Full text of "Respiratory care : the official journal of the American Association for Respiratory Therapy"

APRIL 2000
VOLUME 45

^^^^^^^^^^^HHI^^^^^^^^H

A MONTHLY SCIENCE JOURNAL

44TH YEAR— ESTABLISHED 1956

aJ\ #^

EDITORIALS

Conflict of Interest and Respiratory Care

M%.

ORIGINAL CONTRIBUTIONS

46th International Respiratory Congress

Effects of Respiratory Impedance on the

October 7-10 • Cincinnati, Ohio

Performance of Bi-Level Pressure Ventilators

Reevaluation of Continuous Oxygen Therapy

After Initial Prescription in COPD Patients

Spirometry in Normal Subjects in Sitting,

Prone, and Supine Positions

CASE REPORTS

Persistent Left Superior Vena Cava

1999 DONALD F EGAN SCIENTIFIC LECTURE

Weaning from Mechanical Ventilation: What

Have We Learned?

Introducing the low-volume surfactant.*

Curosurf has established itself as the #1 selling surfactant in Europe'
and has saved thousands of infants born with RDS since 1992.
Now, it's available in the United States.

Curosurf permits you to reduce the volume of administration 37%
(initial dose) and 68% (repeat dose) compared to Survanta® (beractant)
and 12% (initial dose) and 55% (repeat dose) compared to infasuri*
(calfactant).*

Curosurf permits fewer dosing positions and a longer interval between
doses (12 hours) than the market leader.-** For administration, brief
disconnection of the endotracheal tube from the ventilator is required.

Infants receiving Curosurf should receive frequent clinical and laboratory
assessments so that oxygen and ventilator support can be modified to
respond to respiratory changes.

Transient adverse effects seen with the administration of Curosurf
include bradycardia, hypotension, endotracheal tube blockage, and
oxygen desaturation.

Curosurf is conveniently available in two vial sizes (1 .5 mL and 3.0 mL).

We'd like to share the whole clinical story with you. Please call us
at 800-755-5560 or visit us at our Web site wvvav.deyinc.com

*Clinical studies have not evaluated if low volume or convenience
features result in superior safety or efficacy on clinically relevant
endpoints.

New for RDS!

GurosurF

(poractant alfa)

Intratracheal Suspension

DEY 2751 Napa Valley Corporate Drive Napa, CA 94558 Please see brief prescribing information on adjacent page.

Circle 138 on product info card

New for RDS!

GurosurF /^ %

(poractant a If a)

Intratracheal Suspension

fccUROSURFj

Pr (poractant altalf
*t Sitratr.iiheal '
5 Suspension

ICUROSLRf

[poraci-int M
lntratr,Ktie.it ■-
Suspension

NDC Number

Description

Concentration

(mE/mL)

mL/Vial

Units
Per Carton

49502-1 80-01 Curosurf

49502-180-03 Curosurf

CUROSURF^

(poractant alfa)

INTRATRACHEAL SUSPENSION

Brief Summary: Please see full package Insert for full prescribing information.

INDICATION AND USAGE

CUROSURF is indicated for the treatment (rescue) of Respiratory Distress Syndrome
(RDS) in premature infants. CUROSURF reduces mortality and pneumothoraces
associated with RDS.

CLINICAL STUDIES

The clinical efficacy of CUROSURF was demonstrated in one single-dose study (Study
1) and one multiple-dose study (Study 2) in the treatment of established neonatal RDS
involving approximately 500 infants. Each study was randomized, multicenter, and con-
trolled. REFER TO PACKAGE INSERT FOR STUDY DESCRIPTION RESULTS.

ACUTE CLINICAL EFFECTS

As with other surfactants, marked improvements in oxygenation may occur within
minutes of the administration of CUROSURF

WARNINGS

CUROSURF is intended for intratracheal use only

THE ADMINISTRATION OF EXOGENOUS SURFACTANTS, INCLUDING
CUROSURF CAN RAPIDLY AFFECT OXYGENATION AND LUNG COMPLIANCE.
Therefore, infants receiving CUROSURF should receive frequent clinical and laborato-
ry assessments so that oxygen and ventilatory support can be modified to respond to
respiratory changes. CUROSURF should only be administered by those trained and
experienced in the care, resuscitation, and stabilization of pre-term infants.

TRANSIENT ADVERSE EFFECTS SEEN WITH THE ADMINISTRATION OF
CUROSURF INCLUDE BRADYCARDIA, HYPOTENSION, ENDOTRACHEAL TUBE
BLOCKAGE, AND OXYGEN DESATURATION. These events require stopping
Curosurf administration and taking appropriate measures to alleviate the condition.
After the patient is stable, dosing may proceed with appropriate monitoring.

PRECAUTIONS
General

Correction of acidosis, hypotension, anemia, hypoglycemia, and hypothermia is rec-
ommended prior to CUROSURF administration.

Surfactant administration can be expected to reduce the severity of RDS but will not
eliminate the mortality and morbidity associated with other complications of prematurity.

Sufficient infomation is not available on the effects of administering initial doses of
CUROSURF other than 2.5 mL/kg (200 mg/kg), subsequent doses other than
1.25 mL/kg (100 mg/kg), administration of more than three total doses, dosing more fre-
quently than every 12 hours, or initiating therapy with CUROSURF more than 15 hours
after diagnosing RDS. Adequate data are not available on the use of CUROSURF in
conjunction with experimental therapies of RDS, e.g., high-frequency ventilation.

CARCINOGENESIS, MUTAGENESIS, IMPAIRMENT OF FERTIUTY

Studies to assess potential carcinogenic and reproductive effects of CUROSURF or
other surfactants, have not been conducted.

Mutagenicity studies of CUROSURF which included the Ames test, gene mutation
assay in Chinese hamster V79 cells, chromosomal abenation assay in Chinese ham-
ster ovarian cells, unscheduled DMA synthesis in HELA S3 cells, and in vivo mouse
nuclear test, were negative.

ADVERSE REACTIONS

Transient adverse effects seen with the administration of CUROSURF include brady-
cardia, hypotension, endotracheal tube blockage, and oxygen desaturation.

80
80

1.5
3

The rates of common complications of prematurity observed in Study 1 are shown
below in Table 3.

TABLE 3

COMPLICATIONS OF PREMATURITY

CUROSURF 2.5 mUkg

CONTROL**

(200 mg/kg)

n=66

n=78

Acquired Pneumonia

Acquired Septicemia

Bronchopulmonary

Dysplasia

Intracranial Hemorrhage

Patent Ductus Arteriosus

Pneumothorax

Pulmonary Interstitial

Emphysema

"Control patients were disconnected from the ventilator and manually ventilated for 2
minutes. No surfactant was instilled.

Immunological studies have not demonstrated differences in levels of surfactant-anti-
surfactant immune complexes and anti-CUROSURF antibodies between patients
treated with CUROSURF and patients who received control treatment.

OVERDOSAGE

There have been no reports of overdosage following the administration of CUROSURF.

In the event of accidental overdosage, and only if there are clear clinical effects on the
infant's respiration, ventilation, or oxygenation, as much of the suspension as possible
should be aspirated and the infant should be managed with supportive treatment, with
particular attention to fluid and electrolyte balance.

Dosing Precautions

Transient episodes of bradycardia, decreased oxygen saturation, reflux of the surfac-
tant into the endotracheal tube, and airway obstruction have occurred during the dos-
ing procedure of CUROSURF These events require interrupting the administration of
CUI^OSURF and taking the appropriate measures to alleviate the condition. After sta-
bilization, dosing may resume with appropriate monitoring.

HOW SUPPLIED

CUROSURF* (poractant alfa) Intratractieal Suspension (NDC Numbers: 49502-
180-01 [1.5 mLj; 49502-180-03 [3 mL]) is available in sterile, ready-to-use rubber-stop-
pered clear glass vials containing 1.5 mL (120 mg phospholipids) or 3 mL (240 mg
phospholipids) of suspension. One vial per carton.

Rx only

,DEYs

Manufactured for DEY by

Cliiesi Farmaceutid, S.p.A.

26/A Via Palermo & 96 Via San Leonardo

Parma. Italy 43100

03-572-00(BRS) 2/00

1 . IMS Retail and Provider Perspective 2/00. 2. Refer to Survanla* prescribing information.
Survanta* is a registered trademarl( of Ross Products Division. Infasurf is a registered trademark of
Forest Phamiaceuticals, Inc.

signal ^tradlpon pulee oximet;ry

..:^-/^:- ■- ■.■4'.immi-~>- ^ ^

• The only pulse oximetry technology clinically
proven accurate during motion and low perfusion

• Virtually eliminates false alarms

• More reliable in detecting true alarms

Continuous monitoring (no freezing or alarm management)

accurate monitoring wi-ien you need it most

motion etudy

low perfuBion etudy

SpO; System ^

•Mwi

OXISMART XL

N-395

N-200

SpO^System ^llffliof

I OXISMART

1 N-295

N-200

True Hypoxemias Missed

37%

47%

True Hypoxemias IVIissed 0%

33.3%

33.3<'/<

False Aiarms

18%

57%

Drop Out Rate 0.8%

9.9%

9rlormance of Three Pi

17.8«/<

iilse Oximolt

Motion on llw

} Portormance of 17 Pi

ilse Oximeters.

Source: 8ark(

)r SJ. NovaK S. Morgan S. The P<

riwiwinuu ■•! pwsiBi lorm ai ine aocieiy lof lecnnoiogy in Anestrtesioiogy (STA) meeting in Durino Low Pi
Orlando, FL. January 2000.

Briusion in Volunleers. Aneslhesii

3logy 1997:87(3A):A40

wxAfw. masimo.com

Instruments and sensors timtaininf,' Masinio SKI' t('chn(il());.v aiv idcnlificH with the Masimo SET logo.
Look Cor the Masimo SKT desiRnntion to cnsuic accurate pidse oximetry when needed most.

02000 Mii«im<.C.».|».nilirm. MiwitnoJiKT and on> fiilfrall) ru|<i«K!nHl triuli'iimrkn of Mii»iiiiii Cciriirmilioii. OXISMAUT XL. N.:ltl.'i. N-ml .iiirl N-axi iir.' Inufi-nm

Circle 131 on product info card

i4iii:Ba:ii:B»M

FOR INFORMATION,
CONTACT:

AARC Membership or Other AARC
Services

American Association for

Respiratory Care

11030 Abies Ln

Dallas TX 75229-4593

(972) 243-2272 • Fax (972) 484-2720

http;//www.aarc.org

Therapist Registration or
Technician Certification

National Board for Respiratory

Care

8310Nieman Rd

Lenexa KS 66214

(913) 599-4200 • Fax (913) 541-0156

http://www.nbrc.org

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Programs

Committee on Accreditation for

Respiratory Care

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Euless TX 76040

(817) 283-2835 • Fax (817) 354-8519

http://www.coarc.com

Grants, Scholarships, Community
Projects

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Foundation

11 030 Abies Ln

Dallas TX 75229-4593

(972) 243-2272 • Fax (972) 484-2720

Government Affairs —

Cheryl West MHA (703-548-8506)

State Government Affairs —

Jill Eicher MPA (703-548-8538)
1225 King St, Second Floor
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Fax (703) 548-8499

RE/PlRATORy
Q\RE

RESPIRATORY CARE (ISSN 0020-1324. USPS 0489-
190) is published monthly by Daedalus Enterprises Inc. at
1 1030 Abies Lane, Dallas TX 75229-4593. for the Amer-
ican Association for Respiratory Care. One volume is
published per year beginning each January. Subscription
rates are $75 per year in the US; $90 in all other countries
(for airmail, add $94).

The contents of the Journal are indexed in Hospital and
Health Administration Index, Cumulative Index to Nurs-
ing and Allied Health Literature, EMBASE/Exerpta Med-
ica, and RNdex Library Edition. Abridged versions of
RESPIRATORY CARE are also published in Italian,
French, and Japanese, with permission from Daedalus En-
terprises Inc.

Periodicals postage paid at Dallas TX and at additional
mailing offices. POSTMASTER: Send address changes to
RESPIRATORY CarE, Membership Office. Daedalus En-
terprises Inc, 1 1030 Abies Lane. Dallas TX 75229-4593.

@ Text printed on acid-free paper.

Printed in the United States of America

APRIL 2000 / VOLUME 45 / NUMBER 4

EDITORIALS

Conflict of Interest and RESPIRATORY CARE
by David J Pierson — Seattle, Washington

ORIGINAL CONTRIBUTIONS

388

Effects of Respiratory Impedance on the Performance of

Bi-Level Pressure Ventilators

by Alexander B Adams, Peter L Bliss, and John Hotchkiss — St Paul, Minnesota

Reevaluation of Continuous Oxygen Therapy After Initial Prescription

in Patients with Chronic Obstructive Pulmonary Disease

by Yuji Oba, Gary A Salzman, and Sandra K Willsie — Kansas City, Missouri

390

401

spirometry in Normal Subjects in Sitting, Prone, and Supine Positions ** j m

by Gary M Vilke, Theodore C Chan, Tom Neuman, and Jack L Clausen — San Diego, California 407

CASE REPORTS

411

417

Persistent Left Superior Vena Cava: Case Report and Literature Review

by Bipin D Sarodia and James K Stoller — Cleveland. Ohio

1999 DONALD F EGAN SCIENTIFIC LECTURE

Weaning from Mechanical Ventilation: What Have We Learned?
by Martin J Tobin — Maywood, Illinois

LETTERS TO THE EDITOR

Are Digital Distance Learners Learning or Just Distant?

by Keith B Hopper— Atlanta, Georgia * » a

response by Shelley C Mishoe — Augusta, Georgia "f i L

BOOKS, FILMS, TAPES, & SOFTWARE

Fatal Asthma (Sheffer AL, editor)

reviewed by Randy Baker — Augusta, Georgia

Emergency Asthma (Brenner BE, editor)
reviewed by Jay D Eisenberg — Portland, Oregon

Clinical Simulations in Respiratory Care (Barnes TA)

reviewed by Glen R Kuck — Lama Linda, California

Basic Clinical Lab Competencies for Respiratory Care:
An Integrated Approach, 3rd ed (White GC)

reviewed by Jeff Anderson — Boise, Idaho

437
439
439

440

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iHlli:lfl:^:il»M

CONTINUED,

ALSO
IN THIS ISSUE

447

AARC Membership ^^^H
Application ^^^|

370

Abstracts from ^^^H
Other Journals ^^^|

456

Advertisers Index ^^^H
& Help Lines ^^H

456

Author ^^^1
Index ^^^1

444

Calendar ^^^|
Events ^^^|

445

Call For Open ^^H
Forum Abstracts ^^H

449

Manuscript ^^H
Preparation Guide ^^H

453

MedWatch ^^M

443

New Products ^^^|

455

Notices ^^^1

RE/PIRATORy
CME

A Monthly Science Journal
Established in 1956

The Official Journal of the

American Association for

Respiratory Care

RESPIRATORY CARE Journal has

been selected by the Literature

Selection Technical Review

Committee of the National Library

of Medicine to be indexed and

included in Index Medicus and

MEDLINE, which is available online

in the U.S. and throughout the

world. All articles in the Journal

beginning with the January 2000

issue will be included.

Win A Free Tri^ to the

2000 AARC International

Respird^ry Qmgress m

Cincinnati, Ohio, October 7-10

All you have to do is request information from the advertisers in this issue.

How to Enter

To receive information from advertisers in this issue, simply fill out the postage-paid
Product Information card and drop it in any US mailbox. Your name will automatically
be entered in a sweepstakes drawing for the Grand Prize which includes round-trip
airfare for two to Cincinnati, Ohio from any domestic US airport, 4 nights, hotel
accommodations, and one registration to the 46th International Respiratory
Congress. To enter you must circle the numbers for the product information that you
would like to receive, and provide all the information requested. Cards may also be
faxed to (609) 786-4415 or enter Online by requesting product information at
http://www.pub-serv.com/rs/m120/ Official Sweepstakes rules may be requested by
e-mail at info@aarc.org.

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The LTVIOOO is ideal for weaning and chronic use, for children and
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EDITORIAL OFFICE

600 Ninth Avenue, Suite 702

Seattle WA 98 104

(206) 223-0558

Fax (206) 223-0563

www.rcjoumal.com

EDITOR IN CHIEF

David J Pierson MD FAARC
Harbon'iew Medical Center
University of Washington
Seattle, Washington

MANAGING EDITOR

Ray Masferrer RRT

ASSISTANT
EDITOR

Katharine Kreilkamp

ASSOCIATE EDITORS

Richard D Branson RRT

University of Cincinnati
Cincinnati, Ohio

Charles G Durbin Jr MD

University of Virginia
Charlottesville, Virginia

Dean R Hess PhD RRT FAARC

Massachusetts General Hospital
Harvard University
Boston, Massachusetts

James K StoUer MD

The Cleveland Clinic Foundation

Cleveland, Ohio

EDITORIAL
ASSISTANT

EDITORIAL BOARD

Linda Barcus

COPY EDITOR

Matthew Mero

PRODUCTION

Kelly Piotrowski

PUBLISHER

Sam P Giordano MBA
RRT FAARC

MARKETING

Dale L Griffiths

Director of Marketing

Tim Goldsbury
Director, Advertising Sales

Beth Binkley
Advertising Assistant

RE/PIRATORy
QVRE

A Monthly Science Journal
Established in 1956

The Official Journal of the

American Association for

Respiratory Care

Alexander B Adams MPH RRT

Regions Hospital
St Paul. Minnesota

Thomas A Barnes EdD RRT
FAARC

Northeastern University
Boston. Massachusetts

Michael J Bishop MD

University of Washington
Seattle, Washington

Bartolome R Celli MD

Tufts University
Boston, Massachusetts

Robert L Chatbum RRT
FAARC

University Hospitals of Cleveland
Case Western Reserve University
Cleveland. Ohio

James B Fink MS RRT FAARC

Hines VA Hospital
Loyola University
Chicago, Illinois

Luciano Gattinoni MD

University of Milan
Milan. Italy

John E Heffner MD

Medical University of South Carolina
Charleston. South Carolina

Mark J Heulitt MD

University of Arkansas
Little Rock, Arkansas

SECTION EDITORS

Leonard D Hudson MD

University of Washington
Seattle. Washington

Robert M Kacmarek PhD RRT
FAARC

Massachusetts General Hospital
Har\'ard University
Boston, Massachusetts

Toshihiko Koga MD

Koga Hospital
Kuruine, Japan

Marin HKoUefMD
Washington University
St Louis, Missouri

Patrick Leger MD
Clinique Meaicale Edouard Rist
Paris. France

Neil R Maclntyre MD FAARC
Duke University
Durham. North Carolina

John J Marini MD

University of Minnesota
St Paul, Minnesota

Shelley C Mishoe PhD RRT
FAARC

Medical College of Georgia
Augusta, Georgia

Marcy F Petrini PhD

University of Mississippi
Jackson, Mississippi

Joseph L Rau PhD RRT FAARC

Georgia State University
Atlanta, Georgia

Catherine SH Sassoon MD

University of California Irvine
Long Beach, California

John W Shigeoka MD

Veterans Administration Medical Center

Salt Lake City, Utah

Arthur S Slutsky MD

University of Toronto
Toronto, Ontario, Canada

Martin J Tobin MD

Loyola University
Chicago, Illinois

Jeffrey J Ward MEd RRT
Mayo Medical School
Rochester, Minnesota

Robert L Wilkins PhD RRT
Loma Linda University
Loma Linda, California

STATISTICAL CONSULTANT

Gordon D Rubenfeld MD

University of Washington
Seattle. Washington

Hugh S Malhewson MD
Joseph L Rau PhD RRT FAARC
Drug Capsule

Charles G Irvin PhD

Gregg L Ruppel MEd RRT RPFT FAARC

PFT Comer

Richard D Branson RRT
Robert S Campbell RRT FAARC
Kittredge 's Comer

Jon Nilsesnien PhD RRT FAARC
Ken Hargett RRT
Graphics Comer

Patricia Ann Doorley MS RRT
Charles G Durbin Jr MD
7"^^/ Your Radiologic Skill

Hols of the Trade

Learn more about the topics presented in this issue.

Bi-Level Pressure Ventilation

NPPV in Acute and Long-Term Care

Addresses patient selection guidelines, when to initiate NPPV,
clinical applications of NPPV, ventilator and interface selections,
modes of ventilaiton, weaning strategies, and complications and
limitations. By Donna Wemhoff, BS, RRT, CPFT. 40-min. audiotape.
Item PAD866 $15.00 ($20.00 Nonmembers)

Application of Positive Airway Pressure Without Intubation
Covers short-term application in the inpatient setting in the
treatment of acute, life-threatening conditions and elective, long-
term application in home care. Includes a discussion of bi-level
positive airway pressure. Featuring Robert M. Kacmarek, PhD,
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Item VC32 $49.95 ($99.00 Nonmembers)

COPD

Chronic Obstructive Pulmonary Disease (COPD) Simulation

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The Latest Word in the Treatment of COPD

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Spirometry
Diagnostic Training and Competence Assessment Manual for
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Pulmonary Diagnostics Section features: quality control, diffusing
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Uniform Reporting Manual for Diagnostic Services
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This manual identifies diagnostic procedures commonly
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Its 219 pages contain nine sections with 149 procedures including
procedure descriptions, time standards, applicable clinical practice
guidelines; and suggested CPT codes. Spiral-bound book, 1999.
Item PM88 $99.00 ($135.00 Nonmembers)

Basic Spirometry and Pulmonary Function Testing

Discusses the rationale for the use of basic PFT and the techniques
and use of the basic forced exhalation spirograph. Details how
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capacities and presents the use of the spirogram as a method to
document the difference between obstructive and restrictive lung
disorders. CAI Software. Requires Windows 3.1 or higher.
Item PELS $65.00 (multi-installation license is an additional $65.00

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Abstracts

Summaries of Pertinent Articles in Other Journals

Editorials, Commentaries, and Reviews to Note

End of Life Decisions in Intensive Care — Levin PD, Sprung CL. Intensive Care Med 1999
Sep;25(9):893-895.

Ultrasound-Aided Thoracentesis in Intensive Care Patients — Keske U. Intensive Care Med
1999 Sep;25(9):896-897.

Proportional Assist Ventilation — Kuhlen R, Rossaint R. Intensive Care Med 1999 Sep;25(9):

1021-1023.

Wean from the Tube Not Necessarily from the Ventilator — Bach JR. Chest 1999 Nov;l 16(5);
1498-1499.

Athletes and Doping: Effects of Drugs on the Respiratory System — Dekhuijzen PN, Machiels
HA, Heunks LM, van Der Heijden HF, van Balkom RH. Thorax 1999 Nov;54(l 1):1041-1046.

The Wizard of Odds: Bayes Theorem and Diagnostic Testing — Diamond GA. Mayo Clin Proc
1999 Nov;74(ll);l 179-1 182.

Medical Innovation and the Critical Role of Health Technology Assessment — Perry S, Thamer
M. JAMA 1999 Nov 17;282(19):1869-1872.

Extracorporeal Membrane Oxygenation for Patients with Refractory Ventricular Arrhyth-
mias — Cohen MI, Gaynor JW, Ramesh V, Karl TR, Steven JM, Posner J, et al. J Thorac
Cardiovasc Surg 1999 Nov;l 18(5):961-963.

Pulmonary Placental Transmogrification: Diagnosis and Treatment — Brevetti GR, Clary-
Macy C, Jablons DM. J Thorac Cardiovasc Surg 1999 Nov;l 18(5):966-967.

Using the Intubating Laryngeal Mask Airway (LMA-Fastrach) for Blind Endotracheal
Intubation in Patients Undergoing Cervical Spine Operation — Nakazawa K, Tanaka N, Ish-
ikawa S, Ohmi S, Ueki M, Saitoh Y, et al. Ane.sth Analg 1999 Nov;89(5):1319-1321.

Randomized, Controlled Trial of Low-Dose
Inhaled Nitric Oxide in the Treatment of
Term and Near-Term Infants with Respira-
tory Failure and Pulmonary Hypertension —

Cornfield ON, Maynard RC, deRegnier RA,
Guiang SF 3rd, Barbato JE, Milla CE. Pediat-
rics 1999 Nov, 104(5 Pt 1): 1089- 1094.

Recent reports indicate that inhaled nitric oxide
(iNO) causes selective pulmonary vasodilation,
increases arterial oxygen tension, and may de-
crease the use of extracorporeal membrane ox-
ygenation (ECMO) in infants with persistent
pulmonary hypertension of the newborn
(PPHN). Despite these reports, the optimal dose
and timing of iNO administration in PPHN re-
mains unclear. OBJECTIVES: To test the hy-
potheses that in PPHN 1) iNO at 2 parts per
million (ppm) is effective at acutely increasing
oxygenation as measured by oxygenation index

(OI); 2) early use of 2 ppm of iNO is more
effective than control (0 ppm) in preventing
clinical deterioration and need for iNO at 20
ppm; and 3) for those infants who fail the initial
treatment protocol (0 or 2 ppm) iNO at 20 ppm
is effective at acutely decreasing OI. STUDY
DESIGN: A randomized, controlled trial of iNO
in 3 nurseries in a single metropolitan area.
Thirty-eight children, average gestational age
of 37.3 weeks and average age < 1 day were
enrolled. Thirty-five of 38 infants had echocar-
diographic evidence of pulmonary hypertension.
On enrollment, median OI in the control group,
iNO at ppm, (n = 23) was 33.1, compared
with 36.9 in the 2-ppm iNO group (n = 15).
RESULTS: Initial treatment with iNO at 2 ppm
for an average of 1 hour was not associated
with a significant decrease in OI. Twenty of 23
(87%) control patients and 14 of 15 (92%) of
the low-dose iNO group demonstrated clinical

deterioration and were treated with iNO at 20
ppm. In the control group, treatment with iNO
at 20 ppm decreased the median OI from 42.6
to 23.8, whereas in the 2-ppm iNO group with
a change in iNO from 2 to 20 ppm, the median

01 did not change (42.6 to 42.0). Five of 15
patients in the low-dose nitric oxide group re-
quired ECMO and 2 died, compared with 7 of
23 requiring ECMO and 5 deaths in the control
group. CONCLUSION: In infants with PPHN,
iNO 1): at 2 ppm does not acutely Improve
oxygenation or prevent clinical deterioration,
but does attenuate the rate of clinical deterio-
ration; and 2) at 20 ppm acutely Improves ox-
ygenation in infants Initially treated with ppm,
but not In infants previously treated with INO at

2 ppm. Initial treatment with a subtherapeutic
dose of INO may diminish the clinical response
to 20 ppm of iNO and have adverse clinical
sequelae.

