratio of providing public access 
for automatic defibrillators remains 
undetermined. Hopefully, this con- 
ference will provide guidance in this 

Pepe: To answer the question that was 
asked by Henry (Halperin): we can 
look at some inferential studies on en- 
ergy levels.'- For example, the defib- 
rillation comparison study examining 
360 and 1 75 joules was done in Seattle 
when I was there.' Defibrillation rates 
were actually equal, but more people 
receiving the higher energy level came 

back with a high-degree AV block. 
The inference was that it's more of a 
stun (or whatever) to the conduction 
system. There have been several other 
opinions, however. Equally impres- 
sive, are arguments from those on the 
other side who say you're more apt to 
defibrillate faster and get more re- 
sponse if you use higher energy 
levels.- So, it's still up for debate. As 
you expressed, I think it needs to be 
studied. Another thing I was going to 
add, is the issue of widespread defibril- 
lation with pads (which is sort of a re- 
quirement with the automated defibril- 
lators in terms of design). Traditional 
hard paddle design for defibrillation is 
different, especially in terms of provid- 
ing adequate transthoracic pressure. 
Success rate doesn't seem to be as 
good in animals when you use the pads 
versus when you use paddles. One of 
the implications of a recent animal 
study done by Dave Persse and Chuck 
Brown,^ was that if you apply more 
pressure, even with pads you would 
have had a better conversion rate. 
Therefore, there may be a subtle de- 
sign flaw with the typical automated 
defibrillator. They may provide an ad- 
vantage in time-to-defibrillation, but a 
disadvantage in conversion success. 
One of the reasons why 1 raise this 
issue is because of what the Seattle 
data show over the years. Even with 
the addition of EMT-D (emergency 
medical technician defibrillation) into 
the picture as well as e;irly automated 
defibrillation by first responders. those 
two changes have not led to a dramatic 
increase in survival rates there. I be- 
lieve this is kind of an interesting thing 
to talk about and debate. 

1. Weaver WD. Cobb LA, Copass MK. 
Hallstrom AP. Ventricular fibrillation: 
a comparative trial using 1 75 J and 320 J 


Respira TORY Care • April '95 Vol 40 No 4 


shocks. N Engl J Med 1982:307: 1 101- 

2. Dallas: American Heart Association. 
Textbook of Advanced Cardiac Life 
Support. 1987:1-248 and 1994: 4-6. 

3. Persse DE, Dzwonczyk R. Brown CG. 
The effect of applied pressure to self- 
adhesive defibrillator pads on counter- 
shock success (abstract). Ann Emerg 
Med 1994:23:621. 

Aufderheide: The lack of a dramatic 
increase in survival rates following 
emergency medical technician-defib- 
rillation (EMT-D) programs may par- 
tially be explained by Milwaukee's 
time-to-defibrillation data previous- 
ly.' Successful resuscitation rapidly 
and exponentially declines within the 
first several minutes following car- 
diac arrest. If you reduce average de- 
fibrillation times from 8 to 7 minutes, 
you will see little difference in sur- 
vival rate at this point on the expo- 
nential curve. You are only going to 
make a major difference when you re- 
duce time to defibrillation from 3 min- 
utes to 2 minutes, or 2 minutes to 1 .' 

1 . Hargarten KM, Stueven HA, Waite EM. 
Olson DW, Mateer JR, Aufderheide 
TP, Darin JC. Prehospital experience 
with defibrillation of coarse ventricular 
fibrillation: a ten-year review. Ann 
Emerg Med 1990:19:157-162. 

Durbin: On a slightly different topic 
that you brought up — in respiratory 
care we often deal with new technol- 
ogy introduced into the market place 
without adequate standardization of 
what terms mean and what the me- 
chanical or electronic components ac- 
tually do. Is there an effort to stan- 
dardize the technology of automatic 
defibrillators — the sensitivity, what 
capabilities they have, and how they 
actually behave, so that if you buy 
one off the shelf you know it meets a 

Aufderheide: There are two types of 
automated external defibrillators 
(AEDs) — fully-automated and semi-au- 
tomated. Fully automated defibrilla- 

tors require only that the operator at- 
tach the defibrillatory pads and turn 
on the device. The device then ana- 
lyzes the rhythm; if ventricular fibril- 
lation is present, the device will 
charge its capacitors and deliver a 
shock. Semi-automated devices re- 
quire additional operator steps, in- 
cluding pressing the Analyze control 
to initiate rhythm analysis and press- 
ing the Shock control to deliver the 
shock. The shock control is pressed 
only when the device identifies ven- 
tricular fibrillation and advises the 
operator to press the Shock control. 

Of the AEDs currently available, 
one device requires a signal amplitude 
of > 1.5 mm and another requires > 
2.0 mm. The difficulty is that a device 
that is sensitive to very fine ventricular 
fibrillation will probably have lower 
specificity and may misdiagnose sig- 
nal noise as ventricular fibrillation. 
Furthermore, optimal sensitivity/spe- 
cificity may vary, depending on the 
clinical setting and the operator. When 
used by trained and experienced EMS 
personnel, the AED may have high 
sensitivity and low specificity because 
the operators are able to verify cardiac 
arrest and react to and minimize signal 
noise. In settings where operators have 
had little experience with cardiac ar- 
rests, a device with low sensitivity and 
high specificity may be preferred. 

Shock-advisory AEDs may theo- 
retically be safer because they never 
enter the analysis mode unless acti- 
vated by the operator, and they leave 
the final decision to deliver the shock 
to the operator. This potential in- 
crease in safety is more theoretical 
than real. Clinical experience sug- 
gests the devices are equally safe 
with or without a human operator to 
push the Shock button.' 

To summarize, the technology has 
been standardized to the point of pro- 
ducing two types of devices — fully- 
and semi-automated. Computerized 
rhythm analysis has variable sensitiv- 
ity and specificity for the detection of 
ventricular fibrillation depending on 

the device. The final impact of the 
application of the device will also be 
affected by the clinical scenario in 
which it is used. Clinical experience 
to date suggests little difference in 
outcome based on the type and mod- 
els of devices u.sed.' 

1, Stults KR, Cummins RO. Fully auto- 
matic versus shock advisory defibrilla- 
tors-what are the issues? J Emerg Med 
Serv 1987:12:71-73. 

Durbin: Just to respond to that. My 
biggest concern is that if we see pub- 
lished data, will it be important to 
know which device, specifically, was 
used in order to evaluate the outcome 
of that particular intervention? 

Aufderheide: Preliminary clinical 
studies appear to demonstrate no sig- 
nificant difference in outcome fol- 
lowing cardiac arrest based on differ- 
ences in the type of automatic exter- 
nal defibrillators applied. Nonetheless, 
I think it is valuable to identify the 
type of device used and its clinical 
setting and incorporate that into how 
you interpret that study's findings. 

Kaye: Again I want to commend you 
on your review. It's not a criticism, 
but, in my old age I have learned to 
get simpler and simpler. First, we 
have to remember that this group is 
addressing the issue of resuscitation 
in acute care hospitals. We must not 
get misled or led down the path with 
all of these issues about Should 
Mama be taught to defibrillate Dad in 
the house if he's a high-risk patient? I 
think we have to be careful. Sec- 
ondly, there's no question that if the 
patient appears dead, which means 
pulseless and apneic and resuscita- 
tion is appropriate, the first thing is to 
determine whether V-fib (ventricular 
fibrillation), is present, and then to 
defibrillate. In hospital I've become 
an evangelist — all first responders 
must be trained to operate an AED 
(automated external defibrillator). 
AEDs are no longer experimental. I 




think we have to be very careful we 
don't get misled into becoming too 
cerebral. The science is there. Early 
defibrillation is the answer. AEDs 
work. AEDs should be in every hos- 
pital to be used by every first respon- 
der. They should be as available as 
fire-extinguishers. We should move 
beyond the issues of are they safe, are 
they accurate? They're safe. They're 
accurate. If you can assess when the 
person's apneic and pulseless, put the 
device on and shock. 

Aufderheide: I believe the currently 
available literature supports advocat- 
ing the use of AEDs by every trained 
first responder in every hospital. I 
also believe that AED use by un- 
trained lay bystanders cannot be ad- 
vocated until a national consensus 
has been reached regarding the many 
medical, social, and legal issues. 

Kaye: In-hospital. 
Aufderheide: Oh, in-hospital. 
Kaye: My concern is in-hospital. 

Pepe: I want to echo what Bill (Kaye) 
said because I think a lot of times when 
we have codes, staff on the floor pull 
out a crash cart and don't even know 
how to use the defibrillator because 
they haven't used it a lot. AEDs are so 
intuitive that it should be a much better 
thing to use on the crash cart than what 
we currently have. The second thing I 
want to say in regard to defibrillation is 
that I think it's a dynamic process. In 
some ways it can be very simplistic to 
say that you should always defibrillate 
as the first intervention. In the first few 
minutes after cardiac arrest, when there 
is very coarse V-fib and a lot of energy 
left in the heart, it is plausible that 
countershock is the first thing you 
should do. On the other hand, it may be 
that after 10 minutes of ventricular fib- 
rillation, you may have to do other 
things first.' You may have a certain 
amount of salvage potential at 10 min- 

utes, and the shock is only going to 
turn on (depolarize) the heart with the 
last bit of energy that it has left. As a 
result, it doesn't start up again (like a 
radio with dying batteries). Better to 
somehow provide perfusion for the 
coronary arteries, first. So I think in the 
future we may want to be able to look 
at the V-tlb waveform in real time.- On 
a scale of 1 - 1 0. if the score is 8 or 9 or 
10, you should shock first. However, if 
the score is 1 or 2, you may do other 
things first — intubate, give epineph- 
rine, and "sweeten up the myocardi- 
um, "-As Jim Niemann and Dave 
Persse would say-and then shock. I 
believe that'll be an interesting para- 
digm to investigate down the line. 

1. Niemann JT, Cairns CB, Sharma J, 
Lewis RJ. Treatment of prolonged ven- 
tricular fibrillation: immediate counter- 
shock versus high-dose epinephrine 
and CPR preceding countershock. 
Circulation 1992;85:281-287. 

2. Brown CG. Griffith RF, Van Ligten P. 
Hoekstra J, Nejman G, Mitchell L, 
Dzwonczyk R. Median frequency: a 
new parameter for predicting defibrilla- 
tion success rate. Ann Emerg Med 

Mathews: I hate to bring us back to 
the prehospital situations, but it's al- 
ready been brought up, and there's 
something that we really need to ad- 
dress — What do you do with these de- 
vices if they are out there in the public? 
When the patient moves or dies, do we 
find these things in estate sales, garage 
sales, at auction? It's really not funny, 
because we have at least one bar in the 
Kansas City area with an oxygen con- 
centrator they picked up at a garage 
sale. They are now selling oxygen for 
$2 for about 5 minute's use. We've 
talked to the FDA. and they won't do 
anything about it. They're not too wor- 
ried about oxygen. 

The other thing is, and this is 
something we discussed at length at 
the AARC's Home Care Equipment 
Consensus Conference that we did in 
Bethesda, Maryland. Was it in 1988. 
Sam'.' I believe so. One focus group 

concentrated on tracking. We talked a 
lot about how to track medical instru- 
ments after they are in the home.' 
There are ventilators out there in 
garage sales. This is an issue that you 
must think of. when you're putting 
something into the public's hands 
that's as potentially dangerous as an 
AED with no way of tracking it. 

1. American Association for Respiratory 
Care. Final report on the concensus 
meeting on home respiratory care 
equipment, September 29-30. 1988. 
Dallas: American Association for 
Respiratory Care 1989:20-24. 

Barnes: I agree with Bill and I think 
we should really focus on acute care 
hospitals for this conference. I'd be 
really interested, Tom, in your feel- 
ings about, not laypeople, but health 
care professionals using AEDs. Do 
manual defibrillators have enough 
advantages to recommend their use in 
hospitals? Are there studies out there 
showing that staff don't know how to 
use some models of manual defibril- 
lators because they can't go from one 
model to the next? Does that mean 
we should be using only AEDs in 

Aufderheide: The National Heart, 
Lung, and Blood Institute has issued 
a consensus opinion that all first re- 
sponders should have defibrillation 
capability.' It seems logical to me 
that autoinated external defibrillators 
are an ideal biotechnology to imple- 
ment for in-hospital cardiac arrest 
teams. One would expect this tech- 
nology to reduce the impact that vari- 
ations in defibrillation skills of first 
responders would have on cardiac ar- 
rest victims. However. I know of no 
prospective, in-hospital, randomized 
studies evaluating cardiac arrest out- 
come with the use of inanual versus 
automatic defibrillators' 

I. Ornalo JP, Aufderheide TP, Wynn J, 
Anderson PB. Working Group Report: 
Present and I-uture Prehospital Manage- 


RiiSPiRATORY Care • April '9."^ Vol 40 No 4 


merit. In; Proceedings of the National 
Heart, Lung, and Blood Institute Sym- 
posium on Rapid Identification and 
Treatment of Acute Myocardial Infarc- 
tion. JH LaRosa, MJ Horan. and ER 
Passamani, eds. U.S. Department of 
Health and Human Services, National 
Institutes of Health. 1991:140. 

Halperin: This has to do with the 
FDA. Although the medical commu- 

nity is firmly convinced of the utility 
of automatic defibrillators, the FDA 
actually isn't. The reason they aren't 
is because the companies that make 
them typically label them to say that 
they are safe and effective and that 
they will respond to V-fib. But, occa- 
sionally, they don't. The problem that 
Physiocontrol got into (as well as 
some other defibrillator companies) is 

the fact that they labeled them that 
they would convert V-fib. But, occa- 
sionally, they don't. So I think it's up 
to the medical community — and 
maybe up to us — to define criteria 
that says that the automatic defibrilla- 
tor is good enough. Without that guid- 
ance, the FDA will be very rigid and 
will limit the dissemination of this 
very valuable technology. 

41st Annual Convention and Exhibition 
December 2-5 • Orlando, Florida 

Respiratory Care • April '95 Vol 40 No 4 


Compression Techniques and Blood Flow during 
Cardiopulmonary Resuscitation 

Henry R Halperin MD, Nisha C Chandra MD, Howard R Levin MD, 
Barry K Rayburn, MD, and Joshua E Tsitlik MD 







Basic & Clinical Science 

A. The Pumps 

B. Modifiers of the Pumps 

1. Abdominal Pressure 

2. Circumferential Chest 


3. Active Chest Decompression 

C. The Vascular Load 
Therapeutic Options 

A. Optimizing the Pumps 

B. Optimizing the Vascular Load 

C. Invasive Adjuncts for Improving 

Blood Flow during CPR 
Monitoring the Effectiveness of CPR 
The Future 

A. The Nature of the Pump 

B. Improving Standard Chest Compression 

C. Alternative Compression Techniques 

D. Improving Adjunctive Therapy 

Portions of this manuscript appear in Halperin HR. Mechanisms of fore- 
ward flow during external chest compression. In: Paridis N. Halperin H. 
Nowak R, eds. Cardiac arrest: the pathophysiology and therapy of sudden 
cardiac death. Baltimore: Williams & Wilkins (in press). 

Drs Halperin and Tsitlik are Associate Professors of Medicine and 
Biomedical Engineering. Dr Chandra is Associate Professor of Medicine. 
Peter Belfer Cardiac Mechanics Laboratory. The Johns Hopkins 
University School of Medicine, Baltimore. Maryland. Dr Levin is 
Assistant Professor of Medicine, Columbia University School of 
Medicine. New York. New York, and Dr Rayburn is Assistant Professor 
of Medicine, Bowman Gray School of Medicine. Winston-Salem. North 

Reprints: Henry R Halperin MD. Peter Belfer Cardiac Mechanics 
Laboratory. The Johns Hopkins University School of Medicine, 
Cardiology . Blalock 524, 600 N Wolfe Street. Baltimore MD 2120.";. 

Vest-CPR technology has been licensed to Cardiologic Systems Inc. in 
which the authors and the Johns Hopkins University hold equity. By the 
policies of the Johns Hopkins Univeristy. the equity is being held in es- 
crow until a trigger date that has been set by the Johns Hopkins 
Univeristy Committee on Conflict of Interest. 


Laboratory and clinical studies have shown that restora- 
tion of cardiac function after cardiac arrest is related to the 
level of coronary perfusion generated during resuscitation. '■- 
It is also clear that adequate cerebral perfusion is critical for 
preservation of brain function.' There is, therefore, a critical 
need for methods that can augment the blood flow that can 
be generated during resuscitation. A key factor in determin- 
ing these methods is understanding the mechanisms of flow 
that are operative during resuscitation because it may be 
possible to optimize flow by exploiting those mechanisms. 

Fluid movement in any hydraulic system results from the 
interaction of a pump, or driving force for fluid movement, 
and a load. Pumps that appear to be operative during chest 
ct)mpression include direct cardiac compression,^ and in- 
trathoracic pressure lluctuation.'' It is important to determine 
the nature of the pump because the method of chest com- 
pression for optimizing flow may be different, depending on 
the pump that is operative.' 


Ri si'iKAioRV Caki-: • aXpril "95 Vol 40 No 4 

Compression Techniques & Blood Flow 

Cardiac Compression Pump 


Intrathoracic Pressure Pump 


Fig. 1. Schema of the cardiac-compression pump (left panel) and the intrathoracic-pressure pump (right panel). The cardiac-compression- 
pump model postulates that chest compression causes the heart to be compressed between the sternum and vertebral column. Presumably, 
blood is squeezed from the heart into the arterial circulation during chest compression, with the cardiac valves preventing retrograde blood 
flow. Also presumably, air moves out of the lungs (upper right arrow), venting intrathoracic pressure. With chest relaxation, the heart expands 
and fills with blood. The intrathoracic-pressure-pump model postulates that chest compression causes a rise in intrathoracic pressure (large 
arrows), that is transmitted to the intrathoracic vessels. Blood flow out of the thorax is presumed to result from the differential transmission of 
intrathoracic vascular pressure to the extrathoracic arteries and veins. Veins at the thoracic inlet (leading into the right heart) collapse, which 
prevents transmission of intrathoracic venous pressure to the extrathoracic veins. With chest relaxation, intrathoracic pressure drops, with 
return of venous blood from the peripheral circulation into the thoracic venous system. LH = left heart; RH = right heart. 

For optimizing flow, it may also be important to under- 
stand the effects of a number of techniques that may en- 
hance the pump's performance. These techniques include 
(1) abdominal compression,* (2) circumferential chest com- 
pression,^ and (3) sternal force applied during chest relax- 
ation (active decompression).** Newer methods of improving 
blood flow, based on these techniques, are currently being 

In addition, the vascular load during resuscitation may 
have profound effects on coronary and cerebral blood flow."* 
Increases in peripheral resistance may preferentially shunt 
flow to the heart and brain, whereas low peripheral-resis- 
tance states may lead to vascular collapse with reduction of 
flow.' A detailed understanding of how the vascular load af- 
fects blood flow and how the vascular load can be altered, 
may be useful in determining methods for optimizing flow. 

Basic & Clinical Science 

The Pumps 

The cardiac-compression-pump model postulates that 
chest compression does not cause intrathoracic pressure to 

rise. Instead, the heart is compressed between the sternum 
and vertebral column"* (Fig. 1). It is presumed that blood is 
squeezed from the heart into the arterial circulation during 
chest compression, with the cardiac valves preventing ret- 
rograde blood flow. With release of chest compression, the 
heart expands and fills with blood. However, the intratho- 
racic-pressure-pump model suggests that chest compres- 
sion causes a rise in intrathoracic pressure, which is trans- 
mitted to the intrathoracic vasculature (Fig. 1).-'' Blood 
flow out of the thorax is presumed to result from the differ- 
ential transmission of intrathoracic vascular pressure to the 
extrathoracic arteries and veins. With release of chest com- 
pression, intrathoracic pressure drops, and venous blood 
from the periphery returns to the thoracic venous system. 

Current evidence suggests that the intrathoracic pres- 
sure pump is probably responsible for most of the driving 
force for blood movement during standard external chest 
compression, although the cardiac compression pump 
probably contributes, to some extent. Some newer meth- 
ods for improving blood flow during cardiopulmonary re- 
suscitation (CPR) appear to exert their benefit by modify- 
ing the pump to augment the vascular pressures that are 

Respiratory Care • April '95 Vol 40 No 4 


Compression Techniques & Blood Flow 

Fig. 2. Interposed abdominal counterpulsation during human car- 
diopulmonary resuscitation. During chest compression, force is re- 
leased from the abdomen. During chest relaxation (upward arrow), 
force is applied to the abdomen (Downward arrow). Reprinted, with 
permission, from Reference 1 1 . 

Modifiers of the Pumps 

Abdominal Pressure. Abdominal pressure influences the 
intrathoracic pressure pump directly because manipulation 
of abdominal pressure can affect the level of intrathoracic 
pressure generated.'" Manipulation of abdominal pressure 
during chest relaxation, termed interposed-abdominal-com- 
pression CPR or abdominal-counterpulsation CPR (Fig. 2), 
has been studied extensively."" In addition to the increase 

in intrathoracic pressure, it is presumed that abdominal com- 
pression, delivered between chest compression, compresses 
the aorta and produces greater retrograde aortic blood 
flow.'- As with intra-aortic balloon pumping, the resulting 
increase in aortic pressure appears to augment coronary 
blood flow. The results of animal studies of interposed-ab- 
dominal-compression techniques have been variable, and 
abdominal mechanics may be quite different in man than in 
animals. In man, direct compression of the aorta by abdomi- 
nal compression may be more effective than in the dog. 
Increasing intrathoracic pressure during chest relaxation 
may prolong the duration of intrathoracic pressure, which 
could augment coronary flow.''' Alternatively, right atrial 
pressure may be raised relative to aortic pressure, which 
could decrease coronary flow. However, hemodynamic data 
in humans are not available. 

Recently, improved survival in humans with interposed- 
abdominal-compression CPR was reported." However, the 
force and frequency of chest compression was not controlled, 
either in the group receiving abdominal compressions or in 
the group receiving standard manual CPR, so that the contri- 
bution of the abdominal compressions themselves cannot be 
determined. This approach requires further investigation. 

Circumferential Chest Compression. Circumferential 
chest compression has been suggested as a more effective 
way of generating intrathoracic pressure fluctuation (Fig. 3).' 

Vest CPR CI 

Fig. 3. Thoracic vest system for CPR (upper-left), and standard manual CPR (upper-right). The vest contains a bladder that is inflated and 
deflated by the pneumatic system. Defibrillation can be accomplished during chest compression through the flat defibrillator electrodes 
(dashed circles) under the vest. The electrocardiogram signals are transmitted through the same electrodes. The lower panels are trans- 
verse sections of the midthorax during vest and manual CPR. Thoracic size during chest relaxation is shown by the solid lines. The arrows in- 
dicate force applied to the thorax during chest compression. With vest inflation, there is a relatively uniform decrease in thoracic dimensions. 
With manual CPR, the sternum is displaced during compression as indicated by the arrow, and the lateral thorax can bulge, thereby increas- 
ing lung volume and reducing the level of generated intrathoracic pressure. Reprinted, with permission, from Reference 7. 


Rhsi'ir.m'ory Carl • April "95 Vol 40 No 4 

Compression Techniques & Blood Flow 

This technique is generally accomplished with a pneumat- 
ic vest,^ and has been termed vest CPR. The increased in- 
trathoracic pressure fluctuation appear to be mediated 
through increased chest compression force,' and through 
increased airway collapse during chest compression, 
which traps air in the lungs.''* Increased chest compression 
force raises intrathoracic pressure relative to the reduction 
in lung volume, assuming air trapping occurrs. By reduc- 
ing expiratory air flow, air trapping could also increase the 
efficiency with which vest pressure is transmitted to the in- 
trathoracic space. Any decrease in expiratory airflow 
would reduce the amount of chest deformation at any level 
of vest pressure. At the reduced amount of chest deforma- 
tion, less of the force applied to the chest would be needed 
to compress the elastic structures of the thorax, resulting in 
greater transmission of vest pressure to the intrathoracic 

When used late in cardiac arrest, vest CPR has been 
shown to augment aortic pressure and coronary perfusion 
pressure in humans (Fig. 4),' and to increase short-term 
survival. A multicenter clinical trial is ongoing to deter- 
mine whether the hemodynamic benefits of vest CPR, 
when started early in cardiac arrest, can improve long-term 

Active chest decompression. Active, rather than passive, 
decompression of the chest has been reported to augment 
vascular pressures'-'' and promote the return of spontaneous 
circulation.'^ The technique, termed active-compression-de- 
compression (ACD) CPR, utilizes a suction-cup device to 
pull up on the chest during chest relaxation. The mechanisms 
operative during ACDs have not been well characterized, but 
this technique may produce greater chest expansion and air 
entry between compressions, increasing the amount of air 
trapped in the lungs and augmenting intrathoracic pressure 
that is generated. '■" In addition, the active decompressions 
may induce negative intrathoracic pressure between com- 
pressions, augmenting venous return and enhancing the for- 
ward flow produced by cardiac compression or by intratho- 
racic pressure fluctuation. Few data are available on the level 
of chest compression force used with this technique. 
Therefore, it is not known whether reported benefit for active 
decompression CPR results simply from an increased total 
force (peak compression-to-peak decompression force) ap- 
plied to the chest. For example, if a 400 N compression force 
and a 100 N decompression force are applied to the chest, is 
it simply equivalent to applying 500 N of compression force 
or does the decompression force have unique and separate 
physiologic effects that improve blood flow? Results of 
studies reported, to date, have not resolved these issues. 

ACD devices used to apply the active compressions and 
decompressions may also give the rescuer a mechanical 
advantage in performing chest compression, resulting in 

X ao. 

E «• 

l:^V-y^^y^~V~- ".XJ^XTXT 

Fig. 4. Vascular pressure recordings during manual and vest CPR 
in 2 patients (A and B), reproduced from digital recordings. 
Compared with manual CPR, Record A shows one of the largest 
changes in aortic pressure and the aortic right-atrial pressure (coro- 
nary perfusion pressure) produced by vest CPR, whereas Record B 
shows one of the smallest changes. Continuous line is aortic pres- 
sure and the dashed line is right-atrial pressure. Reprinted, with 
permission, from Reference 7. 

substantially higher sternal forces being applied than with 
standard manual CPR.** These increased forces may aug- 
ment the generated intrathoracic pressure or enhance car- 
diac compression, increasing short-term survival. How- 
ever, if trauma results, long-term survival may be reduced. 
Because the physiology of active-decompression CPR re- 
mains unclear, further study of this technique is needed. 

Tiie Vascular Load 

As with the intact circulation, the vascular load during 
external chest compression is probably determined by the 

Respiratory Care • April '95 Vol 40 No 4 


Compression Techniques & Blood Flow 

resistance and compliance of the arteries. However, these 
values during CPR may be substantially different from 
those of the intact circulation, due to changes in neural-hu- 
moral conditions, ischemia, administered drugs, and me- 
chanical maneuvers, such as applying pressure to the ab- 

The arterial (systemic vascular) resistance (SVR) ap- 
pears to be the most critical loading factor that influences 
coronary and cerebral blood flow. Studies have shown that 
administering drugs that increase SVR increase coronary 
perfusion pressure and blood flow and cerebral blood flow 
and promote return of spontaneous circulation (Fig. 5).'^'* 
Increased SVR likely decreases the runoff of blood into 
the peripheral circulation during chest compression, main- 
taining higher levels of aortic pressure, regardless of the 
nature of the pump. The dependence of the newer tech- 
niques of increasing blood flow on SVR has not been de- 

Therapeutic Options 

The goal of external-chest-compression CPR, when de- 
fibrillation fails or is not indicated, is to maximize the gen- 
erated coronary and cerebral blood flow. Restoration of 
native cardiac activity and preservation of brain function 
are directly related to these flows. Cerebral and coronary 
flows should be maximized by optimizing the driving 
force for blood movement, and the loading conditions. 

Optimizing the Pumps 

For intrathoracic pressure fluctuations, the amount of 
lung volume reduction produced by chest compressions 
appears to be critical. By Boyle's law, the more lung vol- 
ume is reduced, the more intrathoracic pressure will rise. 
In current clinical practice, lung volume is reduced by the 
standard anteroposterior sternal displacement technique, 
although other techniques are being studied that may prove 
to be more effective.^ "•' ' For maximizing cardiac compres- 
sion, however, the amount of lung volume reduction is 
probably not important. The major determinant of cardiac 
compression is likely the amount of anteroposterior chest 
displacement, although the exact determinants of cardiac 
compression are unknown. Whether the driving force for 
blood flow is intrathoracic pressure fluctuation or direct car- 
diac compression, the force of chest compression is a critical 
determinant of blood flow (Fig. 6), and the quality of chest 
compression will likely be a major factor in the effective- 
ness of CPR. 

The ability of even properly performed chest compres- 
sions to generate adequate levels of intrathoracic pressure 
during cardiac compression is probably marginal because 
onlv about \5'/i of cardiac-arrest victims survive. However, 

chest compression is the only technique for CPR that is 
widely available, and many lives are saved each year by the 
application of standard CPR. Proper chest compression re- 
quires that the arms of the rescuer be locked relatively 
straight and that the whole body be used in the compres- 
sions. Often, only the arms are used for chest compression, 
which is extremely tiring, and likely does not generate suffi- 
cient compression force. 

Whereas the amount of chest compression force or lung 
volume displacement appears to be a major determinant of 
the level of generated vascular pressure." chest compres- 
sion must be applied at the optimal rate and compression du- 
ration. Blood flow due to intrathoracic pressure fluctuation 
should be insensitive to rate over a wide range but depen- 
dent on the compression duration."'''-" However, if direct 
compression of the heart plays a major role, blood flow 
should be dependent on rate but above some threshold 
should be insensitive to compression duration. The current 
recommendation of a compression rate of 80- 100/min prob- 
ably maximizes blood flow from either pump as much as 
possible. At that rate, the compression duration tends to be 
around 50%,-' which is optimal for blood movement by in- 
trathoracic pressure fluctuation.-" The compression rate of 
80- 100/min is near the maximum that can be administered 
for any length of time by a rescuer and maximizes the num- 
ber of stroke volumes delivered to the circulation by the car- 
diac-compression pump.-" During studies of standard CPR, 
myocardial and cerebral blood flow were increased when 
the compression duration (percent of cycle in compression) 
was increased from 1 5% to 45%, but were unchanged when 
the rate was increased from 60 to 150/min (Table 1 )." This 
duration-dependence of flow and rate insensitivity suggest 
that blood flow was due to changes in intrathoracic pressure. 

Effect of Constant-Force Chest-Compression Rate and 
Duration on Myocardial and Cerebral Blood Elow in 8 Dogs 
during Manual Cardiopulmonary Resuscitation (CPR). Data 
are mean (SEM) in mL ■ min ' • 100 g'." 










25 (6) 
11 (4) 

3.1 (7)' 

.32 (5)' 

* M60S = manual CPR at 60 comprcssions/min with short duration (com- 
pression for 15% of cycle); M60L = manual CPR at 60 compres- 
sions/min with long duration (45% of cycle); Ml SOL = manual CPR at 
ISOcompressions/min with long duration, p < 0,01 vs M6()S; tp < 0.02 
vs M60S. 

The level of generated va.scular pressures can likely be 
affected by techniques that modify the pump, including ab- 
dominal compression,"-- airway manipulations,'"-' cir- 


Respiratory Care • April "95 Vol 40 No 4 

Compression Techniques & Blood Flow 

cumferential chest compression,'-''-'' and active decompres- 
sion.*'"' The efficacy of abdominal compression, circumfer- 
ential chest compression, and active chest decompression 
have not been definitively determined, so that their use in 
routine practice is not recommended. The only technique 
that should be used routinely at this time is airway inflation 
between chest compressions. This airway inflation is used 
for ventilation, but It can also augment vascular pressures 
generated by the intrathoracic-pressure pump. Lung infla- 
tion prior to chest compression can increase the amount of 
air trapped in the lungs during chest compression,'"* thereby, 
augmenting the generated intrathoracic and vascular pres- 
sures, and improving the efficiency of CPR. 

Optimizing tlie Vascular Load 

Peripheral resistance is probably the component of the 
vascular load that has the largest effect on blood flow. 
Numerous studies have shown that vascular pressures are 
augmented and produce increased flow to the heart muscle 
and brain when vasoconstrictors are used (Fig. 5).-^-" This 
increased flow appears to be mediated through a-adrenergic 
agonism,'^"*-'' which increases SVR and decreases runoff 
of blood to the peripheral circulation. Decreased runoff 
slows the decay of arterial pressure during the release phase 
of chest compression, thereby raising aortic pressure, my- 
ocardial perfusion pressure (aortic pressure minus right-atri- 
al mean release-phase pressure), and cerebral perfusion 
pressure (carotid pressure minus mean intracranial pres- 


"o S I 1 I 1 


■40 It 

on '° ° 

■30 o -^ 


■20 5 .£ 

0) ■ 

10 S^ 



Fig. 5. Effect of epinephrine on myocardial and cerebral flows in 
dogs (n = 8). Flows were measured with radioactive microspheres. 
Flows were significantly different with (czi) and without {^M) 
epinephrine; p < 0.05.' 

The vasoconstrictor used most is epinephrine,'^ which 
has both a- and /J-agonist effects. It is clear that the a-ago- 
nist effects are responsible for the improved blood flow to 
vital organs. The utility of the /3-agonist effects, however, is 

controversial. Some investigators believe that P agonism is 
detrimental because of increased myocardial work."--' 
whereas others believe that P agonists offer benefit by in- 
creasing inotropy.'^ The efficacy of epinephrine compared 
with other vasoconstrictors remains to be determined. 

The use of increased doses of epinephrine to augment 
vital organ flow during CPR (especially later in resuscita- 
tion when tissue acidosis, hypoxia, and ischemia may be 
more profound) is gaining much interest. The exact role of 
high-dose epinephrine has not been determined because of 
conflicting clinical and laboratory data.*''' By increasing 
peripheral vascular resistance, increased doses of epineph- 
rine can increase blood flow to the heart muscle and 
brain.-'-''' Increased doses of epinephrine may, however, 
have direct toxic effects on tissues, and may exacerbate is- 
chemic damage to other tissues by shunting blood away 
from them. The utility of high-dose epinephrine in favorably 
altering the loading conditions during extemal-chest-com- 
pression CPR is, therefore, questionable. 

In contrast to increasing blood flow to the myocardium 
and brain, increased SVR can reduce total cardiac output. 
Cardiac output is reduced because the increases in SVR are 
greater than the increases in generated vascular pressures 
that are secondary to the increases in SVR.-'-'^ This de- 
creased cardiac output can explain the observation that 
end-tidal carbon dioxide tension (Petco:) can with 
increased doses of epinephrine.-' Petco: has been studied as 
a noninvasive method of determining the adequacy of resus- 
citation because it appears to correlate with cardiac output 
and resuscitation success in some circumstances." 

In addition to the effects of vascular resistance and com- 
pliance on blood flow during CPR, it appears that the blood- 
volume status contributes independently. If excessive vol- 
ume is present in the vascular spaces during CPR, the ve- 
nous pressures tend to be elevated during the release-phase 
of chest compression, which can reduce the coronary perfu- 
sion pressure. '** This finding strongly suggests that exces- 
sive volume should not be infused during resuscitation. If 
insufficient volume is present, however, forward flow ap- 
pears to be impeded by induced arterial collapse. Selective 
arterial infusion does appear to be of value in reversing this 
arterial collapse.'' 

Invasive Adjuncts for Improving Blood 
Flow during CPR 

Cardiac assist devices or cardiopulmonary bypass may 
be useful in prolonged arrests, when it is believed that the 
patient is still viable, as in cardiac arrest due to hypothermia 
or to drug overdose. assist devices, if they can be 
placed expeditiously, may also be u.sed in patients who are 
candidates for heart transplantation. In patients who experi- 
ence cardiac arrest in the catheterization laboratory because 
of cardiac ischemia, emergency angioplasty may be used to 

Respiratory Care • April "95 Vol 40 No 4 


Compression Techniques & Blood Flow 

reduce ischemia and restore viability to the heart muscle. In 
this circumstance, angioplasty must be done quickly to limit 
ischemic damage. Standard CPR during angioplasty is gen- 
erally not possible, although cardiopulmonary bypass or 
possibly vest CPR may be used. In patients with more ex- 
tensive coronary disease who experience cardiac arrest, 
emergency bypass surgery may be considered, if CPR is 
judged to be providing adequate blood flow and the patient 
is an excellent candidate. A major problem with 
sending patients in cardiac arrest to cardiac surgery is that ir- 
reversible brain damage may have been sustained during the 
arrest, which may eliminate any benefit from emergency 
surgery. Finally, intra-aortic balloon pumps may be used 
immediately after resuscitation to provide circulatory assis- 
tance to the stunned heart, until it can recover. The potential 
neurologic status of the patient must be considered when de- 
ciding whether to institute such invasive therapy. 

Monitoring the Effectiveness of CPR 

Interest in using invasive and noninvasive techniques to 
determine the effectiveness of CPR exists. The reason is 
that if a particular CPR technique is found to be ineffec- 
tive, a different technique could then be performed to in- 
crease the chances of successful resuscitation. These dif- 
ferent CPR techniques could be more invasive ones, such 
as open-chest cardiac massage,''^-" or cardiopulmonary by- 
pass.'*- Even though Petco^ correlates with cardiac output 
and has been suggested as a means for determining the ef- 
fectiveness of CPR," myocardial and cerebral blood flows 
are more strongly correlated with return of spontaneous 
circulation than is cardiac output. Moreover, cardiac out- 
put can be reduced by vasoconstrictors, which are given to 
increase cerebral and myocardial flow because the vaso- 
constrictors increase SVR. Therefore, measures of cardiac 
output can only correlate with the effectiveness of CPR if 
the SVR does not change. With periodic use of epineph- 
rine, it is likely that SVR varies substantially during the 
course of CPR. And measures of cardiac output are proba- 
bly unreliable indicators of the efficiency of CPR. 

Measurement of coronary perfusion pressure is proba- 
bly the best method of monitoring the effectiveness of 
CPR, because of the direct correlation with restoration of 
spontaneous circulation.- The disadvantage of this tech- 
nique is that arterial and venous pressure-measuring 
catheters must be in place during CPR, and the delays in 
placing these catheters can be substantial. Coronary perfu- 
sion pressures < \5 mm Hg predict failure of resuscitalivc 
measures, whereas coronary perfusion pressures > 15 mm 
Hg predict successful resuscitation.- If the resuscitation 
team plans to substitute invasive techniques when standard 
resuscitative measures fail, then placement of catheters for 
measuring coronary perfusion pressure is a reasonable 

Tlie Future 
The Nature of the Pump 

Controversy continues as to the nature of the pump oper- 
ative during external chest compression. Future studies 
could potentially resolve that controversy, but it now seems 
that the driving force for blood flow produced by standard 
external chest compression is some combination of intratho- 
racic pressure fluctuation and direct cardiac compression. 
Whereas standard external chest compression does not ap- 
pear to allow selective utilization of intrathoracic pressure 
or cardiac compression, it is likely that more clever ways of 
applying force to the patient's heart and thoracic blood ves- 
sels that are based on exploiting specific mechanisms will 
be developed in the future. 

By its more focused application of force, cardiac com- 
pression is probably more efficient than intrathoracic pres- 
sure fluctuation for moving blood, given .some amount of 
pressure rise. However, it remains to be determined whether 
external CPR can compress the heart enough to generate ad- 
equate vascular pressures.'' It is also unclear how to specifi- 
cally augment cardiac compression during noninvasive CPR 
because the determinants of the effectiveness of cardiac 
compression have not been defined. These issues must be 
clarified with further research. 

Improving Standard Chest Compression 

One way of increasing blood flow is simply to increase 
chest-compression force. Clearly, some minimum amount 
of chest-compression force must be applied to generate 
blood flow (Fig. 6)." Ineffective CPR probably occurs be- inadequate chest-compression force is applied. In rou- 
tine clinical practice, no objective method exi.sts for a res- 
cuer to determine whether chest compressions are adequate. 
The American Heart Association recommends that the ster- 
num be displaced 1.5-2 inches during chest compression."*' 
but it is unknown whether that amount of chest compression 
is routinely applied or whether that amount of compression 
is optimal. We have frequently observed that chest compres- 
sions are performed with substantially less sternal displace- 
ment than recommended and with inconect rate or compres- 
sion duration. More emphasis should be placed on assuring 
that adequate chest compression is pertormed, even if more 
training is required. However, retention of skills is limited 
and even well-trained rescuers have no objective way of 
judging whether chest compression is adequate during CPR. 
The widespread use of gauges or other measuring aids may 
increase the likelihood that chest compression is performed 
properly. Whereas it is probably true that "any CPR" (ie, 
any blood flow) is better than no CPR, the available data 
suggest veiy strongly that "better CPR" (ie, CPR that gener- 


Ri-;siMRATORY Care • APRIL "95 VOL 40 No 4 

Compression Techniques & Blood Flow 

ates more blood flow) will improve survival.'"''^ The 
chance that ischemia will be relieved or that drugs will be de- 
livered adequately is low if there is insufficient blood flow 
generated during CPR. Increasing the force of chest com- 
pression beyond that normally used may improve blood flow 
and survival. However, it has not been determined whether 
increased sternal force would have more of an effect on im- 
proving blood flow and enhancing survival or on increasing 
trauma and limiting survival. External chest compression 
could also be modified by altering the point or points of force 
application and the rate of the force rise. Studies should be 
performed to investigate the influence of changes in chest- 
compression force on blood flow and survival. 

Force (N) 

Force (N) 

Fig, 6 (A) Correlation between normalized myocardial perfusion 
pressure and applied sternal force with manual CPR at 60 compres- 
sions/min with prolonged compression duration, in dogs. The perfu- 
sion pressure for each dog is expressed as a percent of the perfu- 
sion pressure obtained at a sternal force of 400 N for that dog. (B) 
Correlation between normalized cerebral perfusion pressure and 
applied sternal force with manual CPR at 60 compressions/min with 
prolonged compression duration. Normalization was performed as 
in A, Reprinted, with permission, from Reference 1 , 

Alternative Compression Techniques 

Understanding and exploiting the specific mechanisms 
of blood flow that operate during external chest compres- 

sion are probably the most important ingredients for devel- 
opment of improved compression techniques because these 
techniques can exploit specific mechanisms of flow. 

Circumferential chest compressions (vest CPR)' may be a 
more efficient way of generating vascular pressures and flow 
because the magnitude of the reduction in lung volume is 
critical for generation of intrathoracic pressure rises. The ad- 
vantage to reducing lung volume with a circumferential 
rather than a point compression is geometric rather than lin- 
ear, as Boyle's law would suggest (PV = k). Lung volume 
decreases roughly as the square of the decrease in the radius 
of a circle proscribed by the circumference of the chest from 
its relaxed state (ri) to its compressed state (ri) — 
(P[(r^2~'^i)^'^2]^ = ^")- Circumferential compression may 
also allow increased force to be used because the force is dis- 
tributed over a much larger area than with point compres- 
sion. However, because only preliminary data are available, 
the role of vest CPR in treating cardiac arrest remains un- 

With the circumferential vest, there appears to be more 
transmission of intrathoracic pressure to the abdomen than 
with standard CPR. The effect of this rise in abdominal pres- 
sure is unclear, although coronary flow could probably be in- 
creased by reducing this transmission of pressure to the ab- 
domen. The design of the vests could be improved so that the 
amount of transmitted pressure to the abdomen is reduced. 
Umiting its harmful effect on coronary blood flow. 

Another potential method of optimizing intrathoracic 
pressure changes is through increased air trapping. Increased 
air trapping is achieved by inflating the lungs prior to each 
chest compression or by active chest decompressions.*'* The 
active decompressions might result in greater chest expan- 
sion and filling with air between compressions, so that the 
next compression causes a greater rise in intrathoracic pres- 
sure and. thus, greater blood flow. Because the role of active 
decompressions remains to be determined, more studies are 
needed to assess the hemodynamic effects of this method and 
its potential effect on mortality. 

Finally, application of force to the abdomen during chest 
relaxation may augment vascular pressure." Animal studies 
using abdominal compressions have shown variable results, 
and few objective hemodynamic data are available in hu- 
mans. Further studies of this technique are needed. 

Improving Adjunctive Therapy 

The effectiveness of CPR may be improved by using 
drugs or mechanical techniques to favorably modify the 
pump or the load. Such interventions may increase peripher- 
al resistance to levels higher than those currently achieved, 
favorably alter the distribution of arterial compliance (in- 
trathoracic vs extrathoracic), increase air trapping, and aug- 
ment venous return. 

Respiratory Care • April "95 Vol 40 No 4 


Compression Techniques & Blood Flow 

Peripheral resistance may be increased to higher levels 
by using increased doses of epinephrine or other vasocon- 
strictor drugs. It is clear that the a effects of epinephrine in- 
crease peripheral resistance.'**-'' However, controversy per- 
sists as to the utility of the P effects. Some investigators be- 
lieve that P agonism is detrimental because it increases 
myocardial work.-' ■" whereas others believe that p agonism 
offers benefit by increasing inotropy." Increased doses of 
epinephrine may also have direct toxic effects on tissues, 
and may exacerbate ischemic damage to other tissues by 
shunting blood away from them. The roles of different dos- 
ing regimens of epinephrine and of other vasoconstrictor 
drugs are currently under investigation. 


The level of coronary perfusion generated during resusci- 
tation of cardiac arrest is, clearly, an important determinant 
of resuscitation success. Therefore, optimizing the compo- 
nents of coronary perfusion — the pump and the load — is 
key to improving patient survivability following cardiac ar- 
rest. Research that fully characterizes these components and 
perfects current techniques and develops new ones is clearly 
needed and is, in part, underway. 


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Compression Techniques & Blood Flow 

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Halperin Discussion 

Hamill: I have one question about the 
vest CPR. One of my concerns with 
some of the standard procedures are 
the rib fractures and chest trauma, par- 
ticularly in the elderly. What is the in- 
cidence of chest-wall trauma with the 

Halperin: The vest spreads the force 
out around the chest. It uses more force 
than standard CPR does, and I think 
that's why it generates higher pres- 
sures. But it turns out that the local 
force on any one portion of the chest is 
only one third of what it is with stan- 
dard CPR. So. in fact, there's been 
very little trauma that's been noted 
with the vest in the clinical trials.' 

Halperin HR, Tsitlik JE, Gelfand M. 
Weisfeldt ML, Gruben KG, Levin HR. 
et al. A preliminary smdy of cardiopul- 
monary resuscitation by circumferential 

compression of the chest with the use of 
a pneumatic vest. N Engl J Med 1993; 
329(1 1):762-768. 

Hamill: I guess I find that very appeal- 
ing because I'm always concerned 
when I'm doing CPR on elderly pa- 
tients. If I give them a flail sternum 
then they may end up dying on the 
ventilator, anyway. 

Halperin: If the patient already has rib 
trauma from, say, BLS that occurred 
first; we don't know how or whether 
the circumferential compressions in- 
crease or decrease that. 

Branson: I don't want to throw you 
off of the blood flow discussion al- 
ready, but it was interesting to me that 
(and you discussed Boyle's law) that 
your tracheal pressures are 40 cm HiO 
during compression CPR? Have you 
studied the airflow into the trachea 
with the compression, and is that 

enough so that you don't even need to 
ventilate the patient? 

Halperin: You're referring to vest 

Branson: Yes. 

Halperin: That's an excellent point. 
Actually, because of time considera- 
tions, I didn't use a couple of slides 
that show data related to that. We've 
already studied air movement during 
CPR.' It turns out that this very inter- 
esting phenomenon of air trapping oc- 
curs. When you inflate the vest initial- 
ly, there's a rush of air out of the tra- 
chea, and then airflow stops. This is 
assuming that the lungs have been in- 
flated. Let's look at the scenario — 
you're giving the 5th compression, you 
inflate the lungs, and then the vest in- 
flates. What happens is that air comes 
rushing out, then it stops, and when 



Halperin Discussion 

you release the vest, more air comes 
out. In addition, the higher the vest 
pressure, the less air comes out of the 
chest, paradoxically. So, what that says 
is that when the vest inflates, it collaps- 
es the airways, and traps air in the 
lungs. This is actually why the vest 
works. Because air is no longer vented 
out, intrathoracic pressure can rise, 
then, in relation to how much the chest 
is compressed. If air just kept coming 
out of the chest, it wouldn't matter how 
much you compressed it, intrathoracic 
pressure wouldn't rise. We also did 
some cineradiographic studies where 
we instilled tantalum into the airways 
of animals, and visualized that the air- 
ways actually collapsed.' Now. the 
ventilation issue is only starting to be 
investigated. Nisha Chandra and others 
are very interested in how much venti- 
lation is really needed during CPR, and 
whether chest compression itself 
moves enough air to provide adequate 
ventilation and oxygenation. Those 
studies are ongoing.- But, suffice it to 
say that the blood gases are no worse 
with vest CPR than they are with stan- 
dard CPR. 

1. Halpenn H, Brower R. Weisfeldt ML, 
Tsitlik J. Chandra N, Cristiano L, et al. 
Air trapping in the lungs during cardio- 
pulmonary resuscitation in dogs: a mech- 
anism for generating changes in intratho- 
racic pressure. Circ Res 1989;65(4):946- 

2. Chandra N, Halperin H, Gruben K, 
Tsitlik J. Ventilation and oxygenation 
during cardiopulmonary resuscitation. 
Circulation, (in press) 

Branson: We recently did a study 
looking al compliance in CPR victims 
and found that during regular chest 
compression, sometimes you can de- 
velop l.'SO-mL tidal volumes from the 
compression and then the relaxation of 
the chest wall.' 1 wonder if the same 
thing occurs with active compression- 
decompression, whether that actually 
increases tidal volume, and whether 
ventilation would be necessary at all. 
combined with continuous oxygen in- 
su mill ion. 

1. Davis K, Johannigman JA. Johnson RC, 
Branson RD. Lung compliance follow- 
ing cardiac arrest. Acad Emerg Med 
1995:(in press). 

Halperin: Clearly, that is very likely 
with the active compression-decom- 
pression CPR. A couple of groups 
have looked at airflows and tidal vol- 
umes, mainly Ahmid Idris in Gaine- 
sville, and they have presented prelimi- 
nary data that show that there's almost 
twice the airflow with active compres- 
sion-decompression CPR than there is 
with standard CPR, which is a very in- 
teresting finding. But again, the 
amount of ventilation required for 
CPR has to be defined in order to de- 
termine if that amount of ventilation is 

Pepe: There were two issues I wanted 
to raise. The first is the issue of 
whether brain, heart, and peripheral 
blood flow are separate. In other 
words, if we're making compressions 
that also raise superior vena cava pres- 
sure are we decreasing cerebral perfu- 
sion pressure? What's happening 
there? I want to know whether you 
have looked at such possible .sequelae 
with your devices. And I think that's a 
kind of potential problem that happens 
with the basic CPR that we do. The 
second issue that 1 wanted to raise has 
to do with ventilation. Sometimes, 
with positive-pressure ventilation, we 
often overzealously inflate people be- 
cause we're taught that we're supposed 
to titrate acidosis. But we also know 
that we don't have that much COj pro- 
duction during circulatory arrest. As a 
result, you may need very little ventila- 
tion, period.' One of the things I'm 
concerned about is the auto-PEEP ef- 
fect caused by too much positive-pres- 
sure ventilation during CPR, both be- 
fore and after return of spontaneous 
circulation. During CPR, overzealous 
ventilation may even be obstructive to 
cardiac output, to some extent. 

I. American Heart Association. I*mer- 
gcncy Care Comniillco. Suhcommillcc 

on ACLS. Adult advanced cardiac life 
support (ACLSl. Part III. Guidelines for 
cardiopulmonary resuscitation and emer- 
gency cardiac care. JAMA October 28, 
2. Pepe PE. Marini JJ. Occult positive end- 
expiratory pressure in mechanically ven- 
tilated patients and airflow obstruction: 
the Auto-PEEP effect. Am Rev Resp Dis 

Halperin: In terms of the brain blood 
flow issues, I think you are referring to 
the question of whether intracranial 
pressure rises, reducing brain blood 
flow. Or is it whether we have looked 
at brain flow per se? 

Pepe: I'm just saying that in the past 
we have traditionally looked at aortic 
pressure versus the right-atrial pres- 
sure, in CPR studies to determine what 
the circulatory pressure is doing. At the 
same time, we should also be paying 
attention to cerebral perfusion pres- 
sure, meaning the difference between 
what's going up in the aorta and what's 
coming down off the jugular bulb or 
something further up, intracranially. 

Halperin: Clearly, you have to get the 
heart back. I think that's the impetus 
for a lot of people who are looking at 
that. Brain blood flow is a little more 
difficult to quantify. I don't think jugu- 
lar bulb pressure is an adequate indica- 
tor of pressure because in- 
tracranial pressure can be much higher, 
and that's the downstream pressure. 
We do have some measurements. It 
turns out that very little intrathoracic 
pressure is transmitted to the intracra- 
nial space, if intracranial pressure is at 
a reasonable level. If intracranial pres- 
sure is high for some reason, like with 
an hypoxic insult, or maybe a pro- 
longed down time, then intracranial 
pressure rises dramatically when in- 
trathoracic pressure rises. This excess 
rise of intracranial pressure reduces 
cerebral blood flow. But, in all of the 
animal studies we've done in which 
we've measured intracranial pressure, 
we set more cerebral blood flow with 


Respiratory Care • April '94 Vol 39 No 4 

Halperin Discussion 

higher aortic pressures, and there does 
not seem to be a down side to that. 

1. Halperin H. Tsitlik J. Guerci A, Mellits 
ED. Levin H. et al. The detenninants of 
blood flow to vital organs during car- 
diopulmonary resuscitation in dogs. Cir- 
culation 1986;73(3):539-550. 

Durbin: I am concerned about volume 
status and venous return during all of 
these maneuvers. I noticed your right 
atrial pressures were in the range of 10 
cm H2O in the lowest indicator-case 
and 20-30 cm H2O in the highest cases. 
The new recommendations in ACLS 
are to infuse volume if you don't get 
good circulatory return, because hypo- 
volemia may be a problem. There's 
still a reluctance in clinicians to give 
large volumes of fluid to patients re- 
ceiving CPR. What's your opinion on 
optimal fluid status and how does that 
fit with your research? 

Halperin: There was one more com- 
ment 1 wanted to make on Paul's 
(Pepe) question. For all the CPR tech- 
niques we've ever studied, if the brain 
is viable, there's always more brain 
blood flow than heart blood flow. On 
your question about volume status, in 
our own studies in which we've mea- 
sured blood flows, we've always found 
that if the volume status is low, then 
myocardial and cerebral blood flows 
are compromised. Interestingly, 
though, if the volume status is exces- 
sively high, then blood flow can actu- 
ally be reduced under those circum- 
stances, as well. So there has to be 
some optimal volume status. I think 
what happens is that if the volume sta- 
tus is excessively high, you wind up 
getting a lot of pulmonary edema. 
Pulmonary edema is common during 
CPR. But I think the high volume sta- 
tus actually induces more pulmonary 
edema and more hypoxia, and this will 
reduce blood flow. In addition, 
Ditchey' did some work during which 
he volume-loaded, and actually found 
out that more of the volume goes to the 
venous side rather than to the arterial 

side. Therefore, excessive volume re- 
duces coronary perfusion pressure. 
Certainly, there's a caveat about using 
excessive volume, but I think we only 
use excessive volume in patients who 
are failing CPR anyway. Therefore, I 
don't really know how big a problem 
that is. 

1. Ditchey RV. Lindenfeld J. Potential ad- 
verse effects of volume loading on perfu- 
sion of vital organs during closed-chest 
resuscitation. Circulation 1984:69:181- 

Boudin: I would like to know if you 
could make a recommendation on the 
use of the intra-arterial balloon pump 
during cardiac arrest — is it beneficial 
to leave it on and, perhaps synchro- 
nize the manual chest compressions in 
an attempt to improve coronary and 
cerebral blood flow or should it be 
turned off? 

Halperin: So this is in patients that 
already have intra-arterial balloon 

Boudin: Right. They're already in 

Halperin: That's a tricky question. 
The problem is that the motion inside 
the chest during CPR is enormous. If 
you do cineradiography of the chest 
during chest compressions, the heart 
and the intravascular structures move 
a lot more than you would think. So, 
one of the problems with intra-aortic 
balloon pump catheters being in place 
is that there's a real risk of trauma. To 
synchronize balloon pump catheters 
with chest compressions is probably 
possible. In our own experience, the 
balloon pump seems to have a fairly 
trivial effect, compared to what CPR 
does. Balloon pumps on their own 
generate about 40 mm Hg pressure. 
CPR, if you're doing it well, gener- 
ates 80 mm Hg pressure. In our own 
experience, we haven't really seen 
much of an additive effect, and I think 
that's related to the fact that it is very 

difficult to synchronize. But I don't 
want to diminish the enthusiasm for 
invasive-type techniques. There's a 
lot of excitement with aortic occlu- 
sion techniques, with which, rather 
than having the balloon counterpuls- 
ing and letting the volume out in be- 
tween compressions, it actually oc- 
cludes the aorta, for maybe a minute, 
and volume is infused while CPR is 
going on. Now, those particular 
catheters, I think, are less stiff than 
balloon pump catheters, but all those 
techniques are currently under inves- 
tigation. My own clinical bias is that 1 
don't think there is evidence that the 
balloon pump really does anything, 
and I think there's as much chance 
that it could impede as enhance flow. 
I wouldn't recommend doing much 
with the balloon pump. 

Sanders: This is an excellent review 
of the various techniques of CPR. I 
wonder if one of the issues that maybe 
you are emphasizing is finding diver- 
gent outcomes for the same CPR tech- 
nique in different environments. For 
example, ACD CPR showed benefit 
in one city and no benefit in another. 
We must question our underlying as- 
sumption that there should be one 
standard CPR technique for all pa- 
tients. We all have different body 
habitus, which may mean different 
mechanisms of blood flow when CPR 
is applied. Even in your very elegant 
studies'- looking at the coronary per- 
fusion pressures with vest CPR, most 
of the coronary perfusion pressures 
went up, but there were several pa- 
tients whose coronary perfusion pres- 
sures decreased or stayed the same. 
Maybe, it's time that we treat patients 
as individuals, use the CPR technique 
that obviously optimizes perfusion in 
each patient. Some patients may ben- 
efit most from vest CPR, others from 
rapid-rate chest compressions, and 
others from intra-arterial catheter 
CPR. This concept depends on havin 
monitoring tools to assess the effi- 
ciency of CPR. 



Halperin Discussion 

1. Chandra NC, Tsitlik JE, Halperin HR. 
Guerci AD, Weisfeldt ML. Observations 
of hemodynamics during human car- 
diopulmonary resuscitation. Crit Care 
Med l990;l8(9):929-934. 

2. Halperin HR, Tsitlik JE, Gelfand M, 
Weisfeldt ML, Gruben KG. Levin HR. 
et al. A preliminary study of cardiopul- 
monary resuscitation by circumferential 
compression of the chest with use of a 
pneumatic vest. N Engl J Med 1993; 
329(1 1):762-768. 

Halperin: Those are excellent com- 
ments, I agree with you. I don't know 
what I can do about it now, but I think 
that should be addressed by future re- 

Rubenfeld: I was wondering if you 
could comment on the effectiveness 

of just a tight thoracic binder. Sup- 
pose you inflate the vest to whatever 
pressure and then continue giving 
standard CPR? 

Halperin: We haven't done that. The 
theory would be that maybe it would 
restrict the bulging at the side. I think 
the major problem with standard 
CPR is the fact that it can't deliver 
enough energy. Let me just give you 
an example. A conditioned Olympic 
bicyclist can generate 200 watts con- 
tinuously. We're not conditioned 
Olympic bicyclists. So we generate 
less power than that. Now, with the 
CPR vest, we're using 1,000 watts to 
compress the chest — and that only in- 
creases coronary perfusion pressure 

by about 50 percent. The issue is, 
how much would a minor increase in 
the amount of standard chest com- 
pression by some clever maneuver 
improve coronary perfusion? I'm not 
saying that vest CPR is the ultimate, 
but I think that all of these standard- 
CPR-type improvements have very 
small effects due to the fact that it's 
related to how much energy is avail- 
able to move blood. The heart re- 
quires only 3 watts in order to pump 
blood. We're applying 1,000 watts, 
with the vest, in order to move one 
tenth of the amount of blood that the 
heart moves. So, clearly, people 
weren't designed to move blood that 
way. I don't know what the answer 
might be. 

41st Annual Convention and Exhibition 
December 2-5 • Orlando, Florida 


Respiratory Care • April '94 Vol 39 No 4 

Practice Guidelines for Airway Care during Resuscitation 

Michael J Bishop MD 






Practice Guidelines — An Overview 

A. Why Have Guidelines? 

B. How Does a Guideline Differ from a Standard of Care? 

C. What GuideHnes Currently Exist? 
Guidelines for Airway Management 

A. Equipment Guidelines 

1. Experience with Airway Management Equipment 

2. Equipment Needed To Ascertain Tube Position 

B. Personnel Guidelines: Who Should Manage the Airway? 
Guidelines for Managing the Difficult Airway 


"Code Blue"or "Code 199" — whatever the euphemism 
used in your hospital — is a call that gets your adrenaline 
pumping and an exciting and dramatic event for health- 
care practitioners. Despite the variable outcome data for 
in-hospital resuscitations, the opportunity to return life to 
someone whose vital functions have ceased creates in all 
of us the desire to perform at our best. Clearing and main- 
taining a patent airway is critical during resuscitation — 
"airway" is the "A" in the ABCs of resuscitation. Perhaps 
because of the importance of opening the airway, it is a 
skill that often becomes a topic of controversy or of 'turf 
wars. Failure to manage the airway adequately tends to 
lead to criticism, recriminations, and a significant number 
of expensive medical malpractice actions.' Such failures 
are especially likely to occur during intubations outside 
the operating room when conditions are not well-con- 

Dr Bishop is Professor, Departments of Anesthesiology and Medicine 
(Pulmonary and Critical Care, adjunct). University of Washington School 
of Medicine and the Veterans Affairs Medical Center, Seattle, 

The author has no financial interest in any of the products mentioned in 
the text. 

A version of this paper was presented by Dr Bishop during the Journal 
Conference entitled, "Resuscitation in Acute Care Hospitals" held in 
Cancun, Quintana Roo, Mexico, October 1994. 

trolled, patients are more likely to be on the floor or on soft 
beds, vomitus may be present, and other conditions may be 

Establishing guidelines or using already established 
guidelines is a mechanism for providing optimal patient 
care and limiting controversy at the time of a cardiac ar- 
rest. If personnel, equipment, and procedures are identified 
and catalogued in advance, events proceed more smoothly. 

In this article, I discuss existing guidelines for airway 
management, with special emphasis on guidelines for re- 
suscitation. I also discuss the questions of who should be 
responsible for airway management during resuscitation 
and what latitude is available to individual hospitals for 
making qualified personnel available. Finally, I review the 
recently published American Society of Anesthesiologists 
(ASA) Practice Guidelines for Management of the Diffi- 
cult Airway.'' 

Practice Guidelines — An Overview 

Why Have Guidelines? 

The purposes of guidelines are ( 1 ) to assist the practi- 
tioner in making the appropriate decisions and (2) to limit 
the number of times we reinvent the wheel regarding opti- 
mal practice. Guidelines are generally created by a group 
of experts whose combined experience far exceeds that of 
any of the individuals involved in their development. That 
experience is then readily transmitted by means of guide- 

Respiratory Care • April '95 Vol 40 No 4 


Guidelines For Airway Care 

lines to the practitioner who may only occasionally en- 
counter a given situation. A difficult airway is a relatively 
rare event but one with the potential for catastrophic out- 
come. Studying guidelines that exist for such events can 
better prepare the clinician to respond to such events and 
improve patient outcome. Practice guidelines are not in- 
tended to serve as standards, ■* and their use does not guar- 
antee a desirable patient outcome. As medical knowledge 
evolves, guidelines need to be revised. 

How Does a Guideline Differ from a 
Standard of Care? 

Medical malpractice litigation often revolves around 
the '"standard of care." The standard of care is not a written 
code but is defined on an ad hoc basis by a judge or jury in 
such cases.' Established by the testimony of medical ex- 
perts, the standard may vary from region to region, state to 
state, or even within states. 

Guidelines permit a practitioner to exercise judgment 
within reasonable limits. However, when a guideline be- 
comes routinely used by a group with expertise in that spe- 
cialty, it becomes a de-facto standard. '' The practice of 
using exhaled COi to determine endotracheal-tube (ETT) 
placement is an example of the evolution of a de-facto 

Does such a standard apply across medical specialties? 
The presumption of the courts has been that there is free 
exchange across specialties. If a certain practice has be- 
come standard among specialists in a field, practitioners in 
other specialties are held to the same standard. As guide- 
lines are created, there is latitude for the exercise of indi- 
vidual judgement. However, once such guidelines are rou- 
tinely used by the majority of practitioners, they tend to be 
viewed by the courts and other authorities as a standard of 
care, and major deviations will need to be defended. 

What Guidelines Currently Exist? 

Existing guidelines relevant to airway management 
during resuscitation include the Advanced Cardiac Life 
Support (ACLS) Guidelines published by the American 
Heart Association'' and the American Association for 
Respiratory Care (AARC) Clinical Practice Guideline for 
Resuscitation in Acute Care Hospitals (RACH).^ Both of 
these sources address the training of individuals involved 
in airway management during resuscitation and the equip- 
ment that is used for airway management. However, the 
RACH Guideline applies only to the hospital setting. The 
ASA Practice Guidelines for Management of the Difficult 
Airway* specifically address airway management in areas 
of the hospital where anesthesia is administered — a space 
in a health-care facility that is specifically equipped and 

intended for the delivery of anesthetic care."* However, the 
pivotal role played by anesthesiologists in airway care is 
already leading to the application of these guidelines for 
airway management in areas of the hospital other than the 
operating room (OR). The higher prevalence of difficult- 
to-manage-airway events that occur outside the OR dic- 
tates the expanded application of the Guidelines. 

Guidelines for Airway Management 

Equipment Guidelines 

Guidelines are generally conservative and recognize the 
need to prove that a device is effective before advocating 
its routine use. ACLS Guidelines classify devices as Class 
I (usually indicated, always acceptable) and Class II (ac- 
ceptable, of uncertain efficacy, and may be controversial). 
Class II devices are further divided into Ila (the weight of 
evidence favors the use of the device) or Class lib (may be 
helpful and probably not harmful). Oral and nasopharyn- 
geal airways and endotracheal tubes are Class I devices 
and are clearly efficacious when used early in resuscita- 
tion. Alternative airway techniques including esophageal 
obturator airways, pharyngotracheal lumen airways, and 
Combitubes (esophageal-tracheal Combitube, or ETC) are 
all considered Class lib devices. Given the bias of the 
medical literature towards positive results, using newer de- 
vices with caution seems reasonable. 

Table 1 . Techniques for Management of the Difficult Airway 

I. Techniques for difficult intubation 

Alternative laryngoscope blades 
Awake intubation 
Blind intubation (oral or nasal) 
Fiberoptic intubation 
Intubating stylet/tube changer 
Light wand 
Retrograde intubation 
Surgical airway access 

II. Techniques for difficult ventilation 

Esophageal-tracheal Combitube 
Intratracheal jel slylel 
Laryngeal mask 

Oral and nasopharyngeal airways 
Rigid ventilating bronchoscope 
Surgical airway access 
Transtracheal jet ventilation 
Two-person mask ventilation 

IMPORTANT This tabic dispUiys cmnmonly cilcd techniques, li is not a compre- 
hensive list. The order of presentation is alphabetical and does not imply preference 
for a given technique or sequence of use. Combinations of techniques may be em- 
ployed. The techniques chosen by the practitioner in a particular case will depend 
upon specific needs, preferences, skills, and clinical constraints, (Repnnicii from 
Reference 4. with permission, ) 


RiispiRATORY Care • April "95 Vol 40 No 4 

Guidelines For Airway Care 

The ACLS Guidelines favor early tracheal intubation 
stating, "As soon as practical during the resuscitative ef- 
fort, the trachea should be intubated by trained person- 
nel.'"^ AARC RACH Guideline is similar and avoids rec- 
ommending newer, untested airway-management devices.' 
Equipment recommendations cover artificial airways and 
devices for their placement. The AARC Guideline lists de- 
vices for tube placement including a variety of laryngo- 
scope blades, stylets, forceps, fiberoptic bronchoscopes, 
tube-changing stents, and light wands. 

ASA Guidelines do not take a stand as to efficacy, but 
list "commonly cited techniques" for dealing with difficult 
intubation and/or ventilation (Table 1).^ These include 
such devices as the ETC and the laryngeal mask airway 
(LMA). The ASA guidelines also include suggested con- 
tents for a portable difficult airway management kit (Table 
2)."* Whereas some of the suggested devices such as retro- 
grade intubation equipment'* are unlikely ever to be sub- 
jected to rigorous scientific scrutiny, the assumption is that 
they may be reasonable alternatives in the hands of a 
skilled operator who understands how to use them safely. 

Experience with Airway-Management Equipment. The 

ETC (Fig. P) is a double-lumen tube that enables ventilation 
whether the tube is placed in the esophagus or in the tra- 
chea."^" One lumen resembles an esophageal obturator air- 
way with a blind distal tip and proximal perforations for the 
delivery of ventilation gas. The 100 mL pharyngeal cuff pre- 
vents this gas from escaping via the mouth or nose. The sec- 
ond lumen resembles a conventional endotracheal tube and 
its distal cuff around the tube tills the lumen of the trachea or 

esophagus. Most of the time, the ETC comes to rest in the 
esophagus, and ventilation is accomplished via the pharyn- 
geal perforations. Should the tube come to rest in the trachea, 
the second lumen can be used like a conventional ETT. 

Table 2. Suggested Contents of the Portable Storage Unit for Manage- 
ment of the Difficult Airway 

1 . Rigid laryngoscope blades of alternate design and size from those rou- 
tinely used. 

2. Endotracheal tubes of assorted size. 

3. Endotracheal tube guides. Examples include (but are not limited to) 
semirigid stylets with or without a hollow core for jet ventilation, light 
wands, and forceps designed to manipulate the distal portion of the en- 
dotracheal tube. 

4. Fiberoptic intubation equipment. 

5. Rettograde intubation equipment. 

6. At least one device suitable for emergency nonsurgical airway ventila- 
tion. Examples include (but are not limited to) a transtracheal jet venti- 
lator, a hollow jet ventilation stylet, the laryngeal mask, and the 
esophageal-tracheal Combitube. 

7. Equipment suitable for emergency surgical airway access (eg, cricothy- 

8. An exhaled CO: detector. 

IMPORTANT; The items listed in this table represent suggestions. The contents of 
the portable storage unit should be customized to meet the specific needs, 
preferences, and skills of the practitioner and health-care facility. (Reprinted from 
Reference 4. with permission.) 

At this point in 1995, experience with the ETC remains 
limited. In a comparison with mask ventilation in patients 
undergoing routine abdominal surgery, all patients could 
be ventilated, and the oxygen tension was actually better 

Fig. 1 . The esophageal-tracheal Combitube (ETC) Is shown in place in both the esophageal (A) and tracheal (B) positions. If the tube comes 
to rest in the esophagus, ventilation takes place via perforations in the tube between the two cutfs. If proper ventilation does not result via this 
lumen, then the positive pressure source is switched to the second lumen, which presumably rests In the trachea. Although the concept 
seems foolproof, malfunction can result, (C) if the perforations are below a level at which ventilation gas can be delivered to the trachea 
(Reprinted from Reference 9, with permission). 

Respiratory Care • April '95 Vol 40 No 4 


Guidelines For Airway Care 

Fig. 2. The laryngeal mask airway is inserted without a laryngo- 
scope and has an inflatable rim that provides a low-pressure seal 
over the glottic opening. 

using the ETC than using an ETT." This is presumably be- 
cause as exhalation is retarded by the small openings in the 
airway for gas egress, a positive pressure in the lungs re- 
sults. Although these data sound encouraging, a study using 
this as a first-line device for paramedics found that the tube 
was inserted successfully only 71% of the time.'- The fail- 
ures were attributed to a lack of skill retention after the ini- 
tial training. However, with routine use, these skills would 
likely improve. A study of the efficacy of ETC use by in- 
tensive care nurses found that in emergency situations, the 
airway was routinely secured rapidly, ventilation was suc- 
cessful,'^ and there were no adverse effects from its use. 
The reason for the varying results from different centers is 
unclear. However, the successful reports have come from 
the ETC-development group in Vienna, and their experi- 
ence with the ETC probably accounts for their relatively 
greater skill and, therefore, success with the device.'"" 

Laryngeal mask airways (LMAs, F-^ig. 2) have achieved 
great popularity among anesthesiologists in Europe and 
more recently in the United States.''' The mask is made of 
soft rubber with an inllatable rim that fits over the laryn- 
geal inlet and is connected to a wide-bore reinforced tube 
by a connector similar to those used with ETTs. The mask 
is generally placed without direct visualization and can be 

used for positive pressure ventilation with peak pressure 
up to approximately 20 cm HiO. Experience with LMAs 
during resuscitation is limited, and potential difficulties in- 
clude the risk of aspiration and the inability to generate 
high ventilating pressures such as would be needed for pa- 
tients with poorly compliant lungs. 

Several studies have been carried out using the LMA 
for resuscitation. After a period of training, paramedics 
u.sed the LMA 41 times and reported that only 2 patients 
could not be ventilated." No other problems were noted 
and the author commented that the staff adopted the device 
enthusiastically. In a multicenter study, ward nurses were 
trained and used the LMA in 164 cases of cardiac arrest.'^ 
Successful placement occurred in 71% on the first inser- 
tion and 26% of the time on the second insertion. 
Satisfactory chest expansion occurred in 86% of cases. 
The mean interval between cardiac arrest and successful 
LMA placement was 2.4 minutes. As it turns out, aspira- 
tion was not a major problem. Pulmonary aspiration of 
gastric contents was suspected to have occurred during the 
procedure in only 3/164 patients, and only 1 of these had 
clinical evidence of aspiration. Although satisfactory chest 
expansion was not achieved in 14% of the cases, the au- 
thors suggest LMAs as an alternative to bag and mask ven- 
tilation but do not suggest that they should replace tracheal 
intubation. A third study compared the ease of establishing 
an airway in surgical patients using either an LMA or an 
ETT.'^ The practitioners included nurses, paramedics, and 
respiratory therapists, all of whom had some basic training 
in tracheal intubation and brief instruction in the use of the 
LMA. These relatively untrained individuals had far 
greater success ventilating the patients using the LMA. 
Based on the results of this study, the LMA seems a rea- 
sonable alternative in cases of failed intubation. 

As with all airway devices, a period of training is re- 
quired prior to use of the LMA. In an Australian study, 10 
junior physicians were asked to ventilate the lungs of 50 
anesthetized patients using either an LMA or a bag and 
mask; the ventilation-failure rate was significantly greater 
using the LMA and the time required to establish adequate 
ventilation was substantially longer.'** 

The use of transtracheal jet ventilation (TTJV) has been 
widely advocated as a ventilation alternative in cases of 
failed intubation.''' For the most part, it is a simple and ef- 
fective way of delivering oxygen to the trachea during 
those frightening moments when the patient cannot be in- 
tubated or ventilated by mask. The key requirements for 
TT.IV are that a high-pressure oxygen source and proper 
connectors be available because compliant tubing cannot 
accomodate the fiows that are generated in the relatively 
small-caliber catheter. The system components needed to 
deliver TTJV should be part of the emergency airway kit 
for in-hospital resuscitation. 


Ri:,SI>IRAT()RY Cari- • APRIL '^.S VOL 40 No 4 

Guidelines For Airway Care 

As with all emergency airway techniques, caregivers 
must understand and be competent to perform the key 
steps in TTJV application. The most important of these is 
that the catheter's position in the trachea be confirmed by 
unrestricted aspiration of air prior to initiating TTJV. It is 
also critical that its position be secured and firmly main- 
tained because a misplaced catheter, emitting rapid pulses 
of gas at high-pressure, represents a significant hazard to 
the patient. These caveats regarding catheter placement are 
necessary because of a number of reports of instantaneous 
and massive subcutaneous emphysema during TTJV, mak- 
ing any further efforts to manage the airway completely 
unsuccessful, (personal communication Fredrick W 
Cheney MD, 1995). 

For patients in cardiac arrest, the alternative devices de- 
scribed all appear to have some utility. However, tracheal 
intubation is still the gold standard for airway management 
during cardiac arrest, and the use of ETC, LMA, and other 
such devices should be reserved for situations in which tra- 
cheal intubation has failed.-'' 

Equipment Needed To Ascertain Tube Position. 

Regardless of the method used to establish a patent airway, 
the single most important facet of airway management is 
recognition of whether the ETT is indeed in the trachea. 
ACLS guidelines note that 

. . . determining whether the tube is in the esophagus or tra- 
chea should be the primary end-point of training and clini- 
cal use of all invasive airway techniques. This key skill is 
required for the successful use of any of these devices. 
Training and supervision intluence the long-term impact 
of these devices more than factors related to the actual de- 

The AARC Guideline also states the need to confirm 
ETT placement.' The ASA position on the subject is actu- 
ally delineated in a statement of Standards for Basic 
Anesthetic Monitoring-' that reads. 

When an endotracheal tube is inserted, its correct position- 
ing in the trachea must be verified by clinical assessment 
and by identification of carbon dioxide in the expired gas. 

The ASA standard is based on the identification of 
esophageal intubation as a correctable source of catas- 
trophic and costly patient outcomes.' The ASA standard 
also reflects the failure of traditional methods of identify- 
ing tube location such as observation of moisture in the 
tube, breath sounds, palpation, and visualization. -- 

Although the overwhelming consensus supports the 
need to distinguish between esophageal and tracheal tube 
placement, the ASA may have been overzealous in identi- 
fying exhaled COt as the only clear standard for confirm- 
ing ETT placement. During resuscitation, it is often not 

practical to monitor exhaled CO2. Chemical sensors are 
available but are relatively expensive. Furthermore, under 
circumstances encountered during resuscitation, exhaled 
CO2 measurement is 100% specific — ie, when it is high, 
the ETT can only be in the trachea. However, low cardiac- 
output states may prevent excretion of enough CO2 for 
confirmation — ie, low exhaled CO2 may mean that the 
ETT is misplaced or that cardiac output is low. A multi- 
center study of colorimetric determination of exhaled CO2 
in 227 patients ( 144 in cardiac arrest) found that the device 
was 100% sensitive and 100% specific in patients who 
were not in cardiac arrest. However, during arrest the sen- 
sitivity fell to 69%.-' 

Fortunately, recognition of the importance of assessing 
tracheal intubation has spurred ingenious new methods 
that may be equally effective or even more effective in the 
circumstances encountered during resuscitation. For the 
immediate future, the most promising of these is the use of 
a self-inflating bulb syringe, also known as an esophageal 
detector device (Fig. 3).-'* This device works on the princi- 
ple that the trachea will not collapse when a negative pres- 
sure is applied to it because of its relatively rigid wall, 
whereas the compliant esophagus wall will collapse over 
the end of a rigid tube if a negative pressure is applied. The 
procedure is: a bulb syringe is applied to the end of an ETT 
and compressed. A clue as to the location of the tube is 
given by the noise during this maneuver — silent, if in the 
trachea and flatus-like, if in the esophagus. The more im- 
portant finding is whether the bulb reinflates. It should not 
reinflate if the tube is in the esophagus but does reinflate if 
the tube is in the trachea. The initial description of this de- 
vice included 100 surgical patients in whom the trachea 
and esophagus were intentionally intubated and a blinded 
observer asked to judge whether the ETT was in the tra- 
chea or in the esophagus.-"* The test was 100% sensitive 
and specific — ie, all observers made correct judgments on 
all trials. Subsequent studies have found that the reliability 
of the test is not affected by prior inflation of the stomach 
(as often occurs during resuscitation),-' nor does the pres- 
ence of a nasogastric tube or ETT-cuff deflation affect the 
results.-* A more recent study reconfirmed 100% sensitivi- 
ty, specificity and positive predictive value in 500 pa- 

As with capnography, the esophageal detector device 
may be unreliable if there is severe airway obstruction or if 
the ETT is kinked.-** Slow refill of the syringe has been re- 
ported in morbidly obese patients and in patients with de- 
creased expiratory reserve volume.-"^ The device may not 
be useful in small children because of their more-compli- 
ant tracheas.-'" 

In the future, we may use devices that provide comput- 
erized analysis of temperature" or waveform'- as C02-in- 
dependent methods of detecting tube location, offering an 

Respiratory Care • April '95 Vol 40 No 4 


Guidelines For Airway Care 

1. Assess the likelihood and clinical impact of basic management problems. 

A. Difficult Intubation 
B- Difficult Ventilation 
C. Difficulty with Patient Cooperation or Consent 

2. Consider the relative merits and feasibility of basic management choices: 

Non-Surgical Technique for Initial 
Approach to Intubation 

Surgical Technique for Initial 
Approach to Intubation 

Awake Intubation 

3, Develop pnmary and alternative strategies: 

Awake Intubation 

Attempts Successtul" 






1. Returning lo spontaneous 


2 Awakening the patient 

3 Calling lor help 



'atient Anesthetized, Iniubalion Unsuccesslul, 

Alternative Approaches 

f ^ 


Multiple Attempts 

If Mask 


■a. Inti 


Call tor Help 

1 1 

Mask Aneslhesia Patientc 



Emergency Non-Surgic 

^ Airway Venlialliond 






a Other options include (but are not limited lolsurgety 

intillralion or regional nerve blockade, or intubation attempts after 
b Alternative approacbes to difficult intubation include (but are not lir 
awake intubation, blind oral or nasal intubation, fiberoplic intubatic 
light wand, retrograde inlupation, and surgical airway access 

d Options lor emergency non-surgical ainway 

largngeal mask ventilation, or esophageal-l 
e Options lor establishing a definitive airway 1 

spontaneous ventilation, tracheotomy. 


e not limited to): transtracheal Jet 

Fig. 3, The Difficult Airway Algorithm developed by the American 
Society of Anesthesiologists, (Reprinted from Reference 4, with 

advantage tor cardiac arrest patients in whom exhaled CO2 
may not be detectable, even when the trachea has been 

successfully intubated. 

Personnel Guidelines: Who Should 
Manage the Airway? 