370

Respiratory Care • April 2000 Vol 45 No 4

Incorporating Palliative Care into Critical
Care Education: Principles, Challenges, and
Opportunities (review) — Danis M, Federman
D, Fins JJ. Fox E. Kastenbaum B, Lanken FN,
et al. Crit Care Med 1 999 Sep;27(9):2005-20 1 3.

OBreCTIVE: To identify the goals and meth-
ods for medical education about end-of-life care
in the intensive care unit (ICU). DATA
SOURCES AND STUDY SELECTION: A sta-
tus report on palliative care, a summary report
of recent research on palliative care education,
articles in the medical literature on end-of-life
care and critical care, and expert opinion were
considered. DATA EXTRACTION: A working
group, including specialists in critical care, pal-
liative care, medical ethics, consumer advocacy,
and communications, was convened at the
"Medical Education for Care Near the End of
Life National Consensus Conference." A mod-
ified nominal group process was used to de-
velop a consensus. DATA SYNTHESIS: In the
ICU, life and death decisions are often made in
a crisis mode or in the face of uncertainty, and
may necessitate the withholding and withdrawal
of life-supporting technologies. Because criti-
cal illness often diminishes the capacity of pa-
tients to make decisions, clinicians must often
make decisions in conjunction with surrogates,
rather than with patients. Discontinuity of care
can threaten trusting relationships, and cultural
diversity can have a particularly powerful im-
pact on choices for care. In the face of these
realities, it is possible and appropriate to give
compassionate palliative care to dying patients
and their families in the ICU. CONCLUSIONS:
Teaching care of the dying in the ICU should
emphasize the following: a) the goals of care
should guide the use of technology; b) under-
standing of prognostication and treatment with-
holding and withdrawal is essential; c) effective
communication and trusting relationships are
crucial to good care; d) cultural differences
should be acknowledged and respected; and e)
the delivery of excellent palliative care is ap-
propriate and necessary when patients die in the
ICU.

Results of a Collaborative Quality Improve-
ment Program on Outcomes and Costs in a
Tertiary Critical Care Unit — Clemmer TP,
Spuhler VJ. Oniki TA. Horn SD. Crit Care Med
1999Sep;27(9):1768-1774.

OBJECTIVE: To demonstrate that by using the
knowledge and skills of the primary care pro-
vider and by applying statistical and scientific
principles of quality improvement, outcomes
can be improved and costs significantly reduced.
DESIGN: A before and after quasi-experimen-
tally designed trial using historical controls plus
an analysis of costs in areas not influenced by
intensive care unit (ICU) practice to control for
possible secular changes. SETTING: A tertiary
ICU. PATIENTS: All patients admitted to the

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above-mentioned ICU from January 1, 1991,
through December 31, 1995. INTERVEN-
TIONS: a) A focused program that applied sta-
tistical and scientific quality improvement pro-
cesses to the practice of intensive care, b) An
organized effort to modify the culture, thinking,
and behavior of the personnel who practice in
the ICU. MEASUREMENTS: Severity of ill-
ness. ICU and hospital lengths of stay. ICU and
hospital mortality rates, total hospital costs as
analyzed by the cost center, and measures of
improvement in specific areas of care. MAIN
RESULTS: Significant improvement in glucose
control, use of enteral feeding, antibiotic use,
adult respiratory distress syndrome survival, lab-
oratory use, blood gases use, radiograph use,
and appropriate use of sedation. A severity ad-
justed total hospital cost reduction of $2,580,98 1
in 1991 dollars when comparing 1995 with the
control year of 1991. with 87% of the reduction
in those cost centers directly influenced by the
intervention. CONCLUSIONS: A focused qual-
ity improvement program in the ICU can have
a beneficial impact on care and simultaneously
reduce costs.

Lung Transplantation in Very Young In-
fants— Huddleston CB, Sweet SC. Mallory GB,
Hamvas A, Mendeloff EN. J Thorac Cardio-
vasc Surg 1999 Nov;II8(5):796-804.

INTRODUCTION: Established successes with
adult lung transplantation have laid the founda-
tion for extension of this therapeutic modality
to infants and children dying of end-stage pul-
monary disease. The purpose of this report is to
convey our experience with 19 infants under-
going lung transplantation before the age of 6
months. METHODS: Six patients with predom-
inantly pulmonary vascular disease and 13 pa-
tients with primarily pulmonary parenchymal
disease have undergone bilateral sequential lung
transplantation at our institution since 1990.
Mean age at transplant was 104 ± 44 days, and
mean weight was 4.9 ± 1.6 kg. RESULTS:
Although early mortality (32%, 6/19) was higher
than that previously reported for older pediatric
age groups, long-term survival was similar (44%
at a maximum follow-up of 6 years). Although
anastomotic complications and infections oc-
curred at a rate approximating that seen in older
pediatric age groups, episodes of acute rejec-
tion appear to occur with decreased frequency.
Similarly, at a mean follow-up of 3 years, only
2 (15%) of 13 long-term survivors have evi-
dence of bronchiolitis obliterans. The functional
residual capacity, as measured on infant pulmo-
nary function tests, has gradually increased as
the children have grown, suggesting that lung
growth is occurring. CONCLUSIONS: Bilat-
eral lung transplantation is a viable alternative
in infants dying of end-stage pulmonary dis-

Respiratory Care • April 2000 Vol 45 No 4

371

Abstracts

ease. Efforts directed toward avoiding the com-
plications that lead to early posttransplant mor-
tality combined with the seemingly lower
incidence of early and late rejection may pro-
vide long-term results better than those in other
age groups.

Clinical Predictors and Outcomes for Pa-
tients Requiring Tracheostomy in the Inten-
sive Care Unit— Kollef MH, Ahrens TS, Sh-
annon W. Crit Care Med 1999 Sep;27(9):1714-
1720.

OBJECTIVE: To identify clinical predictors for
tracheostomy among patients requiring mechan-
ical ventilation in the intensive care unit (ICU)
setting and to describe the outcomes of patients
receiving a tracheostomy. DESIGN: Prospec-
tive cohort study. SETTING: Intensive care units
of Barnes-Jewish Hospital, an urban teaching
hospital. PATIENTS: 52 1 patients requiring me-
chanical ventilation in an ICU for >12 hours.
INTERVENTIONS: Prospective patient sur-
veillance and data collection. MEASURE-
MENTS AND MAIN RESULTS: The main
variables studied were hospital mortality, dura-
tion of mechanical ventilation, length of stay in
the ICU and the hospital, and acquired organ-
system derangements. Fifty-one (9.8%) patients
received a tracheostomy. The hospital mortality
of patients with a tracheostomy was statistically
less than the hospital mortality of patients not
receiving a tracheostomy (13.7% vs. 26.4%; p =
0.048), despite having a similar severity of ill-
ness at the time of admission to the ICU (Acute
Physiology and Chronic Health Evaluation
[APACHE] II scores. 19.2 ± 6.1 vs. 17.8 ±
7.2; p = 0.173). Patients receiving a tracheos-
tomy had significantly longer durations of me-
chanical ventilation ( 1 9.5 ± 15.7 days vs. 4. 1 ±
5.3 days; p < 0.001) and hospitalization (30.9 ±
18.1 days vs. 12.8 ± 10.1 days; p < 0.001)
compared with patients not receiving a trache-
ostomy. Similarly, the average duration of in-
tensive care was significantly longer among the
hospital nonsurvivors receiving a tracheostomy
(n = 7) compared with the hospital nonsurvi-
vors without a tracheostomy (n = 124; 30.9 ±
16.3 days vs. 7.9 ± 7.3 days; p < 0.001). Mul-
tiple logistic regression analysis demonstrated
that the development of nosocomial pneumonia
(adjusted odds ratio |AOR], 4.72; 95% confi-
dence interval |CI1, 3.24-6.87; p < 0.001), the
administration of aerosol treatments (AOR,
3.00; 95% CI, 2.184.13; p < 0.001), having a
witnessed aspiration event (AOR, 3.79; 95%
CI, 2.30-6.24; p = 0.008). and requiring rein-
tubation (AOR. 2.21; 95% CI, 1.. 54-3. 18; p =
0.028) were variables independently associated
with patients undergoing tracheostomy and re-
ceiving prolonged ventilatory support. Among
the 44 survivors receiving a tracheostomy in
the ICU, 38 (86.4%) were alive 30 days after
hospital discharge and 31 (70.5%) were living
at home. CONCLUSIONS: Despite having

longer lengths of stay in the ICU and hospital,
patients with respiratory failure who received a
tracheostomy had favorable outcomes compared
with patients who did not receive a tracheos-
tomy. These data suggest that physicians are
capable of selecting critically ill patients who
most likely will benefit from placement of a
tracheostomy. Additionally, specific clinical
variables were identified as risk factors for pro-
longed ventilatory assistance and the need for
tracheostomy.

Determination of Airway Humidiflcation in
High-Frequency Oscillatory Ventilation Us-
ing an Artificial Neonatal Lung Model: Com-
parison of a Heated Humidifler and a Heat
and Moisture Exchanger — Schiffmann H,
Singer S, Singer D, v Richthofen E, Rathgeber
J, Zuchner K. Intensive Care Med 1999 Sep;
25(9):997-1002.

Objective: Thus far only few data are available
on airway humidiflcation during high-frequency
o,scillatory ventilation (HFOV). Therefore, we
studied the performance and efficiency of a
heated humidifier (HH) and a heat and moi.sture
exchanger (HME) in HFOV using an artificial
lung model. Methods: Experiments were per-
formed with a pediatric high-frequency oscilla-
tory ventilator. The artificial lung contained a
sponge saturated with water to simulate evap-
oration and was placed in an incubator heated
to 37 degrees C to prevent condensation. The
airway humidity was measured using a capac-
itive humidity sensor. The water loss of the
lung model was determined gravimetrically. Re-
sults: The water loss of the lung model varied
between 2.14 and 3.1 g/h during active humid-
ification; it was 2.85 g/h with passive humidi-
fication and 7.56 g/h without humidification.
The humidity at the tube connector varied be-
tween 34. 2 and 42.5 mg/L, depending on the
temperature of the HH and the ventilator setting
during active humidification, and between 37
and 39.9 mg/L with passive humidification.
Conclusion: In general, HH and HME are .suit-
able devices for airway humidification in HFOV.
The performance of the ventilator was not sig-
nificantly influenced by the mode of humidifi-
cation. However, the adequacy of humidifica-
tion and safety of the HME remains to be
demonstrated in clinical practice.

Application of Mortality Prediction Systems
to Individual Intensive Care Units — Patel PA.
Grant BJ. Intensive Care Med 1999 Sep;25(9):
977-982.

Objective: To evaluate the predictive accuracy
of the severity of illness scoring systems in a
single institution. Design: A prospective study
conducted by collecting data on consecutive pa-
tients admitted to the medical intensive care
unit over 20 months. Surgical and coronary care
admissions were excluded. Setting: Veterans Af-

fairs Medical Center at Buffalo, New York. Pa-
tients and participants: Data collected on 302
unique, consecutive patients admitted to the
medical inten.sive care unit. Interventions: None.
Measurements and results: Data required to cal-
culate the patients" predicted mortality by the
Mortality Probability Model (MPM) II. Acute
Physiology and Chronic Health Evaluation
(APACHE) 11 and Simplified Acute Physiology
Score (SAPS) 11 scoring systems were collected.
The probability of mortality for the cohort of
patients was analyzed using confidence interval
analyses, receiver operator characteristic (ROC)
curves, two by two contingency tables and the
Lemeshow-Hosmer chi-square statistic. Pre-
dicted mortality for all three scoring sy.stems
lay within the 95% confidence interval for ac-
tual mortality. For the MPM II, SAPS II and
APACHE II, the c-index (equivalent to the area
under the ROC curve) was 0.695 ± 0.0307 SE,
0.702 ± 0.063 SE and 0.672 ± 0.0306 SE,
respectively, which were not statistically differ-
ent from each other but were lower than values
obtained in previous studies. Conclusion: Al-
though the overall mortality was consistent with
the predicted mortality, the poor fit of the data
to the model impairs the validity of the result.
The observed outcoume could be due to erratic
quality of care, or differences between the study
population and the patient population in the orig-
inal studies. The data cannot be u.sed to distin-
guish between these possibilities. To increase
predictive accuracy when studying individual
intensive care units and enhance quality of care
assessments it may be necessary to adapt the
model to the patient population.

Improved Prognosis of Acute Respiratory
Distress Syndrome 15 Years On — Jardin F,
Fellahi J. Beauchet A. Vieillard-Baron A. Lou-
bieres Y. Page B. Intensive Care Med 1999
Sep;25(9):9.36-941.

Objective: Evaluation of the impact of low-vol-
ume, pressure-limited ventilation on the recov-
ery rate of acute respiratory distress syndrome
(ARDS). Design: Prospective observational
clinical study with historical control. Setting:
University hospital intensive care unit (ICU).
Patients: We studied two groups of. respectively,
33 and 37 ARDS patients separated by 15 years
("historical". June 1978-April 1981. and "re-
cent". October 1 993-June 1 996). Method: ARDS
was defined as the presence of bilateral chest
infiltrates and a Pao./Fio. ■'^''o of less than 200
mm Hg under controlled ventilation regardless
of PEEP level. Any cardiac participation was
excluded by right heart catheterization in the
"historical" group and by echo-Doppler exam-
ination in the "recent" group. The origin of
ARDS was principally pulmonary (ARDS,,) in
both groups (26/33 and 29/37. respectively), and
secondarily extrapulmonary (ARDS^^p) (7/33
and 8/37, respectively ). In the "historical" group,
normocapnia was the major goal for respiratory

372

Respiratory Care • April 2000 Vol 45 No 4

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Abstracts

support and was achieved in all patients regard-
less of airway pressure levels. In contrast, end-
inspiratory plateau pressure in the "recent"
group was limited to 30 cmHjO under respira-
tory support, regardless of P^^o, level. The "his-
torical" and "recent" ARDS groups were com-
pared with regard to therapeutic procedure and

outcome. Results: Normalization of P„

,(36:

6 mm Hg) in the "historical" group required
high airway pressure (end-inspiratory plateau
pressure at 39 ± 4 cm HjO) and high tidal
volume (13 mL/kg). Respiratory support used
in the "recent" group was less aggressive, with
lower airway pressure (end-inspiratory plateau
pressure 25 ± 4 cm H^O) and tidal volume (9
mL/kg) resulting in "permissive" hypercapnia
(51 ± 10 mm Hg).Mortality rates significantly
decreased from 64 % in the "historical" group
to 32 % in the "recent" group (p < 0.01). This
decrease concerned only ARDSp, which was
markedly predominant in both groups. Conclu-
sion: Mortality due to ARDS of pulmonary or-
igin has declined in our unit over the last 15
years. Low-volume, pressure-limited (protec-
tive) ventilation seems the most likely reason
for improved survival, despite hypercapnia.

Withdrawal of Life Support: Who Should
Decide? Differences in Attitudes among the
General Public, Nurses and Physicians —

Sjokvist P, Nilstun T, Svantesson M, Berggren
L. Intensive Care Med 1 999 Sep;25(9):949-954.

Objective: To examine the attitudes of the gen-
eral public regarding who should decide about
the withdrawal of life support and to compare
these attitudes with those of intensive care per-
sonnel. Design: Nationwide postal questionnaire
survey. Setting: Sweden. Participants: One thou-
sand one hundred ninety-six randomly selected
persons from the Swedish population register,
339 nurses and 121 physicians from 29 ran-
domly selected intensive care units (ICUs). Mea-
surements and results: Respondents' answers to
questions related to two clinical scenarios: one
with a conscious and competent patient and one
with an unconscious patient. The response rates
were 64% for the general public, 86% for the
nurses and 88% for the physicians. Concerning
the competent patient, 48% of the public, 31%
of the nurses and 8% of the physicians were of
the opinion that a decision about continued ven-
tilator treatment should be made by the patient
alone or together with the family, but without
the physician. The vast majority of physicians
(87%) wanted to make the decision themselves,
either alone or together with the patient or fam-
ily. Concerning the incompetent patient, 73%
of the general public and 70% of the nurses
advocated a joint decision made by the family
and the physician together. The majority of the
physicians (61%) regarded themselves as the
sole decision-maker, a view supported by only
5% of the public and 20% of the nurses. Con-
clusions: While existing Swedish guidelines rec-

ommend that the physician should be the sole
decision-maker, the general public favour more
patient and family influence on the decision to
withdraw life support as compared with inten-
sive care physicians.

Advances in Respiratory Monitoring during
Mechanical Ventilation — Jubran A. Chest
1999 Nov; 116(5): 14 16- 1425.

This review provides an update on the various
techniques that are available to monitor patients
during mechanical ventilation with an emphasis
on clinical observations and applications in crit-
ically ill patients.

Prevalence, Etiologies and Outcome of the
Acute Respiratory Distress Syndrome among
Hypoxemic Ventilated Patients — Roupie E,
Lepage E, Wysocki M, Fagon J, Chastre J, Drey-
fuss D, et al. Intensive Care Med 1999 Sep;
25(9):920-929.

Objective: To evaluate the prevalence and out-
come of the acute respiratory distress syndrome
(ARDS) among patients requiring mechanical
ventilation. Design: A prospective, multi-insti-
tutional, initial cohort study including 28-day
follow-up. Settings: Thirty-six French intensive
care units (ICUs) from a working group of the
French Intensive Care Society (SRLF). Patients:
All the patients entering the ICUs during a 14-
day period were screened prospectively. Hy-
poxemic patients, defined as having a Pao,/Fio2
ratio (P/F) of 300 mmHg or less and receiving
mechanical ventilation, were classified into
three groups, according to the Consensus Con-
ference on ARDS: group I refers to ARDS (P/F:
200 mm Hg or less and bilateral infiltrates on
the chest X-ray); group 2 to acute lung injury
(ALI) without having criteria for ARDS (200 <
P/F • 300 mm Hg and bilateral infiltrates) and
group 3 to patients with P/F of 300 mm Hg or
less but having exclusion criteria from the pre-
vious groups. Results: Nine hundred seventy-
six patients entered the ICUs during the study
period, 43 % of them being mechanically ven-
tilated and 213 (22 %) meeting the criteria for
one of the three groups. Among all the ICU
admissions, ARDS, ALI and group 3 patients
amounted, respectively, to 6.9 % (67), 1.8 %
(17) and 13.3 % (129) of the patients, and rep-
resented 31.5 %, 8.1 % and 60.2 % of the hy-
poxemic, ventilated patients. The overall mor-
tality rate was 41 % and was significantly higher
in ARDS patients than in the others (60 % vs 3 1
% p < 0.01). In group 3, 42 patients had P/F
less than 200 mm Hg associated with unilateral
lung injury; mortality was significantly lower
(40.5 %) than in the ARDS group. In the whole
group of hypoxemic, ventilated patients, septic
shock and severity indices but not oxygenation
indices were significantly associated with mor-
tality, while the association with immunosup-
pression revealed only a trend (p = 0.06). Con-

clusions: In this survey we found that very few
patients fulfilled the ALI non-ARDS criteria
and that the mortality of the group with ARDS
was high.

Risk Factors for Central and Obstructive
Sleep Apnea in 450 Men and Women with
Congestive Heart Failure — Sin DD, Fitzger-
ald F, Parker JD, Newton G, Floras JS, Bradley
TD. Am J Respir Crit Care Med 1999 Oct;
160(4):1 101-1 106.

In previous analyses of the occurrence of cen-
tral (CSA) and obstructive sleep apnea (OSA)
in patients with congestive heart failure (CHF),
only men were studied and risk factors for these
disorders were not well characterized. We there-
fore analyzed risk factors for CSA and OSA in
450 consecutive patients with CHF (382 male,
68 female) referred to our sleep laboratory. Risk
factors for CSA were male gender (odds ratio
[OR] 3.50; 95% confidence interval [CI], 1.39
to 8.84), atrial fibrillation (OR 4.13; 95% CI
1.53 to 1 1. 14), age > 60 yr (OR 2.37; 95% CI
1.35 to 4.15), and hypocapnia (Pco, < 38 mm
Hg during wakefulness) (OR 4.33; 95% CI 2.50
to 7. 52). Risk factors for OSA differed by gen-
der: in men, only body mass index (BMI) was
significantly associated with OSA (OR for a
BMI > 35 kg/m-, 6.10; 95% CI 2.86 to 13.00);
whereas, in women, age was the only important
risk factor (OR for age > 60 yr, 6.04; 95% CI
1.75 to 20.0). We conclude that historical in-
formation, supplemented by a few simple lab-
oratory tests may enable physicians to risk strat-
ify CHF patients for the presence of CSA or
OSA, and the need for diagnostic polysomnog-
raphy for such patients.

Technologic Advances in the Treatment of
Obstructive Sleep Apnea Syndrome — Loube
DI. Chest 1999 Nov;l 16(5): 1426-1433.

Among adult patients with obstructive sleep ap-
nea syndrome (OSAS), adherence to continu-
ous positive airway pressure (CPAP) treatment
is approximately 40%, according to recent well-
designed studies that evaluated outcomes other
than adherence as a primary end point. This
finding suggests the need for the improvement
of the adult OSAS treatment approach, either
by improving adherence to CPAP treatment or
by developing effective alternatives to CPAP.
Technologic advances have allowed for the de-
velopment of new treatments for OSAS that
include automatic CPAP and innovative airway
procedures. Studies evaluating the application
of these new technologies are reviewed. These
technologic advances can be viewed as possible
improvements over the existing treatment ap-
proach only if the risks and benefits of each
new treatment are well understood by OSAS
patients and their physicians.

374

Respiratory Care • April 2000 Vol 45 No 4

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A Randomized Clinical Trial of Continuous
Aspiration of Subglottic Secretions in Car-
diac Surgery Patients — KolletMH. SkubasNJ,
Sundt TM. Chest 1999 Nov;l 16(5): 1339- 1346.

Study objectives: To determine whether the ap-
plication of continuous aspiration of subglottic
secretions (CASS) is associated with a decreased
incidence of ventilator-associated pneumonia
(VAP). DESIGN: Prospective clinical trial.
SETTING: Cardiothoracic ICU (CTICU) of
Barnes- Jewish Hospital, St. Louis, a university-
affiliated teaching hospital. PATIENTS: Three
hundred forty-three patients undergoing cardiac
surgery and requiring mechanical ventilation in
the CTICU. INTERVENTIONS: Patients were
assigned to receive either CASS, using a spe-
cially designed endotracheal tube (Hi-Lo Evac;
Mallinckrodt Inc; Athlone, Ireland), or routine
postoperative medical care without CASS. RE-
SULTS: One hundred sixty patients were as-
signed to receive CASS, and 183 were assigned
to receive routine postoperative medical care
without CASS. The two groups were similar at
the time of randomization with regard to demo-
graphic characteristics, surgical procedures per-
formed, and severity of illness. Risk factors for
the development of VAP were also similar dur-
ing the study period for both treatment groups.
VAP was seen in 8 patients (5.0%) receiving
CASS and in 15 patients (8. 2%) receiving rou-
tine postoperative medical care without CASS
(relative risk, 0.61%; 95% confidence interval,
0.27 to 1 .40; p = 0. 238). Episodes of VAP
occurred statistically later among patients re-
ceiving CASS ([mean ± SD] 5.6 ± 2.3 days)
than among patients who did not receive CASS
(2.9 ± 1 .2 days); (p = 0.006). No statistically
significant differences for hospital mortality,
overall duration of mechanical ventilation,
lengths of slay in the hospital or CTICU, or
acquired organ system derangements were found
between the two treatment groups. No compli-
cations related to CASS were observed in the
intervention group. CONCLUSIONS: Our find-
ings suggest that CASS can be safely adminis-
tered to patients undergoing cardiac surgery.
The occurrence of VAP can be significantly
delayed among patients undergoing cardiac sur-
gery using this simple-to-apply technique.

Inhalation of Nitric Oxide in Acute Lung In-
jury: Results of a European Multicentre
Study — Lundin S, Mang H, Smithies M. Sten-
qvist O, Frostell C. Intensive Care Med 1999
Sep;25(9):91 1-919.

Objective: To determine whether inhalation of
nitric oxide (INO) can increase the frequency
of reversal of acute lung injury (ALI) in nitric
oxide (NO) responders. Design: Prospective,
open, randomised, multicentre, parallel group
phase III trial. Setting: General ICUs in 43 uni-
versity and regional hospitals in Europe. Pa-
tients: Two hundred and sixty-eight adult pa-

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tients with early ALI. Interventions: NO
responders were patients whose Pj,o, increased
by more than 20 % when receiving 0, 2, 10 and
40 ppm of INO for 10 min within 96 h of study
entry. Responders were randomly allocated to
conventional treatment with or without INO.
INO, 1-40 ppm, was given at the lowest effec-
tive dose for up to 30 days or until an end point
was reached. The primary end point was rever-
sal of ALI. Clinical outcome parameters and
safety were assessed in all patients. Results:
Two hundred and sixty-eight patients were re-
cruited, of which 1 80 were randomised NO re-
sponders. Frequency of reversal of ALI was no
different in INO patients (61 %) and controls
(54 %; p > 0.2). Development of severe respi-
ratory failure was lower in the INO (2.2 % )
than controls (10.3 %; p < 0.05). The mortality
at 30 days was 44 % for INO patients, 40 % for
control patients (p > 0.2 vs INO) and 45 % in
non-responders. Conclusions: Improvement of
oxygenation by INO did not increase the fre-
quency of reversal of ALI. Use of inhaled NO
in early ALI did not alter mortality although it
did reduce the frequency of severe respiratory
failure in patients developing severe hypoxae-
mia.

Structural Models for Intermediate Care Ar-
eas (review) — Cheng DC, Byrick RJ. Knobel
E. Crit Care Med 1999 Oct;27(10):2266-2271.