Who should manage the patient's airway during in-hos- 
pital resuscitation? In teaching hospitals, it often seems 
that everyone wants 'to get in on the act". In community 
hospitals, there may be no anesthesiologist on duty during 
off-hours or the anesthesiologists may all be occupied in 
the operating room." The key questions then are ( 1 ) Who 
is available? (2) Who has the educational background'.' and 

(3) Who has the skills? 

Whereas no specific guidelines are available, the ACLS 
manual^ states. 

As soon as practical during the resuscitative effort, the tra- 
chea should be intubated by trained personnel... who either 
perform intubations frequently or are retrained frequently. 

Further, in teims of the use of alternative airway devices, 
the manual states. 

Training and supervision influence the long-term impact of 
these devices more than factors related to the actual devices. 

Endotracheal intubation is within respiratory therapists' 
scope of practice by virtue of their training, but intubation 
by therapists is dependent on local and regional practice. 
Kacmarek^"* notes that almost all registry-level respiratory 
therapy programs instruct students in the technique. 
However, he cites textbooks to support this statement, and 
there are no data that document the extent of this training. 
Certainly all therapists are routinely trained in evaluation 
of tube placement, tube inanipulation, and measurements 
of cuff pressures and volumes. 

Numerous articles have been wiitten on the question of 
who should perfoim tracheal intubation. Most of these arti- 
cles assess the likelihood of the tube ending up in the trachea 
with various comparisons made as to whether the letters 
after the intubator's name are MD, RRT, or EMT. What con- 
clusions can we draw based on the existing literature? 

The frequency of failed intubation in the anesthesia lit- 
erature is generally well under l^r.^'"" Of course, these in- 
tubations are performed under well-controlled conditions 
in the operating room, and that level of success may not be 
possible in other settings. Given that the rate of failed intu- 
bations is low, any study conducted to demonstrate a true 
difference in intubation-skill level among categories of 
personnel would require an enormous number of patients. 
For example, if anesthesiologists had a true intubation-fail- 
ure rate of 2%, and paramedics had a rate of 4%, a sample 
of approximately 1 ,000 patients would need to be studied 
test to whether this 100% difference in failure rate was sta- 
tistically significant at the p < 0.05 level! Thus, the most 
likely conclusion of such studies is that there is no differ- 
ence in failure rate when, in fact, insufficient numbers of 
patients may have limited the investigator's ability to ex- 
pose such a difference. 

One of the most widely cited papers supporting intuba- 
tion by nonanesthesiologists found no difference in com- 
plication rates during emergency-room intubations 
whether the procedure was perforined by anesthesiology 
staff or by emergency department staff." Further analysis 
of their findings reveal several critical flaws. This study 
did not show which group is more competent. There were 
complications in 20 of 23 patients intubated by the emer- 


Ri:,spiKAT()RY Care • April "95 Vol 40 No 4 

Guidelines For Airway Care 

gency-department personnel and 14 of 23 intubated by the 
anesthesiology staff; the difference was not significant. 
Given that the complication rate was nearly 43% higher in 
the emergency department group, these data could be in- 
terpreted as supporting the routine use of anesthesiologists. 
However, the power of the study was unsufficient to reach 
a definitive conclusion. 

Most physicians receive little training in airway man- 
agement. Therefore, the alternative provider to an anesthe- 
siologist should be someone specifically trained in these 
skills, rather than a physician without training in airway 
management. Placing an ETT expeditiously is a psy- 
chomotor skill that can be taught to nonphysicians. 
Certified registered nurse anesthetists routinely perform 
tracheal intubation. Since the 1970s, paramedics in some 
regions have been trained in intubation. In 1977, DeLeo'** 
reported 91% intubation success by paramedics in the field 
compared to 89% success for physicians. Paramedics" suc- 
cess in other studies have generally ranged from 90 to 
98%.'' One study found that unsuccessful intubations by 
field personnel were generally in patients who could not be 
intubated by emergency room physicians.'"' 

What data do we have on the intubation success of res- 
piratory therapists? In 1981, McLaughlin and Scott report- 
ed that 50 consecutive patients were intubated by respira- 
tory therapists under emergency conditions.-" The thera- 
pists had each performed 12 OR intubations and two 
supervised emergency intubations prior to the start of the 
study. Of these cases, 19% required more than 5 minutes 
for intubation, a surprisingly large number. However, 25 
different therapists were involved in the program, raising 
the possibility that even though the initial training was ad- 
equate, there may have been insufficient opportunities for 
skills retention. 

A second 1981 study in a community hospital found a 
complication rate of 18% when respiratory therapy person- 
nel performed intubations and 57% when a physician at- 
tempted the intubation.'' Many of the complications expe- 
rienced by both groups were due to esophageal placement 
of the ETT. This study, overall, reports the greater success 
of nonphysician intubation providers compared to that of 
nonanesthesiologist physicians. 

At Duke University Medical Center (Durham NC), respi- 
ratory therapists have performed intubation for many years. 
According to a recent study,''- they were successful in 79 1 of 
833 intubations (95%). A key feature of this service was that 
a core group of respiratory therapists had been selected and 
trained in airway management techniques and support. In a 
large institution, having a highly trained subgroup of respi- 
ratory therapists may be a useful strategy. 

The Respiratory Care Department at Butterworth 
Hospital (Grand Rapids MI) published their experience as 
backup providers of tracheal intubation following failed 

attempts by other professionals.'*-' Their success rate of 
90% is remarkable given that none of these was a first at- 
tempt. When the respiratory therapist failed to intubate, 
patients were intubated by an anesthesiologist or required 
a tracheotomy. The providers in this study all performed 
12-15 successful OR intubations and maintained their 
skills by performing a minimum of 15 intubations every 2 

Clearly, the majority of intubations can be performed 
successfully by respiratory therapists. What is an accept- 
able intubation-failure rate? Obviously, 10% is too high if 
all patients die as a result of the failed intubation. 
However, if intubation failure (ie, esophageal intubation) 
is recognized immediately, consequences can usually be 
minimized by returning to mask ventilation. In rare cases, 
surgical access to the airway may be required. In the last 
10 years, with the introduction of reliable devices for de- 
tecting esophageal intubation, unrecognized ETT mis- 
placement has been reduced, and the reported rates of ini- 
tial intubation failure become less worrisome. 

Whether respiratory therapists should be providers of 
intubation services on a routine basis should be weighed 
against the alternatives. It seems reasonable that the most 
skilled practitioners in the hospital provide intubation. Few 
would argue that anesthesiologists, accustomed to intubat- 
ing the trachea many times a day, would have the highest 
skill level. However, their services are costly and in de- 
mand in the OR, limiting their availability. Given these re- 
alities, the practitioner with the most experience and who 
is most familiar with intubation and airway maintenance 
procedures should probably be designated. With appropri- 
ate training and skill maintenance, this practitioner is often 
the respiratory therapist. 

A final argument in support of the role of respiratory 
therapists in airway management is their ability to manage 
the airway should intubation fail. Compared to other 
groups of health-care providers, respiratory therapists have 
substantially more training and experience in bag-and- 
mask ventilation. 

There are no legal precedents as to who should manage 
the airway or who should perform tracheal intubation. A 
search of a legal database (Westlaw) revealed no appellate 
decisions bearing directly on this question. However, what is 
clear is that nonphysician personnel who undertake medical 
services are subject to the same standards of performance as 
the physicians who would usually perform them.^ The only 
legal decision relating to a failed intubation was the case of a 
patient who experienced cardiac arrest, the respiratory thera- 
pist failed to intubate, and the patient was intubated by a 
physician. The hospital was found liable for the original 
failed intubation, but the basis of the liability was not the 
issue of the intubator, but the lack of immediate availability 
of a size-4 Macintosh laryngoscope blade."" 

Respiratory Care • April '95 Vol 40 No 4 


Guidelines For Airway Care 

Guidelines for Managing the Difficult Airway 

Failure to manage a patient's airway successfully can 
result in severe adverse outcomes, including brain injury, 
myocardial injury, airway trauma, and death. Because of 
these risks, failed intubations are frequently associated 
with in-hospital consequences as well as the threat of med- 
ical malpractice litigation. In an effort to minimize such 
adverse actions, the ASA appointed a task force on man- 
agement of the difficult airway. That group, following an 
exhaustive literature search and much discussion, pub- 
lished Practice Guidelines for Management of the Difficult 
Airway. ^ ■"' These Guidelines are intended for use by anes- 
thesiologists in the OR and do not refer specifically to crit- 
ical care or other in-hospital settings. However, the logic 
of having a clear algorithm to call on in an emergency 
seems indisputable. The algorithm suggested is already 
being taught to all anesthesiology residents and is widely 
applied. Given the discussions earlier in this article about 
how guidelines evolve into practice standards, all practi- 
tioners who are responsible for or interested in airway care 
should carefully review these guidelines. 

Many aspects of the difficult airway algorithm (Fig. 4) 
do not apply in the cardiac arrest situation. The initial steps 
in the algorithm (lA, IB, IC) all involve assessing the air- 
way to anticipate potential difficulty with intubation, ven- 
tilation, or patient cooperation. However, these steps are 
not practical when resuscitation is required. Similarly, 
Item 2 of the algorithm — patient-management choices 
such as awake intubation, preservation of spontaneous 
ventilation, or other nonsurgical awake techniques — is 
generally not relevant in emergency situations. 

The relevant portion of the difficult airway algorithm 
that should be adapted for use in the cardiac arrest setting 
is Section 3B: "Intubation Attempts after Induction of 
General Anesthesia." Several key points may be useful. If 
the initial intubation attempts are unsuccessful, a call for 
more experienced help should be issued immediately. It 

Fig. 4. The esophageal detector device can be constructed from a 
self-inflating bulb syringe and an ETT adapter. The bulb reinflates 
promptly if the tube is positioned in the trachea but slowly or not at 
all if the tube is in the esophagus. 

was the hope of the Task Force that putting this instruction 
in the algorithm would encourage practitioners to call for 
assistance as soon as a problem became evident rather than 
continuing to try to place the ETT while the patient's con- 
dition deteriorated. 

At this point, the algorithm splits into a nonemergency 
pathway and an emergency pathway. If mask ventilation is 
adequate, then the nonemergency pathway can be followed. 
This pathway encourages further attempts at intubation 
using different laryngoscope blades, fiberoptic intubation, 
retrograde intubation, or surgical airway access via cricothy- 
rotomy. However, during cardiac arrest, fiberoptic intuba- 
tion and retrograde intubation are likely to be difficult. 

In contrast to the surgical algorithm, the algorithm for 
cardiac arrest needs to be adapted so that if the alternative 
approaches fail, the caregiver moves to the emergency 
pathway. If mask ventilation is inadequate, the emergency 
pathway must be followed. Once again, the importance of 
calling for help is emphasized. At this point, no more than 
one further intubation attempt should be made, and the 
clinician should move quickly to secure an airway by other 
means rather than waiting and placing the patient at risk 
for hypoxic damage. There are several options available 
for emergency nonsurgical airway ventilation. If these fail, 
then an emergency surgical airway should be obtained as 
expeditiously as possible. Options for emergency ventila- 
tion via a nonsurgical airway include (but are not limited 
to) TTJV, LMA, or endotracheal intubation. 

Finally, notice that the pathways all end with confinna- 
tion of intubation by exhaled COt. As discussed earlier, this 
may not always be reliable in the arrest situation and use of 
the esophageal detector device should be considered. 


Existing guidelines for equipment and personnel have 
been described. In addition, the ASA guidelines on manage- 
ment of the difficult airway have been presented as an ex- 
ample of the type of algorithm that might be used for man- 
agement of the difficult airway. Whereas guidelines are not 
standards, it is important to recognize that as guidelines are 
adopted by more and more practitioners, they become "stan- 
dards of care" to which we aie all held accountable. 


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Bishop Discussion 

Malinowski: I .support the idea that the 
best person to do the job, if available. 

is the anesthesiologist. Something, 
though, that I noticed, especially in my 
review of the pediatric literature, is that 
when you're talking about success 

rates, oftentimes you're comparing dif- 
ferent environmental conditions. TTie 
operating room versus the freeway can 
be quite different. The same thing is 



Bishop Discussion 

true in the acute care hospital resuscita- 
tion, where I have been handed a laryn- 
goscope after t'lrst-year residents had 
tried to intubate a premature newborn 
five times, and then w(v success rate is 
logged on the data sheet. I've had a 
paramedic student of mine tell me that 
he has sometimes intubated in the pitch 
black when his flashlight batteries 
went out. It is important to recognize 
that maybe we shouldn't ask for simi- 
lar success rates in different environ- 
mental conditions. 

Bishop: I think I actually pointed that 
out in my slides. It's just incredible 
seeing paramedics intubate while 
lying on the floor. I did a study a few 
years ago looking for the force re- 
quired to do the average intubation. 
It's between 10 and 20 pounds. Try 
holding 10-20 pounds when you're 
prone. You can't use the proper mus- 
cles for it. It's very difficult, there's 
no question. Paul (Pepe), you've 
probably been there once or twice. 

Pepe: Look at the published 
paramedic success rates.' They're 
very high, but I also think they really 
reflect the situation in which the 
paramedics are working. Your aca- 
demic centers that publish these 
kinds of results are obviously set up 
to watch the paramedics very careful- 
ly to report these findings. You don't 
find those kinds of results every- 
where in the world. I think that that's 
an important issue to recognize. 

1. Pepe PK, Copass MK. Joyce TH. 
Prehospital endotracheal intubation — 
rationale for training emergency medi- 
cal personnel. Ann Emerg Med 1985; 

2. Pepe PE, Zachariah BS. Chandra N. 
Invasive airway techniques in resusci- 
tation. Ann Emerg Med 1993:22(2. 
Part 2):393-403. 

Bishop: Paramedics can be trained to 
be very good at intubation, but 
they're not going to get to the level of 
skill of the anesthesiologist. How- 

ever, I think you also have to look at 
what the alternatives are. You can't 
spend the money it would take to 
have an anesthesiologist in every ve- 

Pepe: I think you can do very well if 
you're in an urban academic center, 
especially if you use certain deploy- 
ment strategies. For example, in Mil- 
waukee, Houston, and Seattle we 
have all found that if we concentrate 
the paramedics and keep them avail- 
able for resuscitation cases, our suc- 
cess rate improves dramatically.' 
Therefore, we intentionally don't put 
paramedics on every vehicle. We 
strategically deploy them, especially 
because 85-90% of emergency medi- 
cal service calls in an urban center 
only require basic care. If we had 
enough paramedics to staff all the ve- 
hicles to handle this load, individual 
paramedics would never get experi- 
ence.' The second issue is regarding 
the Combitube- There may be a lot of 
auto-PEEP phenomena.' The Combi- 
tube may trap air. That's the same 
issue that I raised with Henry (Hal- 
perin) about what happens when 
we're doing CPR. Are we really not 
getting any cardiac output because 
we're ventilating so much — dramati- 
cally raising intrathoracic pressure? 
Most studies with this device are re- 
ports from the operating room where 
ventilation with the Combitube is 
performed by experts in airway man- 
agement. Prehospital studies are still 
lacking.- Interestingly enough, how- 
ever, people already believe in it so 
much that some Canadian officials 
have considered its use to avoid a 
paramedic system. They want a basic 
EMT (emergency medical techni- 
cian) service that uses automated de- 
fibrillators and Combitubes and not 
have advanced life support personnel 
out there — they think that will be 
more cost-effective.'' So there's been 
a lot of stock put in to a device with- 
out a lot of clinical experience in the 
prehospital setting.- Ihc final thing 

I'd like to comment on is the bag- 
valve-mask issue. I think it's very im- 
portant. We almost threw out the bag- 
valve-mask last year at the ACLS 
ventilation panel meeting because so 
many people on the committee had 
seen a lot of inappropriate use of the 
device. I mean it's just being so poor- 
ly used — people blowing up stom- 
achs and not lungs, and the tech- 
niques are terrible. We really need to 
focus on training people to be able to 
do bag-valve-mask properly. 

1. Curka PA, Pepe PE, Ginger VF, 
Sherrard RC, Ivy MV. Zachariah BS. 
Emergency medical services priority 
dispatch: ability of a computer-assisted 
dispatch triage algorithm to safely 
spare paramedics from responses not 
requiring advanced life support. Ann 
Emerg Med 1993:22:1688-1695. 

2. Pepe PE, Zachariah BS, Chandra N. 
Invasive airway techniques in resusci- 
tation. Ann Emerg Med 1993:22(2, 
Part 2):393-403. 

3. Pepe PE. Marini JJ. Occult positive 
end-expiratory pressure in mechanical- 
ly ventilated patients with airflow ob- 
struction: the Auto-PEEP effect. Am 
RevRespirDis 1982:126:166-170. 

4. Spears T. Life and death — and the bot- 
tom line: the paramedic debate, the 
Ottawa citizen;Sunday. November 21, 

Bishop: I couldn't agree with you 
more. I didn't discuss that but if I had to 
say, based on my experience, what the 
least successful device is, it's the bag- 
valve-mask. I see somebody squeezing 
the bag for a patient with no teeth, and 
the air is all going out the sides. That's 
one of the reasons why, when I get to a 
resuscitation, the first thing I ask for is 
an anesthesia bag. I'm used to getting 
that feedback of seeing gas at least re- 
turn to the bag and getting a feel for the 
patient's compliance and resistance. 
Proper bag-and-mask ventilation may 
be a more difficult skill to acquire than 

Durbin: 1 offer a comment on CO2 
detection and resuscitation and endo- 
tracheal intubation in the absence of 


RESPIRATORY Care • April '95 Vol 40 No 4 

Bishop Discussion 

chest compressions. I guess I feel dif- 
ferently. I would have trouble de- 
fending the use of a homemade CO: 
detection device in a court of law. 
That may be inappropriate. However, 
it is an effective device, and I agree 
with your cost-benefit analysis. 1 
guess maybe I believe that if I pay the 
$5 for the commercial device, then 
the company will go to court with me 
if a problem arises. It's much more 
difficult for me to defend the use of a 
homemade device medically and 
legally, although I have used such a 
device in practice. I have a portable 
COt detector that I carry to all car- 
diac arrests, and as little as 15% of 
normal cardiac output will register on 
the meter. You can, in fact, see the 
fluctuations in CO2 with ventilation. 
It's not a very expensive device, only 
a couple hundred dollars, and so far I 
haven't had it fail me, even with pa- 
tients in asystole receiving just com- 

Hess: I agree with you that perhaps we 
made a mistake when we assumed that 
monitoring exhaled CO2 in a cardiac 
arrest situation would give us the same 
kind of information that we get in the 
operating room. I think we need to be 
careful that we don't make the same 
mistake with the esophageal detector 
device. To my knowledge, all the data 
in the literature has been done on ei- 
ther anesthetized patients in the oper- 
ating room or on cadavers or on ani- 
mals. I don't know of any field studies 
at all that have been done with that de- 
vice. So I guess I would urge caution. 

as perhaps Charlie (Durbin) is, that we 
don't lock on to this device that I per- 
sonally think is very intriguing and has 
a lot of possibilities. I think we need to 
see some data about how well it actu- 
ally works in a cardiac arrest situation. 

Bishop: I agree with you. I just think 
the important point that I'm trying to 
make is that we have to be careful not 
to let our existing standards blind us 
to something that may actually be a 
"better mousetrap.' 

Kaye: Just a question. The device that 
one puts through the endotracheal tube 
with a light on the end of it — is there 
no literature? Why didn't you mention 

Bishop: Lighted stylet. You mean the 

Kaye: Well, in terms of blind intuba- 
tions also. 

Bishop: The lighted stylet is one of 
many alternative methods for intuba- 
tion. If you fail initially at tracheal in- 
tubation, you must look at other ways 
of establishing an airway. 

Hess: But there again, in the operat- 
ing room, you can turn the lights 
down, and I think that works very 
well. If you have a hard time when 
you're intubating somebody outside 
the OR, where you can't shut down 
the lights and see the transillumina- 
tion, then the lighted stylet may not 
work as well. So, again. I think some 

of these devices work very well in the 
controlled environment of the OR. 
The mistake that we make sometimes 
is that we assume they should work 
equally well under all circumstances, 
and we find that they don't. 

Hamill: Body habitus also needs to be 
taken into consideration. People with 
very thick necks, for example, can be 
very difficult to intubate under direct 
vision. Transillumination is also not 
helpful in these patients. 

Bishop: Robin's (Hamill) point is 
well taken. In patients for whom one 
method doesn't work, alternative 
methods often don't work either. 

Sanders: A minor point, but I think 
that some of the problem with the low 
sensitivity from the CO2 devices is 
that they are colorimetric or qualita- 
tive devices. In the animal lab and in 
my clinical experience, the quantita- 
tive devices are much better. Even if 
you get levels of 3 or 4 torr, it means 
that the endotracheal tube is in place. 
CO2 levels in the esophagus should 
be zero. We've actually used CO2 ex- 
cretion as a noninvasive measure- 
ment of cardiac output during CPR. 

Bishop: Oh it's very nice but unfor- 
tunately, when you have somebody 
who's just collapsed in the cafeteria, 
you often don't have that available. A 
CO2 trace is the most definitive way 
to go. But you often don't have that 
available in some in-house arrest sit- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs Used during Resuscitation 

Joseph L Rau Jr PhD RRT 

I. Overview of ACLS Drugs 

A. Perspective on Use of ACLS Drugs in Cardiac Arrest 

B. Classification of Drug Recommendations Used in ACLS 

C. Overview of Drugs and Drug Groups in ACLS 
L Oxygen Therapy 

2. Intravenous Fluids 

3. Morphine Sulfate 

4. Drugs for Control of Heart Rate & Rhythm 

5. Drugs for Control of Cardiac Output & Blood Pressure 
IL Drugs Used in Cardiac Arrest 

A. Epinephrine 

B. Lidocaine 

C. Procainamide 

D. Bretylium 

E. Atropine 

F. Sodium Bicarbonate 

G. Adenosine 

in. Conclusion & Summary 

Overview of ACLS Drugs 

Perspective on Use of ACLS Drugs 
in Cardiac Arrest 

Drugs used in Advanced Cardiac Life Support, or 
ACLS, encompass a wide range of agents and pharmaco- 
logic classes. These agents include oxygen, intravenous 
(l.V.) fluids, morphine sulfate and numerous cardiovascu- 
lar drugs intended for cardiac and hemodynamic regula- 
tion. An in-depth discussion of every agent is beyond the 
scope of this review and could constitute several pharma- 
cology courses. In order to narrow the focus and remain of 
reasonable length, 1 have selected ACLS drugs used for 
cardiac arrest, and more specifically, ventricular fibrilla- 
tion, ventricular tachycardia and asystole. The rationale for 
this selectivity is twofold: to allow adequate depth of treat- 

Dr Rau is Professor and Chair, Department of Cardiopulmonary Care 
Sciences. Georgia State University. Atlanta, Georgia. 

Reprints: Joseph L Rau Chi). Department of Cardiopulmonary Care 
.Sciences, Georgia State University. Atlanta, (ieorgia .^(UO.^ 

ment and to present drugs most likely to be encountered by 
respiratory therapists in the hospital cardiac arrest situa- 
tion. One exception to this basis of discussing only drugs 
used in cardiac arrest is given by adenosine, a relatively 
new agent with a profile that may be of interest to critical 
care practitioners. 

The classification system for drug recommendations in 
ACLS and a brief overview of the range of drug therapy 
included in ACLS is given prior to a detailed discussion of 
individual agents used in cardiac arrest, and of adenosine. 
As the 1992 ACLS guidelines clearly indicate, basic car- 
diopulmonary resuscitation (CPR). defibrillation, and 
definitive airway management logically precede the insti- 
tution of drug treatment.' Drug therapy should follow the 
establishment of these interventions. 

Classification of Drug Recommendations 
Used in ACLS 

The American Heart Association (AHA) has provided a 
staged classification of recommendations for particular 
drug therapies in cardiac arrest and ACLS.' The classes 


R[:spiRA roRY Cark • April '95 Vol 40 No 4 

ACLS Drugs 

Class I: definitely helpful 

Class Ila: acceptable, probably helpful 

Class lib: acceptable, possibly helpful 

Class III: not indicated, may be harmful 
In this review, I use these classes of staged recommenda- 
tion or lack of recommendation when discussing specific 
drugs or the use of certain drugs in specific situations. For 
example, the administration of 100% oxygen as soon as 
possible in cardiac or respiratory arrest or in suspected hy- 
poxemia is given a Class-I recommendation. As another 
example, the prophylactic administration of lidocaine in 
uncomplicated acute myocardial infarction (MI) or is- 
chemia without ventricular premature beats (PVC) is given 
a Class lib recommendation by the American College of 
Cardiology (ACC)/AHA task force. '- 

Table 1. Advanced Cardiac Life Support (ACLS) Agents Used To 
Control Cardiac Rate and Rhythm* 

Lidocaine — used for ventricular ectopy. VT, VF 

PrcK'ainamide — used to control ectopy if lidocaine fails or is contraindicated. 

Bretylium — a secondary agent for VF if lidocaine fails. 

Beta adrenergic antagonist — used to reduce the incidence of VF after MI 
when thrombolytic therapy is not used. 

Atropine — used for sinus bradycardia. 

Isoproterenol — used when a temporary inotropic/chronotropic effect is 

Verapamil/Diltiazem — used for atrial fibrillation, supraventricular tachy- 

Adenosine — used for narrow-complex paroxsymal tachycardia. 

Magnesium — used if magnesium decreased in VF, VT 

* Based on Reference 1 

Overview of Drugs & Drug Groups in ACLS 

Oxygen Therapy. Oxygen, a drug well known to respira- 
tory care personnel, is given a Class-I recommendation in 
emergency cardiac care (ECC) scenarios, as previously in- 
dicated. Adjunct equipment used for oxygen administra- 
tion and airway management is also well known to respira- 
tory care practitioners. 

I.V. Fluids — I.V. fluids include blood, crystalloid solu- 
tions such as Ringer's lactate or normal saline, colloid so- 
lutions such as albumin, and 5% dextrose in water (D5W). 
The two general reasons for using I.V. fluids in ECC are 
for volume expansion in the case of acute blood loss and to 
keep I.V. lines open for drug administration.' 

Morphine Sulfate. The analgesic property of the opioid, 
morphine sulfate, is indicated for the pain of acute ML' In 
addition, morphine dilates veins, thereby increasing the 

venous storage capacity and reducing venous return. This 
effect is beneficial in relieving cardiogenic pulmonary 
edema and reducing myocardial oxygen consumption. The 
patient must be monitored for possible side effects, such as 
respiratory depression and hypotension. 

Drugs for Control of Heart Rate & Rhythm. A number 
of drugs operating by different mechanisms are used to 
manage cardiac dysrhythmias such as ventricular tachycar- 
dia ( VT), ventricular fibrillation( VF), and premature beats. 
A list of drugs used in this category is given in Table 1, 
with a synopsis of their use. Those agents used in cardiac 
arrest, such as lidocaine, are discussed individually. 

Drugs for Control of Cardiac Output & Blood Pressure. 

In addition to controlling disorders of rate and rhythm, cer- 
tain drugs are used to maintain cardiac output and blood 
pressure. In general, agents in this category affect cardiac in- 
otropy or chronotropy, and/or peripheral vascular tone. 
They are used in acute myocardial ischemia, heart failure 
and pulmonary edema, and shock or cardiac arrest. Cardio- 
vascular agents in this category are listed in Table 2, with a 
brief statement of their purpose. As with the antiarrhythmic 
agents, only those drugs used in cardiac arrest, such as 
epinephrine, are discussed individually. 

Table 2. Advanced Cardiac Life Support (ACLS) Agents Used for 
Control of Cardiac Output and Blood Pressure* 

Epinephrine — used in VT, VF. asystole 

Norepinephrine — used for severe hypotension and low peripheral vascular 

Dopamine — used for hypotension with bradycardia 
Dobutamine — used for heart failure 
Amrinone — used for heart failure 

Calcium — used in the presence of increased potassium, decreased 
calcium, or calcium-blocker toxicity 
Digitalis — limited use as an inotrope in ECC 
Nitroglycerin — used for acute angina pectoris 
Sodium nitroprusside — used for heart failure/hypertension 
Sodium bicarbonate — used for metabolic acidosis, increased potassium. 

some drug overdoses 
Diuretics — used with cerebral edema after cardiac arrest and acute 

pulmonary edema 
Thrombolytics — use within 6 hours with chest pain consistent with acute 

Ml if < 70 years old. and > 0. 1 -mV ST elevation 

Drugs Used in Cardiac Arrest 

The drugs that are used in cardiac arrest include those 
used specifically to treat VT, VF, and asystole, including 
pulseless electrical activity (PEA), also termed electrome- 
chanical dissociation (EMD). 



ACLS Drugs 


ACLS Indication. Epinephrine is indicated in ACLS for 
persistent or recurrent VT. VF, and asystole, including 
PEA. This is a Class-I recommendation.' The rationale for 
use of epinephrine in cardiac arrest is based on its alpha 
(a)-adrenergic effect, in order to increase myocardial 
blood flow and aid the return of spontaneous circulation. 

Pharmacology of Epinephrine. Epinephrine was named 
by Abel in 1899, and synthesized around the same time by 
Stolz and Dakin.' It was identified as the active ingredient 
in suprarenal extracts of a pressor substance. Thus, epi- 
nephrine is an endogenous catecholamine, secreted by the 
adrenal glands, and is well known to respiratory care prac- 
titioners as a prototype agent for a number of adrenergic 
bronchodilators. Its structure consists of a catechol nucleus 
and a 2-carbon side chain with a terminal amino group 
(Fig. 1). The hydroxyl attachment on the beta {p) carbon 
(carbon farthest from the amino group) allows for right- 
hand (dextro. d) and left-hand (levo, /) stereoisomers of 
epinephrine. The /-isomers are the naturally occurring 
form physiologically active in humans.'* Epinephrine is in- 
ternationally known as adrenaline. 


/3 a 


Fig. 1. Chemical structure of the stereoisomer, epinephrine. 

The pharmacologic properties of epinephrine are clearly 
described in standard texts of pharmacology, such as 
Goodman and Gilman 's Pharmacological Basis of Thera- 
peutics, 8th edition, or Craig and Stitzel's Modern Pharma- 
cology, 3rd edition. '"* 

Epinephrine stimulates or, ^1, and /J-2 receptors. Stimu- 
lation of cardiac P receptors causes increased contractile 
force, shortened relaxation times, and an increased heart 
rate. Both, /J-1 and j3-2 receptors exist in human heart tis- 
sue, with 15-2 receptors comprising about 157c of the fi re- 
ceptors in the left ventricle, and a substantial number of ^2 
receptors in the atria.'' Both /J- 1 and j3-2 receptors can cause 
a positive inotropic response in the heart. Whether a recep- 
tors are found in the heart is a subject of debate. In a cat 
model, stimulation of a receptors increases the force of 
contraction. Such stimulation can also cause the release of 
adenosine from ischemic myocardium.'' ' 

Table 3 outlines the effect of epinephrine on blood ves- 
sels, in usual doses of around 10 /ug/min given intra- 
venously or subcutaneously (SC).'' 

The effect of epinephrine on blood vessels is dose de- 
pendent, with low doses causing predominantly dilation of 
blood vessels due to /3-2 activation and higher doses result- 
ing in increasing vasoconstriction due to increasing activa- 
tion of a receptors in skeletal-muscle blood vessels. The 
net cardiovascular effects of epinephrine in usual doses are 
summarized in Table 3 and result from the action of the 
drug on both the heart and blood vessels. The increased 
systolic pressure results from stimulation of cardiac P re- 
ceptors, with a positive inotropic effect, increasing cardiac 
output. The decreased diastolic pressure is due to stimula- 
tion of /3-2 receptors in skeletal-muscle blood vessels, re- 
sulting in vasodilation. 

A Summary of ihe Effects of Epinephrine on Blood Vessels 
and the Cardiovascular System 


Receptor Type 


Cutaneous vessels 



Visceral vessels 



Renal vessels 



Coronary vessels 


Skeletal vessels 



Systolic pressure 


increase (++) 

Diastolic pressure 


slight decrease (-) 

Peripheral resistance 


decrease (-) 

Cardiac output 


increa,se (+++) 

Heart rate 


increase (+) 

Rationale for Use in Cardiac Arrest. The beneficial ef- 
fect of epinephrine in cardiac arrest is due to its a-receptor 
stimulating properties, which restore or improve coronary 
blood flow to the myocardium and ultimately result in the 
return of spontaneous circulation (ROSC). 

In 1949, Beck and Rand described the method for re- 
suscitation from cardiac arrest, which is the basis for CPR 
today. Writing in the Journal of the Amercian Medical 
Association, December 24, 1949, they stated: "The resus- 
citation procedure consists of two components. One is 
restoration of the oxygen system; the other is restoration of 
the heart beat.... The lungs must be filled with oxygen, and 
the heart must be squeezed. These procedures must be car- 
ried out without interruption."** They also suggested the 
use of epinephrine for ventricular standstill, using a dose 
of 0.5 mL of 1 : 1 ()()() epinephrine solution, which is 0.5 mg. 

In 1962, Redding and Pearson" systematically looked at 
different techniques of resuscitation, using dogs who were 
asphyxiated by airway occlusion and who subsequently 
went into full cardiac arrest. They used four resuscitative 
techniques, alone or in coinbination: intermittent positive 
pressure ventilation (IPPV), closed-chest cardiac massage 
(CCCM), 1 mg epinephrine in the left ventricle, and exter- 
nal electrical defibrillation. A portion of their results is 
given in Table 4. ll can be seen that a decrease in aortic 


Ri:si'ikATORY Cari; • April "95 Vol 40 No 4 

ACLS Drugs 

pressure is associated with a decrease in survival. After 
full circulatory arrest, when aortic pressure is zero, basic 
CPR consisting of ventilation and CCCM still gave only a 
20% survival rate, whereas the addition of I mg of 
epinephrine resulted in 100% survival with normal function. 

Table 4. Effect of Four Different Resuscitalive Techniques on 
Survival in Dogs 



Survival Rate 

Apneic; aortic pressure 

Apneic; aortic pressure 

50 mm Hg 
Apneic; aortic pressure 

25 mm Hg 
Circulatory arrest. 1 min 
Circulatory arrest. 2 min 

IPPV/air 10/10; normal 

IPPV/air 4/10: normal 

IPPV/air 1/10; normal 

IPPV/air. CCCM 2/ 1 0; normal 

IPPV/air, CCCM. Epi 10/10; normal 

*IPPV/air = intermittent positive pressure ventilation using air; CCCM = closed 
chest cardiac massage; Epi = epinephrine 1 mg. intracardiac. (From Reference 9. 
with permission) 

The question arises. Is the beneficial effect of epi- 
nephrine in cardiac arrest due to its a-adrenergic stimula- 
tion, or to its j3-adrenergic effect? With the dose range 
used in CPR (0.5-1.0 mg I.V.), both a and /3 effects are 
present, a-adrenergic stimulation in the doses used in 
CPR could result in vasoconstriction and increased total 
peripheral resistance (TPR) and increased aortic diastolic 
pressure, resulting in better coronary perfusion, which is 
needed to oxygenate the myocardium and allow a return of 
heartbeat. j3-adrenergic stimulation could increase heart 
rate, myocardial contractile force, and the vigor of ventric- 
ular fibrillation, which may make the heart more respon- 
sive to countershock in defibrillation.'" Is epinephrine, the 
drug of choice in cardiac arrest of all types, acting as a va- 
sopressor with a-adrenergic effects or as a cardiac stimu- 
lant due to its j3-adrenergic effects or perhaps both? 

Effect of Epinephrine on Coronary Perfusion Pressure. 

Coronary perfusion pressure (CPP. the pressure gradient 
between the aorta and the right atrium during the relax- 
ation phase of CPR) has been found to predict the return of 
spontaneous circulation (ROSC) during cardiac arrest and 
resuscitation. ""'- 

Sanders and associates" examined a dog model in 
which VF was electrically induced and allowed to contin- 
ue for 30 minutes, during which time aortic diastolic pres- 
sure was maintained with epinephrine and boluses of 0.9% 
saline solution. Aortic diastolic pressure, and aortic-to- 
right-atrial diastolic pressure (ie, the CPP) were higher at 
all time intervals during the 30 minutes in survivors (n = 7) 
compared to those not surviving (n = 5). Nonsurvivors 

were unable to maintain an aortic diastolic pressure above 
30 mm Hg. Furthermore, CPP was in the range of 25-30 
mm Hg for all survivors after the first 3-minute measure. 
The authors also noted that survivors received a total dose 
of epinephrine of 3.4 ± 1.7 mg (mean ± SD), compared to 
11.1 ±2.1 mg given to nonsurvivors. These data are con- 
sidered subsequently in the discussion of high-dose 
epinephrine in cardiac arrest. 

A more recent study by Paradis and co-workers'- in the 
Journal of the American Medical Association 1 990, report- 
ed CPP in 100 patients with nontraumatic, prehospital, or 
emergency room cardiac arrest. Twenty-four patients had a 
ROSC. defined as development of spontaneous aortic 
pulse waveforms with a systolic blood pressure greater 
than 60 mm Hg for more than 2 minutes. Initial CPP was 
1.6 ± 8.5 mm Hg (mean ± SD) in patients without ROSC, 
compared to 13.4 ± 8.5 mm Hg in those with ROSC. 
Maximal CPP was 8.4 ± 10 mm Hg in those without and 
25.6 ± 7.7 mm Hg in those with ROSC, respectively. No 
patients with a mean CPP < 15 mm Hg had ROSC; 79%, 
or 1 1 of 14 patients with a maximum CPP > 25 mm Hg had 
ROSC, and. in general, the proportion of patients with 
ROSC increased as maximal CPP increased. The studies of 
Sanders and associates" and Paradis and associates'- both 
showed the importance of CPP in establishing heart action 
for the return of circulation. 

The importance of a CPP > 25 mm Hg, seen in Paradis 
et al's study is consistent with results of Downey and asso- 
ciates," who found that a CPP of 28 mm Hg was needed to 
maintain blood flow above zero in the inner portions of the 
left ventricle (endocardium), with a fibrillating heart in a 
dog model." The authors concluded that ventricular fibril- 
lation elevated the compressive stresses in the myocardi- 
um, inhibiting coronary blood flow. The compressional 
force inhibiting blood flow in the outer portion of the my- 
ocardium, or epicardium, was < 15 mm Hg, indicating 
greater compressive forces on the endocardium. 

Niemann gives a short but informative review of cere- 
bral and myocardial perfusion during CPR, and summa- 
rizes the following points: '■* 

• 30% of normal cerebral blood flow is probably need- 
ed to maintain a normal electroencephalogram; 

• > 20 mL/min/lOO g of myocardial blood flow is re- 
quired to meet the metabolic demands of the fibril- 
lating heart; 

• a CPP of > 28 mm Hg is required for endocardial 
perfusion during ventricular fibrillation (based on 
Downey's work)." 

Studies supporting these data are listed in Niemann's re- 

The mechanism by which epinephrine improves CPP 
and. thereby, myocardial blood flow seems to be vasocon- 
striction of the vascular beds.""" As the dose of epineph- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

rine increases, the vasodilation of skeletal muscle blood 
vessels changes to vasoconstriction (Table 3). In a swine 
model examined by Schleien and others,"' the infusion of 4 
fjg ■ kg"' ■ min' of epinephrine during induced cardiac ar- 
rest (fibrillation) and CPR caused increased myocardial 
blood flow, cerebral blood flow, and cerebral oxygen up- 
take by selective vasoconstriction of other vascular beds.'^ 
The contribution of /J-receptor stimulation has been ad- 
dressed in several studies. Opinions have been offered in 
the literature that the /?-agonist effect of epinephrine is re- 
sponsible for restarting the arrested heart. '^■"* The effect 
presumably is due to direct stimulation of the myocardium 
(increasing contractility) and the ventricular pacemakers. 
Two studies designed to determine the relative importance 
of a- and ^adrenergic effects of epinephrine in CPR are 
summarized in Table S.'*^-" The results suggest that block- 
ing P receptors does not lower ROSC rates, but blockade 
of a receptors does. In another study, several of the same 
authors who performed the previous two studies cited 
compared the effectiveness of dopamine, dobutamine, and 
epinephrine in resuscitaton from asyphyxial and fibrillat- 
ing arrest in dogs.-' Dopamine, like epinephrine, stimu- 
lates a and /3 as well as dopaminergic receptors, and like 
epinephrine, a activity increases with increasing dose lev- 
els to increase TPR. Dobutamine is a synthetic cate- 
cholamine with a largely cardiac stimulant effect due to 
strong ^1 activity, but it has little or no effect on vascular 
resistance. The study found a higher incidence of success- 
ful resuscitation in the groups receiving dopamine or 
epinephrine than was found in those receiving dobutamine 
or no drug. There was no difference between the dopamine 
and the epinephrine groups in rate of successful resuscitation. 