OBJECTIVE: To describe structural models of
intermediate care units used for critically ill pa-
tients. DATA SOURCES: Three multidisci-
plinary units with varying structures and func-
tions of intermediate care areas (ICAs) are
described. DATA SYNTHESIS: Advantages
and limitations for each of the three models are
outlined. The structural models described are
the conventional isolated ICA model, the par-
allel model, and the Integrated model of ICA.
CONCLUSION: Each structural model has ad-
vantages and limitations. Selection of the ap-
propriate ICA model for an institution depends
on the specific circumstances and needs of the
institution. Each of the three models can facil-
itate improved utilization of critical care re-
sources.

The Ventilatory Effects of Auto-Positive End-
Expiratory Pressure Development during
Cardiopulmonary Resuscitation — Woda RP,
Dzwonczyk R, Bernacki BL, Cannon M, Lynn
L. Crit Care Med 1999 Oct;27(10):22I2-22I7.

OBJECTIVE: Auto-positive end-expiratory
pressure (auto-PEEP) is a physiologic phenom-
enon defined as the positive alveolar pressure
that exists at the end of expiration. Normally,
the alveolar pressure is near zero at the end of
expiration. However, certain ventilatory and/or
physiologic paradigms can cause the develop-

Respiratory Care • April 2000 Vol 45 No 4

377

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ment of auto-PEEP during cardiopulmonary re-
suscitation (CPR). Auto-PEEP has a detrimen-
tal cardiovascular effect similar to that of
positive end-expiratory pressure that is inten-
tionally applied to the ventilatory circuit in a
mechanically ventilated patient. The connection
between auto-PEEP and its cardiovascular ef-
fects, however, may go undetected. In this study.
the effect that ventilatory factors have on auto-
PEEP in a simulation of patients with lung dis-
ease undergoing CPR was delineated. DESIGN:
A case control study. SETTING: Laboratory of
a university hospital anesthesia department.
SUBJECTS: A baseline quantification of breath-
ing patterns that occur during CPR was ob-
tained by recording observed respiratory rate
and relative tidal volume during treatment of
in-hospital cardiac arrests. MEASUREMENTS
AND MAIN RESULTS: A test lung was set up
to mimic a series of different airway resistances
and lung compliances as would be seen in dif-
ferent types of pulmonary pathology. A sensi-
tivity analysis was performed on each of the
factors of respiratory rate, tidal volume, and
inspiratory/expiratory ratio as to the effect each
of these factors has on the development of auto-
PEEP. Our study suggests that in various com-
binations of airway resistances and lung com-
pliances. auto-PEEP can be generated to
substantial levels depending on the methods of
ventilation performed. CONCLUSION: We
conclude from our findings that ventilation tech-
niques during CPR may need to be altered to
avoid the development of what may be a he-
modynamically significant level of auto-PEEP.

Neural Network Analysis of the Volumetric
Capnogram to Detect Pulmonary Embo-
lism — Patel MM. Raybum DB. Browning JA,
Kline JA. Chest 1999 Nov:l 16(5):1325-1332.

BACKGROUND: Pulmonary embolism (PE)
produces ventilation/perfusion mismatch that
may be manifested in various variables of the
volume-based capnogram (VBC). We hypoth-
esized that a neural network (NN) system could
detect changes in VBC variables that reflect the
presence of a PE. METHODS: A commercial
VBC system was used to record multiple respi-
ratory variables from consecutive expiratory
breaths. Data from 12 subjects (n = 6 PE-H and
n = 6 PE- ) were used as input to a fully con-
nected back-propagating NN for model devel-
opment. The derived model was tested in a pro-
spective, observational study at an urban
teaching hospital. Volumetric capnograms were
then collected on 53 test subjects: 30 subjects
with PE confirmed by pulmonary angiography
or diagnostic scintillation lung scan, and 23 sub-
jects without PE based on pulmonary angiog-
raphy. The derived NN model was applied to
VBC data from the test population. RESULTS:
Seventeen VBC variables were used by the de-
rived NN model to generate a numeric proba-
bility of PE. When the derived NN model was

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applied to VBC data from the 53 test subjects.
PE was detected with a sensitivity of 100%
(95% CI = 89% to 100%) and a specificity of
48% (95% CI = 27% to 69%). The likelihood
ratio positive [LR(-I-)] for the VBC-NN test
was 1.82 and the LR (-) was 0.1. CONCLU-
SION: This study demonstrates the feasibility
of developing a rapid, noninvasive breath test
for diagnosing PE using volumetric capnogra-
phy and NN analysis.

Inhaled Nitric Oxide Does Not Improve Car-
diac or Pulmonary Function in Patients with
an Exacerbation of Chronic Obstructive Pul-
monary Disease — Baigorri F, Joseph D, Arti-
gas A, Blanch L. Crit Care Med 1999 Oct;
27(10):2153-2158.

OBJECTIVE: To determine whether inhaled ni-
tric oxide (NO) improves right ventricular func-
tion in mechanically ventilated patients with se-
vere chronic obstructive pulmonary disease
(COPD). DESIGN: Open, prospective, con-
trolled trial. SETTING: General intensive care
unit of a community hospital. PATIENTS:
Twelve patients with acute respiratory failure
caused by acute exacerbation of COPD requir-
ing mechanical ventilation. INTERVENTIONS:
Insertion of a pulmonary artery catheter modi-
fied with a rapid response thermistor and a ra-
dial arterial catheter. Nitric oxide was then ad-

ministered to the patient via a T piece placed
between the Y piece of the ventilator and the
endotracheal tube. MEASUREMENTS AND
MAIN RESULTS: Hemodynamic andgasomet-
ric variables were recorded before NO inhala-
tion, during administration of inhaled NO (20
ppm, 20 mins). and 20 mins after NO discon-
tinuation. Inhaled NO reduced pulmonary ar-
tery pressure from 26 ± 6 to 22 ± 5 mm Hg
(p = 0.0004), but arterial oxygenation, cardiac
output, and right ventricular ejection fraction
remained unmodified (41% ± 9% vs. 41% ±
8%; not significant). Calculated pulmonary vas-
cular resistance decreased from 453 ± 233 to
348 ± 108 dyne x sec/cm^ X m^ (p = 0.02),
and right ventricular volumes did not change.
Subsequently, right ventricular end-systolic
pressure/volume ratio decreased from 0.52 ±
0.22 to 0.44 ± 0.19 mm Hg/mL/m" (p = 0.0 1).
No significant correlation was observed between
the changes of pulmonary artery pressure (or
pulmonary vascular resistance) and changes of
right ventricular ejection fraction. CONCLU-
SION: Inhalation of NO does not seem to im-
prove either right ventricular function or arte-
rial oxygenation in patients with acute
respiratory failure caused by acute exacerbation
of COPD.

Temperature Measurement in Critically III
Orally Intubated Adults: A Comparison of

Respiratory Care • April 2000 Vol 45 No 4

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Pulmonary Artery Core, Tympanic, and Oral

Methods— Giuliano KK. Scott SS, Elliot S, Giu-
liano AJ. Crit Care Med 1 999 C)ct;27( 1 0):2 1 88-
2193.

OBJECTIVE: Core temperature measurement
using a pulmonary artery (PA) catheter is con-
sidered the gold standard for measuring tem-
peratures in critically ill patients. The objective
of this study was to compare oral and tympanic
temperature measurements (in both the oral and
core equivalence modes) against PA core tem-
perature measurements to determine which
method was the most accurate and reliable in
the absence of a PA catheter. DESIGN: Pro-
spective, descriptive comparative analysis. PA-
TIENTS: Convenience sample of 102 critically
ill orally intubated patients with a PA catheter
in place. SETTING: A 24-bed medical/surgi-
cal/trauma intensive care unit in a university-
affiliated medical center. INTERVENTIONS:
Four experienced intensive care unit nurses were
trained in the use of temperature measurement
with the oral, tympanic (both core and oral equiv-
alence modes were used), and PA core meth-
ods. Simultaneous temperature measurements
were then taken once in each subject using each
method. The potential covariates that were an-
alyzed were mean blood pressure, patient acu-
ity using the Simplified Acute Physiology Score
II, age, sex, ambient rixjm temperature, and ven-
tilator circuit temperature. MEASUREMENTS
AND MAIN RESULTS: The training period
indicated that it took more time to train expe-
rienced nurses in the use of tympanic thermom-
etry than oral thermometry. Descriptive statis-
tics were the following: core, x = 37.33 (SD =
0.89): oral, x = 37.18 (SD = 0.92); tympanic
oral, X = 36.80 (SD = 0.93); and tympanic
core, X = 37.12 (SD = 1.0). Bias averages
were calculated and were significantly different
from for all three methods (oral-PA core, -0. 1 5
[SD = 0.36]; tympanic core-PA core, -0.11
[SD = 0.57], tympanic oral-PA core, -0.52
[SD = 0.53]), indicating that there is some de-
gree of decreased accuracy associated with each
method when compared with PA core. How-
ever, scatter plots using the Bland and Altman
methodology (Altman DG, Bland JM: Practical
Statistics for Medical Research. London, Chap-
man and Hall, 1991) illustrate that the greatest
variability is associated with the tympanic
method. CONCLUSIONS: Temperature mea-
surement is an important piece of clinical data
in a critically ill patient population. We found
oral thermometry to be the most accurate and
reproducible method when a PA core measure-
ment was not available.

Advances in Pulmonary Laboratory Test-
ing—Johnson BD. Beck KC, Zeballos RJ,Weis-
man IM. Chest 1999 Nov;l 16{5):1377-I387.

This review examines emerging technologies
that are of potential use in the routine clinical

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pulmonary laboratory. These technologies in-
clude the following: the measurement of exer-
cise tidal flow-volume (F^) loops plotted within
the maximal FV envelope for assessment of
ventilatory constraint during exercise; the use
of negative expiratory pressures to asses expi-
ratory flow limitation in various populations and
under various conditions; the potential use of
expired nitric oxide for assessing airway in-
flammation; and the use of forced oscillation
for assessment of airway resistance. These meth-
odologies have been used extensively in the
research setting and are gaining increasing pop-
ularity and clinical application due to the avail-
ability of commercially available, simplified,
and automated systems. An overview of each
technique, its potential advantages and limita-
tions will be discussed, along with suggestions
for further investigation that is considered nec-
essary prior to extensive clinical use.

The Influence of Access to a Private Attend-
ing Physician on the Withdrawal of Life-
Sustaining Therapies in the Intensive Care

Unit— Kollef MH, Ward S. Crit Care Med 1 999
Oct;27(10):2l25-2I32.

OBJECTIVE: To assess the influence of patient
access to a private attending physician on the
withdrawal of life-sustaining therapies in a med-
ical intensive care unit (ICU). DESIGN: Pro-

spective cohort study. SETTING: A university-
affiliated teaching hospital. PATIENTS: A total
of 501 consecutive patients admitted to the med-
ical ICU during a 5-month period. INTERVEN-
TIONS: None MEASUREMENTS AND MAIN
RESULTS: Among patients dying in the med-
ical ICU, those without a private attending phy-
sician (n = 26) were statistically more likely to
undergo the active withdrawal of life-sustain-
ing therapies than patients with a private at-
tending physician (n = 87) (80.8% vs. 29.9%;
relative risk = 2.70; 95% confidence interval =
1.86-3.92; p < 0.001). Despite having similar
predicted mortality rates by Acute Physiology
and Chronic Health Evaluation II score (60.5%
± 27.0% vs. 66.1% ± 21.3%; p = 0.280), pa-
tients dying in the medical ICU without a pri-
vate attending physician had statistically shorter
hospital and ICU lengths of stay, a shorter du-
ration of mechanical ventilation, and fewer to-
tal hospital costs and charges compared with
patients with access to a private attending phy-
sician. Multiple logistic regression analysis, con-
trolling for severity of illness, demographic char-
acteristics, and patient diagnoses, demonstrated
that lack of access to a private attending phy-
sician (adjusted odds ratio = 23.10; 95% con-
fidence interval = 9.10-58.57; p < 0.001) and
the presence of a do-not-resuscitate order while
in the ICU (adjusted odds ratio = 7.33; 95%
confidence interval = 3.69-14.54; p = 0.004)

Respiratory Care • April 2000 Vol 45 No 4

381

Abstracts

were the only variables independently associ-
ated with the withdrawal of life-sustaining ther-
apies before death. CONCLUSIONS; Patients
dying in a medical ICU setting without access
to a private attending physician are more likely
to undergo the active withdrawal of life-sus-
taining therapies before death than patients with
a private attending physician. Health care pro-
viders should be aware of possible variations in
the practice of withdrawal of life-sustaining ther-
apies in their ICUs based on this patient char-
acteristic.

Interobserver Variability in Applying a Ra-
diographic Definition for ARDS — Rubenfeld
GD, Caldwell E, Granton J, Hudson LD, Mat-
thay MA. Chest 1999 Nov; 1 1 6(5): 1 347- 1353.

CONTEXT; Acute lung injury (ALI) and ARDS
are currently defined by the American-Euro-
pean Consensus Conference (AECC) definition
criteria, which contain a radiographic criterion.
The accuracy or reliability of this consensus
radiographic definition has not been evaluated,
and no radiographic definition of ALI-ARDS
has been evaluated by a large international group
of experts. OBJECTIVE; To study the interob-
server variability in applying the AECC radio-
graphic criterion for ALI-ARDS. DESIGN: Sur-
vey. PARTICIPANTS: A convenience sample
of 2 1 experts selected from participants attend-
ing the 1997 Toronto Mechanical Ventilation
Workshop and from members of the National
Institutes of Health ARDS Network. Outcome
measures: Participants reviewed 28 randomly
selected chest radiograph from critically ill, hy-
poxemic (P^oj/fraction of inspired oxygen ra-
tio, < 300) patients and decided whether the
radiograph fulfilled the AECC definition for
ALI-ARDS. RESULTS: Interobserver agree-
ment in applying the AECC definition for ALI-
ARDS was moderate (kappa = 0.55; 95% con-
fidence interval, 0.52 to 0.57). Thirteen
radiographs (43%) showed nearly complete
agreement (defined as 20 or 2 1 readers in agree-
ment). Nine radiographs (32%) had a five dis-
senting readers. The percentage of radiographs
interpreted as consistent with ALI-ARDS by
individual readers ranged from 36 to 71%. Par-
ticipants commented that mild infiltrates, pleu-
ral effusions, atelectasis, isolated lower lobe in-
volvement, radiographic technique, and
overlying monitoring equipment posed the most
difficulties. CONCLUSIONS; The radiographic
criterion used in the current AECC definition
for ALI-ARDS showed high interobserver vari-
ability when applied by expert investigators in
the fields of mechanical ventilation and ARDS.
This variability may result in differences in ALI-
ARDS populations at different clinical research
centers and may make it difficult for clinicians
to apply the results of clinical trials to their
patients. Modifications to the radiographic cri-
terion or annotated reference radiograph may

improve the reliability of future definitions for
ALI-ARDS.

Tidal Breathing Parameters in Young Chil-
dren: Comparison of Measurement by Re-
spiratory Inductance Plethysmography to a
Facemask Pneumotachograph System —

Manczur T, Greenough A, Hooper R, Allen K,
Latham S, Price JF, Rafferty GF. Pediatr Pul-
monol 1999 Dec;28(6):436-441.

The ratio of expiratory time at tidal peak flow
to total expiratory time (1^,^,^) correlates with
conventional measures of airway obstruction. It
is usually assessed using a facemask and pneu-
motachograph system which may be poorly tol-
erated in young children and hence limits the
usefulness of this technique. We therefore de-
termined in young asthmatic children the accu-
racy of tp,j./t^, using an uncalibrated respiratory
inductance plethysmograph (RIP), and com-
pared the results with those from a facemask-
pneumotachograph system. We also assessed
whether age influenced the agreement between
measurements using the two devices. Forty-
seven children aged between 1 month and 12
years were recruited: 39 were inpatients recov-
ering from an acute wheezy episode, and 8 were
recruited from the asthma clinic. All were re-
ceiving bronchodilators. Tidal breathing param-
eters tpi^^t,, the duty cycle (t|/t,„,), and respira-
tory rate were initially measured using the
Respitrace® alone and then simultaneously with
both the Respitrace and the facemask-pneumo-
tachograph system. Eight children did not tol-
erate the facemask, and in two others it was
impossible to analyze the Respitrace trace due
to artifacts. In the remaining 37 children, the
reliability coefficients and coefficients of vari-
ation of the two techniques were similar. Sim-
ilar values of t,/t,„, and respiratory rate were
obtained using the two devices. The mean tp„/t^
obtained using the Respitrace was lower than
with the facemask-pneumotachograph system
(p < 0.0 1 ), although this was age group-depen-
dent (p < 0.05), as the difference was less ap-
parent in the I to 2-year-old children than in
other age groups. Application of the facemask-
pneumotachograph system did not significantly
influence the results obtained using the Respi-
trace. We conclude that uncalibrated respira-
tory inductance plethysmography can measure
tidal breathing parameters as reliably as a face-
mask-pneumotachograph system in young asth-
matic children, and is better tolerated than the
pneumotachograph system. The results obtained
using the two devices are not interchangeable.

Compliance in Asthma — Cochrane GM, Home
R, Chanez P. Respir Med 1999 Nov;93(ll);
763-769.

Low rates of compliance with medication pose
a major challenge to the effective management
of most chronic diseases, including asthma. The

high medical and social costs of non-compli-
ance, and the apparent lack of effective meth-
ods for dealing with it, has stimulated renewed
interest in this complex issue. Two broad cat-
egories of non-compliance have been identi-
fied, namely unintentional (or 'accidental') and
intentional (or 'deliberate'). Unintentional non-
compliance may result from poor doctor-patient
communication or a lack of ability to follow
advice. Intentional non-compliance occurs when
the patient knows what is required but decides
not to follow this to some degree. Healthcare
professionals need to be aware of the various
issues affecting compliance in all patients. The
reasons for non-compliance are many and var-
ied, and include factors such as complexity of
the treatment regimen, administration route, pa-
tient beliefs about therapy and other psycholog-
ical factors. Improvement in patient compliance
with therapy will require better doctor-patient
communication, improved patient education, the
tailoring of therapy to the individual and pos-
sible novel strategies such as offering feedback
to the patients on their level of compliance.

The Effects of Time Delay and Temperature
on Capillary Blood Gas Measurements —

Dent RG. Boniface DR, Fyffe J, Yousef Z. Re-
spir Med 1999 Nov;93(ll);794-797.

Monitoring of blood gas measurements is an
important part of the assessment of patients with
chronic lung disea.se. Increasingly, this is being
done in the patients' homes by specialist nurses.
This makes it important to know the effect of
time delay and storage temperature on the reli-
ability of capillary blood gas analysis results. In
this study, the effect of a delay of I and 2 h and
of storage at both room temperature and in ice,
on blood stored in glass capillary tubes was
investigated. Samples, initially taken from the
earlobes, were transferred to glass capillary
tubes and used to provide duplicate initial sam-
ples for immediate analysis, and then single
samples at 1 and 2 h stored at room temperature
or in ice. The duplicate baseline measurements
showed good reproducibility. There was a small,
but statistically significant, increase in P^oj
when samples were stored in capillaries at room
temperature, or in ice, both at 1 and 2 h. Small
changes in Pq, were not statistically significant,
either in ice or at room temperature. None of
the changes was considered to be sufficient to
be of clinical significance, thus supporting the
use of capillary blood sampling even when there
might be a delay of 1-2 h and transport is at
room temperature, as might be the case when
taking domiciliary samples.

Flow Triggering Added to Pressure Support
Ventilation Improves Comfort and Reduces
Work of Breathing in Mechanically Venti-
lated Patients — Barrera R, Melendez J, Ah-
doot M, Huang Y, Leung D, Groeger JS. J Crit
Care 1999 Dec;l4(4):l72-I76.

382

Respiratory Care • April 2000 Vol 45 No 4

PURPOSE: The purpose of this study was to
measure the effect of flow triggering (FT), added
to pressure support ventilation (PSV), during
spontaneous breathing in intubated patients.
MATERIALS AND METHODS: A prospec-
tive observational study was conducted at a
Comprehensive Cancer Center, University Hos-
pital. Fourteen consecutive critically ill, me-
chanically ventilated patients on PSV with pos-
itive end-expiratory pressure were studied. Flow
triggering was added to PSV in spontaneously
breathing ventilated patients. RESULTS: Re-
spiratory rate (0. minute ventilation (V;;), pa-
tient work of breathing (WOBp), respiratory
drive (Po i). rapid shallow breathing index (f/
V-]-), tidal volume (V^^) and a visual analog scale
of breathing effort and comfort all improved.
There was a large decrease in WOBp and Pq i
when flow triggering was added to PSV
(p<0.001). There was a moderate decrease in
f/V| during the same procedure (p<0.01).
Twelve patients felt subjectively better with the
intervention. CONCLUSIONS: Flow triggering
offers an excellent complement to PSV because
it improves patient comfort and reduces the mag-
nitude of the inspiratory effort as well as the
delay time between inspiratory muscle contrac-
tion and gas flow. It augments gas exchange at
no metabolic cost to the patient while reducing
the work of breathing.

Cystic Fibrosis Lung Disease: Tlie Role of
Nitric Oxide — Grasemann H, Ratjen F. Pediatr
Pulmonol 1999 Dec;28(6):442-448.

This review summarizes current knowledge
about the role of nitric oxide (NO) in cystic
fibrosis (CF) lung disease. NO is endogenously
produced by a group of enzymes, the NO syn-
thases (NOSs). There are three isoforms of NOS,
each encoded by different genes: neuronal
(nNOS), immune or inducible (iNOS), and en-
dothelial (eNOS) nitric oxide synthase. They
all form NO and L-citrulline by enzymatic ox-
idation of L-arginine. This reaction requires a
number of cosubstrates, including molecular ox-
ygen and tetrahydrobiopterin. It is not known
whether all three isoenzymes are constitutively
expressed in cells of the respiratory tract and
that their gene expression is inducible. NO pro-
duction by iNOS, the "high-output" NOS, is
stimulated by bacterial lipopolysaccharide
(LPS) as well as proinflammatory cytokines
such as interleukin (IL)-l gamma, IL-2, inter-
feron (IFN)-gamma, and tumor necrosis factor
(TNF). In contrast to nNOS and eNOS, activa-
tion of iNOS does not require an increase in
intracellular Ca"^ concentration.

Questionnaire Survey of California Consum-
ers' Use and Rating of Sources of Health
Care Information Including the Internet —

Pennbridge J, Moya R, Rodrigues L. West J Med
1999 Nov-Dec;171(5-6):302-305.

OBJECTIVE: To understand how Califomians
use and rate various health information sources,
including the Internet. RESEARCH DESIGN:
Computer-assisted telephone interviews
through which surveys were conducted in En-
glish or Spanish. SUBJECTS: A household sam-
ple generated by random digit dialing. The sam-
ple included 1(X)7 adults ( 18-1- ), 407 (40%) of
whom had access to the Internet. MAIN OUT-
COME MEASURES: Past health information
sources used, their usefulness and ease of use;
future health information sources, which are
trusted and distrusted; and concerns about in-
tegrating the Internet into future health infor-
mation seeking and health care behaviors. RE-
SULTS: Physicians and health care providers
are more trusted for information than any other
source, including the Internet. Among those with
Internet access, a minority use it to obtain health
information, and a minority is "very likely" to
use e-mail to communicate with medical pro-
fessionals or their own doctors and nurses, to
refill prescriptions, or to make doctor appoint-
ments. Also, most of those with Internet access
are "unlikely" to make their medical records
available via the Internet, even if securely pro-
tected. CONCLUSIONS: The public, including
frequent Internet users, has major concerns about
the confidentiality of electronic medical records.
Legislation may not assuage these fears and a
long-term, open and collaborative process in-
volving consumers and organizations from all
the health care sectors may be needed for full
public assurance.

Noninvasive Ventilation for Treatment of
Acute Respiratory Failure in Patients Un-
dergoing Solid Organ Transplantation: A
Randomized Trial — Antonelli M, Conti G,
Bufi M, Costa MG, Lappa A, Rocco M, et al.
JAMA 2000 Jan 12;283(2):235-241.

CONTEXT: Noninvasive ventilation (NIV) has
been associated with lower rates of endotra-
cheal intubation in populations of patients with
acute respiratory failure. OBJECTIVE: To com-
pare NIV with standard treatment using supple-
mental oxygen administration to avoid endotra-
cheal intubation in recipients of solid organ
transplantation with acute hypoxemic respira-
tory failure. DESIGN AND SETTING: Pro-
spective randomized study conducted at a 14-
bed, general intensive care unit of a university
hospital. PATIENTS: Of 238 patients who un-
derwent solid organ transplantation from De-
cember 1995 to October 1997, 51 were treated
for acute respiratory failure. Of these, 40 were
eligible and 20 were randomized to each group.
INTERVENTION: Noninvasive ventilation vs
standard treatment with supplemental oxygen
administration. MAIN OUTCOME MEA-
SURES: The need for endotracheal intubation
and mechanical ventilation at any time during
the study, complications not present on admis-
sion, duration of ventilatory assistance, length

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Respiratory Care • April 2000 Vol 45 No 4

383

A Continuing Education Program
of tlie American Association
for Respirator>- Care

lannTggaBiirii

Continuing Education Credit.
i\ll in the Convenience of Your Facility.
No Planes. No Long Lines. No Hotel Rooms,

atoiy Ilierapists Earn i Hour of CE Credit for Each Program
Nurses Earn i.a Hours of CE Credit for Each Program

Professor's Rounds topics Oi

just what your staff orderei

Each program has been careful

selected from the suggestioi

participants provided afti

previous programs. Yoursta

will learn about the "hot topic;

presented by experts on eac

subject. All in the convenieni

of your ownfaciliti

And, your staff will earn th

continuing education cred

they need as required b

licensure and regulator

requirements

Eight Hot Topics

Program #i

Pulmonary Rehabilitation: What You Need to Know

Live Videoconference - March 7, 11 :30 a.m.-i:oo p.m. Central Time
Teleconference with Videotape - April 4, 11:30 a.m.-i2:oo Noon Central Time
Presenters: Julien M. Roy, BA, RRT, FAACVPR, and Richard D. Branson, BA, RRT
What constitutes a sound pulmonary rehabilitation program? How do you go about
setting up a rehab program? What's the role of assessment in developing an exercise
prescription for the rehab of your patients? What are the issues surrounding
reimbursement and what does the future hold? l.eam the answers to these questions
and gain an appreciation for the importance of pulmonary rehabilitation to your
facility and your patients.

Program #3

Drugs, Medications, and Delivery Devices of

Importance in Respiratory Care

Uve Videoconference - April 25, 11:30 a.m.-i:oo p.m. Central Time
Teleconference with Videotape - May 16, 11:30 a.m.-i2:oo Noon Central Time
Presenters: James B. Fink, MS, RRT, FAARC and David J. Pierson, MD, FAARC
Aerosol therapy is delivered to nearly 80% of respiratory patients. There are a
number of new medications in development for both local and systemic
administration to those patients. Which device to use, how to negotiate care
plans, and how to educate both patients and caregivers are all topics that will be
discussed. Perhaps of critical importance is getting the most medication delivered
to the patient's lungs, which leads to a discussion of selecting the correct delivery
device.

Program #5
Pediatric Ventilation:

Kids Are Different

Live Videoconference - July 25, 11:30 a.m.-i:oo p.m. Central Time
Teleconference with Videotape - August 15, 11:30 a.m.-l2:oo Noon Central Time
Presenters: Mark Heulitt. MD, FAAP, PCCP and Richard D. Branson, BA, RRT
There are significant differences in the anatomy and physiology of the respiratory
systems between adults and children, posing problems for the practitioner attempting
to mechanically ventilate a pediatric patient. Once the process is underway, the
capabilities of the available mechanical ventilators and how they affect children
pose additional problems. Children are so different, you need to stop and reassess
actions you would normally take with an adult patient.

Program #7

Managing Asthma: An Update

Live Videoconference - September ig, 11:30 a.m.-t:oo p.m. Central Time
Teleconference with Videotape - October 17, 11:30 a.m.-i2:oo Noon Central Time
Presenters: Patti Joyner, RRT, CCM and Mari Jones, MSN, RN, FNP, RRT
Asthma management Ls a hot topic for discussion. Everyone wants to implement a
program at his or her facility. What will make a program work, and how do you know
if it's succes.sful? This program will provide you with the information you have been
looking for in order to implement a program and determine how succes.sful the
program really is. You will be given guidance on how to analyze outcomes measures
from a successfiil program.

Program #2

Pediatric Asthma in the ER

Live Videoconference - March 28, 11:30 a.m.-v.oo p.m. Central Time
Teleconference with Videotape - April 18, 11:30 a.m.-i2:oo Noon Central Time
Presenters: Timothy R. Meyers, BS, RRT and Thomas J. Kallstrom, RRT, FAARC
The prevalence of pediatric asthma has increased dramatically in the last few years.
The National Asthma Education and Prevention Program has prodded guidelines for
management of pediatric asthma. This program will discuss these issues as well as the
role of care paths in the management of the disease. Additionally, there have been
some significant advances in coping with pediatric asthma in the ER.

Program #4

Cost-Effective Respiratory Care: You've Got to Change

Live Videoconference - May 23, 11:30 a.m.-v.oo p.m. Central Time
Teleconference with Videotape - June 20, 11:30 a.m.-i2:oo Noon Central Time
Presenters: Kevin L. Shrake, MA, RRT, FACHE, FAAMA, FAARC and Sam P.
Giordano, MBA, RRT, FAARC

Practitioners frequendy confuse the implementation of protocol treatment and case
management. Both programs, if successfully implemented, can lead to cost savings.
The problem most practitioners face is how to identify where costs are avoided and
resources are conserved. Perhaps most critical is ensuring that the correct care is
delivered at the proper time. The health care practitioner is key to the ultimate success
of these programs.

Program #6

What Matters in Respiratory Monitoring:

What Goes and What Stays

Live Videoconference - August 22, 11:30 a.m.-i:oo p.m. Central Time
Teleconference with Videotape - September 26, 11:30 a.m.-i2:oo Noon Central Time
Presenters: Dean R. Hess, PhD, RRT, FAARC and Richard D. Branson, BA, RRT
The health care provider has an array of monitoring devices available in managing a
patient. With all that technology available, which device is appropriate? What about
those displays on ventilators? The availabihty of graphics during mechanical ventilation
can provide a wealth of information. When is it essential? Under what circumstances
should you pay close attention to those displays in the assessment of your patient?

Program #8

Routine Pulmonary Function Testing: Doing It Right

Live Videoconference - November 7, 11:30 a.m.-i:oo p.m. Central Time
Teleconference with Videotape - Decembers, 11:30 a.m.-i2:oo Noon Central Time
Presenters: CarlD. Mottram, BA, RRT, RPFTand David J. Pierson, MD, FAARC

Pulmonary function testing at the bedside is being increasingly utilized as a diagnostic
tool. Is it always appropriate? How can you a.s.sure competency of the person conducting
the test? How can you assure quality assurance outside the pulmonary fiinction
laboratory? This program will provide you with the information you need to assure that
this diagnostic lest is properly conducted outside the laboratory.

Accreditation

Respiratory Care:

Each program is approved for i hour of continuing education credit by Continuing Respiratory Care Education (CRCE). Purchase of
videotapes only does not earn continuing education credit. Registrants must participate in the live program or the telephone seminar
to earn continuing education credits.

Nursing:

Each program is approved for 1.2 hours of continuing education credit by the Texas Nurse Association. Purchase of videotapes
only does not earn continuing education credit. Registrants must participate in the live program or the telephone seminar to earn
continuing education credits.

Live Videoconference Requirements

Sites must have satellite reception capabilities (with moveable dish), video monitor, a telephone, and an individual to proctor the
program. Participants will view a live 90-minute satellite television broadcast with a live call-in question-and-answer session.
Program materials for the live program include satellite coordinates, toll-free telephone number, continuing education packet,
attendance log and reproducible course materials, post-test with answers, evaluation, and certificate of attendance.

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Sites must have a video monitor, a VCR, a telephone with speaker phone, and an individual to proctor the program. Participants
will receive and view a 90-minute videotape and then call a toll-free number for a live 30-minute call-in question-and-answer
session. Program materials for the telephone session include the toll-free telephone number, continuing education packet,
attendance log, videotape and reproducible course materials, post-test with answers, evaluation, and certificate of attendance.

Registration

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Single Programs: $245 per facility ($215 for AARC Members)

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Late Registration Fee: $15 (If registering within one week of program)

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Abstracts

of hospital stay, and intensive cai^ unit mortal-
ity. RESULTS: The 2 groups were similar at
study entry. Within the first hour of treatment.

14 patients (70%) in the NIV group, and 5 pa-
tients (25%) in the standard treatment group
improved their ratio of the P^q^ to the fraction
of inspired oxygen (F,o,). Over time, a sus-
tained improvement in P„o, to F|q, was noted in
12 patients (60%) in the NIV group, and in 5
patients (25%) randomized to standard treat-
ment (p = 0.03). The use of NIV was associ-
ated with a significant reduction in the rate of
endotracheal intubation (20% vs 70%; p =
0.002), rate of fatal complications (20% vs 50%:
p = 0.05), length of stay in the intensive care
unit by survivors (mean [SD] days, 5.5 [3] vs 9
[4]; p = 0.03), and intensive care unit mortality
(20% vs 50%; p = 0.05). Hospital mortality did
not differ. CONCLUSIONS: These results in-
dicate that transplantation programs should con-
sider NIV in the treatment of selected recipients
of transplantation with acute respiratory failure.

Randomised Controlled Trial of Effective-
ness of Leicester Hospital at Home Scheme
Compared with Hospital Care — Wilson A,
Parker H, Wynn A, Jagger C, Spiers N, Jones J,
Parker G. BMJ 1999 Dec 1 1;319(7224):1542-
1546.

Objective: To compare effectiveness of patient
care in hospital at home scheme with hospital
care. Design: Pragmatic randomised controlled
trial. Setting: Leicester hospital at home scheme
and the city's three acute hospitals. Participants:
199 consecutive patients referred to hospital at
home by their general practitioner and assessed
as being suitable for admission. Six of 102 pa-
tients randomised to hospital at home refused
admission, as did 23 of 97 allocated to hospital.
Intervention: Hospital at home or hospital in-
patient care. Main outcome measures: Mortal-
ity and change in health status (Barthel index,
sickness impact profile 68, EuroQol, Philadel-
phia geriatric morale scale) assessed at 2 weeks
and 3 months after randomisation. The main
process measures were service inputs, discharge
destination, readmission rates, length of initial
stay, and total days of care. Results: Hospital at
home group and hospital group showed no sig-
nificant differences in health status (median
scores on sickness impact profile 68 were 29
and 30 respectively at 2 weeks, and 24 and 26
at 3 months) or in dependency (Barthel scores

1 5 and 1 4 at 2 weeks and 1 6 for both groups at
3 months). At 3 months' follow up, 26 (25%) of
hospital at home group had died compared with
30 (31%) of hospital group (relative risk 0.82
(95% confidence interval 0.52 to 1 .28)). Hos-
pital at home group required fewer days of treat-
ment than hospital group, both in terms of ini-
tial stay (median 8 days v 14.5 days, p=0.026)
and total days of care at 3 months (median 9
days v 16 days, p=0.031). Conclusions: Hos-

pital at home scheme delivered care as effec-
tively as hospital, with no clinically important
differences in health status. Hospital at home
resulted in significantly shorter lengths of stay,
which did not lead to a higher rate of subse-
quent admission.

Smoking Cessation and Tobacco Control: An
Overview — Emmons KM. Chest 1999 Dec;
116(6Suppl):490S-492S.

Cigarette smoking is an intractable public health
problem and the single largest risk factor for a
variety of malignancies, including lung cancer.
Worldwide, about 3 million people die each
year of smoking-related disease, and this is ex-
pected to increase to > 10 million deaths per
year. The Agency for Health Care Policy and
Research has published a clinical practice guide-
line detailing available outcome data for vari-
ous smoking cessation strategies. In particular,
it has been recommended that all patients be
screened for smoking status on every health-
care visit, and that all patients who smoke be
strongly advised to quit and offered assistance
to do so. Health-care providers play a vital role
in the effort to reduce the prevalence of smok-
ing by delivering smoking cessation advice, sup-
porting community-based efforts to control to-
bacco, and becoming involved in the tobacco
control debate.

Effect of Continuous Positive Airway Pres-
sure vs Placebo Continuous Positive Airway
Pressure on Sleep Quality in Obstructive
Sleep Apnea — Loredo JS, Ancoli-Israel S,
Dimsdale JE. Chest 1999 Dec; 1 16(6): 1545-
1549.

STUDY OBJECTIVES: Continuous positive
airway pressure (CPAP) therapy has become
the treatment of choice for obstructive sleep
apnea (OSA). However, the efficacy of CPAP
therapy has not been evaluated against a suit-
able control. We investigated the effectiveness
of CPAP therapy in improving sleep quality in
patients with OSA. We hypothesized that CPAP
improves sleep quality. PATIENTS: Forty-eight
CPAP-naive OSA patients were evaluated. None
were receiving antihypertensive medications,
and none had major medical illnesses. DESIGN:
Patients were randomized to receive either
CPAP or placebo CPAP (CPAP at an ineffec-
tive pressure) for 7 days in a double-blind fa.sh-
ion. Forty-one patients completed the protocol.
Sleep quality variables, arousals, sleep arterial
oxygen saturation (S^q,)- ^nd respiratory dis-
turbance index (RDI) were assessed at baseline,
after 1 day of treatment, and after 7 days of
treatment. Repeated ineasures analysis of vari-
ance was used to evaluate the effects of treat-
ment, time, and the interaction of the two. RE-
SULTS: As expected, CPAP lowered RDI and
number of arousals, and increased S^q^ over

time (p = 0.00 1 ). Contrary to expectations, both
CPAP and placebo CPAP had comparable ef-
fects on sleep quality as as.sessed by sleep ar-
chitecture, sleep efficiency, total sleep time, and
wake after sleep onset time. CONCLUSIONS:
This study confirms the effectiveness of CPAP
in lowering the number of arousals and the RDI,
and in raising S.,o,. However, our data suggest
that short-term CPAP is no different than pla-
cebo in improving sleep architecture. Further
evaluation of the effectiveness of CPAP using a
suitable placebo CPAP in prospective random-
ized studies is needed.

Exacerbation of Acute Pulmonary Edema
During Assisted Mechanical Ventilation Us-
ing a Low-Tidal Volume, Lung-Protective
Ventilator Strategy— Kallet RH. Alonso JA,
Luce JM, Matthay MA. Chest 1999 Dec; 1 16(6):
1826-1832.

STUDY OBJECTIVES: To assess the magni-
tude of negative intrathoracic pressure develop-
ment in a patient whose pulmonary edema
acutely worsened immediately following the in-
stitution of a low-tidal volume (V^.) strategy.
DESIGN: Mechanical lung modeling of patient-
ventilator interactions ba.sed on data from a case
report. SETTING: Medical ICU and laboratory.
PATIENT: A patient with suspected ARDS and
frank pulmonary edema. INTERVENTIONS:
The patient's pulmonary mechanics and spon-
taneous breathing pattern were measured. Sam-
ples of arterial blood and pulmonary edema fluid
were obtained. MEASUREMENTS: A standard
work-of-breathing lung model was used to
mimic the ventilator settings, pulmonary me-
chanics, and spontaneous breathing pattern ob-
served when pulmonary edema worsened. Com-
parison of the pulmonary edema fluid-to-plasma
total protein concentration ratio was made. RE-
SULTS: The patient's spontaneous V,- demand
was greater than preset. The lung model re-
vealed simulated intrathoracic pressure changes
consistent with levels believed necessary to pro-
duce pulmonary edema during obstructed
breathing. A high degree of imposed circuit-
resistive work was found. The pulmonary edema
fluid-to-plasma total protein concentration ratio
was 0.47, which suggested a hydrostatic mech-
anism. CONCLUSION: Ventilator adjustments
that greatly increase negative intrathoracic pres-
sure during the acute phase of ARDS may
worsen pulmonary edema by increasing the
transvascular pressure gradient. Therefore,
whenever sedation cannot adequately suppress
spontaneous breathing (and muscle relaxants are
contraindicated), a low-V^- strategy should be
modified by using a pressure-regulated mixie of
ventilation, so that imposed circuit-resistive
work does not contribute to the deterioration of
the patient's hemodynainic and respiratory sta-
tus.

386

Respiratory Care • April 2000 Vol 45 No 4

Success in their world is measured breath by breath thus
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Editorials

Conflict of Interest and Respiratory Care

A primary purpose of science is the formulation and
testing of hypotheses about the world around us, and the
purpose of a science journal is to report and explain the
results of tests of these hypotheses. Data published by a
journal and the interpretation of those data must be the
truth, and to the extent that a journal's contents deviate
from what is strictly true it fails its mission and its readers.
Anything that distorts the testing of hypotheses, or the
interpretation of the results of this testing, is considered to
be a form of bias, and is therefore antithetical to the fun-
damental nature of science.'

Borland's Medical Dictionary^ defines bias as "devia-
tion of results or inferences from the truth." The potential
for bias is everywhere in science. A lack of appropriate
controls, inadequate sample sizes, and other defects in
study design introduce bias, as do the selective reporting
of data and the use of inappropriate statistical tests. Bias
on the part of investigators, authors, or manuscript review-
ers can stem from family and personal relationships, aca-
demic pressure, politics, religious beliefs, and a host of
other sources. The form of bias that tends to receive the
most attention in scientific publishing, though, especially
from the general public, is that involving money, in which
reported results deviate from the truth as a result of a
financial relationship between the author and the product
studied. Much of what editors do is for the purpose of
reducing bias in what their journals publish.

A major part of this activity focuses on the identifica-
tion of conflicts of interest. In its Uniform Requirements
for Manuscripts Submitted to Biomedical Journals, the
International Committee of Medical Journal Editors ("The
Vancouver Group") states that "conflict of interest for a
given manuscript exists when a participant in the peer
review and publication process — author, reviewer, and ed-
itor — has ties to activities that could inappropriately in-
fluence his or her judgment, whether or not judgment is in
fact affected."' Another definition is that offered by Thomp-
son,'' who says that conflict of interest is "a set of condi-
tions in which professional judgment concerning a pri-
mary interest (such as patients' welfare or the validity of
research) tends to be unduly influenced by a secondary
interest (such as financial gain.)"

Unfortunately, different journals use the term inconsis-
tently. Richard Smith, Editor of The British Medical Jour-
nal, agrees with The Vancouver Group in its statement that
the presence of conflict of interest does not necessarily

mean the presence of bias: "conflict of interest is a con-
dition not a behaviour.'"* However, others equate the con-
flict of interest with bias, either explicitly or by implica-
tion,* and some maintain that any conflict of interest is
unethical.^ Relationships today between the participants in
science and the for-profit world are both widely prevalent
and hugely variable, and it seems harsh to imply the au-
tomatic existence of bias whenever there is a relationship
that could conceivably pervert the scientific process. In an
attempt to clarify this issue, the Annals of Internal Medi-
cine uses the term "dual commitment" in its Information
for Authors, to refer to financial interests that might affect
the conduct or reporting of an author's work; conflict of
interest would exist if the latter had in fact occurred.**

For the reader, as well as for editors and reviewers,
being aware of financial conflict of interest and the risk of
bias is important. No one knows its true prevalence. Krim-
sky et al examined identifiable financial interests among
all academic scientists with addresses in Massachusetts
who were first or senior author of a paper published in
1992.^ In addition to researching the medical literature, the
authors used records on patent applications and lists of the
officers and advisory board members of biotechnology
firms in Massachusetts. They found that 34% of the au-
thors studied appeared in one or more of the other data-
bases, and that 15% of them had a financial interest di-
rectly relevant to one of their publications.

It is clear that financial conflict of interest can lead to
bias in scientific publications. Barnes and Bero studied
106 review articles on the health effects of passive smok-
ing published between 1980 and 1995.'° They used records
of funding and other support from tobacco industry sources
to examine the authors' affiliations in relation to the con-
clusions drawn in the articles about whether passive smok-
ing was harmful. Thirty-seven percent of the articles con-
cluded that passive smoking was not harmful to health,
and 29/39 (74%) of these were by authors with tobacco
industry affiliations. In multiple logistic regression analy-
ses controlling for article quality, peer review status, arti-
cle topic, and year of publication, the only factor associ-
ated with the conclusion that passive smoking was not
harmful was whether the author was affiliated with the
tobacco industry (odds ratio, 88.4; 95% confidence inter-
val, 16-476, p < 0.001).

Journals vary substantially in how they deal with con-
flict of interest."'- Most require authors and reviewers to

388

Respiratory Care • April 2(X)0 Vol 45 No 4

Conflict of Interest and Respiratory Care

disclose financial relationships with manufacturers or other
businesses dealing with products in the area of the manu-
script under consideration. A few, however, explicitly do
not. Nature is one of the latter, citing the assumptions that
conflict of interest is unavoidable and that the avoidance
of bias cannot be guaranteed by disclosure: "virtually ev-
ery good paper with a conceivable biotechnological rele-
vance. . . has at least one author with a financial interest —
but what of it?"'-'

However it is defined, conflict of interest is everywhere
in science, and respiratory care is no exception. In fact,
because of its reliance on equipment and devices, and the
integral role played by industry in its research and publi-
cations, respiratory care (the subject area)''* is probably as
vulnerable to bias resulting from conflict of interest as any
field in health care.

What steps does Respiratory Care take to deal with
conflict of interest? Its Manuscript Preparation Guide '-^
asks authors of submitted manuscripts to disclose any li-
aison or financial arrangement they have with a manufac-
turer or distributor whose product is addressed in the manu-
script, or with the manufacturer or distributor of a competing
product. The Journal requires that materials and experi-
mental methods be described in sufficient detail that the
reader could duplicate the work, and seeks to include suf-
ficient primary data in the results section of any original
research article that reviewers and readers can assess the
appropriateness of the conclusions drawn. Respiratory
Care accepts only articles whose subjects lie well within
its defined specialty area, and attempts are made to find
reviewers who are expert on the specific topic involved.
Each original research paper is evaluated by at least 3
out-of-office referees, plus a statistical consultant where
appropriate. Reviewers are unaware of the identity or in-
stitution of the author.

Still, the problem of conflict of interest will not go
away. The purpose of disclosure is to make the issue of
conflict of interest public, "so that all relevant observers
become aware of it and can modify their opinions on the
credibility of statements of the conflicted person accord-
ingly."'*' As pointed out by Krimsky and Rothenberg,"
this mitigates but does not resolve the conflict, and the

reader must always be aware of the possibility of bias due
to conflict of interest in any published article.

David J Pierson MD FAARC

Editor in Chief
Seattle, Washington

10.

REFERENCES

(editorial) Ann Intern Med 1997;

1. Davidoff F. Where's the bias?
l26(12):986-988.

2. Dorland's illustrated medical dictionary. Philadelphia: WB Saun-
ders, 28th edition; 1994; pp. 89:812.

3. International Committee of Medical Journal Editors. Uniform re-
quirements for manuscripts submitted to biomedical journals. Respir
Care 1997;42(6):623-634.

4. Thompson DF. Understanding fmancial conflicts of interest. N Engl
J Med l993;329(8):573-576.

5. Smith R. Conflict of interest and the BMJ (editorial). BMJ 1994;
308(6920):4-5.

6. Rumsey TS. One editor's views on conflict of interest. J Anihi Sci
1999;77(9):2379-2383.

7. Steinbok P. Ethical considerations relating to writing a medical sci-
entific paper for publication. Childs Nerv Syst 1995; 1 1(6):323-328.

8. Information for authors. Ann Intern Med 2000;132(2):I-1 1-1-13.

9. Krimsky S. Rothenberg LS, Stott P. Kyle G. Scientific journals and
their authors' financial interests: a pilot study. Psychother Psycho-
som I998;67(4-5):194-201.

Barnes DE, Bero LA. Why review articles on the health effects of
passive smoking reach different conclusions. JAMA 1998;279(19):
1566-1570.

Krimsky S, Rothenberg LS. Financial interest and its disclosure in
scientific publications. JAMA l998;280(3):225-226.
Wilkes MS, Kravitz RL. Policies, practices, and attitudes of North
American medical journal editors. J Gen Intern Med 1995;1(X8):
443^50.

void financial 'correctness' (editorial). Nature I997;385(6I66):469.
Pierson DJ. What is respiratory care? (editorial) Respir Care 1998;
43(I):I7-19.
Manuscript preparation guide. Respir Care 2000,45(1): 140-143.

16. Bemat JL, Goldstein ML, Ringel SP. Conflicts of interest in neurol-
ogy (editorial). Neurology 1998;50(2):327-331.

Correspondence: David J Pierson MD FAARC, Editor in Chief, Respi-
ratory Care, 600 Ninth Avenue. Suite 702, Seattle WA, 98104-2038.
E-mail: pierson@aarc.org

Respiratory Care • April 2000 Vol 45 No 4

389

Original Contributions

Effects of Respiratory Impedance on the Performance of Bi-Level

Pressure Ventilators

Alexander B Adams MPH RRT, Peter L Bliss BME, and John Hotchkiss MD

BACKGROUND: Noninvasive positive pressure ventilation (NPPV) has been studied in several
settings and shown to reduce patient morbidity associated with endotracheal intubation. Intoler-
ance to NPPV has been estimated at 25-33%, a substantial proportion of attempts to ventilate
noninvasively. Bi-level pressure ventilators (BPVs) have been designed for NPPV, yet their response
to changes in respiratory impedance has not been extensively evaluated. To determine responses of
BPVs to changing impedance conditions, we tested 4 BPVs to evaluate the potential for intolerance.
We also developed a mathematical model for BPV performance that accounted for impedance
conditions, leak, pressure settings, and inspiratory flow cutoff level. METHODS: Four BPV models
at the same settings were challenged to ventilate a triggered test lung under a range of impedance
conditions while measuring tidal volume (Vj) and intrinsic positive end-expiratory pressure (auto-
PEEP). The model was used to predict V^ and auto-PEEP under normal, restrictive, and obstruc-
tive conditions. RESULTS: The BPV models tested delivered Vj in a similar manner. V^ decreased
with decreased compliance and increased resistance. Auto-PEEP developed with increased resis-
tance and compliance. The model predicted a V^ delivery dependent on inspiratory flow cutoff
level. For the obstructive condition, the model predicts an optimal V^ delivery within a specific
inspiratory flow cutoff range that becomes narrower with increasing resistance. CONCLUSIONS:
Vx delivery and auto-PEEP generated by BPVs are highly dependent on the prevailing impedance
condition. Though there are differences between BPV models, generally, performance was similar
between the models tested. This report suggests that knowledge of both respiratory system imped-
ance and the performance of the BPV in use are required to attend to inadequate V^ delivery and
auto-PEEP generation. Furthermore, the model predicts a relatively narrow range for inspiratory
flow cutoff that provides adequate ventilatory support without causing hyperinflation in patients
with obstructive conditions. [Respir Care 2000;45(4):390-400] Key words: noninvasive mechanical
ventilation, mathematical modeling, bi-level pressure ventilator.

Background

Noninvasive positive pressure ventilation (NPPV) has
been studied in several clinical settings: chronic respira-

Alexander B Adams MPH RRT, Peter L Bliss BME, and John Hotchkiss
MD are affiliated with Regions Hospital, Healthpartners, University of
Minnesota, St Paul, Minnesota.

This research was supported by American Heart Association grant
#99301 84N and National Institutes of Health grant SCOR HL-50512.

Correspondence: Alexander B Adams, Pulmonary Research, Regions
Hospital, 640 Jackson Street, St Paul MN 55101. E-mail:
alex.b.adams@Health Partners.com.

tory failure,' acute respiratory failure,^-'' nocturnal hy-
poventilation,''-* restrictive lung disease,^-* chronic ob-
structive pulmonary disease,'"'° as a postextubation bridge
to unassisted ventilation,"-"* and for acute lung injury/
acute respiratory distress syndrome.'-'' NPPV allows many
patients to avoid intubation and its associated morbidity
and mortality.'-" Unfortunately, a significant proportion
of NPPV attempts fail,'*-'"' suggesting that further analy-
sis of the causes of NPPV intolerance is warranted.