Table .'). Influence of a- and /J-Adrenergic-Receptor Stimulation on 
the Return of Spontaneou.s Circulation (ROSC) and 
Successful Resuscitation in Cardiac Arrest in Dogs 


Drug Treatment 


Otto et al-"* 

a-blockade epinephrine. I mg I.V. 0/8 

/}-blockade epinephrine, I nig I.V. 6/8 

r> & /i-blockade epinephrine, I mg I.V. 0/8 

control (no blockade) epinephrine. I mg I.V. 7/8 


a-blockade isoproterenol. I mg .1/1 1 

/^-blockade phenylephrine. 10 mg 10/10 

Control (no blockade) epinephrine, I mg 10/10 

* AH dugs received closed chcsi cardiac massage (C'CCM I ;iiul .irtiricial vcnhlalK 

after 5 minutes of asphyxia! arrest, 
t All dogs received CCCM and artincial venlilaiutn iilicr ?> njiniiics of asphyxial i 


Yakaitis and co-workers-- investigated the effect of 
epinephrine 1 mg I.V. when used with artificial ventilation 
(AV), closed-chest cardiac massage (CCCM), and defibril- 
lation in mongrel dogs. They found that epinephrine did 
not affect the energy level (ie, the charge) needed for suc- 
cessful defibrillation, but the longer the duration of fibril- 
lation, the lower the success rate of defibrillation. 
However, they did find that after 2 minutes of fibrillation, 
epinephrine became increasingly important for successful 
resuscitation, in conjunction with AV, CCCM, and defib- 

In summary, the studies cited suggest that the efficacy 
of epinephrine in re-establishing heart action during car- 
diac arrest is due to its vasopressor effect, mediated by a- 
adrenergic stimulation. This action leads to an elevation of 
diastolic pressure and a re-establishment of coronary blood 
flow, resulting in successful resuscitation. 

Possible Adverse Effects. Epinephrine has the potential 
for adverse effects during resuscitation due to its strong j5- 
adrenergic action.'" The /^adrenergic effect increases the 
vigor of ventricular fibrillation, which increases myocar- 
dial oxygen consumption during VF. This also increases 
intraventricular pressure during fibrillation. In 1988, 
Ditchey and Lindenfeld-' measured left ventricular my- 
ocardial blood tlow during CPR in dogs, with a bolus I.V. 
dose of 1 mg epinephrine, followed by 0.2 mg/min.-' 
Although myocardial blood flow was significantly higher 
with epinephrine compared to a control group, myocardial 
lactate concentration increased significantly in both 
groups, and more in the epinephrine group. Myocardial 
adenosine triphosphate (ATP) decreased significantly and 
comparably in both groups. The authors concluded that 
epinephrine, even in large doses, may fail to improve the 
balance between myocardial oxygen supply and demand 
during CPR, even though coronary blood flow is substan- 
tially increased. The problem seems to be the effect of 
epinephrine on regional distribution of blood flow in the 
myocardium. The ventricular wall can be divided into the 
inner portion, or subendocardium, and the outer portion, or 
subepicardium. In the study by Ditchey and Lindenfeld,-' 
coronary blood flow was equal in the subendocardium and 
the subepicardium of the left ventricle prior to cardiac ar- 
rest and treatment with epinephrine. However, during CPR 
with epinephrine, subendocardial blood flow fell to .^3 ± 9 
mL • min ' • lOOg"' (mean ± SEM), whereas subepicardial 
flow was 60 ± 14 niL ■ min ' ■ lOOg '. This pattern of re- 
gional myocardial blood flow may not relieve myocardial 
ischemia. Usual autoregulatory mechanisms in the beating 
heart distribute a generally higher flow to the subendocar- 
dial than to the subepicardial layers.-'' The inner myocardial 
layers have a higher rate of oxidative metabolism, require 
an increased oxygen uptake, are subject to greater mechani- 


Respiratory Care • April "95 Vol 40 No 4 


cal stress, and have a higher capillary density than subepi- 
cardial layers.-' These combined metabolic and blood flow 
factors may increase the vulnerability of the subendocardi- 
um to ischemic damage. In the previous reference, Opie 
gives the figure of 71 mL • min^' • 100g~' for subendocar- 
dial blood flow compared to 57 mL • min~' ■ lOOg"' for 
subepicardial flow, in normal hearts.-'' 

Comparison of Epinephrine with a Agonists. Related to 
the question of regional distribution of coronary blood 
flow with epinephrine, Livesay -'' and associates compared 
the effects of epinephrine and methoxamine on myocardial 
blood supply and metabolic demands. Methoxamine is a 
relatively pure a-adrenergic agonist, with little /J-receptor 
stimulation. As a result, methoxamine would be expected 
to cause the favorable vasoconstriction seen with 
epinephrine but not provide any stimulation of cardiac ji- 
receptors, with subsequent positive inotropic effect. This 
study was complex, and involved two phases: CPR and a 
steady-state condition of cardiac fibrillation with car- 
diopulmonary bypass. During the fibrillation phase on by- 
pass, the authors found that left ventricular oxygen uptake 
increased from 9.5 ± 1.1 mL ■ min"' ■ lOOg"' (mean ± 
SEM) in controls to 13.0 ± 1.4 mL ■ min"' ■ lOOg"' with 
epinephrine, compared to 7.8 ± 0.8 mL • min"' • lOOg' 
with methoxamine. The ratio of subendocardial to subepi- 
cardial coronary blood flow (endo/epi) was 0.79 ± 0.09 
mL • min"' • lOOg"' (mean ± SEM) in controls, but fell to 
0.48 ± 0.04 mL • min"' • lOOg"' with epinephrine, and re- 
mained at 0.72 ± 0.07 mL • min"' • lOOg"' with methoxam- 
ine. The inotropic effect of epinephrine resulted in an in- 
crease in metabolic demand, seen with increased oxygen 
uptake, but a 53% decrease in left ventricular subendocar- 
dial blood flow. In the study,-'' an intraventricular balloon 
measured pressure in the left ventricle during fibrillation, 
with both methoxamine and epinephrine. Epinephrine, but 
not methoxamine, significantly increased intraventricular 
pressure due to the increased vigor of fibrillation with 
epinephrine. This result compromises coronary blood flow 
and m.ore so in the subendocardium than the subepicardi- 
um, a result in agreement with the quantitation of intramy- 
ocardial compression in the fibrillating heart by Downey 
and associates." The authors concluded that the ^adrener- 
gic effect of epinephrine augmented the vigor of fibrilla- 
tion, increased cardiac oxygen demands, and impeded 
subendocardial blood flow. The inotropic properties of 
epinephrine may increase metabolic demands when the 
oxygen supply is limited, worsening the myocardial oxy- 
gen supply-demand balance. 

A study by Brown and associates^'' reported in 1987 in 
the Annals of Emergency Medicine, examined the effect of 
high-dose phenylephrine, a pure a agonist, on cerebral 
blood flow during CPR, using a swine model. The study 

compared epinephrine 0.2 mg/kg, to phenylephrine 1.0 
mg/kg and 10 mg/kg. Epinephrine 0.2 mg/kg was signifi- 
cantly better than phenylephrine 1 .0 mg/kg in improving 
regional cerebral blood flow, but there was no difference 
between this dose of epinephrine and phenylephrine 10 
mg/kg. The authors concluded that large doses of either 
epinephrine or phenylephrine might be needed to maintain 
cerebral blood flow during CPR. The dose of epinephrine 
in their study is higher than the standard dose of 0.5-1.0 mg. 

Results such as those obtained by Livesay and 
associates-* would suggest that epinephrine should be re- 
placed as the drug of choice in cardiac arrest by pure a-ago- 
nists, such as methoxamine or phenylephrine, in order to 
avoid the unwanted /3-adrenergic effects of epinephrine dur- 
ing cardiac arrest. However, other studies have not support- 
ed such replacement. In 1990. Paradis and Koscove-** gave a 
thorough review of epinephrine in cardiac arrest, which in- 
cluded an examination of the literature on replacement of 
epinephrine with other agents. One of the studies they cite 
was a comparison by Turner and associates of epinephrine 
and methoxamine, in EMD in human subjects.-'' This 
prospective trial found no difference resulting from admin- 
istration of 10 mg of methoxamine and 1 mg of epinephrine. 
Another study compared 0.5 mg epinephrine with 5.0 mg 
methoxamine in prehospital ventricular fibrillation, and 
found a higher ROSC on arrival at the emergency depart- 
ment and a trend toward greater survival with epinephrine.^" 
The critical review of Paradis and Koscove-** pointed out the 
methodologic limitations of studies that have examined 
drugs and drug dosage during cardiac arrest in human sub- 
jects: the dose of epinephrine may have been too low to be 
effective in some studies, equipressor doses of different 
drugs may not have been used, sample size was often too 
small to detect a true difference (Type-II error), and clinical- 
ly relevant end points were not always chosen. Based on the 
results of such studies, it is not clear that pure a-adrenergic 
drugs should be chosen over epinephrine. 

Other considerations can affect the decision to replace 
epinephrine as the drug of choice in cardiac arrest. Ralston 
and co-workers" reported an interesting finding when com- 
paring regional blood flow with and without epinephrine in 
a dog model of CPR and VF. The epinephrine group not 
only had a significantly greater blood flow to the heart and 
brain but also to the adrenal glands. The investigators specu- 
lated that exogenous epinephrine may cause a positive feed- 
back response that results in additional release of endoge- 
nous epinephrine. In a study reported in 1968, Redding and 
Pearson^- also found that the rate of 24-hour survival in 
methoxamine-treated animals was poor, following VF.'- In 
addition, pure a-agonists such as methoxamine may pro- 
voke increased or prolonged vasoconstriction, depending on 
the pharmacokinetics of the particular drug. Increased pe- 
ripheral vascular resistance may compromise organ perfu- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

sion and increase afterload in a heart already impaired by is- 
chemic injury. Finally, the pharmacokinetics of drugs dur- 
ing cardiac arrest and CPR is largely unknown and may be 
somewhat variable due to the many factors present in the 
acute CPR situation." 

It is important to define patient situations in which al- 
ternatives to epinephrine are desirable. An abstract by 
Tang and associates'^ may have provided one example of 
such a situation: patients who exhibit marginal blood gases 
during CPR, indicating hypoxemia and hypercarbia. Tang 
and associates'"* found evidence that epinephrine may in- 
crease intrapulmonary shunting in a rodent model. When 
epinephrine 30 pg/kg was injected into the right atrium, 
CPP increased, but this was accompanied by a striking de- 
crease in PO2 and PCO2 in blood sampled from the aorta, 
with no change in the atrial blood. Considering that this is 
a rat model, the results only suggest further investigation 
in humans, inviting comparison with a agonists in the 
presence of intrapulmonary shunting. 

Use of High-Dose Epinephrine in Cardiac Arrest. The 

first report of the use of epinephrine in cardiac arrest is at- 
tributed to Crile and Dolley in 1906,-'-^ who used doses av- 
eraging 200 yug/kg in dogs. Beck and Rand** suggested the 
use of 0.5 mL of a 1:1,000 solution (0.5 mg) of 
epinephrine in asystole, in their 1949 publication on car- 
diac arrest during anesthesia, and in fact had stated: "Large 
doses of epinephrine should not be used." Redding and 
Pearson's work'' published in 1962 and previously refer- 
enced, also stated that epinephrine 1 mg was given intra- 
cardiac in their investigation of resuscitation. Current 
ACLS guidelines recommend use of a 1-mg dose of epi- 
nephrine given LV., which is not based on body size.' In a 
1989 editorial, Michael Callaham, associate editor of 
Annals of Emergency Medicine, questioned the orthodoxy 
of the then-current 1986 ACLS guidelines and the fixed 
epinephrine dose.''' Published studies have provided data 
supporting the use of higher doses of epinephrine. In 1988, 
Koscove and Paradis" reported the successful use of 5 mg- 
doses of epinephrine, following failure of the standard 1- 
mg dose to resuscitate in two individuals. The first case, a 
59-year-old woman in HMD, survived intact neurological- 
ly and was di.scharged. In the second case, a 71 -year-old 
man originally in asystole was returned to sinus tachycar- 
dia. Further aggressive therapy was discontinued at the 
family's request and the patient died. Perhaps more telling 
than these case reports are animal studies by Brown and 
colleagues''* using a swine model, which are summarized 
in Table 6. 

The standard dose of epinephrine was considered to be 
0.02 mg/kg in their studies. This is based on the fact that a 
translation of the 1-mg dose for a 50-kg person would be 
0.02 mg/kg.'""' In the 3 as listed in Table 6, the dif- 

Table 6. A Summary of Two Studies by Brown and Co- Workers '"■''' in 
an Animal Model. Suggesting That Higher than Standard 
Doses of Epinephrine in Cardiac Arrest May Be Beneficial. 

Regional Brain Blood Flow: (mL min ' lOOg ')" 

0.02 mg/kg 
NSR Epi 

0.2 mg/kg 
NSR Epi 

2.0 mg/kg 
NSR Epi 

Left cerebral cortex 40 3 
Right cerebral cortex 38 4 

Regional Myocardial Blood Flow: (mL 

34 13 
31 14 

min' lOOg^')"' 

36 12 

37 12 

0.02 mg/kg 
NSR Epi 

0.2 mg/kg 
NSR Epi 

2.0 mg/kg 
NSR Epi 

Endocardial 215 2 
Epicardial 168 2 
Total MBF 189 2 

180 176 
160 104 
156 113 

rine dose; MBF = 

126 133 
98 120 
105 94 

*NSR = normal sinus rhythm; Epi = epineph 

myocardial blood 

ference is significant between the 0.02 and 0.2 mg/kg 
doses for regional brain and myocardial blood flow, but 
not the difference between the 0.2 and the 2 mg/kg dose. 
Brown and associates"* noted that neuronal survival ap- 
pears to require cerebral blood flowrates approaching 10- 
15 mL ■ min"' • lOOg"', based on electroencephalographic 
data. Both the 0.2 and the 2 mg/kg dose levels provided > 
12 mL • min"' ■ lOOg ' of blood flow to the right and left 
cerebral cortices. Total myocardial blood flow (MBF) was 
only 1.8 mL • min"' • lOOg"' in the 0.02 mg/kg group, but 
well above the minimally required 20 mL ■ min"' ■ lOOg"' 
level for a tlbrillating heart in the other two groups.''' No sig- 
nificant differences were noted in systolic and diastolic aortic 
pressures among the three dose levels, at a 0.05 significance 
level. In further work. Brown'*" and associates found that the 
standard dose of epinephrine, 0.02 mg/kg. failed to provide 
the minimal MBF needed (16-25 mL ■ min' ■ lOOg"') to 
meet oxygen demands in VT and CPR. in a swine model. 
The ratio of subendocardial-to-subepicardial blood flow 
went from 1.69 during normal sinus rhythm, to 0.66 with 
epinephrine and CPR, indicating poor allocation of blood 
to the subendocardial region of the heart. Lindner and co- 
workers'*' also found that CPP, MBF, and resuscitation 
success were increased in a pig model when epinephrine 
was given at a dose up to 0.045 mg/kg compared to 0.015 
mg/kg, but larger doses up to 0.09 mg/kg did not lead to 
further improvement. Success in resuscitation was defined 
as a return to coordinated electrical activity, with a blood 
pressure greater than 90/40 mm Hg for at least 5 minutes. 

Based on results such as these, other studies have inves- 
tigated the outcome of higher doses of epinephrine in re- 
suscitation of humans. Lindner and co-workers'*- randomly 
allocated 68 adults in cardiac arrest (asystole and HMD) to 
either a standard 1 -mg-dose group or to a high-dose 5-mg 
group, with epinephrine. Resuscitation was considered 



ACLS Drugs 

successful when there was a ROSC. defined as a systolic 
blood pressure above 80 mm Hg with or without use of 
dopamine, for at least 12 hours. Their results can be sum- 
marized as follows; 

Standard High 

1-mg dose (%) 5-nrig dose (%) 

Success after 1st dose 
Success after full ACLS 
Hospital discharge rates 




The authors stated that the hospital discharge rate was not 
significantly different between the two groups, probably 
because of the prolonged brain ischemia already present 
before resuscitation was begun. Stiell and associates'*^ re- 
ported a randomized, double-blind trial of 1 mg versus 7 
mg of epinephrine in 650 adult patients suffering cardiac 
arrest either prehospital or in-hospital.^' They found no 
significant difference in either the group overall or the in- 
hospital group for 1-hour survival or for discharge from 
the hospital. For in-hospital arrests, the discharge rate was 
4.8% for the high-dose group, and 7.1% for the standard 
dose group (p = 0.52). Callaham and associates"" also re- 
ported no significant difference in overall survival of 762 
prehospital cardiac arrest (asystole or EMD) patients given 
either 1 mg or 15 mg of epinephrine, or 1 1 mg of nore- 
pinephrine, which possesses greater a-adrenergic-stimu- 
lating properties than epinephrine. However their study did 
show a significantly greater rate for field resuscitation with 
the high-dose (20%) versus low dose (11%) epinephrine. 

The animal studies cited, with their optimistic results, 
bring out an important consideration in research on CPR 
techniques: ROSC and/or successful defibrillation do not 
equate to the ultimately desirable outcome of CPR, which 
is a return of the individual to pre-arrest baseline and neu- 
rologic normality. 

Some interesting data have been provided by Paradis 
and co-workers in a 1990 abstract on high-dose epi- 
nephrine.'''' They measured the increase in plasma levels of 
epinephrine in samples from the aortic arch, with no 
epinephrine and with 1 and with 0.2 mg/kg doses (14 mg 
in a 70-kg person) in 28 human subjects during CPR at 2.5 
and 5 minutes. Sample levels peaked at 2.5 minutes after 
epinephrine was introduced into the right atrium, with the 
following results: 

Before epinephrine: 
Standard dose: 
High dose: 

Aortic Sample, Epinephrine Level 

1.40 ± 1.80ng/mL 
1.52 ± 1.62ng/mL 
3.93 ± 2.89 ng/mL 

The authors did not explain what the measure of dispersion 
was, whether standard deviation or standard error, although 
this is presumably a standard deviation. The standard dose 
gave a 100-fold increase in blood level, but 14 times this 
dose (high-dose) resulted in only a 2.3-fold increase (actu- 
ally 2.58) in plasma levels. These data suggest that there is 
not a linear relationship between epinephrine dose levels 
and arterial drug levels, and to achieve a certain increase in 
blood levels, a proportionately greater dose is needed. It 
may be that increased doses of epinephrine increase the 
volume of distribution of the drug. The interpretation and 
application of these data are problematic. Is there little re- 
turn with increased epinephrine doses, supporting the stan- 
dard 1-mg dose? Or. does this indicate the need for much 
larger doses than previously considered? Animal studies, 
with doses increased from 0.2 mg/kg to 2 mg/kg, do not 
seem to support the latter. Perhaps the disappointing out- 
come with higher dose epinephrine is related to the data 
observed by Paradis and co-workers."" 

Recommendations of AHA for ACLS. The 1992 ACLS 
guidelines published in the Journal of the American Medical 
Association have concluded that 1 mg epinephrine I.V. con- 
tinues to be the first agent in cardiac arrest.' However, a 
higher dose, 5 mg or approximately 0.1 mg/kg, is given a 
Class-lib recommendation (acceptable, possibly helpful), 
and should be considered only after the 1 mg dose has 

Lidocaine (Xylocaine) 

ACLS Indication. Lidocaine, also known by the name lig- 
nocaine, is considered the drug of choice in treating ven- 
tricular ectopy, VT, and VF. The drug is recommended by 
ACLS guidelines for VT and VF that persist after defibril- 
lation and epinephrine, for control of premature ventricular 
contractions (PVCs), and for wide-complex paroxysmal 
supraventricular tachycardia (PSVT), or tachycardias of 
uncertain type.' Although data have shown that prophylac- 
tic administration of lidocaine reduces the incidence of pri- 
mary VF in the presence of known MI, routine prophylac- 
tic administration in suspected MI remains questionable. 
The ACC/AHA Task Force gives the prophylactic admin- 
istration of lidocaine in uncomplicated acute MI or is- 
chemia without PVCs a Class-lib recommendation (ac- 
ceptable, possibly helpful). '"- 

Pharmacology of Lidocaine. Lidocaine was first synthe- 
sized in 1943 and used as a local anesthetic, prior to its 
subsequent use as an antiarrhythmic agent in the 1950s.''* 
The structures of lidocaine, procainamide, and the anes- 
thetic procaine are shown in Figure 2. Lidocaine and pro- 
cainamide are both members of the local group of anes- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

thetics, consisting of a lipopiiilic aromatic-ring structure 
connected to a hydrophilic amine by an amide linkage. The 
presence of the amide linkage instead of the ester linkage 
that is found in procaine makes lidocaine and pro- 
cainamide resistant to degradation by plasma esterase en- 
zymes. Procaine is known to be effective against cardiac 
dysrhythmias but is rapidly hydrolyzed by plasma butyryl- 
cholinesterase and has a short duration of action.''^ Local 
anesthetics interfere with generation of an action potential 
(AP) by blocking sodium conductance, thus blocking the 
large, transient, voltage-dependent rise in the permeability 
of the cell membrane to sodium ions. This action is the 
basis for the effect lidocaine has on ventricular dysrhyth- 

O P2H5 

H2N^ />-C-0-C-CH2-CH2-N 




/=\ Ti P2H5 

<C )^NH-C-CH2-N 




Fig. 3. An Illustration of the five phases of an action potential for a 
cardiac muscle cell. The slow influx of calcium ions delays the re- 
polarization process begun with the rapid pumping of sodium ions, 
indicated by the dotted lines. See text for a detailed description. 
Abbreviations: ERP, effective refractory period; RRP, relative re- 
fractory period; SNP, supranormal period. 






Fig. 2. Chemical structures of the local anesthetic procaine and its 
two congeners lidocaine and procainamide, both of which are used 
as antiarrhythmic agents. 

A brief review of cardiac electrophysiology with a 
focus on the AP of myocardial cells rather than pacemaker 
cells such as the sinoatrial (SA) node, can illustrate the ef- 
fect of drugs such as lidocaine or procainamide. Several 
texts offer excellent discussions of this topic.'''''' '*'' In the 
heart, myocardial contraction normally occurs in an inte- 
grated, synchronized fashion. Following an automatic de- 
polarization, or 'firing,' of the SA node, largely mediated 
by an influx of calcium ions, a wave of depolarization is 
conducted by atrial tissue, specialized tissues of the atri- 
oventricular (AV) node. Bundle of His, Purkinje fibers, 
and, ultimately, myocardial muscle tissue. With depolar- 
ization, atrial and then ventricular contraction occur. The 
resting membrane potential of atrial and ventricular mus- 
cle fibers and of the specialized conducting fibers of the 
His-Purkinjc system, is approximately -90 mV. An AP for 
ventricular muscle cells is illustrated in Figure 3. 

When, in response to a stimulus, AP reaches a threshold 
of -70 mV, a rapid influx of sodium ions causes depolar- 
ization and a reversal of the transmembrane potential to 
approximately -1-25 to -1-35 mV (Phase 0) of the cardiac cell 
AP. The cardiac cell then begins to repolarize by pumping 
out the sodium ( 1 ), a process which is slowed by a 
secondary, slower influx of calcium ions through the cell 
membrane. This results in the plateau, or Phase 2 of the 
AP. As the sodium and calcium are returned to the cell ex- 
terior (Phase 3), the transmembrane potential is re-estab- 
lished at -90 mV. and the cells are ready to be stimulated 
and contract again (Phase 4). More specifically, during the 
effective refractory period, no stimulus, regardless of 
strength, produces a propagated response. Following the 
effective refractory period in an AP. there is a relative re- 
fractory period during which a propagated AP can be 
elicited, but a greater than normal stimulus is required. For 
a short time after the relative refractory period, there is 
supranorinal period, when the threshold is slightly lower 
than normal. Normal excitability of a Purkinje fiber or 
ventricular muscle exists from the end of the supranormal 
period to the beginning of the next AP.'' 

With initial dcpt)lari/ation, sodium channels are t)pened, 
and then inactivated until repolarization (Phase 3) returns 
membrane potential beyond -60 mV. Full reactivation oc- 
curs at -90 mV. The refractory period after excitation is 


RF..SPIRATORY Care • April '95 Vol 40 No 4 

ACLS Drugs 

caused by sodium channel inactivation. A new stimulus 
does not elicit a second depolarization until membrane po- 
tential reaches -60 mV and beyond during repolarization."" 
Lidocaine and other antiarrhythmic drugs are usually 
identified using four categories, or classes. This classifica- 
tion scheme for antiarrhythmic agents should not be con- 
fused with the classes of AHA recommendations for these 
drugs. Lidocaine is considered a Class- 1 antiarrhythmic 
and is further categorized as a Class- IB drug. The AHA 
gives lidocaine a Class IIB recommendation for prophy- 
lactic use in uncomplicated acute MI. The subdivision of 
Class 1 agents into 1 A, IB, and IC recognizes differences 
existing among the drugs in this class. Table 7 lists the 
drugs in the four classes of antiarrhythmic agents, and 
summarizes the effects of each. To avoid confusion, arable 
numbers and upper case letters are used to designate an- 
tiarrhythmics by class, in this paper. 

Table 7. Classification and Summary of Major Effects of Antiarrhythmic 




Class lA 


inhibition of sodium influx 


(++) and Phase 0; prolonged APt 


duration; moderate reduction in 
myocardial conduction velocity. 

Class IB 


modest inhibition of sodium influx 


(+) and Phase 0; shortened 


AP duration. 



Class IC 


inhibition of sodium influx (+++) 


and Phase 0; reduction in 


myocardial conduction; 


no change in AP duration. 


Class 2 


reduced rate and cardiac output. 

Class 3 


lengthening of the AP duration and 


the ERP. 


Class 4 


inhibition of calcium channel 



decreased rate and conduction. 


tAP = action potential; ERP = effective 

refractory period. *classified as both lb and 

Ic by Opie 

due to mixed properties.™ 

Lidocaine inhibits the fast inward sodium current to 
slow Phase of the AP, a trait common to all Class- 1 
agents to some degree. However, lidocaine shortens the 
AP duration. In the electrocardiogram (ECG) tracing, QT 
prolongation does not occur. Lidocaine has a greater effect 

on ischemic myocardial tissue and is also more effective 
with high levels of external potassium.''" In diseased my- 
ocardial tissue, lidocaine may promote conduction block 
and convert unidirectional block to a bidirectional block, 
thus inhibiting a re-entry circuit and dysrhythmia. Lido- 
caine acts primarily on disturbances of ventricular origin, 
and has a narrow spectrum of antidysrythmic effects."** The 
drug has no effect on sinus rate in normal blood levels; 
there is a slight decrease in conduction velocity through 
atrial tissue and the AV node. In the His-Purkinje system 
and ventricular muscle, lidocaine depresses the Phase 
upstroke, as previously described, and shortens the AP du- 
ration and the ERP. There is a decrease in the rate of spon- 
taneous discharge in Purkinje fibers. ■'*•■** 

Pharmacokinetics. Lidocaine is more effective adminis- 
tered by injection, either intramuscularly or intravenously, 
than by the oral route. There is high first-pass liver 
metabolism with oral administration.'*'' With parenteral ad- 
ministration, approximately 70% of the drug entering the 
liver from the systemic circulation is metabolized by de- 
ethylation in one pass through the liver. As a result, any 
factor that affects hepatic blood flow affects plasma levels 
of lidocaine in a subject. Factors that are known to slow 
hepatic flow and thereby increase plasma levels include 
treatment with /3-adenergic antagonists, heart failure, and 
age. Cirrhosis and renal disease can also increase plasma 
levels to a toxic range unless dosage is adjusted. Two 
major metabolites of lidocaine have been identified in the 
blood of patients, monoethylglycine xylidide (MEGX), 
and glycine xylidide, formed from the further metabolism 
of MEGX.''*"'** About 90% of a lidocaine dose appears in 
the urine as metabolites."*' The plasma half-life of lido- 
caine is 8 minutes in the initial distribution phase, and then 
100-120 minutes as a steady state is reached. For this rea- 
son, a loading dose of 100-200 mg intravenously or 400 
mg intramuscularly is given, followed by I.V. infusion at a 
rate of 2-4 mg/min for the first 24 hours, in order to 
achieve therapeutic plasma levels in the 2-5 jtvg/mL 
range.'*'-''" Some of the toxic effects of lidocaine may be 
explained by the accumulation of the metabolites during 
infusion. Although the plasma levels of the drug may be 
acceptable, both MEGX and glycine xylidide possess po- 
tent antidysrhythmic and central nervous system effects in 
their own right. ^'""* 

Side Effects. The most common side effects with lido- 
caine are mediated through the central nervous system 
(CNS). Drowsiness may be seen and may be beneficial. 
Additional effects include decreased hearing, paresthesias, 
disorientation, psychosis, muscle twitching, patient agita- 
tion, and seizures.""* Large doses of lidocaine may produce 
bradycardia and hypotension due to myocardial depres- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

sion/'' Asystole and respiratory depression are less com- 
mon but can occur.^' 

Prophylactic Use of Lidocaine in MI. As stated previously, 
the ACC/AHA considers the use of lidocaine in uncompli- 
cated acute MI or ischemia without PVCs a Class-lib recom- 
mendation. The routine prophylactic use of lidocaine in ei- 
ther suspected or confirmed acute MI is questioned. There is 
evidence in the literature that prophylactic lidocaine in sus- 
pected acute MI is effective in reducing occurrences of VF. 
Koster and Dunning'- provided data from a large random- 
ized trial of intramuscular lidocaine for suspected AMI in the 
prehospital phase, in which 8 of 2,987 patients receiving li- 
docaine and 17 of 3,037 controls, developed VF within 1 
hour.'- Lie and co-workers" examined the use of lidocaine in 
confirmed acute MI and found that VF did not occur in 107 
patients receiving lidocaine but did occur in 9 of 105 con- 
trols. A meta-analysis by DeSilva and associates'"* examined 
15 studies reporting the effectiveness of lidocaine in prevent- 
ing VF in acute MI and concluded that lidocaine treatment 
does provide protection against VF in acute MI. TTie question 
that is raised concerning the routine prophylactic use of lido- 
caine in suspected MI or even in confirmed MI becomes one 
of cost-benefit and risk to the patient. Carruth and 
Silverman" have pointed out that routine use of lidocaine 
would have been of no potential benefit in 96.8% of their pa- 
tients studied and would have exposed them to extra expense 
and possible toxicity. Opie et al"' note that "250 patients with 
suspected acute MI must be treated to save one from VF." In 
addition, defibrillation offers an effective treatment in those 
few patients when VF does occur. Koster and Dunning'- 
noted in their large, controlled trial, that epi.sodes of VF were 
successfully treated with electrical defibrillation, and there 
was no difference in death rate between treatment and con- 
trol groups ( 19 versus 21, p > 0.2). Other investigators con- 
clude that prophylactic lidocaine in suspected acute MI can- 
not be advocated"" or that results remain equivocal." 
Although the debate may continue and may be refueled by 
new studies not yet published using monitoring of plasma li- 
docaine levels, the crux of the issue seems to be that ( I ) rela- 
tively few suspected or even confirmed acute MI cases de- 
velop VF, (2) electrical defibrillation is effective when VF 
does occur, and (3) lidocaine administration may be fraught 
with toxicity. 

Procainamide (Pronestyl) 

Procainamide is a .second drug used to control cardiac 
arrhythmias, and is considered a Class- 1 A antiarrhythmic, 
as indicated in Table 7. 

ACLS Recommendation. Procainamide is given an AHA 
Class-Ila (acceptable, probably helpful) recommendation for 

the treatment of PVCs and recurrent VT when lidocaine is 
contraindicated or has failed to suppress ventricular ectopy.' 

Pharmacology of Lidocaine. The pharmacology of pro- 
cainamide is reviewed in standard texts of pharmacology, 
and the following summary is based on Lucchesi's chapter 
on antiarrhythmics in Craig and Stitzel's Modern Pluinna- 
cology.'*^ Procainamide is a congener of procaine (Fig. 2), 
synthesized to avoid the limitations seen with procaine: short 
duration of action, CNS toxicity, and lack of oral effective- 
ness. Procainamide is effective taken orally and is not metab- 
olized by plasma cholinesterase (butrylcholinesterase). 

The earlier review of cardiac APs provides an under- 
standing of the action of procainamide on the heart. 
Procainamide is effective against a wider variety of cardiac 
dysrhythmias than lidocaine, including supraventricular and 
ventricular dysrhythmias such as VF.'" Based on the classi- 
fication presented in Table 7, procainamide is a Class- 1 A 
agent, with properties similar to quinidine. Procainamide 
has a marked inhibitory effect on fast-channel sodium influx 
and prolongs the refractory period, lengthening the duration 
of the AP. Procainamide does not prolong the QT interval to 
the same extent as does quinidine. Both PVCs and VT re- 
spond to procainamide. This drug is also useful in treating 
premature atrial beats (PACs), paroxsymal atrial tachycar- 
dia (PAT), and recent-onset atrial fibrillation.^'* 

Procainamide gives good oral bioavailability (about 
75%), with liver metabolism accounting for its breakdown. 
Peak plasma concentrations are seen at 60-90 minutes with 
oral administration, and 12-45 minutes with intramuscular 
injection. The plasma half-life of 3.5 hours provides rela- 
tively short duration of action, compared to that of quini- 
dine, which is 7-9 hours."' It is important to note that my- 
ocardial levels are 2 to 2 1/2 times those of plasma levels."** 
The drug is eliminated rapidly through the kidneys. 

Side Effects. Procainamide has several cardiovascular ef- 
fects, the most common of which include hypotension, 
heart block, ventricular tachydysrhythmias, and dose-relat- 
ed conduction block. Conduction block, can result in a 
prolonged QRS or QT interval, and the drug should be 
avoided in patients with existing QT prolongation and tor- 
sades de pointes.' •""' Patients with acute Ml are at risk for 
hypotension due to existing pump impairment and should 
be monitored carefully if procainamide is used. Long-term 
use, > 6 months, causes increased antinuclear antibody 
production in > 80% of patients. Approximately one third 
of the patients on long-term use develop a lupus erythe- 
matosus-like syndrome, which clears with discontinuation 
of the drug. For this reason, therapy is usually limited to < 
6 months.^**'" With oral therapy, early side effects can be 
fever and rash, and late side effects can include arthralgia 
and rash."' There is little potential to develop CNS toxicity 


Rli.SPIRATORV Carh • APRIL '95 Voi. 40 No 4 

ACLS Drugs 

with procainamide, unless rapid intravenous administra- 
tion occurs. Because of its duration of action and possible 
side effects, quinidine is preferred to procainamide unless 
patients are intolerant or unresponsive to quinidine. 

Bretylium Tosylate (Bretylol) 

Bretylium tosylate, a third drug used to control cardiac 
arrhythmias, is a Class-3 antiarrhythmic agent (Table 7). 

ACLS Recommendation. Bretylium is recommended for 
use in the treatment of VT and VF resistant and unresponsive 
to defibrillation, epinephrine, and lidocaine, or if lidocaine 
and adenosine have failed to control wide-complex tachycar- 

Pharmacology of Bretylium. Bretylium was introduced in 
1959 to treat hypertension, but proved ineffective due to 
rapidly developing tolerance to its antihypertensive effect.'" 
The subsequent discovery of the antidysrhythmic effects of 
bretylium led to renewed interest, and the drug was marketed 
for treatment of life-threatening ventricular dysrhythmias.-''^ 
My summary of its pharmacologic effects is based on chap- 
ters on antidysrhythmic drugs found in Opie's Drugs for the 
Heart.^^ Antonaccio's Cardiovascular Pharmacology.'*^ and 
Craig and Stitzel's Modem Pharmacology.*^ The older, but 
well-organized review of bretylium tosylate by Koch-Weser 
is also available.-"'^ The drug is a quaternary ammonium com- 
pound (Fig. 4) that has two primary effects on the cardiovas- 
cular system: an effect on adrenergic nerve transmission and 
an effect on the electrophysiology of the heart. The effect on 
adrenergic nerve transmission is biphasic, with an initial re- 
lease of catecholamines into the circulation followed by inhi- 
bition of the release of norepinephrine from adrenergic neu- 
rons. Bretylium has the property of concentrating in postgan- 
ghonic adrenergic nerve terminals to produce this biphasic 
effect. As a result, there is an initial rise in arterial pressure, 
cardiac contractility, and heart rate. Subsequently, within 1 to 
2 hours, the adrenergic-blockade effect produces hypoten- 
sion, the most common cardiovascular effect. Opie refers to 
this as a "chemical sympathectomy. "'•''° 

C /VCH2N+-C2H5 




Fig. 4. Chemical structure of the antidysrhythmic, bretylium. 

Bretylium causes no change or a slight decrease in sinus 
heart rate, once the initial phase of catecholamine release 
ends. In the atria, bretylium causes prolonged AP duration 

and prolonged atrial muscle ERP. In the AV node, large 
doses of bretylium can cause a slowing of nodal conduc- 
tion velocity and an increase in the AV nodal refractory 
period. However, in doses used in humans, the moderate 
increase in conduction and decrease in the AV nodal re- 
fractory period can cause an acceleration of ventricular 
rate in the presence of atrial fibrillation or flutter. At thera- 
peutic concentrations, bretylium causes an increase in the 
AP and the ERP of Purkinje fibers and ventricular muscle 
cells. It is this effect that distinguishes bretylium as a 
Class-3 antiarrhythmic agent (Table 7). Unlike Class- 1 
agents, such as lidocaine, bretylium does not depress the 
upstroke velocity (Phase 0) of the cardiac AP.'' The an- 
tifibrillatory effect of bretylium on the Purkinje system 
and ventricular muscle make this drug attractive in VF. 
Bretylium raises the threshold for ventricular fibrillation 
and also lowers the electrical threshold for successful de- 
fibrillation.'*'* The drug has been reported to produce this 
result in both normal and infarcted dog hearts. In infarcted 
dog hearts, bretylium decreases the disparity in AP be- 
tween normal and diseased myocardial regions, which 
would be significant for its antifibrillatory action. ''° 

In a comparison of bretylium with lidocaine as initial 
drug therapy for 146 cases of out-of-hospital ventricular 
fibrillation, Haynes and co-workers'"' found no significant 
advantage or disadvantage between the two drugs. Con- 
version to an organized rhythm, establishment of pulse, 
number of defibrillatory shocks, and hospital discharge 
were the same for both groups. In the study, a 10-mL bolus 
of the randomly allocated drug (500 mg for bretylium, 100 
mg for lidocaine) was given after the first shock, with a 
follow-up identical dose if fibrillafion persisted or re- 
curred. A different study by Olson and associates*- also 
compared bretylium to lidocaine as first-line antiarrhyth- 
mics for out-of-hospital patients in ventricular fibrillation, 
using doses of 10-30 mg/kg of bretylium and 2-3 mg/kg of 
lidocaine. Their study recorded conversion to an organized 
electrical rhythm, conversion to a rhythm with a pulse, re- 
suscitation rate (admission to the emergency department 
with a pulse), and the save rate (alive at hospital dis- 
charge). The only significant difference between the two 
drugs was the conversion rate to a rhythm with pulse in 27 
of 48 (56%) with lidocaine versus in 15 of 43 (35%) with 
bretylium. The resuscitation rate was 11 (23%) and 10 
(23%) respectively, and the save rate was 5 (10.4%) and 2 
(5%) respectively, for the two drugs. 

A study by Koo and associates*' in 1984 reported that 
bretylium given I.V. in doses of 10-30 mg/kg did not change 
the defibrillation threshold in dogs with a normal, nonis- 
chemic myocardium. Heart rate and blood pressure were 
significantly affected, however. These data raise questions 
about the action of bretylium in ventricular fibrillation. Does 
the drug raise the fibrillation threshold and lower the defib- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

rillation threshold? Euler and Scanlon''' found that bretyh- 
um alone or in combination with the /J-blocker timolol did 
nor significantly change the threshold for VF induced by a 
siiifile-piilse technique but did raise the VF threshold in- 
duced by a train-of-pidses technique.^'* The train-of-pulses 
technique causes local norepinephrine release, more so than 
the single-pulse technique. Because bretylium inhibits the 
release of norepinephrine, it can affect the VF threshold in- 
duced by the train-of-stimuli method more than with the sin- 
gle-pulse method. This, together with the results of Euler 
and Scanlon,''' would support the view that the antifibrillato- 
ry effect of bretylium is mediated by its adrenergic neuronal 
blockade. However, the work of Koo and associates'"' also 
used a brief train of .stimuli to induce fibrillation, placing the 
results of the two studies at odds, and perhaps leaving the 
question of the action of bretylium unresolved. There are 
three possible actions of bretylium causing its effect in ven- 
tricular fibrillation; the early release of catecholamines, 
blockade of postganglionic adrenergic neurons, or its direct 
membrane effect on the AP. It is possible that one or more 
of these may reduce the vulnerability of the infarcted heart 
to VF. Both of the studies utilized normal canine hearts, 
which may also influence their results as applied to the is- 
chemic heart. 

Pharmacokinetics. Bretylium has poor oral bioavailabili- 
ty, which limits its use to parenteral administration. With 
intramuscular injection, peak plasma levels are seen within 
1 hour, and with I.V. administration, the half-life is 7 to 9 
hours.'*'-'''' There is no liver metabolism, with greater than 
90% of the drug being excreted unchanged in the urine. 
The usual dose is 5-10 mg/kg given I.V., to a maximum of 
30 mg/kg, with therapeutic blood levels maintained in the 
0.5 to 1 ,0 yUg/mL range.^^" 

Side Effects. The initial catecholamine release causes a pos- 
itive inotropic and chronotropic effect, which may be haz- 
ardous in acute MI, aggravating existing ischemia and in- 
creasing myocardial oxygen demand.'" The major side ef- 
fect is an induced hypotension, which can compromise the 
hemodynamic status and which results from peripheral va- 
sodilation secondary to the adrenergic blockade.'''''^" Rapid 
I.V. bolus injection can cause nausea and vomiting.'" Brety- 
lium is contraindicated in circulatory shock.'*'''"* 


Atropine sulfate is an old drug that is used in cardiac ar- 
rest or acute MI for its vagolytic properties. 