Patient comfort and tolerance of NPPV are often deter-
mined by technical issues related to the patient-ventilator
interface, ventilator circuitry, and, possibly, ventilator char-
acteristics. Mask characteristics and proper fitting are cru-
cial to patient acceptance of NPPV, so advances in mask
design have improved tolerance. Some circuit and mask

390

Respiratory Care • April 2000 Vol 45 No 4

Respiratory Impedance and Bi-Level Pressure Ventilators

PRESSURE
TRANSDUCER
+ 6 CM H20

PRESSURE
TRANSDUCER
0-50 CM H20

michigan instruments
test-tramng lung

COMPUTER (-

TUBWG
ELECTRONIC SIGNAL

DATAO INSTRU»^ENTS

DI-190

MODULE

/ aaaaaoa
/ aaoaaaa
— / oaaaoBO
/ ooooooo
f oooaaaa

Fig. 1 . Schematic of the test lung circuit. The tested ventilator (one of the 4 bi-level pressure ventilators)
actively ventilates one limb of the test lung. The triggering ventilator only initiates inspiration. A fixed orifice
(4 mm diameter) leak source and linear resister (5, 20, or 50 cm HgO/LVs) are in series in the tested
ventilator circuit. Flow and "lung" pressure were continuously monitored in the tested ventilator circuit.
The driving ventilator was set to simply trigger (and not drive) the test ventilator by use of a similar
compliance setting and a double expiratory valve setup.

configurations can allow rebreathing and carbon dioxide
retention, which is alleviated by increasing positive end-
expiratory pressure.'*-" Circuits with significant expira-
tory valve resistance, which may contribute to patient in-
tolerance, have also been studied.-^

To be well tolerated, bi-level pressure ventilators (BPVs)
designed to deliver NPPV should trigger inspiration easily,
meet patient inspiratory flow demand, provide adequate
volume assistance to ventilation, avoid hyperinflation, and
synchronize support with patient effort. Bunburaphong et
al found that BPVs compare favorably with critical care
ventilators in maximal inspiratory flow rates and inspira-
tory trigger sensitivity.-' Hill et al examined the effect of
certain control settings on providing adequate tidal volume
(V-J-) delivery. 22 The effects of patient impedance charac-
teristics on adequacy of volume assistance and avoiding
hyperinflation have not been well characterized. Because
BPVs use a modified pressure support mode to provide
NPPV, there may be significant interactions between pa-
tient impedance characteristics and the level of volume

support delivered or hyperinflation generated. Furthermore,
the level of inspiratory flow at which the BPV terminates
machine assistance of inspiration (inspiratory flow cutoff,
expressed as a fraction of the peak inspiratory flow) af-
fects the duration of inspiration, delivered Vy, and, prob-
ably, patient comfort. BPVs generally use a flow cutoff at
a higher fraction of peak inspiratory flow than critical care
ventilators (to avoid deleterious prolongation of mechan-
ical inspiration due to mask leaks), possibly rendering the
level of flow cutoff more important than pressure support
ventilation by critical care ventilators.

To clarify the effects of impedance characteristics on
Vj support and hyperinflation, we examined the Vj de-
livered and intrinsic positive end-expiratory pressure (au-
to-PEEP) generated by 4 BPVs in common use, with test
lung simulations spanning a range of impedance charac-
teristics. We also developed a mathematical model of BPV
performance to analyze the relationship between flow cut-
off, mask leak, respiratory system impedance, pressure
settings, and Vy delivery.

Respiratory Care • April 2000 Vol 45 No 4

391

Respiratory Impedance and Bi-Level Pressure Ventilators

BIPAP

Quantum

^'^V

Knightstar

''^<Nc,^0

0. \sh^

^'cO^""

VPAP

" '0 "j-i

Fig. 2. Tidal volume (Vj) delivery by the 4 bi-level pressure ventilators (BPVs) under the 12 impedance
conditions tested. The pattern of Vj delivery was similar among the BPVs: V^^ increased with increasing
compliance and decreasing resistance. At the same impedance levels, the Quantum delivered a
smaller Vj than the other BPVs.

Methods

A test lung system was used to simulate conditions of
typical use (Fig. 1 ). One chamber of a dual-chamber Train-
ing Test Lung (Michigan Instruments, Grand Rapids, Mich-
igan) served as a triggering chamber and was linked to the
BPV test chamber with a lifting bar to allow inspiratory
triggering of the BPV. An open connector (4 mm diame-
ter) was inserted in the triggered test limb circuit to serve
as a leak source. Airway and chamber pressure, as well as
circuit flow, were monitored by pressure differential trans-
ducers (model MP-45, Validyne, Northridge, California)
and a pneumotachometer (Hans-Rudolph. Kansas City,
Kansas). The V^^ delivery capabilities of 4 commercially
available BPVs were tested: BiPAP S/T 30 (Respironics,
Pittsburgh, Pennsylvania), Knightstar 335 (Mallinckrodt,
Pleasanton, California), Quantum (Respironics, Pittsburgh,
Pennsylvania), and VPAP (ResMed, San Diego, Califor-
nia). Appendix 1 describes the inspiratory termination meth-
ods used with each BPV. Each BPV was set at: inspiratory
positive airway pressure = 15 cm HjO, end-positive air-
way pressure = 3 cm HjO, and respiratory frequency =
10/min while ventilating each of the 12 simulated imped-
ance conditions arising from all permutations of 3 inter-
posed linear resistors (5, 20 and 50 cm HjO/L/s) and 4

compliance settings (0.02, 0.05, 0.08, 0. 1 1 L/cm H.O).
Ten consecutive breaths were measured for each permu-
tation while the pressure transducer and pneumotachom-
eter signals were acquired and digitized by a software
program (LabView, National Instruments, Austin, Texas).
An average Vj was calculated after integration of the flow
signals from the 10 measured breaths. Auto-PEEP was
measured by recording the end-expiratory "alveolar" pres-
sure directly from the TTL.

A mathematical model was developed to simplify and
idealize BPV performance and permit systematic investi-
gation of the effects of flow cutoff and leak on V-p and
auto-PEEP under 3 respiratory system impedance condi-
tions: restrictive, obstructive, and normal. The assump-
tions and derivation of the mathematical model are de-
tailed in Appendix 2.

Results

Test Lung Measurements

Figure 2 shows the V-p responses of the 4 BPVs to the
tested impedance conditions. The pattern of response was
similar for each of the BPVs tested, with V-^ increasing
when compliance was increased and resistance decreased.

392

Respiratory Care • April 2000 Vol 45 No 4

Respiratory Impedance and Bi-Level Pressure Ventilators

BIPAP

Knightstar

^ >'

'^c\ih^

Quantum

VPAP

^'^ANcgSO

Fig. 3. Intrinsic positive end-expiratory pressure (autoPEEP) generated by the 4 bi-level pressure
ventilators (BPVs) under the 12 impedance conditions tested. AutoPEEP was generated under condi-
tions of increased resistance and increased compliance (a scenario representing obstructive disease).
The Quantum generated less autoPEEP than the other BPVs, associated with its smaller tidal volume.

The Vj delivered by the Quantum was lower than the V-,-
observed with the other BPVs for the same impedance
conditions. Figure 3 shows the pattern of auto-PEEP de-
velopment among the BPVs tested. Increased compliance
and resistance led to increased auto-PEEP. The Quantum
developed less auto-PEEP than the other BPVs. Figure 4
shows the inspiratory time (T,) developed by the 4 BPVs.
Compared to the other BPVs. T, was less (shorter) for the
Quantum. Similar patterns of response to impedance con-
ditions between the BPVs were less apparent for T,, since
flow cutoff algorithms differ between machines, yet longer
T| was associated with auto-PEEP generation. For the set-
tings tested, the higher fixed inspiratory flow cutoff (75%
of peak flow) was responsible for the decreased Vj, less
auto-PEEP, and shorter T, of the Quantum.

Model Predictions

Figure 5 shows V-,- delivery predicted by the model as a
function of the fraction of inspiratory flow cutoff (k). In the
normal and restrictive simulations, as the flow cutoff increased
(inspiration terminated at higher fractions of peak inspiratory
flow = higher k), Vy declined in a linear fashion. For each k
level, Vy in the normal (higher compliance) scenario is higher

than in the restrictive scenario. In contrast, the obstructive
condition led to the appearance of an optimal flow cutoff.
Values of k higher or lower than this optimal value led to
decreased Vj. The optimum value for k in the obstructive
scenario reflects a balance between the effect on V-p of in-
creasing auto-PEEP at lower k and decreasing V-p at higher k,
as seen in each condition. The decline in V-p is quite steep as
k shifts lower and away from the optimal value, presumably
due to a narrowing pressure difference between alveolar pres-
sure (the increasing auto-PEEP) and inspiratory positive air-
way pressure. As resistance in the obstructive configuration
increases within a clinically relevant range (20-1 20 cm HjO),
the optimal value for k rises to higher percentages of peak
flow (from —35% to —80%) and the range for optimal k
narrows (Fig. 6).

Figure 7 shows the effect of a larger leak on V-p delivery
for the 3 conditions. The presence of a larger leak at the
level of the ventilator-patient interface (mask) had signif-
icant deleterious effects in the obstructive condition. If a
default inspiratory termination time (time cycling) is not
imposed, the presence of a larger leak can significantly
prolong the inspiratory phase and increase auto-PEEP while
diverting flow from the lungs. If a maximal T, termination
is imposed, the system behaves as a partially time-cycled

Respiratory Care • April 2000 Vol 45 No 4

393

Respiratory Impedance and Bi-Level Pressure Ventilators

BIPAP

'^'STA^^SO

Quantum

Knightstar

VPAP

^'ST/VNcg^O

O -0 <>'j.f

Fig. 4. Inspiratory times (T,) for the 4 bi-level pressure ventilators (BPVs) under the 12 impedance
conditions tested. T, tended to be lengthened when intrinsic positive end-expiratory pressure
(auto-PEEP) was generated (ie, with increased compliance and increased resistance). The Quantum
had a shortened T,, associated with its smaller tidal volume, lower auto-PEEP generation, and higher
fixed flow cutoff.

ventilator, generating a constant V-j- at the timed flow cut-
off point. As k increases above the "optimal" value, Vy
again declines linearly.

Discussion

The use of NPPV has been reported to avoid complica-
tions, reduce length of stay, and reduce mortality, yet in
studies comparing NPPV to standard care or the use of
endotracheal intubation, a range of 22-53% or an esti-
mated 25-33% of the patients randomized to NPPV fail to
receive adequate ventilation and eventually require intu-
bation.^'*''' ^2^-29 A detailed analysis of those failing NPPV
has not been reported, but studies have found these pa-
tients to be more ill with pneumonia, hypoxemia, or aci-
dosis. ^''•2''--'' The actual inability to adequately ventilate
the patient or the level of hyperinflation has not been
reported. Impedance characteristics (resistance and com-
pliance) and mask leak magnitude have not been system-
atically reported in patients failing NPPV. Our data sug-
gest that these factors may interact with BPV performance
to affect the level of ventilatory support. Both the test lung
data and the mathematical model predict that patient im-

pedance characteristics will have a major impact on the
level of support provided. The theoretical predictions sug-
gest that the level at which inspiratory flow is terminated
("flow cutoff) may be an important factor in patient in-
tolerance of NPPV, particularly in the setting of obstruc-
tive lung disease.

Critique of the Study

There are several concerns regarding the direct rele-
vance of our findings to the clinical .setting. We did not test
BPV-impedance condition interactions in patients or an
animal model. Instead, we compared the performance of
the ventilators in a precisely controlled mechanical lung
analog. The extent to which the differing levels of support
provided by each ventilator under the same nominal set-
tings and conditions could affect patient tolerance of NPPV
will require testing in patients who have been mechani-
cally well characterized. The mathematical model was not
validated in patients. The model assumes passive inspira-
tion following triggering and passive expiration. The model
incorporates purely linear resistances and compliances.
However, our goal in constructing the mathematical model

394

Respiratory Care • April 2000 Vol 45 No 4

Respiratory Impedance and Bi-Level Pressure Ventilators

0.6

0.5

50.4-

|o.3^

re
■o
i=0.2

0.1

autoPEEP

Normal

• ' 'u . . s

' \ N

I \ N

f '^v Restrictive " *^ ■ ■ . . ,

*"^.

|Obstructive

^
--.. ^

- :

r12

E
o

1-6 ^
m
111

-2

0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9
k, inspiratory flow cutoff (fraction of peak flow)

Fig. 5. The mathematical model prediction of tidal volume (Vj) delivery as a function of k (the inspiratory
flow cutoff), for three scenarios; normal, restrictive, and obstructive conditions. The dashed line rep-
resents intrinsic positive end-expiratory pressure (auto-PEEP) generation (right Y axis) for the obstruc-
tive condition. In the normal and restrictive scenarios, Vj v^/as related linearly to k, with Vj declining as
k increased. As expected, an increased inspiratory positive airway pressure would be required to
deliver "normal" ventilation in the restrictive condition. The obstructive scenario displayed a nonlinear
Vj delivery in relation to k. Vj delivery peaks at a k of approximately 0.3. The decline in Vj at a lower
k was accounted for by a corresponding increase in auto-PEEP.

20 40 60 80 100

resistance (cm H20/L/sec)

120

Fig. 6. The optimal k (inspiratory flow cutoff) for the obstructive
scenario (where k peaks, as identified in Fig. 5) as a function of
resistance. The bold line represents the optimal k. The dashed
lines identify the range for k that delivers a tidal volume of at least
80% of the maximal tidal volume.

0.6-1

Normal

r-^^

Obstructive

1 ^^^^^'

~ «s

1 ^^^1s

0.5-

•

^^^^

1 1

\^*^N^„^^_^

0.4-

1 1

\ ^^^^^

0.3

■ ' " ' ■ ■ sL
."Restrictive | '

■ • ■

\
\

0.2

0.1-

\
\

■ ' ■ ■ ■ ' ' 1 f , . .

■ • ' 1 ' ' ' ' 1 ■ ' ' ' I ' ' ' ' I

0.1 0.2 0.3 0.4 0.5 0.6 0.7 0.8 0.9 1
k, inspiratory flow cutoff (fraction of peak flow)

Fig. 7. The mathematical model prediction of tidal volume (Vj)
delivery as a function of k (inspiratory flow cutoff) (similar to Fig. 5),
with the effect of a larger leak. In this case, the bi-level pressure
ventilators may revert to a time cutoff to allow continuation of
cycling.

Respiratory Care • April 2000 Vol 45 No 4

395

Respiratory Impedance and Bi-Level Pressure Ventilators

was to develop the simplest possible representation of the
patient-ventilator system and to use it to identify interac-
tions that may be of future interest.

Of major importance is the role of the leak during BPV-
patient interaction. We simplified the leak by inserting a
fixed orifice in the physical circuitry and by assigning the
leak a fixed resistance in the mathematical model. In clin-
ical practice, leaks may be multiple, variable, and/or thresh-
old leaks that invoke complex geometric factors that vary
widely. Minimizing leaks is important to, at least, avoid
the ventilation of the leak source. A leak will extend T,,
but leak types and their specific effects on each model of
BPV and the mathematical model were not investigated in
this report.

This investigation did not test, in either the physical or
mathematical models, certain very realistic clinical condi-
tions. The test lung evaluations were not made at elevated
respiratory rates (eg, 20-30/min), which is a common state
for dyspneic patients. In fact, reduced Vj delivery and
auto-PEEP generation (intolerance) would be more likely
at higher respiratory rates, thereby further emphasizing the
importance of our observations. Clinically, expiratory re-
sistance exceeds inspiratory resistance, compliance is not
linear, and most patients exert inspiratory and expiratory
effort. Furthermore, impedance conditions may change with
effective treatment or exacerbation or improvement of the
underlying condition. The.se differences from our assump-
tions may warrant either further simulation testing or, pref-
erably, patient studies.

Possible Implications

These findings suggest that the often-observed NPPV
intolerance in the setting of obstructive disease may have
a partial basis in the dynamic behavior of a system in
which the inspiratory phase is terminated on the basis of
inspiratory flow. The presence of an optimum value for
flow cutoff in the obstructive setting and its mobility under
conditions of changing impedance are in sharp contrast to
the much more predictable behavior of the system under
normal or restrictive conditions, where patient intolerance
is less prevalent. Moment-to-moment variations in patient
impedance characteristics may cause significant moment-
to-moment variability in the level of ventilatory support,
promoting discomfort. Prolongation of the inspiratory phase
due to mask-face leak may cause patient discomfort by
moving k outside the optimal range. Even with an arbitrary
maximal T,, the inspiratory phase may be prolonged be-
yond a comfortable duration and/or require active patient
effort for termination. Given the increasing popularity of
NPPV, further investigation of patient ventilator interac-
tion in this setting may prove fruitful.

The role of the technical aspects of the BPV and its
operator must be emphasized. Though patterns of BPV

performance were similar, differences in performance were
found among the 4 BPVs tested in this study. These dif-
ferences relate to fixed and controllable components of the
flow delivery systems. The flow delivery algorithm, reac-
tion to leaks, and inspiratory termination criteria differ
among machines — affecting flow profile, Vj, auto-PEEP
generation, and T,. Interchanging BPV may require setting
changes to achieve the same level of assistance. Inability
to trigger inspiration, as well as inadequate flow delivery
capacity by a BPV could contribute to patient intolerance,
but these areas have been studied and BPV performance
was found to be adequate compared to critical care venti-
lators.-' Other unresolved and yet to be investigated issues
of BPV performance include aspects of ventilator-patient
synchrony, such as forced or active exhalation.

Conclusions

Intolerance to NPPV is commonly attended to in the
clinical setting by patient encouragement, patience, and
adjusting the mask style, position, or size. This report
suggests that inadequate Vy delivery or significant auto-PEEP
may contribute to NPPV intolerance. Assessing these pos-
sible sources of intolerance requires knowledge of the pa-
tient's respiratory system impedance and of the perfor-
mance and controls of the BPV in use. The dynamic nature
of patient impedance characteristics precludes precise rec-
ommendations for BPV settings and/or BPV model selec-
tion. For patients with obstructive disease, the model pre-
dicts that a relatively narrow range of settings will provide
adequate ventilatory assistance without causing hyperin-
flation.

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Respiratory Impedance and Bi-Level Pressure Ventilators
Appendix 1 . Inspiratory Termination Method

BiPAP S/T 30 — Three seconds or autoTracicing: a traclcing signal is generated by delaying the flow tracing
by 300 ms and reducing it by 15 L/min. When actual flow crosses this tracking signal, the pressure mode
changes.

Knightstar 335 — There are inspiratory termination or cutoff (expiratory sensitivity control) settings of 1
through 5. Settings 2, 3, 4 correspond to stated cutoff levels of 59%, 45%, and 35% of peak flow. The
Knightstar was set at 3 (45%) for this study.

Quantum — 75% of peak flow.

VPAP — A maximum inspiratory time (controllable) or patient effort detected by distal pressure sensing
(accounting for leak compensation).

398 Respiratory Care • April 2(X)() Vol 45 No 4

Respiratory Impedance and Bi-Level Pressure Ventilators

Appendix 2. Model Derivation

Model Description. To further elucidate the behaviors observed in the test lung experiments, we developed a
unicompartmental mathematical model for biphasic, pressure-targeted noninvasive ventilation (Fig. 8). (For the
methods of this derivation, see Gershenfeld N. Finite differences: ordinary differential equations. In: Gershenfeld N.
The nature of mathematical modeling. Cambridge: Cambridge University Press; 1999:67-77.)

The model addressed predicted outcomes of pressure-targeted ventilation in a passive, unicompartmental pulmonary
system where inspiratory resistance (Rj), total expiratory resistance (Re), and compliance (C) were linear. The
expiratory circuitry of the ventilator was assigned a resistance Ry. A leak of resistance Rl was incorporated into the
model proximal to the central airways resistance to simulate the potential for leakage around the mask-face interface.

For simplicity of presentation, this pathway was assumed to have a constant resistance throughout the inspiratory
cycle. Potential limitation of maximal ventilator inspiratory flow rate was also included in the model. For clarity, the
simplest realistic algorithm for the termination of inspiration was modeled: inspiration was terminated either when the
inspiratory flow fell to a preselected fraction of peak inspiratory flow, or when a preselected fraction of the respiratory
cycle time had elapsed.

Ventilator

Lungs

Fig. 8. Mathematical model. See text for definitions.

Model Derivation: Inspiratory Phase. During inspiration, with or without mask leakage, two conditions may exist:
either the system inflates passively as determined by the selected (and attained) airway opening pressure (no flow
limitation), or the flow into the lung plus that through the leak equals the maximal flow capacity of the ventilator (flow
limitation). In the absence of flow limitation, the inspiratory equation is the traditional equation of motion for a given
applied pressure (Pset):

dV/dt = (Ps« - V(t)/C)/Ri, where dV is change in flow, dt is change in time.

(Equation I)

In the setting of flow limitation, the maximal flow from the ventilator (Vm„) equals the sum of the flow into the lung
and the flow through the leak, both of which are determined by the pressure attained (Pjr) at the branch point between
the leak pathway and the airway (within the mask):

V™„ = P.,/RL + (P.„-V(t)/C)/R,.

(Equation 2)

By solving for the attained pressure at the airway opening and substituting into Equation 1, the flow into the lung is
found to be:

dV/dt = (V^ X Rl - V(t)/C)/(RL + R, ),

(Equation 3)

and total flow is equal to maximal flow. Under both conditions, the applied flow (V,p) can be shown to be:

V,p = [(Rl + Rl) X dV/dt + V(t)/C]/RL.

(Equation 4)

Respiratory Care • April 2000 Vol 45 No 4

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Respiratory Impedance and Bi-Level Pressure Ventilators

Appendix 2. Model Derivation (Continued)

Model Derivation: Expiratory Phase. Because expiration was assumed to be passive, the expiratory equation of
motion is:

dV/dt = - (V(t)/C)/[RE + Rl X Rv/(Rl +Rv)].

(Equation 5)

Model Derivation: Integration of Inspiratory and Expiratory Phases. The respiratory cycle was partitioned into
10,000 time steps, and the inspiratory equations were numerically integrated. At each time point. Equation 4 was
solved, and the appropriate inspiratory equation was selected:

(Equation 1 ifV.p<V„

,; Equation 3 ifV,p > V,n„

:)•

The inspiratory phase ended either when Vap fell below a preselected fraction of the maximal total inspiratory flow, or
when a preselected inspiratory time was exceeded. In the former case, the remaining "inspiratory time" was added to
the expiratory phase. The expiratory equation was integrated to solve for end-expiratory volume. The process was
repeated using this value as the initial inspiratory volume until end-expiratory and end-inspiratory volumes were stable
(to allow for the effects of auto-PEEP).

Although intended for qualitative rather than rigorous quantitative comparisons, we attempted to confirm that the
computer model tracked the physical setting. A Mallinckrodt 840 ventilator (Mallinckrodt, Pleasanton, California) that
allows setting of k values was set to simulate conditions to be predicted by the mathematical model. The conditions
tested and predicted included combinations of Ps^t = 10, 15, and 25 cm H2O, PEEP = cm HjO, respiratory
frequency = 10, 12, and 20/min, compliance = 0.02-0. 12 L/cm HjO, R| = 5, 20, and 50 cm HjO/L/s, and the fraction of
inspiratory peak flow cutoff (k) = 0.2-0.45. A Bland-Altman-type plot was constructed for measured versus predicted
Vt, with the x-axis representing a measured VT, not the average of measured and predicted. (Bland-Altman methods
are described in Bland JM, Altman DG. Statistical methods for assessing agreement between two methods of clinical
measurement. Lancet 1986;1 :[8476]:307-3 10.) Average bias was -0.015 ± 0.06 L (Fig. 9). This comparison of
measured and predicted Vj was considered adequate to confirm an acceptance level of validity for the model and its
assumptions.

u.s
0.4

0.3

0.2

0.1

-.•- 5 J.

-. •••

-0.1

• •

>. , .

-0.2

•

-0.3-

-0.4

-OB

-^ . 1 , , , r— ., — ,

0.2

0.4 0.6 0.8
Measured VT

1.2

Fig. 9. Bland-Altman diagram. See text for definitions and discussion.

Model Predictions. Model predictions were then developed for 3 scenarios: obstructive, restrictive, and normal. In all
presented simulations, V^ was 12 cm H2O (equivalent to IPAP = 15 cm H2O, EPAP = 3 cm H2O), frequency was
12 breaths/min, and Rv was 10 cm H2O. In the obstructive configuration, Ri = Re = 20 cm H2O L"' x s ' and

C = 0. 1 Ucm H2O. In the restrictive configuration, Ri = Rg = 5 cm H2O L ' x s ' and C -■
normal configuration, Ri = Re = 5 cm H2O L"' x s"' and C = 0.1 L/cm H2O.

0.03 L/cm H2O. In the

400

Respiratory Care • April 2000 Vol 45 No 4

Reevaluation of Continuous Oxygen Therapy After Initial Prescription
in Patients with Chronic Obstructive Pulmonary Disease

Yuji Oba MD, Gary A Salzman MD, and Sandra K Willsie DO

BACKGROUND: Long-term oxygen therapy improves survival and quality of life in hypoxemic
patients with chronic obstructive pulmonary disease (COPD). The need for long-term oxygen
therapy should be determined when patients are medically stable. The Third Oxygen Consensus
Conference recommended reevaluating patients 1-3 months after continuous oxygen therapy (COT)
is initiated, if initiated when the patient is medically unstable. METHODS: A cross-sectional study
was performed to examine how often orders for COT are reevaluated pursuant to the guidelines
promulgated by the Third Oxygen Therapy Consensus Conference, and to assess the impact that
following these guidelines would have on the cost of COT. RESULTS: Of 226 patients prescribed
home oxygen therapy, 92 had COPD as a primary diagnosis and 57 were prescribed COT. Only 19
(35%) of 55 patients who returned to the clinics were appropriately reevaluated. The rate of
appropriate reevaluation was significantly higher among pulmonary physicians than among pri-
mary care physicians (65% vs 17%; odds ratio: 9.0; 95% confidence interval: 2.5-32). Of 19
patients who were appropriately reevaluated, 11 (58%) were discontinued from COT. The patients
who were discontinued from COT had a significantly higher percent of predicted forced expiratory
volume in the first second than those who were not (34 ± 8.6% vs 25 ± 8.8%; p = 0.04). CON-
CLUSIONS: In our study, most patients were clinically unstable when COT was prescribed, and a
significant number of patients remained on COT without reevaluation. Up to 60% of those patients
could potentially be discontinued from COT if appropriately reevaluated. Referring a patient
initiated on COT to a pulmonary specialist for the proper use of oxygen is strongly recommended.
Reevaluating such patients in a timely fashion and discontinuing unnecessary oxygen concentrators
could possibly save $106-153 million per year in the United States. [Respir Care 2000;45(4):401-
406] Key words: oxygen therapy, home care services, health insurance, reimbursement, obstructive lung
disease, non-drug prescription.

Background

Long-term oxygen therapy (LTOT) is a well-established
treatment and improves survival'- and quality of life'-* in
hypoxemic patients with chronic obstructive pulmonary
disease (COPD). However, LTOT imposes a substantial
economic burden. Close to 800,000 patients in the United
States receive LTOT annually, at a yearly cost of $1.8
billion.'

Yuji Oba MD. Gary A Salzman MD, Sandra K Willsie DO are affiliated
with the Section of Respiratory and Critical Care Medicine. Truman
Medical Center West and University of Missouri-Kansas City School of
Medicine Kansas City, Missouri.

Correspondence: Yuji Oba MD. School of Medicine, Green 5 Unit. Uni-
versity of Missouri-Kansas City. 241 1 Holmes, Kansas City MO 64108-
2792. E-mail: yoba@cctr.umkc.edu.

The Nocturnal Oxygen Therapy Trial and Medical Re-
search Council Working Party studies, which demonstrated
the mortality and morbidity benefits of LTOT, assured
stability of the patients for 1 month before entry,'- and
current recommendations inside and outside of the United
States adopt inclusion criteria from these studies.*-* In
actual practice, oxygen therapy is usually initiated during
hospitalization, while patients are suffering from acute ill-
ness, and they are sent home on oxygen. In this case ox-
ygen therapy is considered "short-term," and the Third
Oxygen Consensus Conference recommended reevaluat-
ing such patients 1-3 months later for the purpose of de-
termining the continued need for oxygen therapy. Because
of substantial improvement in their clinical status, a sig-
nificant number of such patients may not require supple-
mental oxygen.

This study was undertaken to examine how often orders
for COT are reevaluated pursuant to the guidelines pro-

Respiratory Care • April 2000 Vol 45 No 4

401

Reevaluation of Continuous Oxygen Therapy

mulgated by the Third Oxygen Therapy Consensus Con-
ference, and to assess the impact that following these guide-
lines would have on the cost of COT. Various physiologic
and laboratory data were also examined to identify factors
that may predict continuous need for COT after short-term
oxygen therapy.

Methods

With approval from the University of Missouri-Kansas
City Adult Health Services Institutional Review Board, a
cross sectional retrospective study was performed in a uni-
versity-affiliated urban teaching hospital. Home oxygen
therapy was arranged through the department of social
work in all patients in our hospital between January 1,
1996, and July 31, 1998. Two hundred twenty-six patients
who had been prescribed home oxygen therapy were iden-
tified from their records during that period. Medical records
were reviewed and the primary diagnosis for which home
oxygen therapy was required was identified. Patients with
a primary diagnosis of COPD, as defined by the American
Thoracic Society criteria,'" were included in the analysis.
There was enough information to confirm the diagnosis of
COPD in most patients, but when the pulmonary function
test results were not available, clinical diagnosis of COPD
was also accepted. All the medical records were carefully
reviewed by a pulmonary specialist to exclude other pri-
mary diagnoses. Oxygen prescriptions were reviewed to
identify patients on COT. Demographic data, indications
for COT, and clinical stability at the time of initial pre-
scription were recorded. The Medicare criteria (Table 1)
were used to determine if each patient satisfied indications
for COT. Arterial blood gases ( ABGs) obtained at the time
of initial evaluation, and pulmonary function test resuhs
obtained within 6 months before or 3 months after initia-
tion of oxygen therapy were also obtained.

The prevalence of appropriate reevaluation was deter-
mined from outpatient medical records and a telephone
survey. The reevaluation was considered appropriate if the
following criteria were satisfied: (1) Pulse oximetry or
ABG measurement on room air was performed within 1 -3
months after initiation of COT, and (2) COT was discon-

Table 1 . Medicare Criteria for Continuous Oxygen Therapy

PdC), - 55 mm Hg or O, saturation s 88%

PaOj *-■ ^ IT"' Hg plus one of the following:

Edema

Hematocrit > 56%

P pulmonale on EGG: 3 mm in leads II, III, AVE

P^ « arterial oxygen tension.
ECG = clectrocanJiogrdm.

tinued if a patient no longer satisfied Medicare criteria for
COT. Patients who were discontinued from COT but con-
tinued on portable oxygen systems because of exercise
desaturation were considered appropriately reevaluated.
The telephone survey was conducted to confirm the re-
moval of oxygen concentrators in the discontinued group.
Patients were excluded from the analysis of appropriate
reevaluation if they did not return to a clinic for a follow-
up. Physicians were categorized into primary care or pul-
monary physicians, and the prevalence of appropriate re-
evaluation was determined in each group.

Statistical analy.ses were performed using statistical soft-
ware packages (Statistica, StatSoft, Tulsa, Oklahoma, and
Instat, GraphPad, San Diego, California). The Mann-
Whitney test was used to examine the baseline character-
istics between the reevaluation group and the no reevalu-
ation group. Fisher's exact test was used to compare
differences in reevaluation rate between primary care and
pulmonary physicians. Patients who had appropriate re-
evaluation were divided into subgroups for age, arterial
oxygen tension (Pao,)' arterial carbon dioxide tension
(Paco,)' forced expiratory volume in the first second (FEV, ),
vital capacity, residual volume, total lung capacity (TLC),
and diffusion capacity for carbon monoxide. These vari-
ables of interest were then inserted into a multivariate
analysis (factor analysis) to identify which factors best
predicted continuous need for oxygen after short-term ox-
ygen therapy. Using continuous need for oxygen therapy
as a fixed variable and the parameters defined as playing
independent roles in continuous need for COT as depen-
dent variables, we were able to define the relative role
played by each variable in predicting continuous need for
COT. Significance was accepted as p < 0.05.

Results

At Truman Medical Center West, 226 patients were
started on home oxygen therapy between January 1, 1996,
and July 31, 1998. The primary diagnoses were COPD (92
patients, 41 %), cancer (43 patients, 19%), congestive heart
failure (39 patients, 17%), sleep apnea/obesity-induced hy-
poventilation (24 patients, 11%), and other (28 patients,
12%). Of the 92 patients with COPD, 57 (62%) were
prescribed COT, 23 were prescribed oxygen for use during
exercise, and 12 were prescribed oxygen for use at night.
At the time of initial evaluation, room air ABG measure-
ment was performed on 49 of the 57 COPD patients, pulse
oximetry on the remaining 8 COPD patients. Medicare
criteria for COT were satisfied by 54 (95%) of the 57
patients. Table 2 lists the characteristics of the COPD
patients who were prescribed COT. Spirometric data were
available in 41 patients, and lung volumes and diffusion
capacity in 33. Forty-eight patients (84%) were started on
COT during hospitalization for deterioration of respiratory

402

Respiratory Care • April 2000 Vol 45 No 4

Reevaluation of Continuous Oxygen Therapy

Table 2. Characteristics of COPD Patients Receiving COT*

Gender ratio, M:F
Smokers (%)
Mean age (years)
P^, (mm Hg)
Paco; (mm Hg)
FEviA'C (%)
FEV, (L)
FEV, % predicted
VC(L)

VC % predicted
RV % predicted
TLC % predicted
Dlco ^ predicted

26:31

51%

61 ± 8 (45-76)

51 ±5(41-57)

49 ± 8(37-71)

49 ± 1 1 (25-67)

0.92 ±0.32 (0.44-1.76)

32 ± 12(13-79)

1.82 ±0.52(1.02-3.13)

53 ± 14(34-100)

239 ±85 (11 1-359)

126 ± 25(79-186)

27 ± 16(6-67)

COPD = chronic obslnjclive pulmonary disease.

COT = continuous oxygen therapy.

♦n = 57. n = 41 for FEviA'C. FEV,. FEV, <J predicled. VC. and VC » predicted, n = .13

for RV * predicted. TLC ■? predicted, and Dlco * predicted.

Values are mean ± suindard deviation (minimum-maximum).

PjOt = arterial oxygen tension.

■-<x>j

- arterial carbon dioxide tension.

FEV I = forced expiratory volume in the first second.

VC = vital capacity.

RV = residual volume.

TIX = total lung capacity.

Dlco — diffusion capacity for carbon monoxide.

Status. The other 9 patients ( 1 6%) were prescribed COT as
outpatients when they were relatively stable. No patients
prescribed COT as outpatients were hospitalized at the
time of initial evaluation.

Of the 57 patients prescribed COT, 55 (96%) returned to
the clinics for follow-up, where 35 were seen by their
primary care physicians and 20 by pulmonary physicians.
All the primary care physicians were general internists. Of
the 55 patients who returned to the clinics, only 19 patients
(35%) were appropriately reevaluated for the continued
need for COT. Six patients (17%) seen by primary care
physicians and 13 patients (65%) seen by pulmonary phy-
sicians were appropriately reevaluated at follow-up. Nine-
teen patients who were appropriately reevaluated were sim-
ilar at baseline to the 28 patients who were not reevaluated.
The baseline characteristics between the two groups were
as follows. Age: 63.3 ± 8.3 versus 59.4 ± 8.3 (p = 0.15);
Male/female ratio: 35% versus 65% (p = 0.24); P.^q-. 52 ±
4.6 mm Hg versus 50 ± 4.0 mm Hg (p = 0.32);"P3co,
47 ± 7.0 mm Hg versus 50 ± 9.0 mm Hg (p = 0.14)
FEV,: 0.97 ± 0.31 L versus 0.91 ± 0.33 L (p = 0.54)
Forced vital capacity: 1.77 ± 0.62 L versus 1.88 ± 0.50 L
(p = 0.34). The rate of appropriate reevaluation was sig-
nificantly higher among pulmonary physicians than among
primary care physicians (Fisher's exact test: p < 0.01,
odds ratio: 9.0, 95% confidence interval: 2.5-32). Of the
36 patients who were not appropriately reevaluated, 9 were
prescribed COT as outpatients, 6 by pulmonary physicians
and 3 by primary care physicians when they were clini-

cally stable. When those patients who were prescribed
COT as outpatients were excluded, the rate of appropriate
evaluation was still 41% overall, 19% by primary care
physicians and 93% by pulmonary physicians.

Of those 19 patients who were appropriately reevalu-
ated, 1 1 (58%) had substantial improvement in gas ex-
change and were discontinued from COT. Four out of 1 1
patients who were discontinued from COT still required a
portable oxygen system because of significant exercise
desaturation, but oxygen concentrators were removed from
their houses. Table 3 shows a comparison of those discon-
tinued from COT and those who were not. Multivariate
analysis was performed to identify factors to predict con-
tinued need for COT after short-term oxygen. Patients who
were discontinued from oxygen had significantly higher
percent of predicted FEV, than those who remained hy-
poxemic and continued on COT (34 ± 8.6% vs 25 ±
8.8%, p = 0.04, Fig. 1). When the percent of predicted
FEV, was S: 32%, positive predictive value for ability to
discontinue oxygen therapy was 88% and negative predic-
tive value was 64%. The other variables, including age,
Pao,' Paco,. absolute FEV|, vital capacity, residual vol-
ume, TLC, and diffusion capacity for carbon monoxide
were also analyzed but did not reach statistically signifi-
cant difference between the two groups.

Discussion

Between January 1, 1996, and July 31, 1998, COT was
prescribed for 57 COPD patients, with almost equal num-

Table 3.

Comparison of COT Discontinued and Continued Groups
in Patients Who Were Reevaluated

COT

discontinued

continued

(n = 11)

(n = 8)

Mean age (years)

63 ±8

56 ±6

P^o, (mm Hg)*

50 ±3

50 ±4

Paco, (mm Hg)*

50 ±7

52 ± 10

FEV, (L)

0.87 ± 0.22

0.81 ± 0.28

FEV, % predicted

34 ±9

24 ± 8t

VC % predicted

49 ±7

47 ± 12

RV % predicted

207 ± 82

272 ± 78

TLC 9c predicted

126 ± 22

97 ±42

Dlco % predicted

ihetzpy.

30 ± 18

22 ±4

COT - continuous oxygen

Values are mean ± standard deviation.

tp < 0.05.

PaOi ~ arterial oxygen tension.

•Data when COT was initiated.

PaCOi = anerial carbon dioxide tension.

FEV| = forced expiratory

volume in ihe first second.

VC = vital capacity.

RV = residuai volume.

TLC = local lung capacity

Dlco = diffusion capacity

for carbon nuHioxide.

Respiratory Care • April 2000 Vol 45 No 4

403

Reevaluation of Continuous Oxygen Therapy

50
45
40
35

?: 30
>

'^ 25
20
15
10

COT discontinued

COT continued

Median value

Fig. 1. Categorized plot for variable FEV, (forced expiratory vol-
ume in the first second). COT = continuous oxygen tfierapy.

bers of men and women. COPD predominantly afflicts
men, but similar gender ratio was also observed in previ-
ous studies of COPD patients receiving home oxygen ther-
apy."'- It is conceivable that male patients with COPD
died prematurely from comorbid conditions such as coro-
nary artery disease, which occurs in female patients at
older ages.

Our study showed excellent compliance by prescribing
physicians with the current Medicare criteria at initial eval-
uation. More than 80% of the hypoxemic COPD patients
were started on oxygen when they were clinically unstable
following hospitalization, and nearly two thirds remained
on COT without reevaluation. Of those who were appro-
priately reevaluated, close to 60% no longer satisfied the
criteria for COT and were discontinued from COT. Al-
though there might be a possibility that the patients were
reevaluated outside of our clinics, the high discontinuation
rate of oxygen therapy in the reevaluation group makes
this possibility unlikely. The findings in the reevaluation
group could also apply to the population at large, because
the 19 patients who were appropriately reevaluated were
similar at baseline to the 28 patients who were not reeval-
uated. In the Nocturnal Oxygen Therapy Trial and Medical
Research Council Working Party studies, the patients were
initially evaluated when they were clinically stable, blood
gas measurements were repeated during 3-4-week obser-
vation periods, and the patients who did not meet the
criteria at the end of the observation period were excluded
from the study. '^ In the Nocturnal Oxygen Therapy Trial,
45% of hypoxemic COPD patients who were considered
initially stable showed substantial improvement during 1
month of stable outpatient observation, to the point that
COT was no longer indicated.'^ It is obvious that more
patients in our study showed improvement in gas exchange

at the subsequent evaluation, because of their clinical in-
stability at the initial evaluation.

Currently, Medicare has not adopted the recommenda-
tions from the Third Oxygen Consensus Conference re-
garding reevaluation of oxygen therapy after 1-3 months
if patients are medically unstable at the initial evaluation.
Though it is expected that almost all patients who qualify
for COT for the first time are recently discharged from a
hospital and recovering from acute illness,"* Health Care
Financing Administration regulations require retesting and
recertification only if the initial P„q^ is > 56 mm Hg or the
arterial oxygen saturation > 89%. '^ On the other hand,
improvement in oxygenation after 3 months of COT may
be derived from "reparative effect of oxygen" rather than
fluctuation in clinical stability, and in such cases discon-
tinuation of COT can be hazardous and is not justified.'^
Because our study confirmed that most of the patients
were clinically unstable at the initial evaluation, we be-
lieve that initial certification for COT should be restricted
to 3 months, especially in COPD patients. Recertification
with ABG measurement after short-term oxygen would
facilitate cost-effective use of COT, because 40-60% of
these patients may not require COT at reevaluation. Ac-
tually, the British Department of Health and Social Secu-
rity guidelines recommend a repeated ABG measurement
after 3 weeks to confirm stability before LTOT is pre-
scribed.'''

The rate of appropriate reevaluation was significantly
higher among pulmonary physicians than primary care phy-
sicians (65% vs 17%, p < 0.01). It was incidentally found
that pulse oximetry became available in the primary care
clinic during the period of the study, but institution of
pulse oximetry did not change the rate of appropriate re-
evaluation among primary care physicians. (Three patients
out of 18 before vs 3 out of 17 after the availability of
pulse oximetry; Fisher's exact test p = 1.0.) Walshaw et al
reported that compliance with LTOT prescribing guide-
lines is significantly better among pulmonary physicians
than primary care physicians.'* In their study, 24 out of 34
patients (71%) who were prescribed oxygen concentrators
by pulmonary physicians met the Department of Health
and Social Security guidelines for LTOT, compared to 9
out of 27 (33%) by primary care physicians. Better com-
pliance with oxygen therapy is also reported in patients
who were prescribed LTOT by pulmonary physicians."
The British Medical Society now recommends regular fol-
low-up by a pulmonary physician when LTOT is pre-
scribed." In our study, about two thirds of the patients on
COT were managed by primary care physicians. Referring
a patient initiated on COT to a pulmonary specialist is
strongly recommended, not only to facilitate the proper
use of oxygen therapy but also to improve patients' LTOT
compliance.

404

Respiratory Care • April 2000 Vol 45 No 4

Reevaluation of Continuous Oxygen Therapy

Among the patients who were appropriately reevalu-
ated, the patients who were discontinued from COT had
significantly higher percent of predicted FEV, than those
who were not. The other variables in our study did not
reach significant difference by a multivariate analysis. All
patients who met the criteria for COT had higher than
normal residual volume, but 3 patients had TLC < 100%
of predicted. Two of them had significant obesity and one
had congestive heart failure, which could explain super-
imposed restrictive disease and low TLC. Both groups
included one patient whose TLC was < 100% of pre-
dicted. Excluding patients with combined disease from the
statistical analysis did not affect the results. Levi-Valensi
et al'** also found that FEV,, vital capacity, and TLC were
not reliable markers to predict improvement in oxygen-
ation after 3 months of a probation period, which is in
agreement with our study. Our data suggest that the per-
cent of predicted FEV, might be a better predictor of
ongoing need for or ability to discontinue oxygen therapy,
but the results should be contlrmed in a large prospective
study because there was a significant overlap of individual
results from one group to another.

In our study, close to 40% of the patients who were
discontinued from COT still required portable oxygen sys-
tems to compensate for exercise desaturation. In general,
patients who are discontinued from COT but still require
oxygen with exercise do not need a stationary system.
Most of the study patients used an oxygen concentrator for
a stationary system and a compressed gas tank for a por-
table system. Rental of a concentrator usually costs $275-
400 per month, whereas rental of an E-size tank set-up
(tank, gauge, cart, and wrench) costs only $15-30 per
month.^" In a 5-state survey of patients receiving home
oxygen therapy, most physicians did not know what type
of oxygen delivery system the patient was supplied.-' To
avoid unnecessary use of concentrators, prescribing phy-
sicians should be familiar with oxygen delivery systems,
and education of primary care physicians about oxygen
delivery equipment is indispensable. Close to 800,000 pa-
tients receive LTOT in the United States yearly, at a cost
of $ 1 .8 billion.'^ The prevalence of LTOT use in the United
States is 4-10 times higher than in other developed coun-
tries. ^ It is likely that proper reevaluation of COT and
discontinuation of unnecessary stationary systems would
contribute to a significant reduction in health care costs.
Current Medicare statistics-- indicate that an estimate of
new elderly users of home oxygen under Medicare in 1992
was 168,360, and 26% of these new users died in the same
year. Eighty-seven percent of those beneficiaries received
oxygen concentrators and 82% were defined as having
COPD. The estimated relative risk of death associated
with a diagnosis of COPD was 0.45. Our study indicated
that 83% of concentrator users were prescribed COT as
opposed to nocturnal oxygen, only 35% were appropri-

ately reevaluated at follow-up, and 58% of the patients no
longer satisfied the criteria for COT at reevaluation. Tak-
ing these numbers into consideration, it is possible that
approximately 32,000 COPD patients remained on unnec-
essary oxygen concentrators in 1992. Reevaluating such
patients in a timely fashion and discontinuing unnecessary
concentrators could possibly save $106-153 million per
year in the United States.

Conclusions

In our study, most of the patients were prescribed COT
while clinically unstable, and a significant number of pa-
tients were continued on COT without reevaluation, espe-
cially when the patients were seen by primary care phy-
sicians. Referring a patient initiated on COT to a pulmonary
specialist is strongly recommended to ensure the proper
use of oxygen therapy. Up to 60% of those patients can be
discontinued from COT if appropriately reevaluated. Dis-
semination of current guidelines from the Third Oxygen
Consensus Conference and more strict adherence to the
guidelines by the Health Care Financing Administration
would make a significant impact on the cost-effective use
of oxygen therapy. Clinical outcomes of discontinuation of
COT after short-term oxygen are currently unknown; a
prospective study is ongoing at our institution.

ACKNOWLEDGMENTS

The authors are grateful to Betty Hemdon PhD for her assistance in
statistical analyses.

REFERENCES

1. Continuous or nocturnal oxygen therapy in hypoxemic chronic ob-
structive lung disease; a clinical trial. Nocturnal Oxygen Therapy
Trial Group. Ann Intern Med l980:93(3):391-398.

2. I-ong term domiciliary oxygen therapy in chronic hypoxic cor pulmonale
complicating chronic bronchitis and emphysema. Report of the Medical
Research Council Working Party. Lancet 1 98 1;1(8222):68 1-686.

3. Morrison DA. Stovall JR. Increased exercise capacity in hypoxemic
patients after long-term oxygen therapy. Chest 1992; 102(2):542-
550.

4. Krop HD. Block AJ, Cohen E. Neuropsychologic effects of contin-
uous oxygen therapy in chronic obstructive pulmonary di-sease. Chest
1973;64(3);3l7-322.

5. O'Donohue WJ Jr. Plummer AL. Magnitude of usage and cost of home
oxygen therapy in the United States. Chest 1995;107(2);301-302.

6. British Thoracic Society. Recommendations for oxygen concentra-
tors for long term domiciliary oxygen treatment with adults. BTS
News l993:No. II.

7. Siafakas NM. Vermeire P, Pride NB, Paoletti P. Gibson J, Howard
P, et al. Optimal assessment and management of chronic obstructive
pulmonary disease (COPD). The European Respiratory Society Task
Force. Eur Respir J 1995;8(8);I398-1420.

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10.

8. Matthys H, Keller R. Zwick H, Barthlen G. Recommendations and guide-
lines for long-temi oxygen therapy (LTOT) of the International Respir Can;
Club (IRCC). Monaldi Arch Chest Dis 1998;53(1);107-109.

9. Conference Report. New problems in supply, reimbursement, and
certification of medical necessity for long term oxygen therapy. Am
Rev Respir Dis 1990;l42(3):721-724.

Standards for the diagnosis and care of patients with chronic ob-
structive pulmonary disease. American Thoracic Society. Am J Re-
spir Crit Care Med 1995(5 Pt 2);152:S77-SI21.
Morrison D. Skwarski K, MacNee W. Review of the prescription of
domiciliary long term oxygen therapy in Scotland. Thorax 1995;
50(I2):1 103-1 105.

12. Restrick LJ. Paul EA, Braid CM, Cullinan P, Moore-Gillon J.
Wedzicha JA. Assessment and follow up of patients prescribed long
term oxygen treatment. Thorax 1993;48(7):708-713.

13. Timms RM. Kvale PA. Anthonisen NR, Boylen CT, Cugell DW,
Petty TL, Williams GW. Selection of patients with chronic obstruc-
tive pulmonary disease for long-term oxygen therapy. JAMA 1981;
245(24):2514-25I5.

14. Health Care Financing Administration. Coverage issues manual -
durable medical equipment. Home use of oxygen. l993;60-64.

19,

15. Health Care Financing Administration. Medicare carriers manual,
claim processing. HCFA Pub. 14-3: PB 94-954799. 1994: Part 3.

16. O'Donohue WJ Jr. Effect of oxygen therapy on intTeasing arterial oxygen
teasion in hypoxemic patients with stable chronic obstmctive pulmonary
disease while breathing ambient air. Chest 1991;100(4):968-972.

17. Department of Health. Domiciliary oxygen therapy service. Drug
tariff Part X. London HMSO, 1990.

Walshaw MJ, Lim R, Evans CC, Hind CR. Prescription of oxygen
concentrators for long term oxygen treatment: reassessment in one
district. BMJ 1988;297(6655):1030-1032.

Levi-Valensi P, Weitzenblum E. Pedinielli JL, Racineux JL, Duwoos
H. Three-month follow-up of arterial blood gas determinations in
candidates for long-term oxygen therapy: a multicentric study. Am
Rev Respir Dis 1986;133(4):547-55l.

20. Pfister SM. Home oxygen therapy: indications, administration, re-
certification and patient education. Nurse Pract 1995;20(7):44.47-
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21. Office of the Inspector General. Office of Audit Service: Results of
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Audit Control No. A-04-88-02058, 1990.

22. Silverman BG, Gross TP, Babish JD. Home oxygen therapy in Medi-
care beneficiaries, 1991 and 1992. Chest 1997;! 12(2):380-386.

Respiratory Care Open Forum 2000

Respiratory Care welcomes abstracts of scientific reports on any aspect of respiratory care presented as

• an original study

• the evaluation of a method, device, or protocol

• a case or case series

If your abstract is accepted for publication in RESPIRATORY CARE, you will be invited to present it at the 46th
International Respiratory Congress in Cincinnati, Ohio.

See the Call for Abstracts 2000 in this issue for more information.

Deadline for Submission: April 28, 2000

406

Respiratory Care • April 2000 Vol 45 No 4

Spirometry in Normal Subjects in Sitting, Prone, and Supine Positions

Gary M Vilke MD, Theodore C Chan MD, Tom Neuman MD, and Jack L Clausen MD

OBJECTIVE: Determine whether pulmonary function testing is affected by patient positioning.
METHODS: In a descriptive study with measurements made in a sequential but randomized order
at a university-based pulmonary function laboratory, 20 healthy men, ages 18-50 years, were
evaluated with spirometric assessment of forced vital capacity (FVC), forced expiratory volume in
the first second (FEV,), and maximum voluntary ventilation (MW) in the sitting, supine, and
prone positions. Subjects were excluded for body mass index (BMI) > 30 kg/m^ or abnormal
baseline spirometry. RESULTS: Comparing sitting to supine and prone positions, there was a
statistically significant decline in the spirometry values (reported as percent of predicted normal ±
standard error of the mean). FVC was 102% ± 4% while sitting, 95% ± 4% while supine, and 94%
± 4% while prone. FEV, was 104% ± 3% while sitting, 96% ± 3% while supine, and 94% ± 3%
while prone. MW was 115% ± 4% while sitting, 102% ± 4% while supine, and 97% ± 3% prone.
CONCLUSION: In healthy men with BMI < 30 kg/m^, changing from the sitting to supine or prone
position results in statistically significant change in respiratory pattern. However, all spirometry
values in each position were normal by American Thoracic Society definitions. [Respir Care 2000;
45(4):407-410] Key words: pulmonary function testing, forced vital capacity, forced expiratory volume
in the first second, maximal voluntary ventilation, body mass index, spirometry, sitting, prone, supine.