ACLS Recommendation. Atropine sull'ate is given the 
following recommcntlations by the ACC/AHA.' 

Class I — for the treatment of symptomatic sinus 

Class Ila (acceptable, probably helpful) — for in the 
presence of AV block at the nodal level or in ventricular 

Pharmacology. With the renewed interest in anticholiner- 
gic bronchodilation over the last decade, (including the use 
of ipratropium bromide), respiratory care clinicians have be- 
come familiar with this class of drugs. Atropine sulfate is an 
antimuscarinic drug and a naturally occurring alkaloid of the 
belladonna plant, used for hundreds of years in medicine. Its 
structure is shown in Figure 5. Antimuscarinic agents block 
the effects of muscarine, a mushroom extract, at the post- 
ganglionic junctions on glands and smooth muscle of the 
parasympathetic nervous system. Alkaloids such as atropine 
and scopolamine, are organic esters. Atropine is a racemic 
mixture of ^-/-hyoscyamine, which is a combination of trop- 
ic acid and the organic base tropine. The pharmacologically 
active isomer is the levorotatory form.''^ As a tertiary amine, 
the drug is well absorbed across the blood-brain barrier and 
distributes throughout the body. Atropine exerts its anti- 
cholinergic action by competitive antagonism of acetyl- 
choline receptors at parasympathetic postganglionic sites. 
Atropine, in sufficient doses, blocks parasympathetic 
(cholinergic) effects on the sinoatrial (SA) node. By block- 
ing vagally induced bradycardia, atropine accelerates heart 
rate. Atropine also increases conduction velocity in the AV 
nodal portion of the heart and decreases the effective refrac- 
tory period of this conduction system. There is no change in 
the conduction of the His-Purkinje system,'*' and atropine 
has little direct effect on the circulatory system. Although 
cholinergic receptors are present on blood vessels, parasym- 
pathetic fibers do not normally innervate such vessels. As a 
result, atropine produces an effect on peripheral vascular 
tone only in the presence of a cholinergic drug whose effect 
on blood vessels atropine can block. Atropine does produce 
flushing due to vasodilation in the blush area of the skin.*^ 
The effect of atropine on blood pressure when the drug is 
used in sinus bradycardia is through the improvement in car- 
diac output, rather than a change in peripheral vascular tone. 

H2C— CH — CH2 C ^__ 

I / \ II /=\ 

I N-CH3 CH— O — C — CH^d h 

H2C— CH — CH2 CH2OH ^^^ 


Fig. 5. Chemical structure of the antimuscarinic agent, atropine. 

Use of Atropine in Sinus Bradycardia. Dauchot and 
Gravenstein'''' give a detailed review of the incidence and 
etiology of bradycardia following acute Ml, and discuss 


Re.spiratory Care • April "95 Vol 40 No 4 

ACLS Drugs 

the advantages and disadvantages of atropine treatment for 
this condition. •'■' Sinus bradycardia, defined as a heart rate 
of < 60 beats/minute, has been noted to occur in the pres- 
ence of myocardial ischemia after MI and is more often as- 
sociated with an inferior MI. Sinus bradycardia with ac- 
companying hypotension has been treated with vagolytic 
agents such as atropine, to reverse the bradycardia and re- 
store cardiac output and blood pressure. 

The use of atropine in 56 patients with acute MI com- 
plicated by sinus bradycardia and pump failure was evalu- 
ated by Scheinman and co-workers.''* An initial I.V. bolus 
injection of at least 0.5 mg was given to all patients. Heart 
rate increased significantly from 53 ± 8 beats to 85 ± 18 
beats after atropine (p < 0.01). In 27 of 31 patients, there 
was a decrease or abolition of ventricular arrhythmias, in- 
cluding PVCs and accelerated idioventricular rhythm. In 
15 of 17 hypotensive patients, blood pressure was normal- 
ized, and in 1 1 of 13 patients with second- or third-degree 
heart block, there was improvement in AV conduction. 
There were 10 major adverse effects reported in 7 of the 
patients. These included sustained sinus tachycardia, in- 
creased number of PVCs, ventricular tachycardia or fibril- 
lation ( 1 patient), and toxic psychosis in 1 patient. There 
were 4 patients who received more than 2.5 mg within a 2 
1/2 hour period, and all of these experienced the adverse 
effects reported. Normal heart rate of 70- 1 00 beats/minute 
was achieved with single doses in the 0.5-1.0 mg range in 
27 of the 56 patients. Multiple doses were required in 29 of 
the patients, however. The authors concluded that atropine 
was the drug of choice for treating sinus bradycardia with 
hypotension. They advised against the use of atropine for 
sinus bradycardia when hypotension, ventricular irritabili- 
ty, or evidence of pump failure are lacking (ie, with 
asymptomatic bradycardia). 

Chamberlain and associates*^ investigated the dose of 
I.V. atropine needed for maximal vagal inhibition of the 
SA node in 10 healthy volunteers pretreated with propra- 
nolol to negate any sympathetic effect on heart rate.*' They 
found that the supine resting heartrate increased to a peak 
with 1 .8 mg in 3 volunteers, with 2.4 mg in 4, and with 3.0 
mg in the remaining 3. This corresponded to a dose sched- 
ule of 0.025 to 0.041 mg/kg of body weight. There was an 
inverse correlation between the supine resting heart rate 
and the dose of atropine needed for maximal effect (r = - 
0.73). They concluded that a dose of 0.04 mg/kg, or 3.0 mg 
in adults, is sufficient to produce complete vagal blockade 
of the SA node. 

It is also useful to note that small doses of atropine can 
produce cholinergic effects, prior to the anticholinergic ef- 
fect seen as the dose increases.*-'' Kottmeier and Graven- 
stein** studied cumulative doses of both atropine sulfate 
and atropine methyl bromide, a quaternary form with poor 
diffusibility across the blood-brain barrier. The authors 

reasoned that if the cholinergic effect of atropine sulfate is 
mediated by a central vagal stimulation, then this effect 
should not be seen with the methylbromide formulation. 
Using a canine model, they found that low doses of both 
drugs produced an initial slowing of heart rate. They also 
found that an increase in the P-R interval occurred after 
heart rate began to accelerate with increasing cumulative 
doses of atropine, before decreasing to below pre-treat- 
ment values. Their results did not support the view that this 
cholinergic effect of low-dose atropine was centrally me- 
diated. In vagotomized animals, atropine continued to pro- 
long the P-R interval when the distal vagal stump was elec- 
trically stimulated, indicating that the action of the at- 
ropine occurred peripherally at the cardiac site, and not in 
the central nervous system. 

A study by Hayes and associates*' indicated that large 
doses of atropine by the intramuscular route, give the 
same results as small doses given I.V. In their study, 175 
;Ug/kg of atropine sulfate were given to 6 healthy volun- 
teers by intramuscular injection, resulting in ranging 
from 11 to 14 mg. Two minutes after the dose, there was 
slowing of the heart rate, followed by an increase in heart 
rate, and then an AV dissociation. This pattern is consis- 
tent with that found by Kottmeier and Gravenstein*'* using 
a dose range of 0.0003 to 0.003 mg/kg in dogs, with a cu- 
mulative dose ultimately approaching 1 .0 mg/kg. 

Use of Atropine in Asystole. The use of atropine to treat 
asystole is less well supported than its use in sinus brady- 
cardia and hypotension after acute MI. In a prospective 
study in 1981, Coon and associates'" examined the use of 
atropine in 21 prehospital cardiac arrest patients develop- 
ing asystole. Resuscitation was successful in 2 of the 10 
subjects treated with atropine, and 2 of the 1 1 subjects in 
the control group. They concluded that the data failed to 
demonstrate any benefit from use of atropine. Stueven and 
others" reviewed human studies on the use of atropine in 
asystole, and implemented a retrospective review of pre- 
hospital subjects with refractory asystole to resolve the 
issue of atropine's efficacy. They looked at a 4-year-study 
period, involving 170 patients. Of these, 84 remained in re- 
fractory asystole after receiving both epinephrine and bi- 
carbonate. Atropine was given to 43 of the 84 subjects. 
The resuscitation rate in the atropine group was 6 of 43 
(14%) versus of 41 in the control group, with an ob- 
served probability of < 0.04 for the difference. The authors 
also reported that no patient who received atropine for re- 
fractory asystole was discharged alive. 

Side Effects. Atropine sulfate has a number of effects in 
the body due to its efficient distribution as a tertiary amine. 
Side effects are relative to the desired therapeutic effect, 
which in the case of sinus bradycardia or asystole is an in- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

crease in heart rate. As an antimuscarinic drug, atropine 
can cause the following effects: 

Skin — inhibition of sweating, flushing; 

Eye — cycloplegia. mydriasis, increase in intraocular pres- 

Gastrointestinal — decreased salivation, reduced tone; 

Urinary — urinary retention; 

Respiratory — blockade of vagally induced bronchial 

CNS — variable effects, including drowsiness or excita- 
tion, ataxia, hallucinations. 

In the context of resuscitation, possible cardiac side effects 
that can occur and were reported in Scheinman et al's 
study*"^ include sustained sinus tachycardia, increased num- 
ber of PVCs, ventricular tachycardia or fibrillation, and 
toxic psychosis. With myocardial ischemia and acute MI, 
increases in heart rate may increase the myocardial oxygen 
demand and exacerbate ischemia or the zone of infarction. ^- 

Summary — Based on these results, the ACLS recommen- 
dation for atropine in sinus bradycardia is a dose of 0.5 to 
1.0 mg I.V. every 3 to 5 minutes, to a total dose of 0.04 
mg/kg, which gives full vagal blockade.' 

Sodium Bicarbonate 

ACLS Recommendation. The recommendations in the 
1992 Guidelines for sodium bicarbonate administration 
during cardiac arrest ( 1 mEq/kg I.V.) are:' 
Class Ila: (acceptable, probably helpful) 

— for known pre-existing bicarbonate-responsive 

— for overdose with tricyclic antidepressants; 

— to alkalinize the urine in drug overdoses. 
Class lib; (acceptable, possibly helpful) 

— if intubated, with long-arrest interval; 

— after ROSC following long-arrest interval. 
Class III: (not indicated, may be harmful) 

— in hypoxic lactic acidosis. 

Pharmacology of Sodium Bicarbonate. Sodium bicar- 
bonate is an alkalinizing salt, used as a buffer agent, that 
acts by dissociating reversibly to form sodium and bicar- 
bonate ions. The bicarbonate anion combines with free hy- 
drogen ions to form carbonic acid, or H2CO3, which in 
turn dissociates into carbon dioxide and water. Sodium bi- 
carbonate is administered to buffer excess hydrogen ions 
in states of metabolic acidosis in order to maintain a nor- 
mal base excess/deficit. The drug is not indicated for re- 
versal of respiratory acidosis. 

Rationale for Use in Cardiac Arrest. Cardiac output and 
tissue perfusion are low during cardiac arrest and resusci- 
tation until spontaneous circulation can be restored. As a 
result of the reduction in tissue perfusion, oxygen delivery 
is inadequate, and anaerobic metabolism and lactic acid 
production occur at the tissue level despite adequate alveo- 
lar ventilation.^' In the past, sodium bicarbonate has been 
recommended to combat the severe metabolic acidosis ac- 
companying circulatory arrest. In 1968, Redding and 
Pearson^- reported the results of a study examining differ- 
ent drug therapies on dogs in circulatory arrest due to ven- 
tricular fibrillation. They examined drug therapies includ- 
ing 1 mg epinephrine, 20 mg methoxamine hydrochloride, 
and a combination of 1 mg epinephrine and 1.5 g sodium 
bicarbonate. They found that circulation was restored for 7 
of 15 dogs in the epinephrine group, 13 of 15 dogs in the 
methoxamine group, and 13 of 15 dogs in the combination 
drug group. Perhaps more significantly, they also found 
that the 24-hour-survival rate was only 3 of 13 in the 
methoxamine group, but 11 of 13 in the combination 
group. Use of bicarbonate alone to correct metabolic aci- 
dosis gave no better resuscitation results than was obtained 
in the control group receiving no drug therapy. The authors 
concluded that the combination of epinephrine and sodium 
bicarbonate was as effective as the vasoconstricting drug 
methoxamine alone, and survival was better with the com- 
bination, making it preferable. Studies such as that of 
Redding and Pearson" indicating an improved outcome 
with bicarbonate use in ventricular fibrillation were com- 
plemented by other studies, such as that of Gerst and oth- 
ers,^'* who showed that metabolic acidosis lowers the 
threshold for ventricular fibrillation and that alkalosis re- 
verses this. In 1970, Cingolani and associates'^ reported 
that decreases in pH caused by increasing PCO2 produced 
a significant decrease in cardiac contractility. In another 
study, Cingolani and associates'^ reported that either respi- 
ratory or metabolic acidosis, ie a change in pH from 7.36 
to 7.01 and 6.98, respectively, depressed contractility of 
human atrial or ventricular muscle, when examined in 
vitro. These findings support the reversal of acidemia by 
use of a buffering agent. 

Other studies have illustrated a striking difference be- 
tween arterial and mixed venous acid-base status during 
cardiopulmonary resuscitation, following standard guide- 
lines and with use of recommended drug therapy including 
sodium bicarbonate.""* These studies show that during 
CPR an arterial alkalemia is present at the same time that 
acidemia exists in the venous circulation. For example, 
Weil and co-workers'** examined the difference between 
arterial and venous blood gas values during clinical condi- 
tions of cardiac arrest and resuscitation in 16 patients who 
had pulmonary arterial catheters in place. They found mean values: 


Respiratory Care • April "95 Vol 40 No 4 

ACLS Drugs 




Mixed Venous 


The investigators reasoned that these acid-base differences 
are produced by decreases in cardiac output that lead to de- 
creased tissue perfusion and decreased venous return to the 
lungs. CO2 accumulates in the venous circulation and if 
venous blood is unable to return the COi to the lungs, then 
end-tidal CO2 levels should reflect this failure to excrete 
COt. This was, in fact, found to be the case. End-tidal CO2 
concentration fell to less than 20% of the pre-arrest value 
after cardiac arrest.''^ It can be concluded that end-tidal 
CO2 can reflect cardiac output tissue pertusion, and venos- 
tasis during CPR. 

The question is raised What is the effect of sodium bicar- 
bonate on acid-base status during cardiopulmonary resusci- 
tation? An interesting study was pertormed by Adrogue and 
associates,*" to examine the difference between arterial and 
central venous blood in circulatory failure. One of the 
groups they examined consisted of 17 patients who were 
breathing spontaneously prior to cardiorespiratory arrest. 
Standard CPR measures were instituted, with 6 receiving bi- 
carbonate and 1 1 not receiving bicarbonate. Table 8 gives 
partial resuhs from their study, for arterial and venous pH 
and PCO2. with and without bicarbonate. 

Arterial versus Venous Blood Gas Values during Cardiorespir- 
atory Arrest in 17 patients. Treated with and without Sodium 

Without Bicarbonate 
Arterial Venous 

With Bicarbonate 
Arterial Venous 

pH 7.06(0.02) 7.02(0.07) 7.24(0.13) 7.01(0.05) 

PCO: 51.9(4.9) 60.8(4.5) 71.4(16.6) 126.8(21.8) 

HCO3" 15.0(2.0) 15.7(2.0) 33.3(8.9) 29.1(6.0) 

PO: 83.1(15.6) 31.0(4.2) 105.3(47.2) 23.0(6.6) 

*Venous values are central venous samples taken from the superior vena cava. Based 
on daia from Reference 80. Values are means, with SEM in parentlieses. 

It can be seen that there are differences between arterial 
and venous blood values during cardiac arrest, as previous- 
ly noted, and that hypercapnia and acidemia at the tissue 
level are better represented by venous than by arterial 
blood. It can also be .seen that patients who received sodi- 
um bicarbonate had higher arterial and venous levels of 
hypercapnia than those who did not. In their discussion, 
the authors noted that the end-tidal CO2 level increased 
after administration of bicarbonate, consistent with an aug- 
mented production of CO2 during the buffering process. 

Berenyi and associates*' found that administration of 
sodium bicarbonate during CPR caused an increased aci- 

dosis of cerebrospinal fluid (CSF) as compared to no bi- 
carbonate therapy, in a dog study. Cerebrospinal fluid pH 
ranged from 7.30-7.32 with no bicarbonate and from 7.18- 
7.23 with bicarbonate, at 5 and 10 minutes of CPR in the 
model. The decrease in CSF pH with bicarbonate was at- 
tributed to the fact that bicarbonate produces CO2 when 
combining with hydrogen ions at the tissue level. The ex- 
cess CO2 readily diffuses into the CSF, but bicarbonate 
diffuses poorly across the blood-brain barrier. This causes 
the production of unbuffered hydrogen ions in the CSF. 
They concluded that large amounts of bicarbonate during 
CPR may lead to post-CPR cerebral depression. Kette and 
others*- also found that (using controlled experimental 
conditions with a pig model) the administration of buffer 
agents such as bicarbonate did not reverse myocardial aci- 
dosis or improve myocardial resuscitation. An earlier 
study by von Planta and group*' found that PCO2 in car- 
diac vein blood was significantly higher than in mixed ve- 
nous blood during cardiac arrest and CPR. They reasoned 
that this indicated a high CO2 and lactate production in the 
myocardium during ischemia and that this caused myocar- 
dial acidosis during cardiac arrest and CPR. Further in- 
creases in CO2 from administration of buffers and the ease 
with which CO2 diffuses into myocardial cells could wors- 
en intramyocardial acidosis. 

The fact that bicarbonate administration increases ve- 
nous hypercapnia, worsens CSF acidosis, and fails to re- 
verse myocardial acidosis does not support its use in CPR. 
It has been shown that once spontaneous circulation is re- 
stored, the anaerobic generation of lactate is reversed, *- 
and arteriovenous pH and PCO2 gradients are quickly re- 
stored to normal.*'* The effects reported in the various stud- 
ies are consistent with the presence and effects of circula- 
tory failure in cardiac arrest and during CPR, before the 
ROSC. Figure 6 illustrates both the poor cardiac output, 
tissue perfusion, and venous return seen under these cir- 
cumstances, plus the contribution of bicarbonate to in- 
creased CO2 production in the circulation upstream from 
the pulmonary capillaries. 

Inadequate cardiac output causes inadequate tissue perfu- 
sion, poor tissue oxygenation, and anaerobic metabolism 
with lactic acid production. Although arterial values may 
show normal pH, low-to-normal PCO2, and adequate PO2, 
mixed venous blood would show acidemia and low PO2. 
Introduction of bicarbonate into the circulation buffers the 
acidemia and produces CO2, which then accumulates be- 
cause venous return is inadequate. The CO2 produced cannot 
be exchanged in the pulmonary circulation; therefore, be- 
cause pertusion is poor, venous hypercapnia ensues. Because 
this sequence results from lack of circulation, the best treat- 
ment is the restoration of circulation, as several studies have 
indicated.*-'*'' This was further confinned in a study by 
Federiuk and others,*' using bicarbonate treatment in a 

Respiratory Care • April "95 Vol 40 No 4 



porcine model of cardiac arrest. Their study found no differ- 
ence in resuscitation rates with versus without bicarbonate 
therapy during prolonged cardiac arrest. 

minating narrow-complex PSVT.' Although this is not a car- 
diac arrest situation, such arrhythmias are potentially lethal. 
The drug is relatively new, thereby warranting some review. 


Fig. 6. Diagram illustrating changes in ventilation and perfusion 
during cardiac arrest and CPR, and the production of CO2 by bicar- 
bonate administration. See text for detailed discussion. 

Pharmacology of Adenosine. The production and meta- 
bolism of adenosine, and its various pharmacologic/physi- 
ologic effects are well summarized by Van Belle in Chapter 
14 of Cardiovascular Pharmacology and Therapeutics}^ a 
current and authoritative work that should be consulted by 
those needing inore detail. The following summary is based 
on this source and other reviews. **'■** 

Production and Metabolism. It has been known since 1929 
that adenine compounds such as adenosine have significant 
effects on the mammalian heart. Adenosine is formed natu- 
rally in the body from adenosine monophosphate (AMP, or 
cyclic AMP). With normal oxygenation in the heart, adeno- 
sine triphosphate (ATP) is dephosphorylated to adenosine 
diphosphate (ADP) and then to AMP, which is rephosphory- 
lated to ATP (Fig. 7). However, when the myocardial oxy- 
gen demand exceeds supply, as in ischemic heart tissue, 
AMP is not rephosphorylated to ATP, and, instead, adeno- 
sine is formed. The adenosine formed in the cell is transport- 
ed outside the cell into the interstitial space, possibly by sim- 
ple diffusion.'*'' The duration of action of adenosine, whether 
endogenously produced or exogenously administered, is 
fleeting because the half-life is < 5 seconds. During its brief 
existence in the extracellular space, adenosine is thought to 
produce its effects by stimulating the two types of adenosine 
receptors, noted as A] and Ai.*** 

Use of Bicarbonate during ACLS. Based on this under- 
standing of the effect of bicarbonate during CPR, buffer ther- 
apy is recommended in certain circumstances, including pre- 
existing metabolic acidosis, hyperkalemia, and tricyclic or 
phenobarbital overdose. Bicarbonate therapy is recommend- 
ed only after confirmed interventions of defibrillation, car- 
diac compression, intubation, ventilation, and epinephrine 
administration have occurred. The guidelines also state that 
bicarbonate possibly benefits the patient after prolonged ar- 
rest or resuscitative efforts.' 

Adenosine (Adenocard) 

Adenosine is an endogenous adenine nucleoside pro- 
duced by many tissues in the body, including the he;irt. This 
agent exerts a cardioprotective effect in myocaidial ischemia 
and has beneficial antiarrhythmic properties due to its effect 
on the clectrophysiology of the heart. The drug adenosine is 
classified as a Class-4 antiarrhythmic agent (Table 7).''" 


Ischemia & Hypoxia — | 



'-~,^ ^ Transport inhibitor 

■ Inoslne — ^ Hypoxanthlne 


Coronary Vessel Ai , A2 ; 

\ SA, AV + Rate, 
Coronary Vasodilation 

Fig. 7. The generation, metabolism, and primary cardiac effects of 
the adenine nucleoside, adenosine (Adenocard). Ai and Ag are the 
two types of adenosine receptors. SA = sinoatnal (node); AV = atri- 
oventricular (node); ATP = adenosine triphosphate; ADP = adeno- 
sine diphosphate; and AMP = adenosine monophosphate. 

ACLS Recommendation for Adenosine. The ACC/AHA 

guidelines describe adenosine as the drug of choice for ter- 

Adcnosine is ultimately transported by a nucleoside 
transporter into endothelial cells of coronary vessels or 


Rh.simratory Carf- • April '95 Vol 40 No 4 

ACLS Drugs 

back into myocardial cells where it is deaminated into ino- 
sine and hypoxanthine or rephosphorylated to AMP. Any 
adenosine that is not metabolized in coronary blood ves- 
sels can be transported into the systemic circulation to 
exert further effects. Because theophylline can block 
adenosine receptors (Ai, A2), it is a competitive antagonist 
of adenosine. Patients on theophylline products may re- 
quire higher doses of adenosine.'*'' Drugs such as dipyri- 
damole (Persantine), used for angina and as an antiplatelet 
to prevent thromboembolus, are nucleoside-transport in- 
hibitors. Consequently, dipyridamole can block the trans- 
port of adenosine back into cells, increasing the interstitial 
level of adenosine and prolonging its effect.^" 

Pharmacologic Effects. Adenosine exerts a number of ef- 
fects on the electrophysiology of the heart. The drug causes 
slowing of the SA node, depresses AV conduction, and 
prolongs refractoriness, all of which slow the heart rate. 
Adenosine also antagonizes the effect of circulating cate- 
cholamines on the heart and inhibits presynaptic cate- 
cholamine release. In doing so, adenosine antagonizes the 
positive inotropic and chronotropic effects of such chemi- 
cals. In addition, adenosine causes coronary vasodilation, 
improving coronary perfusion. The term cardioprotective 
describes the pattern of effects just outlined: myocardial 
oxygen demand is reduced and oxygen supply is improved 
when ischemia triggers the production of endogenous 
adenosine. Another term that has been used is "homeostatic 
metabolite."'*'' The drug also causes systemic vasodilation, 
with skin flushing and possible lowering of blood pressure. 
Because of its effect in depressing AV-node conduction 
and the fact that most common forms of PSVT involve a 
re-entry pathway through the AV node, adenosine is effec- 
tive in causing enough AV block to terminate a PSVT dys- 

Side Effects. The most common side effects of adenosine 
therapy are skin flushing, dyspnea and chest pain and dis- 
comfort, sinus bradycardia, and decreased blood pres- 
sure. '"•^^"^^ However, because of the rapid metabolism of 
the drug, these effects rarely last beyond 1 or 2 minutes 
and resolve spontaneously.' 

Use & Dose. The recommended initial dose of adenosine in 
PSVT is a 6-mg bolus injected rapidly over 1-3 seconds, 
followed by a 20-mL saline flush of the I.V. line.' A second 
dose of 12 mg should be given if there is no response with- 
in 1-2 minutes. With an appropriate dose, the dysrhythmic 
effect is seen once the drug reaches the AV node."'" 

Adenosine is particularly useful in treating narrow- 
complex tachycardia of uncertain origin. If the narrow- 
complex tachycardia is due to a re-entry circuit involving 
the AV node, adenosine can effectively induce an AV 

block and terminate the dysrhythmia. The diagnosis is then 
confirmed as AV-nodal re-entrant tachycardia, and the 
therapeutic effect is achieved. If the tachycardia is not due 
to an AV-nodal re-entry circuit, but to atrial flutter, atrial 
fibrillation, or atrial or ventricular tachycardia, adenosine 
can produce a short-lived AV block that illuminates the 
dysrhythmia without causing prolonged and severe brady- 
cardia, asystole, or prolonged myocardial depression and 
decreased cardiac output, such as would occur with vera- 
pamil.''"'***'" This advantage is due to its site-specific ef- 
fect, short half-life, and minimal hemodynamic effects.^' 
The extremely short half-life of adenosine (5 seconds) can 
also allow a return of PSVT, requiring additional doses for 
continued effect.'** 

A disadvantage of adenosine is the fact that the endoge- 
nous nucleoside is produced and released at the site of hy- 
poxic injury, localizing and limiting its effect in the body. In 
contrast, the exogenously administered drug has a complete 
systemic effect, limited only by its short duration of action. 

Conclusion & Summary 

In this review, I have focused on the relatively small 
number of drugs used in cardiac arrest, and, specifically, in 
ventricular tachycardia, ventricular fibrillation, and asystole. 
TTiese agents range from older drugs, such as epinephrine 
and atropine, to the more recent agent, adenosine. Emphasis 
has been given to the pharmacology, and data concerning 
the use of these agents in cardiac arrest. Questions concern- 
ing their use have been raised, and where available, data 
have been reviewed suggesting courses of action for these 

• Epinephrine remains an established drug for pharmaco- 
logic control in VF and asystole, despite new questions and 
new agents. Although pure a agonists have shown evidence 
of giving better subendocardial blood flow than 
epinephrine, questions requiring further study remain with 
these agents. Higher doses than the standard, fixed 1 .0 mg in 
cardiac arrest have not been shown to result in better rates of 

• Lidocaine is the drug of choice in treating ventricular 
ectopy, VT, and VF. The prophylactic use of lidocaine in 
suspected acute MI is not supported by a risk-benefit analy- 
sis, and its prophylactic use in confirmed acute MI can be 
debated, given the prevalence of VF in acute MI and the 
success of defibrillation. 

• Procainamide is a second-line drug for treatment of 
PVCs and recurrent VT when lidocaine is contraindicated or 
has failed. 

• Bretylium is another second-line drug for treatment of 
VT and VF unresponsive to defibrillation, epinephrine, and 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Drugs 

• Atropine is useful for treatment of symptomatic sinus 
bradycardia in acute Ml, with a dose of 0.04 mg/kg, or 3.0 
mg. usually sufficient to produce complete vagal blockade 
of the SA node. The efficacy of atropine for asystole is not 
well supported by available data, although the drug is not 
contraindicated and may be helpful. 

• Sodium bicarbonate has not been shown to improve 
mixed venous acidemia indicative of poor tissue oxygena- 
tion, without a ROSC and improved tissue perfusion sec- 
ondary to restored cardiac output. 

• Adenosine is the drug of choice for treatment of nar- 
row complex PSVT, especially of uncertain origin. It is 
rapidly metabolized, with a half-life of only seconds. 


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can Heart Association. Guidelines for cardiopulmonary resuscita- 
tion and emergency cardiac care. III. Adult advanced cardiac life 
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2. ACC/AHA Task Force Report. Guidelines for the early manage- 
ment of patients with acute myocardial infarction: a report of the 
American College of Cardiology/American Heart Association 
Task Force on Assessment of Diagnostic and Therapeutic Cardio- 
vascular Procedures (Subcommittee to develop guidelines for the 
early management of patients with acute myocardial infarction). J 
Am Coll Cardiol 1990:16:249-292. 

3. Hoffman BB. Lefkowitz RJ. Catecholamines and sympath- 
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Rau Discussion 

Sanders: One question about lido- 
caine. I thought it was in the same rec- 
ommendation class as procainamide, 
bretyhum. and magnesium sulfate. In 
your summary and your presentations, 
you make a distinction that it is first 
line, and other antiarrhythmics are 
used if lidocaine is unsuccessful. 
Although there is a lot of experience 
and tradition for the use of lidocaine, I 
am unaware of definitive studies that 
show it to be superior to other antiar- 

Rau: Let me throw in my 2 cents, and 
then, certainly, Fd appreciate com- 
ments from those of you who are more 
directly involved with the ACL.S 
Guidelines. In reference to procaina- 
mide and bretylium, my understand- 
ing is that lidocaine is preferred to 
those drugs for the particular prob- 
lems, V-tach and V-fib (ventricular 
tachycardia and ventricular fibrilla- 

tion).' So, if you're comparing lido- 
caine to bretylium or procainamide, it 
would be a superior drug to those two. 
I welcome any additional information 
about that. 

1 . American Heart Association, Emergency 
Cardiac Care Committee and Subcom- 
mittees. Guidelines for cardiopulmon- 
ary resuscitation and emergency cardiac 
care. Part III. Adult advanced cardiac life 
support. JAMA 1992;268:2199-2241. 

Pepe: When we wrote the Guidelines, 
to some extent we put lidocaine there 
because it has been traditionally used 
and is the most popular choice, but 
there is also a little footnote in the algo- 
rithm that says you can substitute one 
of the other drugs, as well.' The whole 
thing with lidocaine, really has a lot of 
its basis in the study by Lie- in the liter- 
ature about 20 years ago. In that study, 
it seemed that someone having herald- 
ing myocardial infarction symptoms 
and multiple PVCs, who received lido- 
caine seemed to have less V-fib. That's 

the best study we really have around to 
say that lidocaine is clinically useful. 
However, there is some suggestion 
now that giving lidocaine to someone 
after they fibrillate may actually be 
somewhat detrimental.' It's an evolv- 
ing dilemma that we haven't been able 
to elucidate or delineate totally. I'll talk 
more about these studies in some detail 
tomorrow. That's one of the reasons 
why Art (Sanders) is raising this issue. 
We're not so sure that lidocaine should 
be a primary drug. 

American Heart Association. Emergency 
Cardiac Care Committee and Subcom- 
mittees. Guidelines for cardiopulmon- 
ary resu.scitation and emergency cardiac 
care. Pan III. Adult adviuiced cardiac life 
support. JAMA 1992:268:2199-2241. 
Lie KI, Wellens HJ, van Capelle FJ, 
Durrer D. Lidocaine in the prevention 
of primary ventricular fibrillation: A 
double-blind, randomized study of 212 
consecutive patients. N Engl J Med 
Wesley RC, Resh W. Zimmeniian D. 


RESPIRATORY Carf: • APRIL '95 VoL 40 No 4 

Rau Discussion 

Reconsiderations of the routine and pref- 
erential use of lidocaine in the emergent 
treatment of ventricular arrhythmias. 
Crit Care Med 1991;19:1439-1444. 

Barnes: Joe, I have a question about 
the second dose of hdocaine and the 
Heart Association's V-fib algorithm. I 
came across one comment in an ACLS 
book' that said in cardiac arrest the 
metabohsm of hdocaine is slow. If 
you're giving Shock-then-Drug, 
Shock-then-Drug quickly, should you 
be giving the second dose of lidocaine 
or go to an alternate drug because the 
first dose may not have been metabo- 
lized at that point? 

1. Graver K, Cavallaro D. ACLS certi- 
fication preparation, Vol I. St Louis: 
Mosby Lifeline 1993:9. 

Rau: I didn't see data on that in the lit- 
erature I reviewed, but if you look at 
the two-compartment model with lido- 
caine and. again, I would welcome 
other comments, I think you have a 
margin for error at the beginning with 
the patient, although the circulation in 
CPR is still a question. My point is that 
one of the reasons that you get such a 
very short half-life with lidocaine 
when you start the drug is the huge ex- 
travascular space that becomes a stor- 
age depot because the drug diffuses 
into it. It's not just the liver 
metabolism on a first pass. I think the 
question is If you take away the liver 
metabolism with Shock-then-Drug, 
Shock-then-Drug and poor circulation, 
what kind of buildup of lidocaine will 
you see compared to what you see with 
better perfusion and good liver func- 
tion? The reservoir you have, the safe- 
ty reservoir, is the extravascular space. 
Does that outweigh the loss, say, of the 
liver metabolism that might be occur- 
ring in CPR? 1 wish I had seen data on 
that, but I did not. It would be an inter- 
esting thing to look at, if you could 
simulate it in an animal model, where 
essentially you have poor perfusion. Is 
that outweighed by the tissue deposi- 

tion of the lidocaine in a relatively 
short amount of time? It's really after 
24 hours that you worry about lido- 
caine levels and really have to monitor 
the dose and taper it off because it then 
begins to accumulate. So, I don't know 
the answer to your question, but I think 
that's the question that would maybe 
provide the answer or begin to give 
some data. Is anyone else familiar with 
data on this? 

Pepe: In answer to your question, you 
have two separate issues. First, if you 
have a person who has a return of 
spontaneous circulation, it would take 
20 minutes as a rough estimate to use 
up 50 mg once you've loaded with 
250 mg. (eg. 3 mg/kg on an 80-kg guy 
with a normal liver). So it's probably 
not that much of a deal to give extra 
drug after 20-30 minutes prior to es- 
tablishing a lidocaine drip. Most 
paramedics would be at the hospital at 
that point any way. The other ques- 
tion is. What are the pharmacokinet- 
ics during a cardiac arrest? No one re- 
ally knows. You may have a little bet- 
ter information on lidocaine than on 
some of the other drugs but as far as 1 
know, there haven't been any good 
studies about what happens during 
CPR. So, the thing is we don't know 
the answer to that. 

Halperin: In the high-dose epineph- 
rine study of Brown and Pepe,' there 
was a subgroup of patients, about 100 
patients, in whom the study was start- 
ed within 10 minutes of arrest and in 
whom apparently there was a 20% 
versus a 10% survival to hospital dis- 
charge. Now, the numbers were too 
small to achieve statistical signifi- 
cance, but that's a pretty substantial 
difference, and why was that study 
not continued? 

1. Brown C, Martin D, Pepe P. Stueven 
H, Cummins R, Gonzalez E, et al. A 
comparison of standard-dose and high- 
dose epinephrine in cardiac arrest. N 
Engl J Med 1992;327(15):105l-1055. 

Pepe: First of all, we decided up front 
what magnitude of difference we were 
looking for, and what we prospectively 
considered acceptable for alpha-val- 
ues. We looked at the results after the 
study. It was a double-blind study and 
we didn't know as we went along that 
we were going to get a little bit better 
outcome in that subgrouping. Yes, the 
trend was there, but it was not statisti- 
cally significant.' There was a very 
provocative subgroup survival trend, 
however. In fact, it was at the point 
where it was even considered statisti- 
cally significant, if you actually took a 
look at those survivors receiving the 
high-dose epinephrine within 10 min- 
utes, in terms of their neurologic out- 
comes. Again, if you looked at their 
survival rates, there was trend toward 
improvement there as well. The prob- 
lem was that we were criticized regard- 
ing the neurologic outcome criteria, in 
that we used the CPC scores (a cere- 
bral-performance category score) gath- 
ered from charts. So that was one of 
the problems in claiming positive ben- 
efit, and. secondly, the trend towards a 
better outcome was just a trend; it 
wasn't statistically significant using 
the arbitrary values that we prospec- 
tively chose. 1 guess the p values in 
studies with low survival rates may 
need to be re-examined. Also, there are 
new data that may be coming out soon. 
Norm Abramson and others (I was in- 
volved in that study as well) have fin- 
ished a very large study looking at 
large groups of people who got the 
drug within 10 minutes.- 1 think in-hos- 
pital studies could be really important 
to see if you can make a difference in 
the subgroup who gets early attention. 
This comes back to what I talked about 
earlier today, which is that the ampli- 
tude and median frequency of the ven- 
tricular fibrillation waveform may de- 
termine that you need to first get some 
drugs administered to have a better 
chance of getting the patient defibril- 
lated.' I think that Jim Niemann's ani- 
mal study, in which he gave the high- 
dose epinephrine before the first shock. 

Respiratory Care • April '95 Vol 40 No 4 


Rau Discussion 

after 10 minutes of V-fib reinforces 
this concept."* So, bottom line is. Yes, 
there may be something to high-dose 
epinephrine if you give it early on. But 
unfortunately, we're not yet sure, and I 
think it needs to be studied further. 

1. Brown CG, Martin DR. Pepe PE. 
Stueven H, Cummins RD. Gonzalez E, 
Jastremski M. and the Multicenter High- 
dose Epinephrine Study Group. A com- 
parison of standard-dose and high-dose 
epinephrine in cardiac arrest outside the 
hospital: N Engl J Med 199:;327:1051- 

2. Abramson NS. el al. Randomized trial 
of escalating doses of epinephrine (ab- 
stract). Ann Emerg Med. 1995:25:130. 

3. Brown CG, Griffith RF, Van Ligten P. 
Hoekstra J, Nejman G, Mitchell L. 
Dzwonczyk R. Median frequency: a new 
parameter for predicting defibrillation suc- 
cess rate. Ann Emerg Med 1991:20:787- 

4. Niemann JT, Cairns CB. Sharma J. 
Lewis RJ. Treatment of prolonged ven- 
tricular fibrillation: immediate counter- 
shock versus high-dose epinephrine and 
CPR preceding countershock. Circu- 
lation 1992.85:281-287. 

Kaye: Whenever I hear the high-dose 
epinephrine story, I'm reminded of the 
story of the Shroud of Turin. This is not 
a joke; this is a fact. Remember, several 
years ago the Roman Catholic church, 1 
don't know whether it was the head of- 
fice or some subsidiary, allowed the 
Shroud of Turin, which is a cloth that 
purportedly shows the face of Christ, to 
undergo scientific analysis. The scien- 
tists used state-of-the-art technology, 
and the final conclusion was, No, it is 
not the face of Christ because the time 
that the Shroud was produced was sev- 
eral hundred years after the death of 
Jesus Christ. Nevertheless, certain reli- 
gious people, rightly or wrongly, said. 
We still believe it is the face of Christ. 
And the high-dose epinephrine is the 
same issue. We have a bias, a belief, 
that was revealed to us in animal stud- 
ies, and some noncontiolled human 
studies,' that suggested that high-dose 
epinephrine had benefit. It was then 
subjected to the highest science that we 

know, which is multicenter randomized 
studies. All have failed to show any 
benefit of high-dose epinephrine.-^ 
Yet. I am astonished that the AHA still 
says. Well, there are no data that it 
works, but why don't you try it any- 
way. It seems to me the right conclu- 
sion is that there is no benefit. Maybe 
we need to go back and look at the 
doses, the time given, etc, to see if it 
does have a benefit. But I don't see how 
anybody at this point can recommend 
high-dose epinephrine. None of the 
studies has shown that it works. It has 
zero effect. Or are we religious zealots? 

1. Paradis NA Koscove EM. Epinephrine 
in cardiac arrest: a critical review. Ann 
Emerg Med. 1990:19:1288-1301. 

2. Lindner KH. Ahnefeld FW. Prengel 
AW. Comparison of standard and high- 
dose adrenaline in the resuscitation of 
asystole and electromechanical dissoci- 
ation. Acta Anesthesiol Scand. 1991: 

3. Stiell IG. Hebert PC. Weitzman BN. 
Wells GA. Raman S. Stark RM, el al. 
High-dose epinephrine in adult cardiac ar- 
rest. N Engl J Med. 1992:327:1047-1050. 

4. Callaham M. Madsen CD. Barton CW. 
Saunders CE. Pointer J. A randomized 
clinical trial of high-dose epinephrine 
and norepinephrine vs standard-dose 
epinephrine in prehospital cardiac ar- 
rest. JAMA. 1992:268:2667-2672. 

5. Brown CG, Martin DR. Pepe PE, 
Stueven H. Cummins RO Gonzalez E, 
Jasu-emski M, and the Multicenter High- 
dose Epinephrine Study Group. A com- 
parison of standard-dose and high-dose 
epinephrine in cardiac arrest outside the 
ho.spital. N Engl J Med. 1992:327:1051- 

Pepe: Bill (Kaye), if I could qualify 
the report, I think we really do need to 
look more closely at those numbers. 
First of all, in some of the studies we're 
looking at cities with very good EMS 
systems, such as Milwaukee, Seattle, 
Houston. EMS got people there quick- 
ly, and yet. even with witnessed cases 
(when someone saw the collapse and 
called 911 right away), the average 
time for epinephrine administration 
was 17 minutes from the time of col- 
lapse. That's the lime it takes for one to 

get the call, process it, get people there, 
give 2-3 shocks, intubate, and get the 
l.V. line in. It may be that by 17 min- 
utes, epinephrine is of no use at all in 
the general population. But, there may 
be subgroups that we can look at, such 
as the pediatric population or those 
down less than 10 minutes. The prob- 
lem is, as I'll talk about tomorrow, it's 
going to take a lot of numbers to prove 
that speculation. 

Kaye: At the 1992 AHA National 
Conference, when these data were pre- 
sented in their preliminary form, A 
participant made the most cogent re- 
marks. He said, "Perhaps need for 
high-dose epinephrine predicts nonsur- 
vival." Because if you can't restart the 
heart with defibrillation and maybe 
one standard dose of epinephrine, it's 
sayonara. Interesting concept. 

Barnes: I would agree with that last 
comment. I noticed in my review of 
CPR outcomes, several studies in the 
literature that show if you must go to 
the second or third dose of epine- 
phrine, the survival rate drops signifi- 

1. Tonolani AJ. Risucci DA. Rosali RJ. 
Dixon R. In-hospital cardiopulmonary 
resuscitation: patient arrest and resusci- 
tation factors associated with survival. 
Resuscitation 1990:20:1 15-128. 

2. Wong RH, Torzillo PJ. In-hospital car- 
diopulmonary resuscitation: prospective 
survey of management and outcome. 
Anaesth Intensive Care 1987:15:193- 

Sanders: I just want to reiterate that 
most of the clinical studies that Paul 
(Pepe) mentioned, are on out-of-hos- 
pital arrests. I really think a good mul- 
ticenter in-hospital study needs to be 
done to determine the most appropri- 
ate dose of epinephrine. Because there 
were no clinical studies on the dose of 
epinephrine for in-hospital resuscita- 
tion, the data on out-of-hospital ar- 
rests was extrapolated and the recom- 
mendations left the same. 


Respiratory Cari: • April '95 V(u. 40 No 4 

ACLS Systems and Training Programs- 
Do They Make a Difference? 

Paul E Pepe MD 








Evolution of ACLS in Clinical Practice 

The Evidence for ACLS Efficacy 

A. Is Endotracheal Intubation Important? 

B. Do ACLS Drugs Alter Outcome? 

C. So Does ACLS Really Work? 
Reaffirmation of the Practice 
Systems for ACLS 
Rethinking Our Study Designs 


The quality and effectiveness of emergency medical 
services (EMS) systems are frequently judged by cardiac 
arrest survival rates.' ■• In turn, elaborate systems of care 
and specialized training have been widely implemented in 
standardized formats for the purposes of resuscitating vic- 
tims of out-of-hospital sudden cardiac death.' "• Further- 
more, despite the relatively didactic nature of such stan- 
dardized courses, hundreds of thousands of practitioners 
have come to consider training in Advanced Cardiac Life 
Support (ACLS) to be an indicator of clinical expertise.-'' 
This mind-set has been reinforced by the widespread prac- 
tice of requiring successful ACLS course completion for 
clinical credentialing. For example, hundreds of emergen- 

cy care provider organizations, medical schools, and resi- 
dency programs require successful ACLS course comple- 
tion for their employees, students, and house staff, respec- 
tively. In fact, many paramedic programs require ACLS 
'certification' for all of their personnel. 

But, despite the incurred costs, utilization of resources, 
and widespread acceptance as gold-standard medical care, 
few of the many ACLS techniques that we currently use 
are strongly supported by scientifically rigorous clinical 
evidence. Although the empiric use of such techniques ap- 
pears logical or even intuitive at times, solid proof for their 
efficacy in cardiac arrest management is still lacking. In 
this paper, I review the basis for ACLS and, in turn, ask the 
question, Do systems and training programs for ACLS 
truly make a difference? 

Dr Pepe is Professor of Medicine and Pediatrics, Baylor College of 
Medicine, and Director, City of Houston Center for Resuscitation and 
Emergency Medical Services, and Director of Emergency Medical 
Services — Houston, Texas 

A version of this paper was presented by Dr Pepe during the RESPIR- 
ATORY Care Journal Conference "Resuscitation in Acute Care Hospi- 
tals" held in Cancun, Mexico, October 21-23, 1994. The paper is adapted 
in part from Pepe PE. Abramson NS, Brown CG. ACLS — Does it really 
work? Ann Emerg Med 1994;23:1037-1041. 

Reprints: Paul E Pepe MD, Director, City of Houston Center for Resus- 
citation and Emergency Medical Services, 410 Bagby, Suite 300 Houston 
TX 77002. 

Evolution of ACLS in Clinical Practice 

Researchers and clinicians alike are convinced that very 
early defibrillation by electrical countershock is of signifi- 
cant clinical value. '■■* It was recognized by the 1960s that 
many cases of sudden death are associated with a sudden 
electrical short-circuiting of the heart's electrical system, 
leading to ventricular fibrillation (VF) and subsequent sud- 
den loss of heart beat — not massive heart failure as had been 
commonly thought. It was reported in the early 1960s that 
ambulance physicians on the streets of Moscow and Prague 
were converting fibrillating hearts by closed-chest counter- 
shocks, with successful restoration of normal heart beats.' 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Systems 

Western physicians began to recognize the efficacy of both 
in-hospital and out-of-hospital countershock in 1967 when 
the paper of Pantridge and Geddes describing a mobile inten- 
sive care unit appeared in The Lxincet.^ This classic paper 
captured the imagination of certain U.S. researchers who 
began to develop their own methods of delivering early 
countershocks to the hundreds of thousands of Americans 
who sustain sudden and unexpected cardiac arrest in the 
community each year.'--' In fact, they were soon able to 
demonstrate a clear lifesaving effect from early counter- 
shocks, particularly when bystanders immediately performed 
basic cardiopulmonary resuscitation (CPR).' 

Nevertheless, the early pioneer researchers soon found 
that many out-of-hospital cardiac arrest cases did not re- 
quire countershock (ie. ventricular fibrillation was not pre- 
sent), or, even if they did, they still failed to respond to 
countershock and achieve restoration of spontaneous cir- 
culation., in the hospital setting, cardiac arrest 
occurring outside of cardiac monitoring units was not usu- 
ally associated with ventricular fibrillation, and thus coun- 
tershocks were of no value. As a result clinicians simply 
provided chest compressions and breathing techniques, 
generally to no avail, without restoration of circulation. 
Although there were some survivors, the majority failed to 
respond to resuscitative efforts. 

Accordingly, it was surmised that several observed 
physiologic .sequelae of cardiac arrest might explain the 
failure to resuscitate the majority of cardiac arrest patients. 
Among these were severe associated clinical aberrations, 
such as significant oxygenation and ventilation abnormali- 
ties, aspiration of vomitus, lactic acidosis, refractory or 
persistently recurring ventricular fibrillation, bradycardia, 
asystole, and so-called electrical-mechanical dissociation 
(EMD).'* '" In turn, a variety of therapeutic interventions 
were empirically and routinely administered in an attempt 
to reverse these problems,'' including endotracheal intuba- 
tion, positive pressure ventilation, and administration of 
oxygen (for hypoxemia/hypercarbia), sodium bicarbonate 
(for lactic acidosis), lidocaine hydrochloride (for persistent 
VF), epinephrine (for HMD), and atropine sulfate (for 
bradycardia), and a myriad of other pharmacologic and 
procedural adjuncts. The fact that some patients sur- 
vived — coincidentally or not — following these interven- 
tions provided further empiric support for their use. 

However, the sheer volume of proposed therapeutic 
modalities eventually 'begged' for organized instruction, 
resulting in the development of ACLS courses.'' Further- 
more, with the advent of coronary care units (CCU) and 
paramedic programs it was shown that the time to such 
"definitive care" appeared to correlate inversely with out- 
come.' Although this correlation with survival may have 
been simply the effect of early defibrillation alone, most of 
these interventions were provided almost simultaneously 

as components of ACLS. Therefore, time-to-ACLS was 
touted as a key correlate with outcome.' 

In view of the evolving large number of proposed 
ACLS interventions, clinical strategies were necessary. In 
turn, this required protocol development and gave rise to 
specialized educational needs for CCU nurses and 
paramedics who were most apt to first deliver such ACLS 
techniques. Likewise, with the evolution of emergency and 
critical care medicine as recognized academic disciplines, 
formal education in emergency cardiac care became neces- 
sary. By the 1980s, ACLS training programs and aggres- 
sive use of ACLS techniques by clinicians had become 
widespread, both in the U.S. and abroad. - 

The Evidence for ACLS Efficacy 

Despite the widespread use of ACLS techniques, none 
of the individual empiric procedures has much scientific 
support outside of the laboratory. Despite widely accepted 
biases and even some impressive experimental results, 
conclusive clinical data are lacking to support the use of 
any of the individual pharmacologic modalities or airway 
and circulatory adjuncts currently used as standard of care 
for cardiac arrest in the clinical setting." Therefore, I re- 
view each key ACLS intervention to substantiate this 
rather negative position. 

Is Endotracheal Intubation Important? 

For example, most practitioners are convinced that the 
use of endotracheal tubes can save lives.'" Most EMS sys- 
tems reporting high survival rates from cardiac arrest pro- 
vide endotracheal intubation routinely, and their para- 
medics have high success rates for performing this inter- 
vention."^'- Conversely. EMS programs that do not 
provide endotracheal intubation generally have lower sur- 
vival rates. Although the reasons for these differences are 
seemingly intuitive, other factors confound the observa- 
tion. In EMS systems providing this intervention, there 
may also be better response intervals (earlier defibrilla- 
tion) and sophisticated deployment strategies for response 
vehicles (enhanced response times), as well as more inten- 
sive training and medical direction.'- To date, no random- 
ized controlled studies have been performed to demon- 
strate the 'lifesaving' effect of endotracheal intubation. '"■'- 

Let me propose an exercise: If one were to directly ex- 
amine the relationship between endotracheal intubation 
and outcome after cardiac arrest using univariate analysis, 
one would actually find a ncgaiive conelation. In those 
clinical settings in which endotracheal intubation is uni- 
versally utilized, all of the patients not surviving cardiac 
arrest resuscitation would have received this intervention 
during their resuscitation attempt. Meanwhile, many of 


RESPiR.vroKV Cakh • April "9.'^ Vol 40 No 4 

ACLS Systems 

those who did survive would not have received endotra- 
cheal intubation during the resuscitation effort. In many 
cases, patients may achieve immediate restoration of spon- 
taneous circulation after the delivery of early defibrillatory 
countershocks. Quite often, these patients rapidly awaken 
because of the short ischemic interval, making endotra- 
cheal intubation either unnecessary or difficult to perform 
(eg, presence of strong gag reflex in an awakening pa- 
tient). Therefore, this confounding variable resulting from 
early defibrillation and awakening would be the actual rea- 
son for the apparent negative correlation between survival 
and endotracheal intubation — not the intervention itself. If 
we still wished to scientifically demonstrate the value of 
endotracheal intubation, it would probably take a random- 
ized, controlled study comparing endotracheal intubation 
with basic airway management techniques in cardiac arrest 
cases. However, endotracheal intubation is currently cate- 
gorized as a Class I intervention by the American Heart 
Association (AHA)." As a result, such a study would 
probably be considered unethical by some practitioners. 
Therefore, the efficacy of endotracheal intubation will 
probably remain unproven for cardiac arrest management. 

Do ACLS Drugs Alter Outcome? 

A few animal studies have shown potential benefit from 
pharmacologic interventions, particularly epinephrine.""' 
Of primary importance, these animal models have provid- 
ed some insight into the possible pathophysiology of sud- 
den circulatory arrest and its sequelae. Unfortunately, 
however, such information may not be applicable to 
human cardiac arrest. Although several animal investiga- 
tions have compared the use of epinephrine to no 
epinephrine, these studies primarily have examined in- 
travascular pressures and regional flows, and not necessar- 
ily outcome.'''-" Of these studies, only four support the 
benefit of epinephrine, and all of these were performed in 
healthy animals without atherosclerotic disease."''*'*''' 
Furthermore, animals have a different anatomy (eg, chest- 
wall configuration) and physiology (eg, vascular re- 
sponse). Therefore, many of our existing clinical guide- 
lines are extrapolated from animal models that probably do 
not closely simulate adult human disease. 

In terms of clinical studies, to date, no prospective clin- 
ical trials in adults have demonstrated a survival advantage 
from either "standard" doses, or even relatively higher 
doses, of epinephrine.-'-'* In fact, a recent clinical study, 
comparing epinephrine to no epinephrine revealed no sig- 
nificant difference in hospital discharge rates.-"* However, 
this preliminary report has several significant limitations, 
leaving the medical community with inconclusive results. 

Beyond epinephrine, there have been only a handful of 
controlled clinical trials involving any ACLS drug."-'-'' 

Many researchers and clinicians have concurred that there 
are strong inferential data to support the use of lidocaine to 
prevent ventricular fibrillation (VF)."""' However, re- 
searchers have recently become increasingly concerned 
over potential negative effects of lidocaine administration 
once VF has occurred.""'"* Some have also become skepti- 
cal about its use for treating monomorphic ventricular 
tachycardia." And, despite early enthusiasm for sodium 
bicarbonate administration, many researchers have now 
emphasized the potential harmful effects of its use during 
cardiac arrest.''"" Likewise, data are lacking to support the 
lifesaving efficacy of atropine, another drug commonly 
u.sed for treatment of cardiac arrest." 

So, Does ACLS Really Work? 

In defense of ACLS, one could argue that early electri- 
cal countershock has been proven to have a true lifesaving 
effect.'"**' Still, many would no longer classify electrical 
countershock as an advanced technique. With the develop- 
ment and widespread use of automated defibrillators, 
countershocks have now become a skill of the basic life 
support (BLS) provider.' Today, most resuscitologists 
consider early defibrillation to be a BLS function and no 
longer only an ACLS skill. 

Therefore, because none of the other individual thera- 
peutic interventions currently provided by ACLS providers 
(physicians, nurses, respiratory therapists, and para- 
medics) has proven efficacy, one could argue that ACLS is 
an unproven entity. In turn, this statement has dramatic 
philosophical, educational, and economic ramifications. If 
none of the ACLS interventions is of any proven value, it 
might mean that ACLS training courses could be either 
significantly scaled down or eliminated altogether. 

For those still wed to the need for invasive airway pro- 
cedures, researchers are now investigating the possibility 
of training basic emergency medical technicians to per- 
form endotracheal intubation.'- Furthermore, airway tech- 
niques such as the pharyngeotracheal lumen (Respironics, 
Murrysville PA, PTL) airway and the esophageotracheal 
Combitube (Kendall-Sheridan, Argyle NY, ETC) have 
achieved some popularity as potential alternatives for use 
by BLS providers." '- In addition, newer approaches to 
basic CPR may further obviate the need for subsequent 
pharmacologic interventions."*"'*' Such a change in educa- 
tional philosophy would be a fiscal advantage for commu- 
nities that are struggling with the high cost of emergency 
health care. Considering the age and comorbidity of most 
cardiac arrest victims, it makes one consider whether the 
time and effort to train personnel in ACLS is really worth- 

Some governments have, in fact, begun to grapple with 
this very issue. Recently, initiatives in some provinces of 

Respiratory Care • April "95 Vol 40 No 4 


ACLS Systems 

Canada have proposed that EMS personnel provide only 
automated defibrillation and the ETC for out-of-hospital 
cardiac arrest, and, in turn, dismantle any existing ACLS 
services.''- At first glance, one might snicker at the sugges- 
tion that we might also dismantle the well-entrenched 
paramedic (out-of-hospital ACLS) systems in the United 
States. However, this scenario is not so far-fetched. 
Currently (1995), many large private ambulance corpora- 
tions are acquiring smaller services and forming conglom- 
erates. In turn, they are competing with fire departments 
and other government-run EMS organizations for control 
of ambulance transport services throughout the U.S."" 
Their main selling point has been "cost-effectiveness" and 
cheaper operations (less burden on taxpayers), and this 
consideration is very attractive to fiscally strapped munici- 
palities. Although proponents of all-paramedic systems do 
themselves argue cost-effectiveness for the addition of 
ACLS training and ACLS care, it is still conceivable that 
struggling governments would eventually opt for the cost- 
saving approach of contracting only for basic personnel, 
equipped with automated defibrillators and alternative air- 
way devices. Even with public service EMS, budgets 
could be cut or limited accordingly. Without proof for the 
efficacy of other ACLS procedures, hard-line city man- 
agers would have a reasonable basis for limiting services. 

Taking the argument a step further, investigators have re- 
cently demonstrated the ineffectiveness of large urban EMS 
programs in terms of saving out-of-hospital cardiac arrest 
victims, including systems with "all-paramedic" staffing of 
EMS ambulances.'"-'*' The authors have generally claimed 
that certain factors found in cities over 1,000,000 population 
may prevent implementation of successful systems of resus- 
citation.'"''' The authors have generally recommended a 
greater focus on basic life support (bystander CPR) and 
early automated defibrillation by first responders, but still 
held a pessimistic outlook for big cities. ■"•''' 

Considering that about 10% of the entire U.S. popula- 
tion resides in the five largest cities (2 million plus popula- 
tions), this philosophy could forecast the 'downsizing" of 
current paramedic operations. Furthermore, when survival 
rates are only I -2% for cardiac arrest, an entity that accounts 
for only about 1% of all typical EMS responses to 91 1 calls, 
city managers could argue that ACLS is not worthwhile 
when only one out of every 10.000 EMS patients is 
saved. ^■''' Then again, one could argue that ACLS skills 
are used for other critically ill patients such as those with 
injury, congestive heart failure, or seizures (about 5% of 
all EMS calls). Still, the counterargument stands that pro- 
viding an airway, speedy transport, and some noninvasive 
procedures may be just as adequate as any ACLS proce- 
dure.'"'"* More importantly for this discussion, data prov- 
ing the efficacy of ACLS techniques in the prehospital set- 
ting are even sparser for these types of clinical cniergen- 

cies, particularly when one considers long-term outcome 
(ie. does delaying therapy until hospital arrival significant- 
ly harm candidates for thrombolytics, those with supraven- 
tricular tachycardia, or those in status epilepticus?).''*'° 
Intuitively and emotionally, we might say. Yes but, to 
date, that explicit /jwo/' does not exist. 

Reaffirmation of the Practice 

Having set up the "straw man" that ACLS is an un- 
proven entity, it is now time to state the position that 
ACLS does, in fact, enhance survival from cardiac arrest. 
For example, in a recent study by our group" from 
Houston, more than 20% of the survivors of out-of-hospi- 
tal cardiac arrest were those who did not present with VF 
or ventricular tachycardia (VT). Furthermore, fewer than 
10% of these surviving non-VF patients ever required 
electrical countershock during their entire resuscitation ef- 
fort." None of these patients had responded to basic tech- 
niques alone. Therefore, depending on the particular case, 
these patients were resuscitated following the implementa- 
tion of one or more standard ACLS techniques, such as the 
placement of an endotracheal tube and the administration 
of one or more drugs, including epinephrine, sodium bicar- 
bonate, or atropine." One could propose that the BLS co- 
incidentally took effect sometime after the ACLS interven- 
tions, but this speculation seems less plausible given our 
current understanding of basic CPR.-" In turn, if it was not 
the basic CPR alone, it would appear that something about 
the ACLS worked. Indeed, these results are not new, but 
only provide a new perspective on previously published 
data from several EMS systems.'-'-*-''- However, it should 
still be recognized that it is still ven' difficult to pinpoint 
which specific ACLS therapeutic modalities improve sur- 
vival and under what circumstances they make that differ- 

Studies in the pediatric literature have also suggested a 
trend toward better survivorship in the small numbers of 
patients who receive epinephrine within a few minutes 
after arrest. '' Moreover, in an experimental study conduct- 
ed by Niemann et al,'"'' a significant improvement in resus- 
citation rates was demonstrated with high-dose epin- 
ephrine when given prior to de fi brill at ory countershocks. 
Is it possible that the recent clinical trials-' -' of high-dose 
epinephrine failed to demonstrate clinical efficacy because 
the epinephrine was not given prior to countershocks in 
the subgroup of patients with persistent VF? On the aver- 
age in witnessed arrests, the first drug was infused 17 min- 
utes after the arrest during the multicenter study, even 
though the study involved excellent EMS systems.^' 
Maybe our methodology was inconect. Perhaps counter- 
shocks alone are most effective in the first few minutes 
alter circulatory arrest, particularly if bystanders have pro- 


Rhspika roRY C.\Ki- • April "95 Vol 40 No 4 

ACLS Systems 

vided immediate basic CPR. On the other hand, they may 
not be as beneficial as the first intervention if provided 
after prolonged periods of ventricular fibrillation. ''•' 
Perhaps real-time scoring of the VF waveform (median 
frequency and amplitude), something that is now techni- 
cally feasible, can. in the future, tell us whether to provide 
countershocks or ACLS therapy first.''' 

There are other speculations about the value and contri- 
bution of ACLS toward survival in cardiac arrest. A recent 
study'* of first-responder defibrillation demonstrated that 
when basic first-responder crews used automated defibril- 
lation, ACLS providers (paramedics) accomplished endo- 
tracheal intubation, intravenous access, and drug adminis- 
tration 2 to 3 minutes faster than in those situations in 
which paramedics had to provide the electrical counter- 
shocks. Although this study did not specifically examine 
the outcome effect of these ACLS variables, the results do 
raise an interesting question. Are the reported benefits of 
first-responder automated defibrillation multifactorial and 
not just due to the earlier arrival of a defibrillator? Is there 
also an accompanying benefit from the earlier administra- 
tion of ACLS techniques as well?'--"' 

Systems for ACLS 

As for the issue of the evolving recognition of the inef- 
fectiveness of certain EMS systems, particularly those in 
large metropolitan cities, there is a documentable defense. 
Recent experience has demonstrated that cities with a pop- 
ulation of more than a million can also achieve reasonable 
survival rates for cardiac arrest, given proper medical di- 
rection and organization."'-"'* For example, under such 
circumstances, the outcome rate for sudden death associat- 
ed with VF in Houston, Texas (population 2 million), rose 
from the negligible chance of surviving (observed for the 
decade previous to 1983) to the 20% chance of survival re- 
ported for 1988 (witnessed and unwitnessed arrests com- 
bined)." In addition to VF cases, as previously stated, 20% 
of the cardiac arrest survivors in Houston are those assisted 
by ACLS alone (independent of countershock)."" 

Clearly then, ACLS can be justified in an absolute 
sense, both in terms of training and EMS system deploy- 
ment. However, the question may still remain. Is it worth it 
for municipalities to have ACLS services for a handful of 
lives? In response, a counterargument can be made: Can 
we save even more lives with better ACLS research, better 
ACLS training, and better ACLS outcomes analysis? 

Rethinking Our Study Designs 

There are take-home lessons here. Our past approaches 
to clinical and even basic science research regarding car- 
diac arrest probably have been oversimplified. For exam- 

ple, is it possible that some subgroups of patients may ben- 
efit from specific pharmacologic interventions, whereas 
others are harmed? Furthermore, because the exact timing 
of these interventions may be crucial, there is a need for 
multidimensional and technologic approaches to both ex- 
perimental and clinical study design.''"'" In addition, con- 
siderations of clinical factors such as the degree of under- 
lying ischemia, age. patient weight, presenting ECG 
rhythm, routes of drug administration, and the duration of 
circulatory arrest must be taken into account. 

Unfortunately, recent experience tells us that it may 
take thousands of patients to prove clinical efficacy for 
any given intervention when considering such a myriad of 
factors and study subgroups.-'--' It may take the involve- 
ment of entire EMS systems from multiple sites over a pe- 
riod of years to conduct a single study. One must then 
wonder about the cost-benefit ratio of studying interven- 
tions that are directed at those who already have only a 
small chance of long-term survival. Specifically, studies 
show that, even in the best of EMS systems, those who do 
not respond with spontaneous pulses prior to pharmaco- 
logic interventions have only a 4% overall survival rate 
using current standards of care.-' 

Therefore, one might then ask if the pathways to achieve 
these answers (large, long-term, multicentered studies) are 
too costly, too much effort, and too difficult to perform just 
to prove efficacy for a small percentage of patients. 
Resuscitation researchers must also confront these issues in 
an evolving era of health care reform. Furthermore, chal- 
lenges from the U.S. Food and Drug Administration (and 
other federal agencies), regarding the inability to obtain in- 
formed consent from cardiac arrest patients, may also ham- 
per future efforts to resolve these resuscitation issues.*' If 
some new intervention comes along that may improve sur- 
vival chances by 50% or more, documentation will be much 
easier, and we should take the challenge. For now, we have 
no such interventions to study. However, because 1 and oth- 
ers "'-believe that ACLS does indeed work, then thousands 
of lives are 'on the line' annually in the U.S. alone. 


Some components of ACLS do improve outcome for a 
small but significant number of patients.""'- Although 
paramedics and ACLS instructors may have job security 
for the present, there are still no guarantees in an era of 
cost-containment. Therefore, we still need to rethink and 
delineate which aspects of ACLS are truly efficacious, 
during what time interval they are of value, and under what 
conditions they are useful. We can all hope that future re- 
search design will improve in such a way that the efficacy 
and utility of ACLS interventions can be specifically iden- 

Respiratory Care • April '95 Vol 40 No 4 


ACLS Systems 


I thank Drs Leonard Cobb and Michael Copass for iheir mentorship and 
for their continuing originality and leadership in the field of resuscitation 
medicine. I also thank Nina Meher-Homji for her preparation of the 


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13. Pearson JW, Redding JS. The role of epinephrine in cardiac resus- 
citation. Anesth Analg 1963:42:599-606. 

14. Redding JS, Pearson JW. Evaluation of drugs for cardiac resusci- 
tation. Anesthesiology 1963;24:203-207. 

15. Schleien CL, Dean JM, Koehler RC. Michael JR, Chantarojanasiri 
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16. Rothwell-Jackson RL. The adjuvanl use of pressor amines during 
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17. Otto CW, Yakaitis RW, Ewy GA. Effect of epinephrine on defib- 
rillation in ischemic ventricular fibrillation. Am J Emerg Med 

1 8. Pearson J W. Redding JS. Influence of peripheral vascular tone on 
cardiac resuscitation. Aneslh Analg 1965;44:746-752. 

19. Redding JS, Pearson JW. Resuscitation from ventricular fibrilla- 
tion: drug therapy. JAMA l968;203(4):255-260. 

Kosnik JW, Jackson RE, Keats S, Tworek RM, Freeman SB. 
Dose-related response of centrally administered epinephrine on 
the change in aortic diaslohc pressure during closed-chest mas- 
sage in dogs. Ann Emerg Med 1985;14(3):204-208. 
Brown CG, Martin DR, Pepe PE. Stueven H, Cummins RO, 
Gonzalez E, Jastremski M and The Multicenter High-Dose 
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high-dose epinephrine in cardiac arrest outside the hospital. N 
Engl J Med 1992;327:1051-1055. 

Stiell IG, Hebert PC, Weitzman BN, Wells GA, Raman S. Stark 
RM, et al. High-dose epinephrine in adult cardiac arrest. N Engl J 
Med I992;327(15):lO45-105O. 

Callaham M, Madsen CD, Barton CW, Saunders CE. Pointer J. A 
randomized clinical trial of high-dose epinephrine and nore- 
pinephrine vs standard-dose epinephrine in prehospital cardiac ar- 
rest. JAMA 1992:268(19):2667-2672. 

Woodhouse SP, Case C. Cox SV, Boyd P. Weber M. Trial of 
large dose adrenaline vs. placebo in cardiac arrest (abstract). 
Resuscitation 1993:25:89. 

Stueven HA. Thompson B. Aprahamian C, Tonsfeldt DJ. 
Kastenson EH. Lack of effectiveness of calcium chloride in re- 
fractory asystole. Ann Emerg Med 1985;14(7):630-632. 
Stueven HA, Thompson B, Aprahamian C, Tonsfeldt DJ, 
Kastenson EH. The effectiveness of calcium chloride in refractory 
electromechanical dissociation. Ann Emerg Med 1985;14(7):626- 

Haynes RE, Chinn TL. Copass MK, Cobb LA. Comparison of 
bretylium tosylale and lidocaine in management of out of hospital 
ventricular fibrillation: a randomized clinical trial. Am J Cardiol 

Olson DW, Thompson BM, Darin JC, Milbrath MH. A random- 
ized comparison study of bretylium tosylate and lidocaine in re- 
suscitation of patients from out-of-hospital ventricular fibrillation 
in a paramedic system. Ann Emerg Med 1984:13(9, Part 2):807- 

Weaver WD, Fahrenbruch CE, Johnson DD, Hallstrom AP, Cobb 
LA, Copass MK. Effect of epinephrine and lidocaine therapy on 
outcome after cardiac arrest due to ventricular fibrillation. 
Circulation 1 990;82(6):2027-2034. 

Lie Kl. Wellens HJ, van Capelle FJ. Durrer D. Lidocaine in the 
prevention of primary ventricular fibrillation: a double-blind, ran- 
domized study of 212 consecutive patients. N Engl J Med 

Wesley RC Jr. Resh W. Zimmerman D. Reconsiderations of the 
routine and preferential use of lidocaine in the emergent treatment 
of ventricular arrhythmias. Crit Care Med I99I:I9( 1 1 );1439- 

Chow MS, Kluger J, Lawrence R, Fieldman A. The effect of lido- 
caine and bretylium on the defibrillation threshold during cardiac 
arrest and cardiopulmonary resuscitation. Proc Soc Exp Biol Med 
1986:182(1 ):63-67. 

Chow MSS, Kluger J, DiPersio DM, Lawrence R, Fieldman A. 
Antifibrillatory effects of lidocaine and bretylium immediately 
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Dorian P, Fain ES, Davy JM, Winkle RA. Lidocaine causes a re- 
versible, concentration-dependent increase in defibrillation ener- 
gy requirements. J Am Coll Cardiol i986;8(2);327-332. 
Jaffe AS. New and old paradoxes: acidosis and cardiopulmonary 
resuscitation. Circulation 1989;80(4): 1079- 1083. 
von Planta I, Weil MH, von Planla M. Gazmuri RJ, Duggal C. 
Hypercarbic acidosis reduces cardiac resuscitabilily. Crit Care 
Med I99I;I9(9):1 177-1 182. 


Respira TORY Care • April "95 Vol 40 No 4 

ACLS Systems 

37. Guerci AD. Chandra N, Johnson E, Rayburn B. Wumib E. Tsitlik 
J, et al. Failure of sodium bicarbonate to improve resuscitation 
from ventricular fibrillation in dogs. Circulation 1986;74 (6. Part 

38. Kette F, Weil MH, von Planta M, Gazmuri RJ, Rackow EC. 
Buffer agents do not reverse intramyocardial acidosis during car- 
diac resuscitation. Circulation 1990;81(5|: 1660-1666. 

39. Kette F, Weil MH. Gazmuri RJ. et al: Pco; as a predominant 
cause of myocardial acidosis during cardiac arrest (abstract). Crit 
Care Med 1990;18:S246. 

40. Cohen TJ. Tucker KJ. Lurie KG. Redberg RF. Dutton JP. Dwyer 
KA. et al. and The Cardiopulmonary Resuscitation Working 
Group. Active compression-decompression: a new method of car- 
diopulmonary resuscitation. JAMA l992;267(2l):2916-2923. 

41. Halperin HR. Tsitlik JE. Gelfand M. Weisfeldt ML. Gruben KG, 
Levin HR. et al. A preliminary study of cardiopulmonary resusci- 
tation by circumferential compression of the chest with use of a 
pneumatic vest. N Engl J Med 1993;329( 1 1 ):762-768. 

42. Spears T. Life and death — and the bottom line: the paramedic de- 
bate. The Ottawa Citizen 1993. November 21 :A9. 

43. Benson K. Fire fights for EMS delivery — and private providers 
fight back. Emergency I994;23(9):28-31. 

44. Becker LB. Ostrander MP. Barrett J. Kondos GT. Outcome of 
CPR in a large metropolitan area: where are the survivors? Ann 
EmergMed 1991;20(4):355-361. 

45. Lombardi G. Gallagher JE. Gennis P. Outcome of out-of-hospital 
cardiac arrest in New York City. Pre-Hospital Arrest Survival 
Evaluation (PHASE) Study. JAMA l994;27l(9):678-683. 

46. Parmley S. City's fire rescue pushing limit. Philadelphia Enquirer 
1994 August 28: A I .A22-A23. 

47. Wall MJ Jr. Pepe PE. Mattox KL. Successful roadside resuscita- 
tive thoracotomy: case report and literature review. J Trauma 

48. Bickell WH. Wal MJ Jr. Pepe PE. Martin RR. Ginger VF. Allen 
MK, Mattox KL. Immediate versus delayed fluid resuscitation for 
hypotensive patients with penetrating torso injuries. N Engl J Med 

49. Weaver WD. Cerqueira M, Hallstrom AP. Litwin PE. Martin JS, 
Kudenchuk PJ. Eisenberg M. Prehospital-initiated vs hospital-ini- 
tiated thrombolytic therapy: The Myocardial Infarction Triage 
and Intervention Trial. JAMA 1 993;270( 1 0): 1 2 1 1 - 1 2 1 6. 

50. Gausche M. Persse DE. Sugarman T. Shea SR. Palmer GL. Lewis 

RJ. et al. Adenosine for the prehospital treatment of paroxysmal 
supravenUicular tachycardia. Ann Enierg Med 1994;24(2);I83-189. 
Pepe PE. Levine RL, Fromm RE Jr. Curka PA, Clark PS. 
Zachariah BS. Cardiac arrest presenting with rhythms other than 
ventricular fibrillation: contribution of resu,scitative efforts to- 
ward total survivorship. Crit Care Med 1993:21(12): 1838-1843. 
Cummins RO. Graves JR. Horan S. Larsen MP, Crump K. The 
relative contributions of early defibrillation and ACLS interven- 
tions to resuscitation and survival from prehospital cardiac arrest 
(abstract). Ann Emerg Med 1989;18:468-469. 
Goetting MG, Paradis NA. High-dose epinephrine improves out- 
come from pediatric cardiac arrest. Ann Emerg Med I991;20(l): 

Niemann JT, Cairns CB, Sharma J, Lewis RJ. Treatment of pro- 
longed ventricular fibrillation: immediate countershock versus 
high-dose epinephrine and CPR preceding countershock. 
Circulation 1992;85(l):281-287. 

Brown CG, Griffith RF. Van Ligten P. Hoekstra J. Nejman G, 
Mitchell L, Dzwonczyk R. Median frequency: a new parameter 
for predicting defibrillation success rate. Ann Emerg Med 

Hoekstra JW. Banks JR. Martin DR. Cummins RO. Pepe PE. 
Stueven HA. et al. and the Multicenter High Dose Epinephrine 
Study Group. Effect of first-responder automated defibrillation on 
time to therapeutic interventions during out-of-hospital cardiac 
arrest. Ann Emerg Med 1993;22(8):1247-1253. 
Pepe PE, Mattox KL, Duke JH. Fisher PB. Prentice FD. Effect of 
full-time, specialized physician supervision on the success of a 
large, urban emergency medical services system. Crit Care Med 

Becker LB, Pepe PE. Ensuring the effectiveness of community- 
wide emergency cardiac care. Ann Emerg Med 1993;22(2, Part 

Pepe PE. Out-of-hospital resuscitation research: rationale and 
strategies for controlled clinical trials. Ann Emerg Med 1993; 

Menegazzi JJ, Davis EA, Yealy DM, Molner RL, Nicklas KA, 
Hosack GM, et al. An experimental algorithm versus standard ad- 
vanced cardiac life support in a swine model of out-of-hospital 
cardiac arrest. Ann Emerg Med 1993:22(2):235-239. 
Olson CM. The letter or the spirit: consent for research in CPR 
(editorial). JAMA 1994;271(18):1445-1447. 

Pepe Discussion 

Bishop: Every time I get my property 
tax bill (which is due a couple of days 
after I get back), there's a line on it that 
says Emergency Medical Senices. I 
figure that in the 15 years I've been in 
Seattle, I've probably paid somewhere 
between $1,000 and $1,500 on my 
property tax bill for emergency medi- 
cal services, and I haven't gotten to be 
resuscitated once, yet. Has anybody 
actually analyzed, what we're paying 
for life saved? My impression is that 
trauma resuscitation has the best cost- 

benefit ratio. Do you have a comment 
on the cost-benefit ratios? 

Pepe: Yes. Each year in our commu- 
nity, it probably costs each one of our 
citizens about $10 ± $5 to have emer- 
gency medical services, which in- 
cludes the use of fire apparatus for 
medical care as well. Therefore, in 
terms of budget, it's kind of an apples 
and oranges thing. Regardless, I think 
it's one of the best insurance policies 
one can buy. After I found out how 
much money my family spent on 
movie videos alone last year, I decid- 

ed that the EMS was a lot better deal — 
just to have that safety net there. In 
fact, we made 1 60,000 responses last 
year which is about 1 for every 10 
Houstonians. That means that some- 
one in my family may very well re- 
quire EMS sometime in the next 5-10 
years for a car wreck, heart attack, ana- 
phylaxis, or assault. I want them there. 
Art (Sanders) probably knows some of 
the data better than I, but Terry Valen- 
zuela' in Tuscon has looked at the cost 
of saving a cardiac arrest victim from 
sudden death versus the cost of sav- 
ing a life by providing an organ trans- 

Respiratory Care • April "95 Vol 40 No 4 


Pepe Discussion 

plantation or coronary artery bypass. 
Resuscitation cost including in-hos- 
pital care is literally in the thousands 
versus tens or hundreds of thousands 
for other things. So, it's really actually 
one of the more cost-effective health 
care insurances that we can offer. And 
you're right about emergency ser- 
vices for injury because EMS helps 
with trauma patients. But they also 
help with various other cases (hypo- 
glycemia and seizures, for example). 
Clearly it's really a worthwhile ser- 
vice to 'buy' insurance for. I really 
couldn't imagine not having it there. 

A better question may be. Is it 
worth it to train all those paramedics? 
The answer. I believe, is Yes and, as I 
have stated in my talk, 1 think it can 
be done in a cost-effective manner 
because we have done it in Houston. 
One of the problems nationwide has 
been that a lot of places have tried to 
put a "paramedic on every comer," 
and/or they haven't used the fire 
trucks and the resources that they al- 
ready have. It's cost them a lot, with 
no demonstrable benefit. In my opin- 
ion, that's been one of the problems 
in places like Chicago and New York 
and various other cities that have 
published extremely low survival 
rates from sudden death (out-of-hos- 
pital cardiac arrest).-"* So how you 
utilize and deploy your resources 
makes a difference in demonstrating 

1. Valenzuela TD. Criss EA. Spaite D, 
Meislin HW, Wright AL. Clark L. Cost- 
effectiveness analysis of paramedic 
emergency medical services in the treat- 
ment of prehospital cardiopulmonary ar- 
rest. Ann Emerg Med 1990:19(12): 

2. Becker LB, Ostrander M. Barrett J, 
Kondos GT. Outcome of CPR in a Uu'ge 
metropolitan area: where are the sur- 
vivors'.' Ann Emerg Med 1991:20(4): 

3. Lombardi G. Gallagher JE, Gennis P. 
Outcome of out-of-hospital cardiac ar- 
rest in New York city. The pre-hospital 
arrest survival evaluation (Phase) study. 
JAMA March 1 994:27 l:67X-683. 

4. Becker I.B. Pepe PI-!. Ensuring the ef- 

fectiveness of community-wide emer- 
gency cardiac care. Ann Emerg Med 
1993:22(2. Part 2):354-365. 

Aufderheide: Were you able to de- 
termine what aspect of the ACLS 
therapy made the significant contri- 
bution to the successful resuscitation 
of your 44 patients? Of your 44 pa- 
tients, 28 had pulseless ventricular or 
EMD rhythms. It has been proposed 
that up to 53% of successfully resus- 
citated EMD patients have cessation 
of respiratory effort as the primary 
cause for their cardiac arrest.' Per- 
haps simple intubation was the pri- 
mary therapy that saved those pa- 
tients, rather than the drugs and the 
ACLS protocols. 