Background

Patients are placed into many different positions by their
physicians, for various procedures or studies or for re-
straint and safety. The effect of these positions on venti-
latory function has not been well studied in healthy indi-
viduals, though there have been papers evaluating body
positioning in obese patients,'- children,'-* and patients
with underlying disease processes.''"^ In patients with ob-
structive lung disease** and patients with diaphragmatic
paralysis,' decreases in forced vital capacity (FVC) were
noted with change in position from erect to supine. In

Gary M Vilke MD and Theodore C Chan MD are affiliated with the
Department of Emergency Medicine; Tom Neuman MD is affiliated with
the Department of Emergency Medicine and the Division of Pulmonary
Medicine. Department of Medicine; and Jack L Clausen MD is affiliated
with the Division of Pulmonary Medicine. Department of Medicine. Uni-
versity of California San Diego Medical Center, San Diego, California.

This study was supported in part by a grant from the County of San Diego
(Grant #94— 1974R) and by a grant from the General Clinical Research
Center's Program, MOl RR0087. of the National Center for Research
Resources, National Institutes of Health.

tetraplegic patients, FVC was noted to increase with chang-
ing to the supine position,'" but in normal subjects FVC
was noted to decrease with changing from erect to supine
positions.** Spirometry studies have also been performed in
normal subjects comparing standing and sitting positions. "'^
Differences in the lung function of healthy subjects in
the supine or prone positions, compared with sitting, are of
interest because these are the positions usually assumed
during radiographs, general anesthesia, and more severe
illnesses. We have also been involved with many agitated
patients who required restraint to gumeys, in which either
supine or prone positions must be utilized. Some concerns
had been raised by staff about the possibility of inducing
hypoventilation by restraining patients in the 4-point prone
position. We hypothesized that subjects might show spi-
rometric changes from changing from sitting to supine or
prone position, but that these changes would probably be
clinically unimportant. Accordingly, we set out to evaluate
spirometric changes resulting from changing body posi-
tion from sitting to supine or prone position, in a specific
population of healthy, nonobese adult males.

Methods

Correspondence: Gary M Vilke MD. Department of Emergency Medi-
cine, UC San Diego Medical Center. 200 West Arbor Drive #8676, San
Diego CA 92103. E-mail:gmvilke@ucsd.edu.

The experimental study design and protocol were re-
viewed and approved by the Human Subjects Committee.

Respiratory Care • April 2000 Vol 45 No 4

407

Spirometry in Normal Subjects in Sitting, Prone, and Supine Positions

Over a one-month period, we tested 20 healthy male vol-
unteers between 1 8 and 50 years of age. recruited by print
advertisements at local colleges. Participants gave informed
consent and were financially compensated.

Exclusion criteria included any history of pulmonary
disease, asthma, cardiac disease, recreational drug use, or
other significant illness or disability that would limit the
ability to perform the pulmonary function tests (PFTs).
Individuals with a body mass index (BMl, defined as weight
in kilograms divided by height in meters, squared) > 30
kg/m^ were also excluded. All the subjects had no smok-
ing history, either recent or distant.

Initial screening PFTs were performed with a pneumo-
tachograph-type spirometer (CPX-D, Medical Graphics,
St Paul, Minnesota), with calibration prior to each subject,
using a 3 L calibration syringe. Peak expiratory flow rates
and lung volumes (FVC and forced expiratory volume in
the first second [FEV,]) were measured with the volunteer
in the sitting position. Spirometry was performed in ac-
cordance with American Thoracic Society criteria, includ-
ing reproducibility within 5% variability on 3 repeat mea-
surements. I ^ Abnormal PFTs (FVC and FEV , ) were defined
as measurements below 80% of predicted normal for each
subject for that individual's height, age, and race.'"* Ab-
normal results were verified with repeat PFT screening
measurements. Volunteers with confirmed FVC or FEV,
values < 80% of predicted did not participate in the study.

The subjects then underwent PFT in sitting, supine, and
prone positions. Measurements obtained in the 3 positions
included FVC, FEV,, and maximum voluntary ventilation
(MVV). To ensure reproducibility, MVV was repeated
twice, for durations of at least 6 seconds each. In the
sitting position, the subject sat in a chair with his feet flat
on the floor, his back upright against the back of the chair,
and with head facing forward. In the supine position, the
subject lay flat on his back on a medical examination table,
with head facing upwards, arms to the side, legs in full
extension, and feet together. In the prone position, the
subject lay flat on his stomach on a medical examination
table, with head turned to the side, cheek resting on the
examination table, arms to the side, legs in full extension,
and feet together. The order of the supine and prone po-
sitions was randomized to prevent any potential influence
of serial testing on the measurements. Spirometry in the
sitting position was performed last, for comparison with
the initial screening sitting spirometry results, in order to
ensure that no significant change occurred from repeated
measurements.

Statistical analysis incorporated two-way analysis of
variance for repeated measures, and / testing to detect
statistically significant differences between the sitting, su-
pine, and prone PFT measurements. A p value < 0.05 was
considered statistically significant.

Results

Twenty-one subjects were considered for enrollment,
and 20 met screening criteria. One subject was excluded
because his screening spirometry results were in the ab-
normal range.

Our results show statistically significant differences in
PFT readings among the three positions tested. FVC was
significantly lower (p < 0.05) in the supine and prone
positions than in the sitting position. The FVC difference
between the supine and prone position was also statisti-
cally significant (p < 0.05). The magnitude of the change
was: supine versus sitting, -7.1%; prone versus sitting,
-7.9% (Table 1). The p values reported in Table 1 were
obtained using analysis of variance for repeated measures,
with position and time as factors.

FEV, was also significantly lower (p < 0.05) in the
supine and prone positions than in the sitting position, and
the FEV, difference between the supine and prone posi-
tions was statistically significant. The magnitude of the
change was: supine versus sitting, -7.2%; prone versus
sitting. -9.1% (see Table 1).

MVV was also significantly lower (p < 0.05) in the
prone and supine positions. The magnitude of the change
was: sitting versus supine, -9.5%; sitting versus prone,
-14.8% (see Table 1).

Discussion

In 20 male subjects, we found statistically significant
differences between spirometry values taken in sitting, su-
pine, and prone positions. However, although the differ-
ences were statistically significant, the clinical applicabil-
ity is not clear. For FVC, FEV,, and MVV, the lowest
measured percent of predicted was 94%, which is well
within the normal range of the American Thoracic Society
guidelines. Thus, prone or supine positioning of healthy
men with normal BMI and no smoking history appears not
to cause ventilatory compromise.

Several potential physiologic mechanisms would explain
our findings. It has been suggested that the supine position
affects diaphragm function because the subject has more
intra-abdominal pressure keeping the diaphragm from mov-
ing caudal into a position of maximum contraction, and
therefore lung volume and forced capacity are compro-
mised. In the prone position, lung volume is reduced even
more because the anterior ribs are compressed by the weight
of the body and thus cannot fully expand, limiting both
volume and the ability to force air out of the lungs. There
is some research that suggests that position affects venti-
lation and perfusion zones within the lung, another factor
that may be involved in our findings.

Although the changes we found were not clinically rel-
evant in our study of healthy adult men, it is unclear what

408

Respiratory Care • April 2000 Vol 45 No 4

Spirometry in Normal Subjects in Sitting, Prone, and Supine Positions

Table I . Mean Positional Spirometry

Measurement

Position

Value

% Change*

% Pred

p valuet

FVC(L)

Sitting

5.34

102 ±4

Supine

4.96

-7.1

95 ±4

<0.05

Prone

4.92

-7.9

94±4

<0.05

FEV, (L)

Sitting

4.27

104 + 3

Supine

3.96

-7.2

96 ±3

< 0.05

Prone

3.88

-9.1

94 ±3

< 0.05

MVV (L/min)

Silting

169

115 ±4

Supine

153

-9.5

102 ±4

<0.05

Prone

144

-14.8

97 ±3

<0.05

""* change from sitting position.

^ pred = percent of predicted normal ± standard eiTOr of the mean.

tThese p values reflect significance compared to sitting values.

?These p values irtlect supine compared to prone values.

FVC = fortred vital capacity.

FEV I = forced expiratory volume in the first second.

MVV = maximum voluntary ventilation.

<0.05

impact such changes might have on patients with compro-
mised pulmonary function from underlying disease or
trauma, and who are placed into these positions for pro-
cedures or surgery.

Moreno and Lyons" studied total lung capacity of
healthy subjects in the same three positions that we did.
but measured tidal volume, minute ventilation, and oxygen
consumption. They found that minute ventilation was lower
in the supine position (3.455 L/min/m") than in the sitting
position (3.974 L/min/m"), but that minute ventilation in
the prone position (3.927 L/min/m~) was almost as much
as in the sitting position. Other authors have also studied
position-related volume differences, most often incorpo-
rating only supine and sitting positions,'*" or standing, su-
pine, prone, and right lateral decubitus positions.'"' Cortese
et al found no change in phase IV in single-breath oxygen
testing when the subject moved from standing to supine,
prone, or right lateral decubitus position. Navajas et al
noted significant decreases in functional residual capacity,
total lung capacity, and vital capacity when subjects
changed from sitting to supine position. Blair and Hick-
man found that functional residual capacity was lower in
the seated position than in the standing position, and still
lower in the recumbent position.'* A comparison of spi-
rometry values from 235 subjects in standing and sitting
positions showed small differences in FVC and FEV,.
with sitting having higher values." Townsend found
slightly higher FEV, and FVC values in standing subjects
than in sitting subjects.'- Compliance in various positions
has also been evaluated,'^ but in our review of the litera-
ture we did not find any comparisons of spirometry mea-
surements in prone, supine, and sitting positions.

There are limitations to our study. First, we restricted
subjects to healthy men between the ages of 1 8 and 50 and
with BMI < 30 kgjm^. Males were chosen because they

were the patients that most frequently require restraint in
the prone position. As this study had a restricted subject
population, the effects of patient position in women, chil-
dren, the elderly, and patients with cardiopulmonary dis-
ease, BMI greater than 30 kg/m", or other conditions were
not addressed. We found no other publications reviewing
position-related spirometry changes in women.

The positioning of the head to the side in the prone
position could possibly cause air flow obstruction. Al-
though this is the position of patients in the intensive care
unit, surgery, or restraints, it may not reflect the physiol-
ogy of a true prone position as would have been demon-
strated with the head placed straight ahead on a massage-
type table.

Our results were as predicted, with significantly lower
spirometry readings in the supine and prone positions, but
the clinical relevance of this finding in this population of
healthy men is limited because the percent of predicted
values was normal for all subjects. Future studies need to
evaluate whether patients with specific disease processes,
such as asthma, chronic obstructive pulmonary disease, or
congestive heart failure have significant changes in pul-
monary function when position is changed, since this may
be significant for positioning patients for procedures, stud-
ies, or restraining maneuvers.

Conclusion

In healthy men with BMI < 30 kg/m"^, changing from
the sitting position to the supine or prone position results
in statistically significant changes in respiratory pattern;
however, all spirometric measurements in each position
were normal by American Thoracic Society definitions.

Respiratory Care • April 2(X)0 Vol 45 No 4

409

Spirometry in Normal Subjects in Sitting, Prone, and Supine Positions

ACKNOWLEDGEMENTS

The authors would like to thank Carlos Lopez. Jeffrey Johnson, and Paul
Schragg for their help with this project.

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Martin RJ. Herrell N, Rubin D. Fanaroff A. Effect of supine and

prone positions on arterial oxygen tension in the preterm infant.

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6. Romero S, Martin C, Hemendez L, Arriero JM, Benito N, Gil J.
Effect of body position on gas exchange in patients with unilateral
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7. Quinn TJ, Smith SW, Vroman NB, Kertzer R, Olney WB. Physio-
logic responses of cardiac patients to supine, recumbent, and upright
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Allen SM, Hunt B, Green M. Fall in vital capacity with posture. Br J
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Newsom-Davis J. The diaphragm and neuromuscular disease. Am
Rev Respir Dis I979;l 19(2 Pt 2):l 15-117.

Estenne M. De Troyer A: Mechanism of the postural dependence of
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with subjects in .standing and sitting positions. Chest I976;70(l):17-
20.
1 2. Townsend MC. Spirometric forced expiratory volumes measured in
the standing versus the sitting posture. Am Rev Respir Dis 1984;
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Standardization of spirometry - 1994 update. American Thoracic
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Morris JF, Koski A, Johnson LC. Spirometric standards for healthy
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Moreno F. Lyons HA. Effect of body posture on lung volumes.
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Navajas D. Farre R. Rotger MM, Milic-Emili J, Sanchis J. Effect of
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Cortese DA, Rodarte JR, Rehder K, Hyatt RE. Effect of posture on
the single-breath oxygen test in normal subjects. J Appl Physiol
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Blair E. Hickman JB. The effect of change in body position on lung
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Respiratory Care • April 2000 Vol 45 No 4

Case Reports

Persistent Left Superior Vena Cava: Case Report and

Literature Review

Bipin D Sarodia MD and James K Stoller MD

A persistent left superior vena cava (PLSVC) is the most common thoracic venous anomaly. It is a
persistent remnant of a vessel that is present as a counterpart of normal right-sided superior vena
cava (SVC) in early embryological development but normally disappears later. Although it can be
easily diagnosed by the characteristic chest radiographic appearance of a pulmonary artery cath-
eter (PAC) passed through it after being inserted into the left subclavian or jugular vein, its
diagnosis is usually missed by the presence of normal (right) SVC and the passage of the catheter
on the right side. Its diagnosis can be confirmed by many noninvasive and invasive tests, or it is
incidentally diagnosed at thoracic surgery or autopsy. If it is not associated with other congenital
cardiac anomalies, it is usually asymptomatic and hemodynamically insignificant. However, PLSVC
has important clinical implications in certain situations. In this article, we describe a patient with
bilateral SVC (a normal right SVC and a PLSVC) identified by a PAC in the PLSVC and the
pacemaker wires in the right SVC. In addition, we review the literature on prevalence, embryo-
logical development, diagnosis, and clinical implications of PLSVC. [Respir Care 2000;45(4):41 1-
416] Key words: left superior vena cava, congenital defects, pulmonary artery catheter, central venous
catheter.

Introduction

A persistent left superior vena cava (PLSVC) is the
most common thoracic venous anomaly, resulting from the
abnormally persistent patency of an embryological vessel
normally present during the early developmental period. '■-
We describe a patient with a PLSVC identified on a chest
radiograph by a pulmonary artery catheter (PAC) passing
through it. Although most patients with an isolated PLSVC
are asymptomatic and hemodynamically stable, PLSVC
may have important clinical implications in certain situa-
tions. In this article, we review the literature on preva-
lence, embryological development, diagnosis, and clinical
implications of PLSVC.

Bipin D Sarodia MD and James K Stoller MD are affiliated with the
Division of Medicine, Section of Respiratory Therapy, Department of
Pulmonary and Critical Care Medicine, The Cleveland Clinic Founda-
tion, Cleveland, Ohio.

Correspondence; James K Stoller MD, Division of Medicine, Section of
Respiratory Therapy, Department of Pulmonary and Critical Care Med-
icine, A-90, The Cleveland Clinic Foundation, 9500 Euclid Avenue.
Cleveland OH 44195. E-mail: stollej@ccf.org.

Case Summary

An 81 -year-old female ex-smoker was admitted to the
hospital for evaluation of her shortness of breath. Her
medical history included emphysema, mitral valve replace-
ment for mitral stenosis and insufficiency, refractory atrial
fibrillation, and dual-chamber pacemaker insertion for sick
sinus syndrome with symptomatic bradycardia. The chest
radiograph (Fig. 1) was obtained, while the patient was
still in the intensive care unit on a ventilator post-opera-
tively, to confirm the position of the Swan-Ganz PAC
introduced for hemodynamic evaluation after a second mi-
tral valve replacement surgery. The film demonstrates the
typical appearance of a PAC passing through a PLSVC.

Right atrial pressure was 16 mm Hg, pulmonary arterial
pressure was 70/27 mm Hg (consistent with her previous
longstanding mitral stenosis), and pulmonary artery cap-
illary wedge pressure was 20 mm Hg. The PLSVC drain-
ing into the right atrium via a markedly dilated coronary
sinus was diagnosed earlier by transthoracic and trans-
esophageal echocardiographic studies, which did not re-
veal atrial septal defect or any other associated congenital
cardiac anomaly (Fig. 2). The other abnormal findings on

Respiratory Care • April 2000 Vol 45 No 4

411

Persistent Left Superior Vena Cava

Fig. 1. Chest radiograph (antero-posterior view) showing the typical appearance of a Swan-
Ganz pulmonary artery catheter passing through a PLSVC in our patient with double superior
vena cava (SVC) connected by a left brachiocephalic vein. The catheter (black arrows pointing
down and left) passes along the left border of the mediastinum (black arrow pointing left) from
its insertion into the left subclavian vein, and its tip reaches the left pulmonary artery via the
coronary sinus, right atrium, and right ventricle, after forming a sharp hairpin loop (black arrow
pointing down) in the right atrium. The hollow arrows (pointing right and up) point to the
pacemaker wires and electrodes. The pacemaker wires pass downward along the right medi-
astinal border, indicating the presence of a normal SVC, and the electrodes are placed in the
right atrium and right ventricle.

current echocardiogram included mild dilation and dys-
function of the right ventricle, and tricuspid valve regur-
gitation. After the surgery, the St Jude prosthetic mitral
valve was found to be seated well, without mitral regur-
gitation or significant left ventricular outflow gradient, as
compared to the preoperative finding of severe left ven-
tricular outflow obstruction with a gradient of 64 mm Hg
caused by the struts of the prior prosthetic mitral valve.

The patient required a new central venous access (either
a triple lumen catheter or a PAC via subclavian vein or
internal jugular vein) 8 times during the current hospital-
ization. The catheter passed via the normal (right) SVC all
4 times when inserted into the right side, and through the
PLSVC in 3 of the 4 times when inserted into the left side.
On one occasion, the PAC crossed from the left of the

mediastinum into the right SVC, indicating the presence of
a left brachiocephalic vein connecting the two vena cavae
(Fig. 3). The catheters on the left side were reported by the
radiologists (who were unaware of the previous finding of
PLSVC) to be "taking an abnormal course in the medias-
tinum" or "possibly in a PLSVC." The shorter central
venous catheters were reported as "possibly in the left
internal mammary or pericardiophrenic vein."

The patient required a tracheostomy for prolonged ven-
tilator weaning because of poor cardiopulmonary status.
The presence of the PLSVC did not appear to have any
clinical implications in the management of this case, ex-
cept causing confusion about the site of the PAC when
placed in the PLSVC, as seen on the chest radiograph (see
Fig. 1).

412

Respiratory Care • April 2000 Vol 45 No 4

Persistent Left Superior Vena Cava

Fig. 2. Transesophageal echocardiography. Transverse view identifies dilated coronary sinus (CS), w/hich lies
posterior to the left atrium (LA) and drains the persistent left superior vena cava (PLSVC) into the right atrium
(RA). Microbubble echo contrast produced by agitated normal saline injection through right arm vein opacifies
RA and right ventricle (RV), but not the CS, PLSVC, or LA. LV = left ventricle. TV = tricuspid valve.

Discussion

Embryological Development

Normally, the cardinal veins constitute the main venous
drainage system of the embryo (see Fig. 3).^ The anterior
and posterior cardinal veins drain cranial and caudal parts
of the embryo, respectively. In the eighth week of gesta-
tion, the left brachiocephalic vein develops and proceeds
to connect the cranial portions of the two anterior cardinal
veins. The caudal part of the right anterior cardinal vein
becomes the normal (right) SVC, and the left anterior
cardinal vein caudal to the left brachiocephalic vein de-
generates. If this portion remains patent, it forms a PLSVC
that opens into the right atrium via the coronary sinus and,
with the presence of normal right SVC, the patient has a
double SVC. This is commonly associated with a small or
absent anastomosis that forms the left brachiocephalic
vein.^ Rarely, in patients with PLSVC, the right anterior
cardinal vein degenerates, resulting in the absence of a
normal (right) SVC, and the blood from the right side is

carried by the brachiocephalic vein to the PLSVC. In most
of the cases, the PLSVC drains into the right atrium through
the coronary sinus, but in the remaining cases, it drains
into the left atrium, creating a right-to-left shunt.

Prevalence

A PLSVC is an embryological remnant that is the most
common congenital anomaly involving central venous re-
turn in the thorax.'- Its prevalence was 0.3% in a series of
unselected postmortem examinations. Also, PLSVC was
present in 4.4% (12 of 275) of patients undergoing angio-
cardiograms for suspected congenital or acquired cardiac
lesions.** -'' PLSVC was found as an associated anomaly in
2.6% (39 of 1,500) of patients with congenital cardiac
anomalies, and at least 67% of these 39 patients had two
SVC.6 In another study, PLSVC with absent right SVC
was found in 0.15% of patients (6 of 4,100) at cardiac
catheterization for suspected congenital cardiac disease.''
Of a total of 174 cases of PLSVC in the literature, 67

Respiratory Care • April 2000 Vol 45 No 4

413

Persistent Left Superior Vena Cava

Right

Left

Anterior Cardinal Vein

Internal Jugular Vein

Subclavian Vein

Brachiocephalic Vein

Normal (Right)
Superior Vena Cava

Internal Jugular Vein

Azygos Vein — •
Posterior Cardinal Vein Inferior Vena Cava

Subclavian Vein

Brachiocephalic Vein

Persistent Left Superior
Vena Cava

Coronary Sinus Os

Coronary Sinus

Sinus Venosus

Fig. 3. Developmental anatomy of the superior vena cava (SVC). The cardinal veins constitute the main
venous drainage system of the embryo. The internal jugular, subclavian, and brachiocephalic veins are
derived from the anterior cardinal veins on either side. In the eighth gestational week, the left brachio-
cephalic vein connects upper portions of the anterior cardinal veins. Normally, on the right side, the
part caudal to this connection forms the SVC, and its counterpart on the left side degenerates. If this
portion remains patent on the left, it forms a persistent left superior vena cava that opens into the right
atrium via the coronary sinus, and the patient thus has a double SVC.

(39%) had associated significant cardiovascular anoma-
lies, including cardiac septal defects in 59 (88%) of 67 pa-
tients (atrial septal defects in 49 patients, ventricular in 36,
and combined in 26), and 82% had double SVC.»

Diagnosis

Clinical clues that suggest the diagnosis of PLSVC in-
clude:

1 . A shadow of the PLSVC visible on a conventional
chest film as widening of the aortic shadow with a medi-
astinal bulge under the aortic arch, or as a definite strip in
the upper left margin of the mediastinum, with slightly
lower density than the medial mediastinum.**

2. The characteristic left-sided course of the catheter
passing through a PLSVC seen on imaging studies ob-
tained to confirm proper position of a central venous cath-
eter or PAC (especially after left subclavian or jugular

venous insertion, as in our case: see Fig. 1 ).''-'''^-' ' The first
case of Swan-Ganz catheterization through a PLSVC was
reported in 1983.'" Thereafter, few other case reports of
discovery of PLSVC on the plain radiograph after pulmo-
nary artery catheterization have been published. ■'■''■^•' ' How-
ever, PLSVC often goes undetected (especially after right-
sided venous insertion) because the presence of a normal
(right) SVC (as occurs in 82% of cases) allows the catheter
to pass in a normal route.** In one study, only 5 cases of
PLSVC were detected on routine imaging studies of ap-
proximately 4,000 central venous catheters placed. •* When
catheters are imaged in a PLSVC, the presence of a normal
(right) SVC is suggested if the central venous catheter,
pacemaker lead (as in our case: see Fig. 1), or guidewire
can be placed simultaneously along the right side of the
mediastinum.

3. A longer than expected PAC insertion length to ob-
tain the typical pressure wave forms of right ventricle.

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Persistent Left Superior Vena Cava

pulmonary artery, and pulmonary artery occlusion pres-
sures.^'o'- For a person of average build, the insertion
length of the catheter, measured at the skin, passing through
the PLSVC to achieve a pulmonary capillary wedge pres-
sure wave form is 65-70 cm, and the lengths to achieve the
right ventricular and the right atrial pressure wave forms
are approximately 52 cm and 42 cm, respectively, from the
right internal jugular vein.'''- Note, however, that the in-
sertion length can be increased even in the absence of a
PLSVC, as when the catheter coils in the right atrium or
ventricle.

4. The central venous tracing in proximal PLSVC shows
small positive pressure waves (instead of normal a, c, and
v waves) because of compression by the juxtaposed aorta
transmitting pulsations. '-

5. Unusually high computed thermodilution cardiac out-
put values because of blood escaping from the right side of
the heart into the coronary sinus and left atrium.'- How-
ever, this overestimation may go undetected unless an-
other, independent measurement of cardiac output is made
simultaneously.

Techniques to confirm the diagnosis of PLSVC include:

1 . Angiographic examination (venogram) with bolus con-
trast injection in the catheter.'"

2. Two-dimensional transthoracic echocardiography
with injection of contrast material from a peripheral left
arm vein causes early opacification of an abnormally large
coronary sinus before other right-sided chambers, thus sug-
gesting abnormal venous drainage.''' The test may fail to
detect a PLSVC in cases where the coronary sinus is atretic
or absent; in such a rare instance, the blood flow is retro-
grade, from the coronary venous system into the PLSVC,
brachiocephalic vein, and right SVC. in that sequence.