I. Stueven HA, Aufderheide TP. Waite 
EM. Mateer JR. Electromechanical 
Dissociation: Six years prehospital ex- 
perience. Resuscitation 1989:17:173- 

Pepe: Well, we did try to delineate 
who got what and who didn't get 
what.' Was it just intubation? The 
problem was that everybody got the 
mix because when the paramedics ar- 
rived, as I showed you on my slides, a 
couple of the firefighters went right 
to the CPR, while another was getting 
out oxygen and the first drugs. 
Therefore, one paramedic went direct- 
ly to placing the endotracheal tube 
while the other went straight to plac- 
ing the I.V. and injecting the first 
drugs (eg, epinephrine and atropine). 
So, within a minute or two of each 
other, they were getting all of these in- 
terventions. So. I really couldn't say, 
"Alright — he got intubated at 8:03, and 
he came back with pulses at 8:05 — it 
must have been the intubation". Be- 
cause he also got the epinephrine 
around the same time, too. So, we real- 
ly couldn't find out reliably what 
works — we don't know how it works 
or where it works. Almost every one of 
those patients 'got it all' — they even 
got sodium bicarbonate in miuny cases, 
prior to restoration of pulses. Did it still 

hurt the outcome in some other cases? 
Change it all? We told the paramedics 
if patients don't respond to the first 
line of drugs, give them the second 
line. Some of these people came back 
with pulses after the first 5-10 min- 
utes. We did find that our outside 
bounds were that if pulses weren't 
back within about 20 minutes of 
ACLS, then they didn't come back, 
period. However, some responded in 
15-20 minutes. What intervention fi- 
nally 'kicked in"? Was it just the tube 
or the whole 'cocktail' ?'■- 

1. Pepe PE, Levine RL. Fromm RE Jr. 
Curka PA. Zachariah BS. Clark PS. 
Cardiac arrest presenting with rhythms 
other than ventricular fibrillation: con- 
tribution of resuscitation efforts toward 
total survivorship. Crit Care Med 1993; 

2. Menegazzi JJ. Davis EA, Yealy DM, 
Molner RL. Nicklas KA, Hosack GM, et 
al. An experimental algorithm versus 
standard advanced cardiac life support in 
a swine model of out-of-hospital cardiac 
arrest. Ann Emerg Med I993:22(2):235- 

Fluck: One of the thrusts of your talk 
seems to have been resuscitating the 
person who has already 'crashed and 
burned.' The A ARC Clinical Practice 
Guideline for resuscitation empha- 
sizes the prearrest and the postarrest.' 
So you say. Does the ACLS work? 
You're on the scene with somebody 
with bad CHF (congestive heart fail- 
ure), you give them morphine. Lasix, 
nitro, and 'beat feet' to the hospital 
and keep him from crashing. You're 
there and the patient has had a synco- 
pal episode from whatever rhythm, 
and you keep him from going back 
there. 1 think that's an important 
point to make. 

I. AARC Clinical Practice Guideline. Re- 
suscitation in acute care ho.spitals. Respir 
Care 1993:38(111:1179-1188. 

Pepe: Ah, this is clear. 1 made it a big 
point that I'm simply setting up a 
'straw man". I'm absolutely a propo- 


Respiratory Care • April '94 Vol 39 No 4 

Pepe Discussion 

nent of ACLS and one of its greatest 
advocates, as you know.' ' I was on 
the National ACLS committee at the 
Heart Association and helped to au- 
thor the most recent guidelines.' ' What's 
happening here is that I'm setting up 
this argument — Does ACLS work? — 
because it addresses what's happen- 
ing in many places in terms of ques- 
tioning cost-effectiveness. Govern- 
ments look at such things. They ask 
Why should we be spending all this 
money if cab fare would do? You can 
see it coming down the pike."* '' Those 
questions are being asked even about 
CPR. So, Tm actually playing devil's 
advocate because I'm trying to do 
something in defense of ACLS. But, 
clearly, I have to say ACLS works, 
but we don't know why. That's all 
I'm saying. Now if we look at the in- 
terventions you're addressing like 
adenosine, we know that those things 
are "good drugs,' and I believe that they 
change outcomes. Do they really 
change the outcome? Just like plac- 
ing the endotracheal tube, I'd defi- 
nitely want it done for me in an arrest. 
It's a Class-I intervention, by consen- 
sus, but I can't prove its efficacy. And 
that's the real issue. You need to be 
aware of that down the line in health 
care reform. We just need to do a bet- 
ter job of proving how and where. 
That's always the call to duty for 
us — as is the education that goes be- 
hind it. I think that Bill Kaye would 
be the first to agree that that is a real 
problem. Following an algorithm 
doesn't guarantee good care. There 
are EMS systems in which para- 
medics show up and watch people ar- 
rest, and they still can't get them back 
using ACLS and defibrillation. I 
think that a lot of the success that we 
see in many ACLS systems has to do 
with training and how they're trained, 
and where they're trained. Go back to 
the original premise that I told you 
about in Seattle and the other places 
like Miami and Columbus. Think 
about how the original training was 
done.*"^ That incredible intensive ap- 

prenticeship of paramedics, that men- 
torship under expert physicians was 
really the key — that made the differ- 
ence. One of you asked me yesterday. 
Should we have respiratory therapists 
perform ACLS? It's the same princi- 
ple. It doesn't matter what you are or 
what your label is. I don't care who it 
is. If a physician mentor who is an ex- 
pert in that area can teach you these 
tricks of the trade and say to a court 
of law, "I will let these people take 
care of my family and you can hold 
me totally accountable for their ac- 
tions," I think that is a very com- 
pelling argument.* I don't care who 
you are. I would be very happy with 
that scenario. 

1. American Heart Association. Emer- 
gency Cardiac Care Committee and 
Subcommittees. Guidelines for cardio- 
pulmonary resuscitation and emergency 
cardiac care. Part 1: Introduction. JAMA 
October 28. 1992;268:2172-2183. 

2. American Heart Association. Textbook 
of Advanced Cardiac Life Support. 
Dallas, 1987:1-248 and 1994:16-1 to 16- 

3. American Heart Association. Emer- 
gency Care Committee. Subcommittee 
on ACLS. Adult advanced cardiac life 
support (ACLS). Part 111. Guidelines for 
cardiopulmonary resuscitation and 
emergency cardiac care. JAMA October 
28. 1992:268:2199-2241. 

4. Spears T. Life and death — and the bot- 
tom line: the paramedic debate. Ottawa 
Citizen. Sunday. November 21,1 993: A9. 

.">. Benson K. Fire fights for EMS de- 
livery... and private providers fight 
back. Emergency September 1994;23{9): 

6. Pepe PE, Bonnin MJ, Mattox KL. 
Regulating the scope of EMS services. 
Prehosp Disaster Med 1990; 5: 59-63. 

7. Pepe PE, Mattox KL, Duke JH, Fisher 
PB, Prentice FD. The effect of fulltime 
specialized physician supervision on the 
success of a large urban emergency 
medical services system. Crit Care Med 

Fluck: One more thing. We fired up 
an enhanced 91 1 system in Syracuse 
about 2 years ago, and, as of a couple 
of months ago, still somewhere be- 
tween two thirds and three fourths of 

the calls that were automatically rout- 
ed to the 911 center were dialed on 
other numbers. So I think we still have 
a major public education problem, if 
you will. Did you have the same ex- 
perience in Houston? 

Pepe: Yes, at first about 50% of our 
calls were still coming in from the old 
numbers that people had program- 
med, or written on their phones, or what- 
ever. That, of course, meant that we 
had to gather the information from 
them. Today a lot of the calls are 
coming in on cellular phones, which 
means that we get the number of the 
cellular phone company; so, there's 
another evolving problem. There's 
also a double-edged sword with 911. 
There's a person at 911. When we 
put in 911 in 1986, our call volume 
literally doubled because people (es- 
pecially in this era), have nowhere 
else to turn, ie, they don't have a per- 
sonal doctor, and they're disenfran- 
chised from the health-care system. 
For them, there is one person who's 
always there — 91 1. They'll give you 
a quick ride to the hospital wherever 
it may be. That's their impression. 
So, we get calls for lots of things. In 
the middle of that major flood a few 
days ago. I was monitoring all the 
calls for any storm-related incidents. 
In Houston, one EMS unit was dis- 
patched to "an animal bite", so I 
thought. Oh, it's our first deadly 
snake bite. I called the dispatcher to 
confirm my suspicion. Much to my 
amazement, the problem was a cat 
bite. They're calling us out for a cat 
bite! Well, maybe this was a tiger that 
had escaped from the zoo or some- 
thing? No. it was only Garfield! How 
serious is this, right? That stuff hap- 
pens. So, like most drugs, 91 1 can be 
both a blessing and a curse. 

Rubenfeld: To follow up on the 
point that you just made, it sounds 
like one of the ways you make ACLS 
cost-effective is to have this triage re- 
sponse system. How often does that 
fail? In other words, how often does 



Pepe Discussion 

a person requiring ACLS miss that 
care when a BLS unit is first dis- 
patched alone to the scene? 

Pepe: Good question. If you look at the 
November 1993 issue of the Annals of 
Emergency Medicine.' we looked at 
every one of 35.000 consecutive dis- 
patches over 90 days and found that we 
had only 14 cases where we said Oops! 
We really would have liked to have had 
the paramedic get there first.' In fact, 
when we examined those cases a little 
more closely, we felt, pretty confident 
that ACLS wouldn't have changed the 
outcome. Several were people in a car 
wreck who presented apneic and pulse- 
less. Even ACLS wouldn't have 
changed the outcome. In other cases. 

paramedics actually arrived first (after 
updated information was received from 
secondary callers), and that didn't 
change the outcome. 

1. Curka PA. Pepe PE. Ginger VF. 
Sherrard RC. Ivy MV, Zachariah BS. 
Emergency medical services priority dis- 
patch. Ann Emerg Med 1993:22(1 1): 

Rubenfeld: If I could just follow up on 
that. Do you allow any of your 
'triagers' to triage and not to transport? 

Pepe: Oh yes. and the way that works 
is that we do require the basic life sup- 
port folks to contact their supervisor (a 
veteran paramedic who works closely 

with me) and explain the situation and 
make sure we're clear. It's a minor 
problem. If there's any question, one 
of our doctors decides one way or the 
other (on-line by phone or radio). The 
paramedics in Houston are now pretty 
well trained by us. They know what we 
want. We've allowed them to make 
those decisions, and if there's any 
question, they call their supervisor or 
the designated doctor at our trauma 
center. In the case of kids, where the li- 
ability extends for 18 years, we do 
have them automatically call the sys- 
tem-designated pediatrician, just to 
cover ourselves better. We are called 
out on a lot of situations for kids that 
we probably don't need to go out for — 
but that's life. 

41st Annual Convention and Exhibition 
December 2-5 • Orlando, Florida 


Ri;sPiRAT()KV Carh • April '94 Vol 39 No 4 


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Test %ur 
Radiologic Skill 

Patricia A Doorley MS RRT and Charles G Durhin Jr MD, Section Editors 

Removal of a Closed-System, Directional-Tip Suction Catheter 

Robert A Milisch MEd RRT, David S Rho MD, and Sheila A Schell RRT 

Case Summary 

A 67 year-old woman was admitted to the hospital for 
evaluation of two solitary lesions — one in the right-upper 
lobe and one in the right-middle lobe, which were proven 
by needle biopsy to be squamous cell carcinomas. Earlier 
pulmonary function tests were consistent with a diagnosis 
of chronic-obstructive pulmonary disease but not severe 
enough to preclude surgery. She underwent right-upper 
and right-middle lobectomy for the removal of the lesions. 

The first two postoperative days were essentially un- 
eventful, although the patient was recovering slowly. On 
postoperative Day 3. she developed increased shortness of 
breath and decreased oxyhemoglobin saturation. Radio- 
graphs showed infiltrates in the left lung. On the sixth 
postoperative day, she was intubated with an 8-mm-ID en- 
dotracheal tube (ET, Lo-Pro. Mallinckrodt Medical, St 
Louis MO) and placed on a mechanical ventilator (Servo 
300, Siemens Medical Systems, Dan vers MA) due to res- 

Mr Milisch is Program Director. Respiratory Care Practitioner Program, 
Western Wisconsin Technical College; and Dr Rho is Director, 
Department of Anesthesiology, and Ms Schell is a respiratory therapist. 
St Francis Medical Center — La Crosse, Wisconsin. 

Reprints: Robert A Milisch MEd RRT, Respiratory Care Practitioner 
Program, Western Wisconsin Technical College, 304 North Sixth Street. 
La Crosse WI 54601 

The authors have no fmancial interests in any of the products mentioned 
in the text. 

A version of this paper was presented during the OPEN FoRUM as part of 
the AARC Annual Meeting held in Las Vegas, Nevada. December 1994. 

piratory failure that persisted, despite aggressive antibiotic 

Her treatment included inhaled bronchodilator and 
chest percussion and postural drainage (CP&PD). On 
postoperative Day 19, the patient was being ventilated 
using the pressure-regulated volume-control mode with a 
rate of 1 6 breaths/min, tidal volume of 650 mL, PEEP of 7 
cm HiO. and Fdo: of 0.6. Humidification was provided via 
a heated wick humidifier with the airway temperature 
maintained at 32-34° C. Because of the need for frequent 
suctioning, a 14-Fr directional-tip closed-system suction 
catheter (CSSC, Trach Care, Ballard Medical Products, 
Draper UT) had been positioned in the ventilator circuit. 

Following a bronchodilator treatment with metered- 
dose inhaler and CP&PD, the patient was suctioned with 
the directional-tip CSSC. The initial insertion of the suc- 
tion catheter yielded moderate amounts of thick yellow se- 
cretions. After instillation of 3 mL of normal saline, the 
catheter was again inserted. During insertion, the patient 
coughed, and. subsequently, the catheter could not be 
withdrawn. The respiratory therapist repeatedly attempted 
to advance and withdraw the catheter without success. An 
anesthesiologist was immediately called to the room to 
evaluate the situation. 

Because this was a closed-system catheter, ventilation 
was maintained. However, the ventilatory mode was im- 
mediately changed to standard volume-limited with assist- 
control to assure delivered tidal volumes. The Fdo: was in- 
creased to 1.0 to maintain oxyhemoglobin saturations in 
the 90-94% range. Upon arrival, the anesthesiologist or- 
dered a chest radiograph to help with his assessment. The 
radiograph was delivered to the patient's room 10 minutes 
later and is shown in Figure 1. 

How Would You Answer These Questions 

What abnormalities are apparent on the radiograph? 


Rhspiratorv Care • April "95 Vol 40 No 4 

Test Your Radiologic Skill 

Fig. 1 . Anteroposterior chest radiograph of a 67-year-old woman on Day 1 9 of mechanical ventilation for respiratory failure following lung resection. 

What would be the best course of action based on the case summary and the radiograph? 

Answers and Discussion on Next Page 

Respiratory Care • April "95 Vol 40 No 4 


Test Your Radiologic Skill 

Radiographic Abnormalities: It can be seen in Figure 1 
that the radiograph is slightly rotated to the right. Although 
unintentional, the rotation allows for enhanced visualiza- 
tion of tracheal structures. ' The close-up view of the radio- 
graph (Fig. 2) shows that the suction catheter exited the ET 
through the Murphy eye (Arrow 2) near the tip of the tube 
(Arrow 1). The catheter then hooked back (Arrow 3) a dis- 
tance of approximately 3.5 cm toward the vocal cords, 
lodging between the ET and the trachea. There is no medi- 
astinal free air to suggest that the catheter had perforated 
the tracheal wall. 

Other abnormalities on this radiograph include diffuse 
alveolar disease throughout the left lung. Bronchial clips, 
skin staples, and evidence of the fifth-posterior-rib resec- 
tion can be seen in the right hemithorax.The right hemidi- 
aphragm is elevated, consistent with the volume loss that 
resulted from removal of the right-upper and right-middle 

Course of Action: The endotracheal tube was untaped, and the 
cuff on the endotracheal tube was deflated. The tube was advanced 
several centimeters to the level of the carina The suction catheter 
was then rotated and easily removed. After follow-up blood gas re- 
sults had been evaluated, the patient was retumed to her previous 
ventilator settings. 


Closed-system suction catheters have been credited 
with preventing oxyhemoglobin desaturation, hypoten- 
sion, and bradycardia during the suctioning of ventilated 
patients,- ' without compromising the effectiveness of the 
procedure.'' They have also been shown to reduce cost in 
patients who require frequent suctioning. Directional-tip 
CSSCs are credited with the ability to selectively suction 
either the right- or left-main bronchus.' 

The most important aspect of this case is the fact that 
the esse allowed for maintenance of adequate ventilation 
during assessment of the situation. Without a proper as- 
sessment and the time that it required, an initial reaction 
might have been to extubate the patient immediately to 
dislodge the catheter. In this case, the potential for tracheal 
or laryngeal damage was high because the catheter formed 
a hook that was wedged between the ET and the tracheal 
wall. Advancing the endotracheal tube to the level of the 
carina allowed sufficient space for the CSSC to fall into 
the main-stem bronchus and be easily removed without 
trauma to the airway. 

When the suction catheter was removed, it was found to 
have thick secretions at the tip. One possible explanation 
for the incident is that the patient obstructed the ET with a 
mucus plug while coughing, forcing the CSSC to exit 
through the Murphy eye of the ET. Another possibility is 
that tube movement and the high instantaneous pressures 
associated with coughing forced the directional tip of the 
CSSC through the Murphy eye. However, the exact mech- 
anism is a matter of speculation. 

We were unable to find published reports of this type of 
incident. The manufacturer of the CSSC claims no knowl- 
edge of incidents of this type. There has been one report 
from Europe where a CSSC designed for use with an endo- 
tracheal tube (22 inches long) was used on a patient with a 
tracheostomy. In this case it was speculated that the practi- 
tioner attempted to advance the CSSC too far, causing the 
catheter to kink at the carina and hook back toward the 
vocal cords, (personal communication, Ballard Corpor- 
ation, 1994) 


This case describes a technique for removal of a trapped 
suction catheter without extubation, and points out another 
benefit of the closed-system suction catheter. Because a 
CSSC was used, ventilation and oxygenation could be 
maintained, allowing adequate time for a careful assess- 
ment before action was required. We suspect that this type 
of mishap is extremely rare but illustrates that proper as- 
sessment and treatment are essential to patient safety. 


1 . Wilkins R. Krider S, Sheldon R, eds. Clinical assessment in respi- 
ratory care, 3rd ed. St. Louis: Mosby Year Book, 1995:150. 

2. Craig KC, Benson MS. Pierson DJ. Prevention of arterial oxygen 
desaturation during closed-airway endotracheal suction: the effect 
of ventilator mode. Respir Care 1 984;29( 1 ): 1 1 3- 1 01 8. 

3. American Association for Respiratory Care. Clinical practice 
guideline: endotracheal suctioning of mechanically ventilated 
adults and children with artificial airways. Respir Care 1993; 38(5): 

4. White GC. Equipment theory for respiratory care. Albany: 
Delmar Publishers. 1992:237-238. 

5. Kacmarek RM. Mack CW, Dinias S, eds. The essentials of respi- 
ratory care, 3rd ed. St Louis: Mosby Year Book. 1990:430-431. 

f). Witmer MT. Hess D, Simmons M. An evaluation of the effective- 
ness of the secretion removal with the Ballard closed-circuit suc- 
tion catheter. Respir Care l99l;36(8):844-848. 

7. Hart TP. Mahutlc CK. Evaluation of a closed-system, directional- 
tip suction catheter. Respir Care 1992; 37( 1 1 ): 1 260- 1 265. 


Respiratory Carl • April '95 Vol 40 No 4 

Test Your Radiologic Skill 

Fig. 2. A close-up view of the chest radiograph shown in Figure 1 . The arrows point to the tip of the endotracheal tube (1 ), the Murphy eye (2), 
and point at which the suction catheter turned toward the vocal cords(3). The tip of the catheter exited the Murphy eye, turned toward the 
vocal cords, and became wedged between the tube and the tracheal wall, preventing withdrawal. 

Respiratory Care • April '95 Vol 40 No 4 


Books, Films, 
Tapes, & Software 

Listing and Reviews of Books and Other Media 

Note to publishers: Send review copies of books, films, tapes, and software to 
RESPIRATORY CARE, 1 1030 Abies Lane, Dallas TX 75229-4593. 

Respiratory Physiology. 3rd ed, by Allan 
H Mines, Professor of Physiology at the 
University of California at San Francisco. 
182 pages, illustrated. New York: Raven 
Press, 1992. From Raven Press Series in 
Physiology, edited by WiUiam F Ganong. 
Soft-cover $34.00. Hardcover $72.50. 

The author's intention in writing this book 
is to help students taking a course in medi- 
cal physiology to gain a working knowl- 
edge of respiratory physiology. The author 
states that the book will be of interest to 
medical students, allied health students, 
graduate students in physiology, physi- 
cians, and researchers. This book may be 
compared to JB West's, Respiratory 
Physiology. 5th ed (Williams & Wilkins, 
Baltimore), in its coverage and length. 
However, it does not possess the ease of 
reading or extensive illustration present in 
T DesJardins's, Cardiopulmonary Analomy 
and Physiology. 2nd ed (Delmar, Albany). 
It becomes clear on comparison than the 
DesJardins book is oriented towards respi- 
ratory therapy students, rather that toward 
medical smdents and physicians as are the 
West and Mines books. 

The book has eight chapters of text and 
two chapters containing study questions 
and answers. Each chapter has a good intro- 
duction, preparing the reader for the content 
to follow. However, unlike the common 
practice, no chapter objectives are supplied. 
Chapter 1 is an introduction to respiration, 
wherein physiologic symbols, gas transport 
from atmosphere to mitochondrion, control 
of the respiratory system, and lung volumes 
are introduced. Chapter 2 presents the me- 
chanics of breathing, including static and 
dynamic properties, with a detailed section 
on pulmonary surfactant. A noticeable 
omission from Chapter 2 is any mention of 
the work of breathing, a concept that has 
gained wide clinical attention. Chapter 3 
covers ventilation and alveolar gas pres- 
sure, including factors determining dead 
space, Pjcc).- PaO.-. '""1 u^e of the alveolar- 
gas equation. Chapter 4 addresses oxygen 
transport and Chapter 5 carbon dioxide 
transport. Chapter 6 is devoted to acid-base 
balance. Chapter 7 covers gas exchange in 
the lungs, and the text concludes with 
Chapter S on control of breathing. Chapters 

9 and 10 contain challenging application 
and synthesis questions and answers per- 
taining to each chapter. The nature of the 
questions reflects the author's recognition 
that smdents must be able to go beyond 
mere memorization of isolated facts if they 
are to truly understand this material. 

The book's type is small and the mar- 
gins narrow, making it somewhat difficult 
to read. The student may need to outline the 
book as he reads in order to separate out im- 
portant points. Figure and table numbering 
start over with each chapter. Illustrations 
and diagrams from the literature are helpful 
in understanding the text. There is no spe- 
cific anatomy chapter, which is a weakness 
when compared to the West and DesJardins 
books. Formulas are frequently provided, 
but they are embedded in the text, instead 
of being set in display. For example, the 
equation for Boyle's Law begins at the end 
of one line then continues at the beginning 
of the next. Again on Page 29, the author 
discusses alveolar pressures and has the for- 
mula: Ptm = 2T/r + 2 (72 dynes/cm) / (48 x 
10~* cm) -)- 30 x 10-' dynes/cm- run through 
the text, which makes it difficult to sort out 
from the rest of the text and difficult for the 
student to discern its importance. 

Most of the references are dated, being 
from the 1950s and 60s. The body plethys- 
mograph shown in Chapter I is a Mead- 
type with a Krogh spirometer, no longer in 
clinical use. The author speaks of a me- 
chanical respirator on Page 2 1 , presumably 
synonymous with a mechanical ventilator. 
On Page 35, he uses the term "continuous 
positive pressure respiration, abbreviating it 
(CPPR), when I think he means continuous 
positive airway pressure (CPAP). In the 
chapter on mechanics, the author discusses 
Ohm's law but neglects to discuss 
Poiseuille's law, which is clearly more ap- 
plicable to the respiratory systein. 

Although I have no doubts about the ac- 
curacy of the content of this book, I found it 
difficult to read from the perspective of one 
who teaches respiratory physiology to res- 
piratory therapy students. If the book is to 
be used as a text in a respiratory care cur- 
riculum, the instructor may really have to 
work to make this text understandable to 
students. The book is not the best choice for 
undergraduate respiratory therapy students 

because it presumes a basic understanding 
of respiratory physiology, brain stem anato- 
my, physics (such as the gas laws), and 
chemistry (such as the concept of pK). Its 
reading level also appears to be higher than 
that of other respiratory therapy texts, such 
as the DesJardin's text or Scanlan et al, 
Egan's Fundamentals of Respiratory Care 
(CV Mosby Co, St Louis). I would recom- 
mend it for medical and graduate students 
because it provides a concise and accurate 
presentation of respiratory physiology. 
Respiratory therapy faculty may wish to 
refer to it for its in-depth explanations and 
for its challenging questions, as an adjunct 
to those contained in other physiology 

Tim Op't Holt Ed D RRT 

Associate Professor 

Department of Respiratory Care 

& Cardiopulmonary Sciences 

University of South Alabama 

Mobile, Alabama 

Principles and Practice of Pulmonary 
Rehabilitation, edited by R Casaburi MD 
PhD and TL Petty MD. Hardcover, illus- 
trated, 508 pages. Philadelphia: WB 
Saunders, 1993. $75. 

Editors Richard Casaburi PhD MD and 
Thomas L Petty MD have collaborated 
with 64 contributors to produce a useful 
text for many allied health disciplines and 
for physicians. Among the contributing au- 
thors to the text are names like Belman and 
Bums, Kacmarek and Kravetz, Pierson, 
Ries, Selecky, and Tietsort, assuring that 
Casaburi and Petty have gathered a diverse 
group of experts on this subject. The editors 
tell us in the preface that "a major purpose 
of this book is to facilitate a transition to a 
scientific basis for pulmon;iry rehabilita- 
tion. It is intended not only to convey a 
sense of the cuirent status of pulinon;uy re- 
habilitation, but also to point out those iu'eas 
that need further study." The book accom- 
plishes that well. 

The book is divided into four parts. 
Chapter One, "Pulmonary Rehabilitation: 
A Personal Historical Perspective," is writ- 


R[;.spiRATORY Care • April '94 Vol .39 No 4 

Books, Films, Tapes, & Software 

ten by Petty, who has both witnessed and 
contributed significantly to many of the 
major events that have brought pulmonary 
rehabilitation (PR) to the level it is today. 
Part 1: Causes and Consequences of 
Chronic Pulmonary Disease actually begins 
with Chapter 2, addressing the epidemiolo- 
gy of obstructive pulmonary disease. Table 
2- 1 on page 1 1 uses the applicable ICD/9 
codes to quantify morbidity and mortality 
for COPD and asthma, helping cle;ir up the 
confusion inherent to the natural overiap 
that occurs within this group of obstructive 
lung diseases. Chapters 3, 4, and 5 offer 
both a thorough review of normal anatomy 
and physiology and a systematic approach 
to evaluating dysfunction. The references 
following each chapter are extensive. 
Chapter 6, cardiovascular consequences; 
Chapter 7, neurocognitive aspects; and 
Chapter 8, sleep-disordered breathing offer 
extensive reviews of the literature and are 
clearly written. Killian's historical perspec- 
tive on dyspnea in Chapter 8 is as iinportant 
as Petty "s to the overall appreciation of the 
impact of COPD. He concentrates on the 
mechanics of shortness of breath but re- 
minds us that "the practical contributions of 
these techniques to patient management re- 
main to be established." Chapter 10. 
Exercise Tolerance in the Pulmonary 
Patient, contains excellent summary tables, 
and Chapter 1 1 offers a systematic review 
of acute and chronic respiratory failure. All 
these chapters are well referenced. 

The three authors of Chapter 1 2, Course 
and Prognosis in Patients with Chronic 
Airflow Obstruction: Possible Implications 
for Therapy, are from the Netherlands 
where physiotherapists are responsible for 
the exercise component of PR. In contrast, 
in the United States that responsibility has 
most often been shared by RCPs and physi- 
cal therapists, but that may be changing. In 
their initial survey of PR programs in the 
US in 1987, Hodgkin and associates found 
that only 13% of the PR programs had an 
exercise physiologist as a team member; 
that number increased to 45% when the sur- 
vey was repeated in 1992-93.' This chapter 
serves nicely as a summary to Part I and in- 
troduction to Part 2 — Therapeutic 
Modalities in Pulmonary Rehabilitation. 

The authors of Chapter 1 3 divide phar- 
macologic agents by organ-related effec- 
tiveness — those for the lungs and those for 
the muscles of respiration. Table 13-4 of- 
fers excellent infonnation on a question that 

we often forget to ask, "What other medica- 
tions might our COPD patient be taking 
that could affect respiratory muscle func- 
tion?" Chapters 14 and 15 not only review 
the literature, but also emphasize that much 
more research needs to be done to assess 
the effectiveness of assistive modalities 
such as CPT and breathing techniques and 
long-term oxygen therapy. Everything you 
ever wanted to know about the body of re- 
search on exercise training is condensed 
into Table 16-1 in Chapter 16. For the ther- 
apist who struggles with finding the most 
effective way to help the COPD patient in- 
crease function, this 4-page table and this 
chapter may well be worth the price of the 
book! Casaburi succinctly summarizes both 
expected and unexpected results from exer- 
cise programs. In Chapter 17, Belman com- 
plements the preceding chapter in his dis- 
cussion of ventilatory muscle training and 
unloading, using a review of the current lit- 
erature to effectively support the use of 
CPAP in this patient population. 

Chapters 18 and 19 address dyspnea 
and its impact, both psychologically and bi- 
ologically, through an extensive literature 
review. Collectively, the authors appear to 
agree that, at the very least, exercise is as 
good a 'piir as a pill. Authors familiar to 
even infrequent readers of the literature 
contribute to the final chapters of Part 2. In 
Chapter 2 1 , Pierson and Kacmarek review 
home ventilator care, with important em- 
phasis on patient selection and discharge 
planning. Table 20-7 lists the equipment 
needed for home ventilator care, and Table 
20-8 offers a summary of the capabilities of 
seven well-known ventilators designed for 
home use. Who better than Louise Nett to 
speak to nicotine addiction and treatment? 
The patient questionnaires and references 
in her chapter should help any therapist 
who has an interest in developing a smok- 
ing cessation program. 

Part 3: "Components of the Pulmonary 
Rehabilitation Program" left me a little dis- 
appointed. Tiep's chapter on PR program 
organization gives only a brief summary of 
a topic requiring more emphasis. The sec- 
tion on documentation and reporting is only 
two paragraphs, and a review of the index 
does not reveal other references to docu- 
mentation in the entire text. In discussing 
the PR team, there is no mention of 
Hodgkins" survey of programs.' Goldstein 
and co-authors describe candidate evalua- 
tion in only 5 pages, equally divided be- 

tween selection and assessment of candi- 
dates. They do not review the literature, 
choosing rather to describe their own pro- 
gram experience almost exclusively. Chap- 
ter 24, Exercise Prescription, discusses 
candidate criteria and the actual exercise 
evaluation (testing modalities, testing pro- 
tocols, and continuous monitoring during 
the test). The authors then speak to the prac- 
tical steps to ensure safety and success, set- 
ting realistic goals. Table 24- 1 outlines this 
nicely. Chapter 25 begins with a strong 
statement: "Nutritional intervention in PR 
lacks a research-based rationale." The au- 
thors begin by reviewing non-disease-spe- 
cific nutritional assessment tools. Table 25- 
1 then reviews the common complaints and 
recommendations for nutritional support in 
COPD, many of whom. I believe, are mal- 
nourished, not obese, as the text implies. 
Psychosocial issues are common for those 
with COPD, and those who work in this 
field are challenged daily to provide appro- 
priate support. It may be semantics, but 
there will be some disagreement among PR 
groups as to whether we provide "reme- 
dies," as the authors of Chapter 26 suggest, 
or whedner we do our best when we are pro- 
viding a helping hand or lending an ear. 
Biofeedback and relaxation training has its 
supporters, but third-party payers are not 
among them. By reviewing the current lit- 
erature and describing therapy modalities, 
the authors of Chapter 27 make a case for 
selective reimbursement for these modali- 

In a lecture on sexuality a few years 
ago, Paul Selecky, author of Chapter 28, 
began with pictures of Mel Gibson and 
Christi Brinkley. That got the audience's at- 
tention, and this chapter keeps it by 
thoughtfully addressing sexuality issues for 
the COPD patient and the caregivers. The 
final chapter in Part 3 discusses how to 
evaluate the results of PR — how to assess 
outcomes, both physical and psychological. 
The section, "Aspects of Study Design." 
should be enough to whet the appetite of 
those who are interested in such research. 

Part 4 addresses special considerations 
for PR, specific to nonobstructive lung dis- 
ease, asthma, cystic fibrosis, and lung trans- 
plantation. The literature review in Chapter 
33, "The Role of Physical Training in 
Asthma," omits one of the most current and 
significant documents on asthma. The 
National Asthma Education Program 
(NAEP) Guidelines for the Diagnosis and 

Respiratory Care • April '95 Vol 40 No 4 


Books. Films, Tapes, & Software 

Management of Asthma- Conspicuously 
absent as well is any reference to the use of 
a peak flow meter for self-monitoring pre- 
and post-exercise. Information presented in 
Chapters 34-36 point up both opportunities 
and challenges for the RCP as our scope of 
practice increases. 

The final four chapters are a fitting sum- 
mary to this book. Authors with experience 
in a variety of PR settings demonstrate that 
issues of reimbursement and cost-effective- 
ness can be addressed in creative ways. 
Perhaps Kravetz's quote from Jack London 
in Chapter 39, "I shall not waste my days ... 
I shall use my time"" should be the mantra 
for all those who continue to work diligent- 
ly to assure that PR services are available 
for those who can benefit from them. 

This generally thorough and well-refer- 
enced text is worth the price and should be 
considered an important resource for all 
discipUnes involved in pulmonary rehabili- 

Gretchen Lawrence BA RRT 


Pulmonary Services 

Baylor Asthma & Pulmonary 

Rehabilitation Center 

Dallas. Texas 


l.HodgkJn JE, Bickford LS. National pul- 
monary rehabilitation survey. In: Hodg- 
kin JE, guest ed. Pulmonary rehabilita- 
tion symposium. J Cardiopulm Rehab 
1988;8:473. Survey repealed in 1992-93. 
Results presented at the AARC annual 
meeting, 1993, Nashville, Tennessee. 

2.Nalional Asthma Education Program. 
Expert Panel Report. Guidelines for the 
diagnosis and management of asthma. 
National Heart, Lung and Blood Insti- 
tute, National Institutes of Health. Pub- 
lication No. 9 1 -3042. August 1 99 1 . 

Essentials of Anatomy and Physiology, 

2nd edition, by Valerie C Scanlon PhD and 
Tina Sanders, Medical Illustrator. Soft- 
cover, 606 pages, illustrated. $31.9.'). 
Instructor's Guide for Essentials of 
Anatomy and Physiology, 2nd edition, by 
Valerie C .Scanlon PhD. Soft-cover. 134 
pages (furnished free of charge to instruc- 
tors). .Student Workbook for Essentials 

of Anatomy and Physiology. 2nd edition, 
by Valerie C Scanlon PhD and Tina 
Sanders. Medical Illustrator. Soft-cover. 
417 pages, illustrated. $17.95. Philadelphia: 
FA Davis. 1994. 

Essentials of Anatomy and Physi- 
ology is a compact yet coinprehensive in- 
troductory textbook of anatomy and physi- 
ology. In an attempt to make essential texts 
more readable, important concepts are 
sometimes oversimplified and medical ter- 
minology omitted. The authors of Essen- 
tials of Anatomy and Physiology have 
successfully distilled the complex details of 
human structure and function without los- 
ing the concepts and terminology necessary 
for students in the clinical health profes- 
sions. The intended audience for this text 
are students with diverse backgrounds and 
varying levels of educational preparation. 
No prior knowledge of biology or chem- 
istry is assumed, making this text an excel- 
lent choice for a one-semester introductory 
course or for physiologic modules, integrat- 
ed into clinical courses at the community or 
technical college level. 

The book is organized in a traditional 
style with introductory chapters on ana- 
tomic organizational structure and cell and 
tissue structure and function followed by a 
systemic chapter approach. A chapter on 
basic chemistry is included but may be dif- 
ficult to incorporate into a one-semester 
course. In the Instructor's Guide, the au- 
thors suggest a strategy of incorporating 
parts of this chapter as needed throughout 
the course. I recommend the same approach 
with the chapter "Body Temperature and 
Metabohsm," which follows "The Diges- 
tive System." 

Each chapter is well illustrated, with la- 
beled anatomic diagrams and physiologic 
illustrations that reinforce concepts in the 
text. Although the quality and quantity of 
illustrations is adequate for a text of this 
scope, .some instructors will want to use ad- 
ditional illustrative material in teaching 
some of the physiologic concepts. A useful 
addition to the 2nd edition are 104 clinical 
applications, which appear as boxed inserts. 
For cardiopulmonary physiology, inserts 
are included describing cardiovascular 
factors, heart murmurs, electrocardiograms, 
dysrhythmias. vascuUtf disorders, hyperten- 
sion, asthma, hyaline membrane disease. 

pneumothorax, emphysema, and pulmon- 
ary edema. 

Several features of this text are specifi- 
cally directed toward assisting the student 
in organizing and studying the material. 
Each chapter begins with a list of student 
objectives and ends with a sUidy outline 
and review questions that summarize im- 
portant concepts. The Appendix includes 
an extensive glossary of terms, with cross 
references back to the chapters in which the 
terms were introduced. 

Additional material for the instructor is 
included in Instructor's Guide for 
Essentials of Anatomy and Physiology by 
Scanlon. A computerized test bank and 
transparencies package are also available. 
The Instructor's Guide includes useful sug- 
gestions about modifying material for spe- 
cific teaching needs and current topics for 
class discussion. The computerized test 
bank contains test questions for each chap- 
ter in a software package that allows the in- 
structor to modify and add questions. 

The Student Workbook for Essentials 
of Anatomy and Physiology provides stu- 
dents with a useful supplemental learning 
tool. Workbook sections correspond to the 
major chapters of the text. Each section 
contains a useful assortment of sentence- 
completion and matching questions, dia- 
gram exerci-ses. vocabulary crossword puz- 
zles, and comprehensive multiple-choice 
exams. A complete answer key is provided 
at the end of the workbook. 

In this text, the authors have succeeded 
in providing the essential concepts of anato- 
my and physiology necessary for students 
in the clinical health professions. The read- 
ability yet comprehensive presentation of 
information on anatomy and physiology 
make this an excellent introductory text for 
a one-semester course for heath science stu- 
dents at the community and technical col- 
lege level. The accompanying student 
workbook and materials for the instructor 
provide excellent supplements to reinforce 
the textbook material and to assist both the 
student and teacher in the learning process. 

Marilyn A Cairns ScD 

Professor of Cardiopulmon;u7 Sciences 

Special Assistant to the Provost 

Northeastern University 

Boston. Massachusetts 


Respiratory Care • April 'm.'^ Vol 40 No 4 

1995 Call for Abstracts 

Respiratory Care • Open Forum 

The American Association for Respiratory Care and its sci- 
ence journal. Respiratory Care, invite submission of brief 
abstracts related to any aspect of cardiorespiratory care. The 
abstracts will be reviewed, and selected authors will be invit- 
ed to present papers at the OPEN FORUM during the AARC 
Annual Meeting in Oriando, Florida, December 2-5, 1995. 
Accepted abstracts will be published in the November 1995 
issue of Respiratory Care. Membership in the AARC is 
not necessary for participation. 


An abstract may report ( I ) an original study, (2) the evalua- 
tion of a method or device, or (3) a case or case series. 

Topics may be aspects of adult acute care, continuing 
care/rehabilitation, perinatology/pediatrics, cardiopulmonary 
technology, health-care delivery. The abstract may have 
been presented previously at a local or regional — but not na- 
tional — meeting and should not have been published previ- 
ously in a national journal. The abstract will be the only evi- 
dence by which the reviewers can decide whether the author 
should be invited to present a paper at the Open Forum. 
Therefore, the abstract must provide all important data, find- 
ings, and conclusions. Give specific information. Do not 
write such general statements as "Results will be presented" 
or "Significance will be discussed." 

Abstract Format and Typing Instructions 

Accepted abstracts will be photographed. First line of abstract 
should be the title in all capital letters. Title should explain 
content. Follow title with names of all authors (including cre- 
dentials), institutions(s), and location. Underline presenter's 
name. Type or electronically print the abstract single spaced 
in the space provided on the abstract blank. Insert only one 
letter space between sentences. Text submission on diskette is 
encouraged but must be accompanied by a hard copy. 
Identifiers will be masked (blinded) for review. Make the ab- 
stract all one paragraph. Data may be submitted in table form 
and simple figures may be included provided they fit within 
the space allotted. No figures, illusU^ations, or tables are to be 
attached to the abstract form. Provide all author information 
requested at the bottom of abstract form. A clear photocopy of 
the abstract may be used. Standard abbreviations may be em- 
ployed without explanation. A new or infrequently used ab- 
breviation should be preceded by the spelled-out term the first 
time it is used. Any recurring phrase or expression my be ab- 
breviated if it is first explained. Check the abstract for ( 1 ) er- 
rors in spelling, grammar, facts, and figures; (2) clarity of lan- 
guage; and (3) conformance to these specifications. An ab- 
stract not prepared as requested may not be reviewed. 
Questions about abstract preparation may be telephoned to 
the editorial staff of Respiratory Care at (214) 243-2272. 

Essential Content Elements 

Deadline Allowing Revision 

An original study abstract must include ( 1 ) Introduction: 
statement of research problem, quesdon, or hypothesis; (2) 
Method: description of research design and conduct in suffi- 
cient detail to permit judgment of validity; (3) Results: state- 
ment of research findings with quantitative data and statisti- 
cal analysis; (4) Conclusions: interpretation of the meaning 
of the results. A method/device evaluation abstract must 
include ( 1 ) Introduction: identification of the method or de- 
vice and its intended function; (2) Method: description of 
the evaluation in sufficient detail to permit judgment of its 
objectivity and validity; (3) Results: findings of the evalua- 
tion; (4) Experience: summary of the author's practical ex- 
perience or a lack of experience; (5) Conclusions: interpre- 
tafion of the evaluation and experience. Cost comparisons 
should be included where possible and appropriate. A case 
report abstract must report a case that is uncommon or of 
exceptional teaching/learning value and must include ( I ) pa- 
tient data and case summary and (2) significance of case. 
Content should reflect results of literature review. The au- 
thor(s) should have been actively involved in the case and a 
case-managing physician must be a co-author or must ap- 
prove the report. 

Authors may choose to submit abstracts early. Abstracts re- 
ceived by March 1 5 will be reviewed and the authors notified 
by April 22. Rejected abstracts will be accompanied by a 
written critique that should in many cases enable authors to 
revise their abstracts and resubmit them by the final deadUne 
(May 27). 

Final DeadUne 

The mandatory Final Deadline is May 27 (postmark). 
Authors will be notified of acceptance or rejection by letter 
only — to be mailed by August 15. 

MaiUng Instructions 

Mail (Do not fax!) 2 clear copies of the completed abstract 
form and a stamped, self-addressed postcard (for notice of 
receipt) to: 

Respiratory Care Open Forum 

11030 Abies Lane 

Dallas, TX 75229-4593 

Respiratory Care • March '95 Vol 40 No 3 

1995 Respiratory Care Open Forum 

Abstract Form 

13.9 cm or 5.5" 

1 . Title must be in all upper 
case (capital) letters, 
authors" full names and 
text in upper and lower 

2. Follow title with all 
authors' names including 
credentials (underline 
presenter's name), institu- 
tion, and location. 

3. Do not justify (ie, do 
leave 'ragged' right 

4. Do not use type size less 
than 10 points. (See 

reduction samples 

5. All text, tables, and 
figures must fit into the 
rectangle shown. 

6. Submit 2 clean copies. 
This form may be photo- 
copied if multiple 
abstracts are to be 

Mail original & 

1 photocopy 

(along with postage-paid 

postcard) to 

Respiratory Care 
Open Forum 

11030 Abies Lane 
Dallas TX 75229-4593 

Early deadline is 

March 15. 1995 

(abstract received) 

Final deadline is 

May 27. 1995 

{abstract postmarked) 

Presenter's Name & Credentials 

Presenter's Mailing Address 

Presenter's Voice Phone & Fax 

Corresponding Author's Name & Credentials 

Corresponding Author's Mailing Address 

Corresponding Author's Voice Phone & Fax 

This is 14-point type, with 
necessary reduction. 

This is 12-poinl type, with 
necessary reduction. 

This is 10-pointtype, 
with necessary reduction 


Manuscript-Preparation Instructions for 
Authors and Typists 

General Information 

Respiratory Care welcomes original manuscripts related to res- 
piratory care and prepared according to these Instructions. 
Perfection is not required, but efforts in that direction are appre- 
ciated. Computer diskette submissions are encouraged and may 
reduce processing and review time. See requirements in these 

Editorial consultation is available by telephone or letter at any 
stage of planning or writing. Specific guidance (in printed form) 
will be provided on request for writing a research paper, a case 
report, an evaluation, a review, overview, or update or a book 
review; for converting to and from SI units: and for in-house 
manuscript review. For typists, a model manuscript, list of jour- 
nal name abbreviations, and copy of these Instructions is avail- 
able. Write to Respiratory Care, 1 1030 Abies Lane, Dallas TX 
75229-4593, call (214) 243-2272, or fax (214) 484-6010. 

Manuscripts are reviewed by authoritative referees in a double- 
blind manner. Accepted manuscripts may be copyedited for 
clarity and style; authors receive galleys to proofread before 
publication. Published papers are copyrighted by the publisher 
and may not be published elsewhere without permission. 

Publication Categories 

Research Article: A report of an original investigation (a study). 
Evaluation of Device/Method/Technique: A description and 
evaluation of an old or new device, method, technique, or modi- 

Case Report: A report of a clinical case that is uncommon, or 
was treated in a new way, or is exceptionally instructive. All 
authors must have been associated with the case. A case-manag- 
ing physician must either be an author or furnish a letter approv- 
ing the manuscript. 

Review Article; A comprehensive, critical review of the litera- 
ture and state-of-the-art summary of a pertinent topic that has 
been the subject of at least 40 published research articles. 
Overview: A critical review of a pertinent topic about which not 
enough has been published to merit a Review Article. 
Update: A report of subsequent developments in a topic that has 
been critically reviewed in this journal or elsewhere. 
Point of View Paper: A paper expressing personal but substan- 
tiated opinions on a pertinent and controversial topic. 
Special Article: A pertinent paper not fitting one of the forego- 
ing categories may be acceptable as a Special Article. It is advis- 

able to consult the Editor before writing or submitting such a 

Editorial: A paper drawing attention to a pertinent concern; it 
may present an opposing opinion, clarify a position, or bring a 
problem into focus. 

Letter: A signed communication about prior publications in this 
journal or about other pertinent topics. Tables and illustrations 
may be included. Type double-spaced, supply a title, mark "For 

Blood Gas Corner: A brief, instructive case report involving 
respiratory care blood data — with questions, answers, discussion. 
PFT Corner: Like Blood Gas Comer, but involving pulmonary 
function tests. 

Test Your Radiologic Skill: Like Blood Gas Comer, but involv- 
ing pulmonary medicine radiography and including one or more 
radiographs, may involve imaging techniques other than conven- 
tional chest radiography. 

Review of Book, Film, Tape, or Software: A balanced, critical 
review of a recent release. 


Prior and Duplicate Publication: Work that has been pub- 
lished or accepted elsewhere usually should not be submitted. 
In special instances, the Editor may consider such material, pro- 
vided that permission to publish is given by the author and other 
publisher. Please consult the Editor before submitting such 

Authorship: All persons listed as authors should have partici- 
pated in the reported work and the shaping of the manuscript; all 
should have proofread the submitted manuscript; and all should 
be able to publicly discuss and defend the paper's content. A 
paper with collective (corporate) authorship must specify the key 
persons responsible for the article. Authorship is not justified 
solely on the basis of solicitation of funding, collection or analy- 
sis of data, provision of advice, or similar services. Persons per- 
forming such ancillary services may be recognized in the 
Acknowledgments section. 

Conflict of Interest: Authors of research or evaluation papers, 
points of view, or editorial are asked to disclose on the manu- 
script's title page any liaison or financial arrangement they may 
have with a manufacturer or distributor whose product figures 
in the submitted manuscript or with the manufacturer or dis- 
tributor of a competing product. (Such arrangements will not 
disqualify a paper from consideration and will not be disclosed 
to reviewers.) 

Respiratory Care • April '95 Vol 40 No 4 


Instructions for Authors & Typists 

Preparation of the Manuscript 

Details about Sections: 

Note: in addition to reading these Instructions, authors and typ- 
ists can benefit from inspecting papers recently published in 
Respiratory Care and using them as models. 

General Speciflcations 

Type on one side of white bond paper. 2 16X279 mm (8 in.X 1 1 in.) 
with margins of at least 25 mm (1 in.) on all sides of the page. 
Double-space the entire manuscript (three lines per vertical 
inch). Number all pages in upper-right comers. Indent paragraphs 
5 spaces. Do not justify. Do not underline titles, headings, or 
other words. Do not type authors' naines or other identification 
anywhere except on the title page. Repeat title only (no authors) 
on the abstract page. Begin each of the following on a new page: 
title page, abstract, text, product-sources list, acknowledgments, 
reference list, each table, each appendix, list of figure captions. 
Use standard English. Employ the first person and active voice 
(eg, "We believe that pigs can fly") rather than the 'obscure per- 
son" and passive voice (eg, "It is believed that pigs can fly") — 
because the latter obscures the identity of the responsible party 
(the believer). 

Headings in Text: Center main section headings on the page 
and type them in capital and small letters (eg. Introduction, 
Methods, Results, Discussion). Begin subheadings at the left 
margin and type them in capital and small letters (eg. Patients. 
Equipment, Statistical Analysis). Do not underline or darken 
section headings or subheadings. 

Manuscript Structure 

Most kinds of papers have standard parts in a standard order, as 
shown hereafter. However, papers can vary individually, and not 
all papers will have all the parts listed here. 

Research Article: Title Page, Abstract, Introduction, Methods, 
Results, Discussion, Conclusions, Product Sources, 
Acknowledgments, References, Tables, Appendices, Figure 

Evaluation of Device/Method/Technique: Title Page, Ab- 
stract, Introduction, Description of Device/Method/Technique, 
Evaluation Methods, Evaluation Results, Discussion. 
Conclusions, Product Sources, Acknowledgments, References, 
Tables, Appendices, Figure Legends. 

Case Report: Title Page, Introduction, Case Suminary. 
Discussion, References, Tables, Figure Legends. 

Review Article: Title Page, Table of Contents, Introduction. 
Review of the Literature, State-of-the-Art Summary. 
Acknowledgments, References. Tables, appendices, and illustra- 
tions may be included. Other formats may be suitable. 

Point (if View Paper: Title Page, Text, References. Tables and 
illustrations may be iiKludctl. 

Title: Make the paper's title as specific, clear, and yet as short as 
you can. 

Title Page: (a) title of the paper; (b) full names of all 
authors, with academic and credential letters, professional titles, 
and institutional affiliations; (c) name, address (include building 
and/or room number for courier service), telephone number, and 
Fax number of corresponding author; (d) name and address for 
reprint requests; (e) sources of support such as grants, equipment, 
drugs, and supplies; (f) name of organization, location, and date 
of any meeting at which a version of the paper has been present- 
ed; (g) disclosure of financial relations of any author with com- 
mercial products or interests connected with the paper — or with 
competing products or interests; (h) name, title, and affiliation of 
statistical consultant, if any; and (i) disclaimers, if any. 

Abstract: (required only for research articles and evaluations of 
devices/ methods/techniques). The abstract must summarize 
what was studied; why and how it was studied; the results, 
including important data and statistical significance; and con- 
clusions drawn from the results. All information in the abstract 
must also appear in the paper itself Do not cite references in the 
abstract. The abstract for a research article should include the 
following headings (in all capital letters), appropriately placed 
within the abstract and followed by colons: BACKGROUND, 
paper evaluating a device/method/technique should include the 
following headings: BACKGROUND, DESCRIPTION OF 
RESULTS, CONCLUSIONS. The abstract should be all one 
paragraph, not indented, and not longer than 250 words. Center 
title, typed in capital and lower case letters, over abstract. 

Introduction: Briefly describe the background of the work or 
the paper. Cite only pertinent references, and do not review the 
subject extensively. Do not include data or conclusions from 
the work reported in your paper. In a research paper, end this 
section with a clear statement of the research question(s) or 

Methods Section (in a research paper): Describe the selection of 
patients, controls, or laboratory animals. Give details about ran- 
domization. Describe methods for blinding of observations. Give 
numbers of observations. Report losses to observation (eg, 
dropouts or disqualified subjects), listing numbers of subjects or 
data .sets lost, when lost, and why lost. Describe methods in suf- 
ficient detail to allow other workers to replicate your work. Give 
references to established methods; provide references and brief 
descriptions for methods that have been published but are not 
well known; describe new or substantially modified methods, 
give reasons for using them, and evaluate their limitations. 
Report calibration of measuring devices. 

Drugs — Identify precisely all drugs and chemicals used, giving 
generic names, doses, and routes of administration. If desired, 
brand names may be given in parentheses after generic names. 


Rit.spiRATORY Carp. • Ai'RIL "95 Vol. 40 No 4 

Instructions for Authors & Typists 

Commercial Products — Identify any commercial product 
(including model number if applicable) the first time it is men- 
tioned, giving the manufacturer's name, city, and state or coun- 
try — in parentheses in the text. If four or more products are men- 
tioned, do not list any manufacturers in the text; instead, list them 
on a Product Sources page at the end of the text before the 
References. Provide model numbers when available and manu- 
facturer's suggested price if the study has cost implications. 

Ethics — When reporting experiments on human subjects, indi- 
cate that procedures were in accordance with the ethical stan- 
dards of the institution's committee on human experimentation. 
State that informed consent was obtained after the nature of the 
procedure(s) had been explained. Do not use patient's names, ini- 
tials, or hospital numbers in text or illustrations. When reporting 
experiments on animals, indicate that the institution's or any 
national guide or national law on the care and use of laboratory 
animals was followed. 

Statistics — In the last paragraph of the Methods section, identify 
the statistical tests used in analyzing the data, and give the 
prospectively determined level of significance. Cite references to 
support choices of tests. (Cite textbooks or published articles, not 
handbooks of commercial software.) Identify any general-use or 
commercial computer programs used, naming manufacturers and 
their locations. 

Results Section: Present results in logical sequence in the text. 
Tables and illustrations may also present data. Do not repeat in 
the text all the data in the tables or illustrations; emphasize or 
summarize only important observations and trends. Be sure to 
report all the results; do not save some of them for the Discussion 
section. Do not discuss the findings in the Results section. Exact 
p values are preferred in all cases but are essential when values 
are not statistically significant. Do not report original results 
merely as nonsignificant or NS. 

Discussion Section: It may be useful to restate the research 
question(s), but do not repeat in detail the data or other material 
given in the Introduction, Methods, or Results sections. 
Emphasize the new and important aspects of the study and the 
conclusions that follow from them. Present the implications and 
limitations of the findings — including implications for future 
research. Relate the findings to other relevant published work. 
Link the conclusions with the goals of your work, but avoid 
unqualified statements and conclusions not completely support- 
ed by your data. Avoid claiming priority and alluding to work 
that has not been completed. State new hypotheses when war- 
ranted, but clearly label them as such. Recommendations, when 
appropriate, may be included. Provide a clear 'take-away' mes- 
sage for readers — either at the end of the Discussion section or 
in a separate Conclusions section. 

Product Sources Page: WTien four or more commercial products, 
including statistical software, are mentioned in the paper, list manu- 
facturers' names, cities, and states or countries on a Product Sources 
page after the text. For each kind of product, hst the generic term, 
brand name and model number, manufacturer's name, city, and state 

or country. Manufacturer's suggested price should be included when 
the study or evaluation has cost implications. For example: 

Manual Resuscitators: 

BagEasy, Respironics Inc. Murrysville PA, $20.50 

Code Blue. Vital Signs Inc. Totowa NJ, $19.85 


7200, Puritan-Bennett Corp, Ovedand Park KS 

Bear Cub. Bear Medical Systems. Riverside CA 

Acknowledgments Page: On this page you may recognize the 
services of persons who made ancillary contributions to the work 
or the manuscript. Such .services might be advice about method- 
ology; data collection; statistical advice or analysis; equipment 
selection or operation; cooperation as caregiver, patient, or sub- 
ject; manuscript preparation; in-house review; and other services. 
Each acknowledgment must specify the service rendered. Named 
persons must provide written agreement (accompanying submit- 
ted manuscript) to be so recognized. 


Use of References: References are used to support statements of 
fact, to indicate sources of information, or to guide readers to fur- 
ther information. Be careful to make clear in the text the reason 
for a specific citation (ie, do not imply support of a statement of 
fact by citing a reference that simply addresses the issue). Cite 
only sources that have actually been consulted and evaluated by 
the authors. Cite only published or accepted material. Cite orig- 
inal articles in preference to textbooks, review articles, abstracts, 
editorials, or letters. Avoid citing abstracts because some pub- 
lished abstracts have never been subjected to peer review and 
may not support your contention. Make every effort to determine 
whether an abstract has been subsequently published as a full- 
length paper. Avoid citing non-English language sources. When 
citing from a book, specify the page numbers unless you are cit- 
ing the entire book. If you cite a paper that has been accepted but 
not yet published ("in press"), provide a copy of the paper to the 
Editor when you submit your manuscript. 

Do not cite unpublished observations as references. Instead, identify 
written (not oral) communications in parentheses in the text, giving 
the writer's name and location and the date of the communication. 
Infonnation from manuscripts submitted but not yet accepted should 
be cited in the text (in parentheses) as "unpublished observations." 

Citing References in the Text: The first reference you cite is 
Reference I , the next is Reference 2, etc. After the first citation of 
a reference, use its original number if you cite it again later in the 
paper. Cite references by superscript, full-size, arable numerals. 
Do not enclose in parentheses. If a citation numeral is located at 
the end of a phrase or sentence, place the numeral after (outside) 
the comma, semicolon, or period — not before (inside) it. Avoid 
citing references at the end of a phrase or sentence if they pertain 
only to internal parts of the phrase or sentence; instead, cite them 
at the pertinent places within the phrase or sentence (eg. Hess et 
al'-' discovered that . . .."). 

Respiratory Care • April '95 Vol 40 No 4 


Instructions for Authors & Typists 

Listing References: Starting on a new page after the text, list 
the references in numerical order. Do not employ "op cit" or 
"ibid." Type references double-spaced, using the styles of the 
examples given hereafter. List all authors (do not use "et al"). 
In titles of articles and books, capitalize only first words and 
proper names. Abbreviate journal names as in Index Medicus. 
Spell out in full the names of less well known or nonindexed 
journals and periodicals If the cited item is an abstract, editori- 
al, or letter, identify it as such in parentheses following the 
item's title. Provide both first and last complete page numbers. 
Do not leave spaces between dates and volume and page num- 
bers. Obtain authors' names, article and book titles, dates, and 
volume and page numbers from the original cited articles and 
books, not from other articles' reference lists, which often are 
inaccurate. Examples of correct reference listings follow (these 
are single-spaced here but must be double-spaced in a manu- 

Article in a journal carrying pagination throughout 

1. Shepherd KE, Johnson DE. Bronchodilator testing: an 
analysis of paradoxical responses. Respir Care 1988; 

Article in publication that numbers every issue beginning 
with Page 1: 

2. Bunch D. Establishing a national database for home care. 
AARC Times 1991:15(Mar):61,62,64. 

Corporate author journal article: 

3. American As.sociation for Respiratory Care. Criteria for 
establishing units for chronic ventilator-dependent patients 
in hospitals. Respir Care 1988:33:1044-1046. 

Article in journal supplement: (Journals differ in their methods 
of numbering and identifying supplements. Supply sufficient 
information to allow retrieval.) 

4. Reynolds HY. Idiopathic interstitial pulmonary fibrosis. 
Chest 1986:89(3, Suppl):139s-143s. 

Abstract in journal: (Abstracts are not strong references. 
Abstracts more than 3 years old should not be cited. When cited, 
abstracts should be identified as such.) 

5. Stevens DP. Scavenging ribavirin from an oxygen hood to 
reduce environmental exposure (abstract). Respir Care 

Editorial in journal: 

6. Rochester DF. Does respiratory muscle rest relieve fatigue 
or incipient fatigue? (editorial). Am Rev Respir Dis 

Editorial with no author given: 

7. High frequency ventilation (editorial). Lancet 1991: 
1 : 706-708. 

Letter in journal: 

8. Smith DE, Herd D, Gazzard BG. Reversible bronchocon- 
striction with nebulised pentamidine (letter). Lancet 

Paper accepted but not yet published: 

9. Hess D. New therapies for asthma. Respir Care (year, in 

Personal author book: (Specific pages should be cited whenev- 
er possible.) 

10. Nunn JF. Applied respiratory physiology. New York: 
Appleton-Century Crofts, 1969. 

Note: To specify pages in a book, place a colon after the year and 
then list the page(s). Examples: 1969:85 (one page), 1969:85-95 
(series of contiguous pages), 1969:85,95 (separated pages). 

Corporate author book: (Specific pages should be cited when- 
ever possible.) 

1 1 . American Medical Association Department of Drugs. 
AMA drug evaluations, 3rd ed. Littleton CO: Publishing 
Sciences Group, 1977. 

Book with editor(s): (Specific pages should be cited whenever 

12. Guenter CA, Welch MH, editors. Pulmonary medicine. 
Philadelphia: JB Lippincott, 1977. 

Chapter in book: (Specific pages should be cited whenever pos- 

13. Pierce AK. Acute respiratory failure. In: Guenter CA, 
Welch MH. editors. Pulmonary medicine. Phildelphia: JB 
Lippincott. 1977:171-223. 

Newspaper article: 

14. Rensberger B, Specter B. CFCs may be destroyed by nat- 
ural process. The Washington Post 1988 Aug 7;Sect 
A:2(Col 5). 

Dictionary or similar reference: 

15. Pneumohemopericardium. Dorland's illustrated medical dic- 
tionary, 26th ed. Philadelphia: WB Saunders, 1981: 1038. 

Tables: Use tables to display information, compare data, or show 
trends. Start each table on a separate page. Do not construct a 
table with fewer than two lines (rows) or columns of data 
(instead, put the data in the text). Avoid more than 8 columns 
across. Number tables as Table 1, Table 2, etc. consecutively in 
the order of their first mention in the text. Place the number and 
a descriptive title above the table (not on a separate page). Give 
each column a brief heading. Place explanatory matter in foot- 
notes, not in the title or column headings. Explain in footnotes all 
nonstandard abbreviations and symbols used in the table. To key 
footnotes to the table body, use conventional designations (aster- 


Respiratory Care • April '95 Voi. 40 No 4 

Instructions for Authors & Typists 

isk, dagger, double dagger, etc) in consistent order, placing them 
superscript in the table body. 

Double-space all elements of tables, including titles, column 
headings, data, and footnotes. Continue a deep table on following 
pages. Do not use horizontal or vertical rules. Do not submit 
tables as photographs, or reduced in size, or on oversize paper. 
Use the same typeface as in the text. Supply the name and ver- 
sion of any table-building computer program used. 

Appendices: Mathematical calculations, documents, and other 
matter that would clutter the main article can be displayed in 
appendices. Number them as Appendix 1. Appendix 2, etc, and 
refer to them in the text. Give each appendix a descriptive title 
and type it double-spaced throughout. 

Illustrations: Graphs, line drawings, photographs, and radi- 
ographs are called figures. Use only illustrations that clarify and 
augment the text. Number them consecutively as Fig. 1, Fig. 2, 
etc, according to the order in which they are first mentioned in 
the text. Figures for publication must be of professional quality, 
but rough sketches may accompany the submitted manuscript, 
with final figures to be prepared after review. Figures need not be 
photographic reproductions. Clear, clean laser-printer-generated 
figures are acceptable (121-144 dpi). However, the data from 
which the original graphs are generated should be available to the 
editor upon request. Remember that originals that are roughly 7 
5 9 inches will be reduced to less than 50% (3 5 4 in) and origi- 
nals with a horizontal dimension of 9 in will be reduced to less 
than 33%. Photographs must be glossy 5 5 7 to 8 5 10-inch black 
and white prints, unless color is essential. (If color is essential, 
consult the Editor to learn whether negatives, transparencies, or 
prints are required.) In reports of animal experiments, use 
schematic drawings, not photographs. A letter of consent must 
accompany any photograph in which a possibility of identifica- 
tion of a person exists; masking the eyes is not sufficient. 
Lettering and numerals must be neat, uniform in size and style, 
and large enough to remain legible when downsized for publica- 
tion. Do not place titles and detailed explanations on figures; put 
such information in the figure captions. Identify each figure on 
the back with a stick-on label showing figure number, an arrow 
indicating the top, and an abbreviated manuscript title. Omit 
author's name. Cover label with clear tape so ink will not 
smudge other prints. Do not use staples or paper clips, and do not 
write heavily on the backs of prints. 

Radiographs: If possible, submit radiographs as full-size 
copies of films, not as prints. Prints may be acceptable, but full- 
size films are preferable in order to display better detail in pub- 
lished figures. Be sure all figures are cited in the text. If any fig- 
ure has been published before, include copyright-holder's written 
permission to use it. 

Figure Captions: Its caption should, to the extent possible, 
make a figure understandable without referring the reader to the 
text. Type figure captions double-spaced, on a separate page, as 
Fig. 1, Fig. 2, etc. When symbols, arrows, numbers, or letters are 
used to identify parts of a figure, identify and explain each part 
clearly in the caption. In photomicrographs, explain the internal 
scale and method of staining. If a figure has been published 

before, acknowledge the original source in its caption (permis- 
sion must be obtained prior to use, of course). 

Units of Measurement: Give measurements of length, height, 
weight, and volume in metric units appropriately abbreviated. 
Give temperatures in degrees Celsius. Give blood pressures in 
millimeters of mercury (mm Hg). Report hematologic and clini- 
cal-chemistry measurements in conventional metric system and 
in SI units (International System of Units). Show gas pressures 
(including blood gas tensions) in torr. List SI equivalent values, 
when possible, in brackets following non-SI values — for exam- 
ple, "PEEP, 10 cm H20 [0.981 kPa]." For conversion to SI, see 
Respiratory Care 1988;33:861-873 (Oct 1988) and 
1989;34:145(Feb 1989). 

Arithmetic: Carefully double-check all arithmetic before sub- 
mitting the paper. Accuracy is the author's responsibility; errors 
are common! 

Abbreviations and Symbols: Use standard abbreviations and 
symbols. Avoid creating new abbreviations. Avoid all abbrevia- 
tions in the title and unusual abbreviations in the abstract. Use an 
abbreviation only if the term occurs several times in the paper. 
Write out the full term the first time it appears, followed by the 
abbreviation in parentheses. Thereafter, employ the abbreviation 
alone. Never use an abbreviation without defining it. Standard 
units of measurement can be abbreviated without explanation 
(eg, 10 L/min, 15 torr, 2.3 kPa). If you employ a great many 
abbreviations and symbols, provide a double-spaced list of them, 
with their definitions, in alphabetical order. 

Please use the following forms: cm H20 (not cmH20), f (not 
bpm), L (not 1), L/min (not LPM, l/min, or 1pm). mL (not ml), 
mm Hg (not mmHg), pH (not Ph or PH), p > 0.001 (not p>0.001 ), 
s (not sec), Sp02 (pulse oximetry saturation). 

Computer Diskettes: A manuscript may be submitted on a 
Macintosh or IBM-compatible diskette. Macintosh documents on 
3.5 in. diskettes written in Microsoft Word versions 4.0 and 5.0 
are preferred. However, we can convert most documents from 
software (including PC-DOS format) to a Macintosh-Microsoft 
Word document. 

Label each diskette with date; author's name; name of word-pro- 
cessing program and version used to prepare documents; and file- 
name(s). If not enough space is available, list contents on disk 
jacket or an attached note. Do not write on a diskette except with 
a felt-tipped pen. 

Tables and figures must be in their own separate files, with soft- 
ware identified. 

Together with diskette, supply three hard copies of the manu- 
script. Do not paperclip a diskette to its hard copy. 

Proofreading and In-House Review: Have all authors proofread 
the manuscript for content accuracy and language. Consider having 
the manuscript reviewed in-house by colleagues before submitting it. 

Respiratory Care • April '95 "Vol 40 No 4 


Instructions for Authors & Typists 

Submitting the Manuscript 

Use the checklist below to make sure the manuscript is ready for 
mailing. Mail three copies of the manuscript and figures to 
Respiratory Care. 1 1030 Abies Lane, Dallas TX 75229-4593. 
Do not Fax manuscripts. Protect figures with cardboard to pre- 
vent bending. A computer diskette submission must be accompa- 
nied by the requisite three hard copies. Keep a copy of the man- 
uscript and figures in your tiles in case of loss. You will be sent 
an acknowledgment that your manuscript has been received. 

Cover Letter: The manuscript must be accompanied by a cover- 
ing letter signed by all the authors. The letter must specify the 
intended publication category and. when there are two or more 
authors, state that "We, the undersigned, have all participated in 
the work reported, proofread the accompanying manuscript, and 
approved its submission for publication." 
Permissions: The manuscript must be accompanied by copies of 
permissions to reproduce published material (figures or tables); 
to use illustrations of or report sensitive personal information 

about, identifiable persons; or to name persons in the 
Acknowledgments section. 

Author's Checklist: 

l.Does paper fit a listed publication category? 
2. Does the cover letter meet specifications? 
3.1s the title page complete? 

4. Is double-spacing used throughout entire manuscript? 

5. Are all pages numbered in upper-right comers? 

6. Are paragraphs indented 5 spaces? 

7. Are all references, figures, and tables cited in the text? 

8. Are references typed in requested style? 

9. Have SI values been provided? 

10. Has all arithmetic been checked? 

1 1. Have generic names of drugs been provided? 

12. Have necessary written permissions been provided? 

13. Have authors" names been omitted from text and figure 

14. Have copies of "in press" references been provided? 

15. Has manuscript been proofread by all authors? 


Rl;.SPIRAT()RY Care • APRIl. "95 VoL 40 No 4 

Notices of competitions, scholarships, fellowships, examination dates, new educational programs, and the like will be listed here free of 
charge. Items for the Notices section must reach the Journal 60 days before the desired month of publication (January 1 for the March issue, 
February 1 for the April issue, etc). Include all pertinent information and mail notices to RESPIRATORY CARE Notices Depl. 1 1030 Abies 
Lane. Dallas TX 75229-4593. 


June 30 Deadline for Arcf Fellowiships 

The Allen and Hanburys Fellowship for Asthma Education provides $3,500 to allow completion of a 
project encompassing asthma self-management or asthma awareness. The Fellowship also provides airfare and 
one night's lodging to attend the Awards Ceremony at the AARC Annual Convention. 

Three $1,000 fellowships are available. In addition to the cash award, each includes airfare and one night's 
lodging to attend the Awards Ceremony at the AARC Annual Convention. 

• The Lifecare Fellowship is designed to foster projects dealing with mechanical ventilation, especially out 
side of the ICU. 

• The Monaghan/Trudell Fellowship is designed to support projects dealing with the development of cost- 
effective aerosol delivery. 

• The Respironics Fellowship is designed to foster projects dealing with noninvasive ventilatory support. 
For details and specifications for application, contact Lynn Perkins or Joy Rea in the AARC Executive Office 
by phone (214) 243-2272 or FAX (214) 484-2720. 


Vail, Colorado July 14-16, 1995 


October 1-7, 1995 

Open Forum 1995 

It's time to submit your abstracts for possible presentation at the OPEN FORtJM during the AARC Annual 
Meeting in Orlando. Florida, December 2-5, 1995. For information on changes to the rules/instructions, see 
Page 445 of this issue. 

THE NATIONAL BOARD FOR RESPIRATORY CARE— 1995 Examination and Fee Schedule 




July 15. 1995 
November 1 1, 


June 3, 1995 
December 2, 1995 


May 1. 1995 
September 1, 1995 

February I, 1995 
August I, 1995 




June 3, 1995 

April 1, 1995 


December 2, 1995 

September 1, 1995 

Fee Schedule 


— new applicant: 
— reapplicant: 
RRT Wntten and Clinical Simulation 
— new applicant: 
— reapplicant: 
Written Registry Only 
— new applicant; 
Clinical Simulation Only — new & reapplicant: 

— new applicant: 
— reapplicant: 

— new applicant: 
— reapplicant: 
Perinatal/Pediatric Specialty 
— new applicant: 

$ 90.00 
$ 60.00 


$ 90.00 
$ 60.00 

$ 80.00 



CRTT Recredenlialing: 

RRT Recredenlialing: 
Written Registry Examination 
Clinical Simulation Examination 

CPFT Recredentialing: 

RPFT Recredentialing; 

P/P Specialty Credentialing: 

Membership Renewal: 

Credential Verification 
Replacement Certificate 
Copy of NBRC Directory: 1994 

Active Credentialed Practitioners 
Copy of NBRC 1994 Listing of All 

Credentialed Practitioners 




$ 60.00 


$ 60.00 




$ 80.00 





$ 12.00 

$ 2.00 

$ 15.00 

$ 6.00 

$ 25.00 


$ 25.00 


$ 25.00 

8310 Neiman Road • Lenexa, Kansas 66214 • (913) 599-4200 



of Events 

Nol-for-profu organiralions are offered a free advertisement of up to eight lines to appear, on a spaee-available basis, in Calendar of Events in 
Respiratory Care Ads for other meetings are priced at $5.50 per line and require an insertion order. Deadline is the 20th of (he month two 
months preceding the month in which you wish the ud to run, .Submit copy and insertion orders to Calendar of Events, RESPIRATORY CARE. 
I Hl.W Abies Lane, Dallas TX 75229-4593. 


April 12-14 in Overland Park, Kansas. The Kansas 
Respiratory Care Society announces tlie 18th Annual 
Educational Seminar at the Overland Park Marriott, The seminar, 
entitled "Ch , , , Ch , , , Ch , , . Changes in Respiratory Care — Now 
and in the Future," looks at health-care reform as it relates to the 
respiratory care profession. This program is approved for 10 
Category I CRCE credit hours. Contact Pat Munzer, 351 
Woodbury Lane, Topeka KS 66606, (800) 332-0291, extension 

April 17-19 in Bellevue, Washington. The Respiratory Care 
Society of Washington announces the 22nd Annual Pacific 
Northwest Regional Respiratory Care Conference at the 
Bellevue Red Lion Inn, Management, pediatrics, and education 
are featured subjects. The latest in health care equipment will be 
on display for two days. For a brochure, contact Bob Bonner, 
Chair, Health, Education, and PE Division, Highline Com- 
munity College, PO Box 98000, Des Moines WA 98198. (206) 
878-3710, ext 469. 

April 19-21 in Rapid City, South Dakota. The SDRC holds its 
annual convention, with featured speakers including David 
Pierson MD and Jack Wanger MBA RPFT RRT. Mechanical 
ventilation, health care reform, pulmonary function testing, and 
respiratory care protocols are among the topics addressed. The 
program has been approved for 13 hours of CRCE credit. 
Contact Kevin Marr or Michelle O'Toole at (605) 341-8307, 

April 25-28 in Cincinnati, Ohio. Region 11 for Respiratory 
Care (encompassing the Ohio, Kentucky, and Indiana societies) 
hosts its 22nd Annual Meeting, "Charting New Waters," at the 
Albert B Sabin Convention Center and Hyatt Regency Hotel. 
Contact Jeff Jones RRT, 1995 Chairman of Region II, at (513) 

May 10-12 in South Padre Island, Texas. The Rio Grande 
Valley District of the TSRC presents its annual seminar at the 
Sheraton Beach Resort. Featured topics include neonatal and 
adult critical care and methods to enhance development of criti- 
cal pathways, CRCE credit has been requested. The registration 
fee, which includes a banquet ticket, is $50; the cost of the 
scheduled fishing trip is extra. Contact TSRC, PO Box 2048, 
Harlingen TX 7855 1 , The deadline for discount room confirma- 
tion at the Sheraton is April 9; call the resort at (800) 672-4747, 
and iiicnlion ihc seminar to receive a discount rate. 

May 17-19 in Kl Paso, Texas. The Southwest Region of the 
TSRC presents its 24th Annual Seminar at the El Paso Airport 
Hilton The theme is "Thriving in an lira of Change": CRCE 

credit has been requested. Contact Carmen Castillo at Sierra 
Medical Center (915) 747-2771. 

July 14-16 in Vail, Colorado. The AARC presents the Summer 
Forum, with eiTiphasis on management and education topics. 
Consult the April issue of AARC Times for program details and 
registration information. 


April 27-28 in Las Vegas, Nevada. The American Lung 
Association (ALA) of Nevada hosts the 10th Annual 
Respiratory Health Conference at the Tropicana Resort & 
Casino. Contact the ALA of Nevada at (702) 454-2500. 

May 2-3 in Little Rock, Arkansas. Arkansas Children's 
Hospital presents the Diamond Conference on the hospital cam- 
pus. Focus sessions on redefining physiotherapy and redirecting 
ventilatory strategies feature presentations and panel discus- 
sions. Roundtable lunch discussions are also planned. Selected 
abstracts have been chosen for slide presentation. Contact Mike 
Anders RRT at (501) 320-3535 or fax (501 ) 320-341 1. 

May 5-6 in Orlando, Florida. The Alpha, National 
Association (alphapantitrypsin deficiency) hosts its 1995 
National Conference at the Radisson Plaza Hotel, Featured top- 
ics include surgical choices for alpha, patients, new products, 
and alphaj-related diseases. Contact Alpha, National 
Association, 1829 Portland Ave, Minneapolis MN 55404, (612) 

May 20-24 in Seattle, Washington. The American Thoracic 
Society hosts its annual International Conference, featuring a 
variety of symposia and workshops on the prevention and con- 
trol of lung disease. Contact 1995 International Conference, 
American Thoracic Society, 1740 Broadway, New York NY 

June 16-19 in Toronto, Ontario, Canada. The Canadian 
Society of Respiratory Therapists (CSRT) announces its 30th 
Educational Forum at the Royal York Hotel. Workshop topics 
cover management, ventilation, cardiopulmonary diagnostics, 
lung transplantation, and research. Call (416) 368-251 1 or fax 
(416) 368-2884 for more infoimation. 

October 29-Noveniber 2 in New York, New York. The 61st 
Annual International Scientific Assembly sponsored by the 
American College of Chest Physicians (ACCP) at the New York 
Hilton and Towers is entitled "Chest 1995: Prevention and 
Diagnosis of Chest Disease." Contact the ACCP. 3300 Dundee 
Rd, NoiThhrook 11. 60062-2.348. 


Ri^.siMKAKmv Carl • April '95 Vol 40 No 4 

1 995 Annual Convention 

of the American Association for Respiratory Care 
Orlando, Florida • December 2-5, 1 995 

By Tony DalNogare, MD 

ARDS was originally 

described in 1967 and nas 

since undergone much 

scrutiny. This review of ARDS 

discusses the latest 

developments in risk factors 

and treatment. Also covers the 

5 diagnostic criteria that must 

be present to make an accurate 

diagnosis of ARDS, including 

clinical, radiographic, and 

physiologic criteria. 

Item VT31 

VHS (60 minutes) 
%'5S (nonmember $40). 

Add $3.25 tor shipping. 

Call (214) 243-2272 or 

Fax your order to 


American Association for 
Respiratory Care 

11030 Abies Ln. 
Dallas, TX 75229-4593 

Prices subject to change without notice. 

With the 


Service Card, 

you can stop 

searching and 

start buying. 

Get the facts 

on all the 
products and 


advertised in 

this issue 

easily and quickly. 

The computerized 


Service Card 

does it all. 

Simply fill in your 

name and 

address, check 

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boxes, and mail 

or fax it. 


in This Issue 

Aufderheide. Tom P 364 

Bames, Thomas A 346 

Bishop, Michael J 393 

Caims. Marilyn A 444 

Chandra. Nisha C 380 

Durbin. Charles G Jr 335 

Halperin, Henry R 380 

Lawrence. Gretchen 444 

Levin. Howard R 380 

Masferrer. Ray 332 

Milisch, Robert A 438 

Op't Holt. Tim 442 

Pepe. Paul E 427 

Rau. Joseph L Jr 404 

Rayburn. Barry K 380 

Rho. Davids 438 

Sanders. Arthur B 338 

Schell, Sheila A 438 

Tsitlik, Joshua E 380 

in This Issue 

Allen & Hanburys 325-327 

Arbor Technologies 329 

Army Nurse Corps 329 

DHD Diemolding Healthcare Div 314 

Drager Critical Care 321 

HealthScan Products Inc 316; 330-331 

HRInc 322 

Puritan-Bennett Corp Cover 3 

Respironics 319 

Sherwood Medical Cover 4 

Siemens Medical Systems Inc Cover 2 


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II...I.I.I.. .1.1.. 1.11,1. ..I.. I.I.I. I.I. ...II..I..II 

Metabolic monitoring 




El B3Ca □!□ Q 

It's never been easier to have indirect calorimetry for 
your ventilated patients. Easy to use, accurate, and 
continuous, the Puritan-Bennett 7250™ Metabolic 
Monitor works integrally with the 7200' Series Ventilator 
to make metabolic monitoring easy for you. 

i^M^btain information with ease. The 7250 Monitor 
self-calibrates automatically, has a simple 5-key 
interface and requires no water traps or dessicant. 

i Make patient care decisions with accurate 
information. The 7250 Monitor has been validated under 
a broad range of ventilator settings including: FIO2 up 
to 0.8, 20 cmHzO PEEP, and when Flow-by or Pressure 
Control Ventilation is active. 

See the effect of patient activity throughout the 
day with continuous values. The 7250 Monitor measures 
metabolic values continuously, averaging at intervals of 
your choice (from breath-to-breath up to 72 hours) and 
intelligently suppressing artifacts in the data. 

Contact your local Puritan-Bennett representative for 
more information about the 7250 Metabolic Monitor. 
Or, call 1-800-255-6773. 

The 7250 Metabolic Monitor is covered by U.S. patents 5,072,737 and 5,325,861. Other 
patents pending in the U.S.A. and other countries. 7200 is a registered trademarit, and 
7250 is a trademarl< of Puritan-Bennett. 

WE'RE In It For Life 

Circle 83 on reader service card 

3 NEW Technologies in Arterial Blood Sampling 


Arterial Blood Gas System 

NEW, Advanced ASPIR-PULSE Syringe 

Patented design improves filling for both 
Aspiration and Pufsation techniques 

NEW, Purge Guard^ 

One-Handed Safety Needle Venting System 

Patent-pending design allows OneHanded operation 
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Guard the needle point and immediately free the 
other hand to apply pressure at the puncture site 

NEW, Total Ca++ Lyte™ 

Precision Heparin 

A breakthrough patented heparin to maximize the 
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See your Sherwood Medical OR, /Critical Care Sales Representative or call 1-8 

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1-325-7472 for a complete listing of