3. Transesophageal echocardiography, which is more
sensitive than transthoracic studies for the diagnosis of
PLSVC and associated cardiac anomalies, including atrial
septal defect, anomalous connection of pulmonary veins,
and PLSVC draining into the left atrium, hepatic vein, or
inferior vena cava.'-* Transverse cuts through the right
atrium and coronary sinus usually show the dilated coro-
nary sinus and the presence of PLSVC to the left of the left
atrial appendage (as in our case: see Fig. 2).'^

4. First pass radionuclide angiography in the right or left
anterior oblique projection, which may be the noninvasive
study of choice for recognizing PLSVC, with or without
associated intracardiac shunt. '-^

5. Computerized tomography of the chest, because of its
widespread use. may often detect or confirm the presence
of PLSVC, but it may not be satisfactory for visualization
of the exact course and site of connection of PLSVC with
the cardiac chambers.'*

6. Magnetic resonance imaging, which gives more ac-
curate images of the heart than conventional computed
tomography and shows mediastinal structures such as vena

cavae, coronary sinus, and the opening into the right atri-
um.'* Before the widespread application of angiocardio-
graphy and the availability of advanced imaging techniques,
PLSVC was difficult or impossible to diagnose clinically,
and was usually discovered at postmortem examination or
incidentally at the time of cardiac surgery.^**

Clinical Implications

The presence of a PLSVC may have important clinical
implications. For example, placement of a central venous
catheter or PAC into a PLSVC may be mistaken for place-
ment in the other sites occupying positions resembling that
of a PLSVC (eg, the subclavian or carotid artery, the me-
diastinum, pericardium or pleural space, or the left internal
mammary vein, pericardiophrenic vein, or superior inter-
costal vein). Additional clues should be sought to deter-
mine whether the central venous catheter is placed ectopi-
cally. For example, confirmation of an inadvertent
placement in an artery is suggested by assessment of the
pressure waveform and/or the arterial partial pressure of
oxygen. The absence of blood return or the presence of
radiographic features of pneumomediastinum, pneumoperi-
cardium, or pneumothorax suggests placement in the me-
diastinum, pericardium, or pleural space. '^

A second important clinical implication of PLSVC is
that an atrial septal defect is commonly associated with
PLSVC.** The septal defect may predispose to paradoxical
systemic air emboli or arterial thromboemboli and stroke
or other sequelae.

Third, cardiac arrhythmias, including ventricular fibril-
lation, have been reported in patients with PLSVC" Ar-
rhythmias may result from dilatation of the coronary sinus
opening, causing stretching of the atrioventricular node
and His's bundle, especially in cases with absent right
SVC, wherein the coronary sinus serves as the only drain-
age for the flow from the entire SVC.

Fourth, PLSVC may cause difficulty in introducing cen-
tral venous catheters, PACs, or pacemaker or defibrillator
leads because of the narrow opening of the coronary sinus
to reach the right atrium. **'"

Fifth, in some cases of PLSVC, the use of retrograde
cardioplegia (eg, for coronary artery bypass graft surgery)
may cause inadequate myocardial perfusion and thus may
be ineffective.'^

Sixth, during cardiac surgery, it is impxjrtant to recog-
nize that PLSVC may be associated with coronary sinus
ostial atresia. Interruption of the PLSVC, which is the sole
route of coronary venous drainage in this rare anomaly, by
surgical ligation can potentially lead to myocardial isch-
emia and necrosis." Retrograde flow in the PLSVC seen
by Doppler ultrasonography should raise the suspicion of
this diagnosis.

Respiratory Care • April 2000 Vol 45 No 4

415

Persistent Left Superior Vena Cava

Thus, a PLSVC, if associated with other congenital car-
diac anomalies, may have adverse clinical implications
that can be averted by clinical recognition of the anomaly.

ACKNOWLEDGEMENTS

We thank Thomas Dresing MD, Cleveland Clinic, Cleveland, Ohio, for
his valuable assistance in obtaining the transesophageal echocardiographic
image of the patient.

REFERENCES

1 . Edwards JE. Congenital malformations of the heart and great ves-
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2. Edwards JE, DuShane JW. Thoracic venous anomalies. Arch Pathol
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3. Moore KL, Persaud TVN, editors. The cardiovascular system. In:
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4. Leibowitz AB. Halpem NA. Lee M-H, Iberti TJ. Left-sided superior
vena cava: a not-so-unusual vascular anomaly discovered during
central venous and pulmonary artery catheterization. Crit Care Med
1992;20(8):1I19-1122.

5. Cha EM. Khoury GH. Persistent left superior vena cava: radiologic
and clinical significance. Radiology I972;103(2):375-38l.

6. Campbell M, Deuchar DC. The left-sided superior vena cava. Br
Heart J 1954:16:423^39.

7. Pugliese P. Murzi B. Aliboni M, Eufrate S. Absent right superior
vena cava and persistent left superior vena cava: clinical and .surgical
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8. Winters FS. Persistent left superior vena cava: survey of the world
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Menendez B. Garcia del Valle S, Marcos RC, Azofra J. Gomez-

Arnau J. Left superior vena cava: a vascular abnormality discovered

following pulmonary artery catheterization. Can J Anaesth 1996;

43(6):626-628.

Ortega-Carnicer J, Malillos M, Parga G. Swan-Ganz catherization

via left superior vena cava. Chest 1983;84(6):784.

Coblentz MG, Criscito MA, Cohn JD. Persistent left superior vena

cava complicating hemodynamic monitoring catheterization. Crit

Care Med 1978;6(l):32-35.

Horrow JC, Lingaraju N. Unexpected persistent left superior vena

cava: diagnostic clues during monitoring. J Cardiolhorac Anesth

1989,3(5):6I 1-615.

1 3. Stewart JA, Fraker TD Jr. Slosky DA. Wise NK. Ki.sslo JA. Detec-
tion of persistent left superior vena cava by two-dimensional contrast
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14. Podol.sky LA. Jacobs LE. Schwartz M, Kotler MN, loli A. Trans-
esophageal echocardiography in the diagnosis of the persistent left
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15. Cheng CY. Wang DJ, Chen WL, Chang YF, Chang FK, Yang SP,
Shieh SM. Demonstration of persistent left superior vena cava by
first pass radionuclide angiography. Clin NucI Med 1987:12(11):
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16. Boussuges A. Ambrosi P. Gainnier M, Quenee V, Sainty JM. Left-
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17. Gentili DR. Onofrey D, Gabrielson GV, Benjamin E. Iberti TJ. Mal-
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Respiratory Care • April 2000 Vol 45 No 4

1999 Donald F Egan Scientific Lecture

Weaning from Mechanical Ventilation: What Have We Learned?

Martin J Tobin MD

It is a pleasure and honor for me to give the 26th Annual
Donald F Egan Scientific Lecture at the American Asso-
ciation for Respiratory Care. Much of my research career
has focused on weaning from mechanical ventilation, and
a major stimulus for my interest in this subject was an
outstanding review article published in Respiratory Care
by its current editor, Dave Pierson. in the early 1980s.' In
that article, Dave made the subject of weaning exciting.
More importantly, he pointed out many areas about which
we knew nothing. To someone starting an academic ca-
reer, the subject of weaning appeared particularly ripe for
research.

While preparing for this morning's lecture, I took my
copy of Egan 's Fundamentals of Respiratory Therapy from
the shelf. This was the first textbook directed primarily at
respiratory therapists. It was first published in 1969, and
the copy I own is the third edition, published in 1977.- In
the 1 977 edition, Dr Egan wrote that "The separation of a
patient from his ventilator is very nearly pure art." Wean-
ing is still an art in 1999. But over the next half hour, I
hope I can show you that the approach to weaning has a
more scientific basis than was the case 20 years ago.

Pathophysiology of Weaning Failure

A patient failing a weaning trial exhibits the physical
signs of respiratory distress. We see heightened activity of
the stemomastoid muscles, recession of the suprasternal
fossa, recession of the intercostal spaces, paradoxical mo-
tion of the abdomen, tachypnea, and sometimes cyanosis. '
These physical signs tell us the patient is not able to sus-
tain spontaneous ventilation. But to understand why pa-

Martin J Tobin MD is affiliated with the Division of Pulmonary and
Critical Care Medicine, Loyola University of Chicago Stritch School of
Medicine and Hines Veterans Affairs Hospital, Maywood, Illinois.

This article is based on a transcript of the 26th Annual Donald F Egan
Scientific Lecture delivered by Martin J Tobin MD at the 45th Interna-
tional Respiratory Congress of the American Association for Respiratory
Care. Las Vegas. Nevada, December 14. 1999.

Correspondence: Martin J Tobin MD, Division of Pulmonary and Critical
Care Medicine. Loyola University Medical Center, 2160 South First
Avenue. Maywood IL 60153.

tients fail weaning trials, we need to delve into the under-
lying pathophysiological mechanisms. Four anatomical
sites or functions may be involved: respiratory centers,
respiratory muscles, lung mechanics, and gas exchange
function of the lung.'* I'll discuss data pertaining to each
site and indicate how each is important in understanding
why patients fail weaning trials.

We begin with the respiratory centers. A depressed re-
spiratory center drive at the start of the weaning trial will
cause hypoventilation, making weaning failure inevitable.
Another possibility is for the drive to be normal at the start
of the trial, but then to fall during the course of the trial.
It's been suggested that it would be clever for the body to
decrease respiratory center output as a way of avoiding
contractile fatigue of the respiratory muscles. Such a strat-
egy has even been called "central wisdom.'"' Figure 1
shows the total pressure generated by inspiratory muscles,
expressed as pressure-time product, measured by Amal
Jubran in 17 patients who failed a weaning trial.'' All but
one patient showed an increase in pressure generation be-
tween the beginning and end of the T-tube trial. As such,
downregulation of respiratory motor output is not common
in patients who fail a trial of weaning.

Next, we move to the respiratory muscles. We used to
think that maximum inspiratory pressure, which reflects
inspiratory muscle strength, was helpful in predicting which
patients could come off the ventilator. In 100 patients
undergoing a weaning trial, we found no difference in
maximum inspiratory pressure between weaning success
and weaning failure patients.'' As such, respiratory muscle
weakness doesn't appear to be a common cause for failure
to wean. Might the respiratory muscles deteriorate be-
tween the beginning and end of a weaning trial? Yes, if
they develop respiratory muscle fatigue.**

Is it important to know whether these patients develop
muscle fatigue? It's extremely important. Darlene Reid*
has demonstrated electron-microscopic evidence of severe
muscle destruction in hamsters who developed diaphrag-
matic fatigue (Fig. 2). The same process may happen in
weaning failure patients. Patients who fail a weaning trial
already have problems before they commence the trial.
Then, as they fail the trial, they may be developing a new

Respiratory Care • April 2000 Vol 45 No 4

417

Weaning from Mechanical Ventilation: What Have We Learned?

30i

^ 25

E
". 20

■s

•D

2 15-

E
i-

3
OT
M

10-

Start

p < 0.0001

End

Fig. 1 . Values of inspiratory pressure-time product at the start and
end of an unsuccessful trial of weaning in 1 7 patients with chronic
obstructive pulmonary disease. All but one patient showed an
increase in pressure generation between the onset and end of the
trial. (Based on data from Reference 6.)

separate problem — that is, structural damage resulting from
contractile muscle fatigue.

To determine whether muscle fatigue is likely in such
patients, Amal Jubran measured the tension-time index of
the inspiratory muscles (Figure 3).* Tension-time index is
the product of two fractions: the mean pressure per breath
over maximum inspiratory pressure, and the time of inspi-
ration over total respiratory cycle time. She made mea-
surements at the start of a T-piece trial and at its end, about
45 minutes later. None of the weaning success patients
developed a tension-time index above 0.15 — the value that
has been linked with muscle fatigue.* Five of the failure
patients, however, had a tension-time index of 0.15 or
higher by the end of the trial. This observation suggests
that these five patients may have developed inspiratory
muscle fatigue. Tension-time index is an indirect index,
and it doesn't provide concrete evidence that fatigue ac-
tually occurred.

To convincingly detect fatigue, you need to stimulate
the phrenic nerves and measure the contractile response of
the diaphragm." Figure 4 shows measurements obtained
by Franco Laghi in a patient who failed a weaning trial. At
the start of the trial, the patient's twitch transdiaphrag-
matic pressure was around 30 cm HjO, which is normal.
The patient then underwent a T-piece trial lasting a half
hour. Franco repeated the measurements 1 5 min after com-
pleting the trial, and again at 30 and 60 min. The twitch
pressures fell considerably compared with baseline. These
data provide conclusive evidence of diaphragmatic fatigue.

This patient would have developed the type of structural
injury I showed you in the hamster model. Of course, the
data are from only a single patient. Franco is now studying
a larger group of patients to determine the frequency of
fatigue in patients undergoing weaning trials.

The data in Figures 5 and 6 show the stress on the
respiratory muscles in weaning failure patients. This stress
is related to the work the muscles perform. The informa-
tion in Figure 5 represents a huge amount of compressed
data.^ The tracings are ensemble averages of several breaths
from each individual patient. The failure patients had much
larger swings in esophageal pressure by the end of the trial
than at the beginning. Also, the swings in pressure were
much greater in the failure patients than in the success
patients.

Why is work of breathing (WOB) increased in patients
who fail a weaning trial? To answer this question, Amal
Jubran measured inspiratory resistance, dynamic elastance
(which is the inverse of compliance), and auto positive
end-expiratory pressure (auto-PEEP) (see Figure 6).'' She
found that the values for each variable were much higher
in failure patients than in success patients over the course
of a trial. Each variable also deteriorated over time in the
failure patients. That is, patients who fail a weaning trial
display a progressive worsening of their pulmonary me-
chanics, resulting in large increases in their WOB.

Might the pulmonary mechanics be more severely de-
ranged in the failure patients even before they come off the
ventilator? Could you tell, on the basis of mechanics, that
weaning failure is going to be inevitable? To address this
question, Amal Jubran looked at passive lung mechanics
before taking patients off the ventilator.'" Measurements
of airway pressure, transpulmonary pressure, and esopha-
geal pressure, combined with the end-inspiratory occlu-
sion method, allow you to respectively characterize the
overall respiratory system, the lung itself, and the chest
wall. You can also divide respiratory resistance into the
component resulting from ohmic resistance, reflecting air-
way resistance, and the component arising from stress in-
homogeneities in the system, consequent to pendelluft and
viscoelastic forces.

Before performing the T-piece trials, she passively ven-
tilated the patients. Respiratory system resistance was
equivalent in the weaning success and weaning failure
patients (Figure T).'** Moreover, partitioning of resistance
into the components reflecting airway resistance and stress
inhomogeneity revealed no difference between the groups.
That the respiratory mechanics were similar in the two
groups before the start of a trial implies that something in
the act of spontaneous breathing causes the weaning fail-
ure patients to deteriorate over the course of the trial. We
can speculate about mechanisms by which spontaneous
breathing could worsen respiratory mechanics, but to find
the real reason we need further research.

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Weaning from Mechanical Ventilation: What Have We Learned?

Fig. 2. Electron micrograph of the diaphragm in a control hamster (upper) and in a
hamster that had breathed through a resistive load for 6 days (lower). Loading was
achieved by tightening a polyvinyl band around the trachea until swings in esophageal
pressure were -20% of maximal inspiratory pressure; pulmonary resistance was in-
creased 6.5 fold. Compared with the normal structure, the loaded animals developed
sarcomere disruption with loss of distinct A bands and I bands and development of Z
line streaming. (From Reference 9, with permission.)

The fourth, and final, aspect of the pathophysiology is
gas exchange. Some patients fail a weaning trial with no
change in their arterial blood gases, whereas others de-
velop increases in carbon dioxide tension (Pco,) or de-
creases in oxygen tension. The term hypoventilation is
used synonymously with hypercapnia. But when you see
an increase in Pco,- 't doesn't mean that minute ventilation
has necessarily fallen. In a group of patients failing a
weaning trial, we found no relationship between P^q^ and
minute ventilation." Instead, we found that more than
80% of the variance in P^-o, could be explained by the
patients' tidal volume (V^-) and respiratory frequency (Fig-

ure 8). The Ppo, rose because the patients developed rapid
shallow breathing — with inevitable increase in dead-space
ventilation. Alveolar ventilation went down but overall
minute ventilation didn't change.

The hypoxemia that occurs in some patients failing a
weaning trial is usually associated with an increase in
venous admixture. A further factor contributing to the hy-
poxemia is a decrease in mixed venous oxygen saturation
(Figure 9).'- The fall in mixed venous oxygen saturation is
partly the result of the considerable cardiovascular de-
mand experienced by weaning failure patients, as first
shown by Franfois Lemaire.'^ In a classic study, Fran9ois

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419

Weaning from Mechanical Ventilation: What Have We Learned?

Failure

Success

1.0

I-

0.5 -

0.0

— r-

0.5

—1
1.0

0.15

I
0.5

—I
1.0

Pes /P| max

Fig. 3. The relationship between the ratio of mean esophageal pressure to maximum inspiratory pressure
(Pgj/Pimax) and duty cycle (J,/Tjot) i" 1 7 ventilator-supported patients with chronic obstructive pulmonary
disease who failed a trial of spontaneous breathing and 14 patients who tolerated the trial. Circles and
triangles represent values at the start and end of the trial, respectively; closed symbols indicate patients who
developed an increase in Pacoj during the trial. Five of the 17 patients in the failure group developed a
tension-time index of > 0.1 5 (indicated by the isopleth), suggesting respiratory muscle fatigue. N represents
the value in a normal subject. (From Reference 6, with permission.)

E
u

20-

.-e 10.

0-*

100 ms

After trial

15 min

30 min

60 min

Fig. 4. Recordings of transdiaphragmatic twitch pressure (Pa,) in a patient with a C4 spinal cord injury
1 min before a trial of spontaneous breathing and at several intervals after the end of the failed trial
that lasted 30 min. The nadir in twitch pressure was reached 30 min after the end of the trial, and at 60
min twitch pressure was still less than that recorded 10 min before the trial. This finding indicates the
development of contractile muscle fatigue.

420

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Failure Group

Success Group

Start

0.2

UL^ 0.0

End

Start

End

Time, sec

Fig. 5. Ensemble average plots of flow and esophageal pressure {P^ at the start and end of a trial of spontaneous breathing in 17
ventilator-dependent patients with chronic obstructive pulmonary disease who failed the trial and 14 patients who tolerated the trial
and were extubated. At the start of the trial, the inspiratory excursion in P^s was greater in the failure group, and it showed a further
increase by the end of the trial. To generate these plots, flow and Pes tracings were divided into 25 equal time intervals over a single
respiratory cycle for each of the 5 breaths for each patient in the two groups. For a given patient, the 5 breaths from the start of the
trial were then superimposed and aligned with respect to time, and the average at each time point was calculated. The group mean
tracings were then generated by ensemble averaging of the individual mean from each patient. The same procedure was performed
for breaths at the end of the trial. (From Reference 6, with permission.)

showed that weaning failure patients develop an increase
in their pulmonary artery wedge pressure and left-ventric-
ular end-diastolic volume. The increased stress on the car-
diovascular system probably resulted from the increased
WOB. When intrathoracic pressure becomes more nega-
tive, the afterload of the left ventricle increases, which, in
turn, makes it more difficult to maintain cardiac outpuL'^'-*

Prediction of Weaning Outcome

I will now discuss how good we are at predicting wean-
ing outcome. The predictive indices listed by Dr Egan in
1977 are similar to those you see listed today." ' One dif-
ference is his inclusion of a dead space-to- Vj ratio of less
than 0.60 as a helpful predictor of weaning success; few
people today would recommend this measurement. Over
the last 20 years, we have found that the classic variables,
such as maximum inspiratory pressure, minute ventilation,
and vital capacity have very high rates of false positives
and false negatives. '■'' Many indices don't help in telling
us whether or not an individual patient is likely to come

off the ventilator. They are useful, however, in our assess-
ment of the patient who has already failed a trial — to un-
derstand why that patient failed.

In the past, it was felt that the gestalt of an experienced
clinician at the bedside was better at predicting weaning
outcome than physiologic indices. The accuracy of this
gestalt had never been studied until recently. Randy Stro-
etz and Rolf Hubmayr"* asked attending physicians in the
intensive care units of the Mayo Clinic to predict whether
their patients were likely to succeed in a weaning trial. Of
the 3 1 patients in the study, the physicians predicted that
22 would fail the trial. Yet, half of the 22 patients were
successfully weaned. This doesn't mean that clinical as-
sessment is useless. It remains necessary, but it's not suf-
ficient. We need something in addition to clinical assess-
ment.

Some people say you can dispense with weaning pre-
dictors completely, and go directly to some weaning
method, such as a T-tube trial or pressure support. But to
use any weaning approach you have to first think of the
possibihty that the patient might tolerate it. In the study

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Weaning from Mechanical Ventilation: What Have We Learned?

15i

u
(1)

—I

10-

40-,

=rJ

30-

20-

10-

5.0 1

ol"

PS-

• Failure
oSuccess

Start

End

Fig. 6. Inspiratory resistance of the lung (Rjnsp.iJ, dynamic lung
elastance (E^yn.L). and intrinsic positive end-expiratory pressure
(PEEP,) in 17 weaning failure patients and 14 weaning success
patients. Data were obtained during the second and last minute of
the trial, and at one third and two thirds of the trial duration. Be-
tween the onset and end of the trial, the failure group developed
increases in Rmsp.L (p < 0.009), E^ynx (P < 0.0001), and PEEP; (p <
0.0001), and the success group developed increases in E^jy^ l (P <
0.006) and PEEP; (p < 0.02). Over the course of the trial, the failure
group had higher values of Rmspx (P < 0.003), E^jy^i.t (P < 0.006),
and PEEP| (p < 0.009) than the success group. (From Reference 6,
with permission.)

from the Mayo Clinic, we see that half the patients that
physicians thought not ready for weaning actually suc-
ceeded.'" As such, the systematic use of predictors alerts
us to the possibility that some of the patients we think not
ready for weaning are in fact much better than they appear.
From my discussion of the pathophysiology of weaning
failure, it's clear that patients failing a weaning trial ex-
perience huge stresses on their respiratory muscles and
cardiovascular system. These stresses might damage their
heart or respiratory muscles and also cause considerable
anxiety and distress. The measurement of predictive indi-
ces — provided they are reasonably reliable — avoids sub-
jecting patients prematurely to such stresses before they
are able to cope with them.

Several years ago, we noted that patients who went on
to fail a weaning trial developed an increase in respiratory
frequency and a fall in Vj as soon as we took them off the
ventilator (Figure 10)." We reasoned that measuring these
changes might be useful in forecasting weaning outcome.

We subsequently undertook a study, where we mea-
sured frequency and V^^ with simple instrumentation — a

hand-held spirometer — over one minute.'' The measure-
ments were made while patients were disconnected from
the ventilator and breathing room air. We combined the
measurements into an index of rapid shallow breathing,
the frequency-to-V.p ratio. The higher the ratio, the more
severe the rapid shallow breathing, and the greater the
likelihood that the patient would fail a weaning trial. We
tested the accuracy of this index in 1 00 patients, and found
a ratio of 100 breaths/min per liter gave the best separation
of the groups — a value that's easy to remember.

One of the best ways of evaluating the accuracy of any
diagnostic test is to use receiver operating characteristic
curves.'' These curves are created by taking multiple val-
ues of a test measurement, and plotting the true positive
rate against the false positive rate (Figure 11). You then
measure the area under the curve, and this tells you the
overall accuracy of the test. A perfect test has an area
under the curve of 1 .0. A test that's no better than chance
has an area under the curve of 0.50. For our patients, the
area under the curve for minute ventilation was 0.40, mean-
ing that minute ventilation was worse than flipping a coin
at the patient's bedside in predicting weaning outcome.
The other classic index, maximum inspiratory pressure,
had an area of 0.61; it's slightly better than chance in
predicting outcome. The CROP index, which integrates a
number of physiologic variables, was substantially better,
with an area of 0.78. The frequency-to-Vj ratio had an
area of 0.89. This simple index turned out to be the most
accurate predictor.

We answer research questions by making measurements
in groups of patients. But when we leave research and go
back to clinical practice, our focus shifts to a single pa-
tient. That relationship between one patient and one clini-
cian is the soul of clinical medicine. What you really want
to answer is what's the likelihood that the patient in front
of you can come off the ventilator? Let's take a situation
where you have no clue whether a patient is likely to come
off the ventilator. In the language of statisticians, this is a
pre-test probability of 50 per cent.''* If you measure the
frequency-to-Vj ratio and the value is above 100, you
draw a line on Figure 1 2 between the pre-test probability,
50 per cent, and the likelihood ratio, which we know is
0.04 for a frequency-to-V-r ratio above 100.'^ Then, you
continue the line to get the post-test probability, and you
find it's less than 5 per cent. Here you have a patient about
whom you're in total doubt as to clinical outcome; if you
find that the frequency-to-VT ratio is above 100, the in-
formation changes your post-test probability to a less than
5 per cent likelihood that the patient will come off the
ventilator. If the frequency-to-VT- ratio is 80, this has a
likelihood ratio of 7.5,'^ which changes the post-test prob-
ability to nearly 95 per cent. This example illustrates the

422

Respiratory Care • April 2000 Vol 45 No 4

Weaning from Mechanical Ventilation: What Have We Learned?

20-1

o
0)

15-

X
o 10

03
■*-•

CO
(D

0-«

' *min
AR

max.rs

^max.L

max.w

Fig. 7. Maximal resistance (overall column height) of the respiratory system (R,^ax.rs). lung (RmaxiJ. and
chest wall (Rmaxw) in weaning failure (F) and weaning success (S) patients during passive ventilation;
the clear portions of the columns represent minimum resistance (RmJ while the shaded portions

represent additional resistance (AR). No differences in R„

, R„

s, or ARrs were observed between

the groups, nor between the lung and chest wall components. Upward directed bars represent ± SE
(standard error) of R^m, while downward directed bars represent ± SE of AR. (From Reference 1 0, with
permission.)

70 r

PaCOg
(mm Hg)

100

200

300

Tidal volume (ml)

Respiratory frequency (breoths/mln)

Fig. 8. Relationship between tidal volume (Vj) and respiratory frequency with carbon dioxide tension
(P3CO2) '" seven patients who failed a spontaneous breathing trial. Pacoj was significantly correlated
with Vt (r = 0.84, p < 0.025) and frequency (r = 0.87, p < 0.025): 81 % of the variance in P^oo^ could
be explained by the changes in these two variables (From Reference 1 1 , with permission.)

Respiratory Care • April 2000 Vol 45 No 4

423

Weaning from Mechanical Ventilation: What Have We Learned?

100

Mech Vent

Spontaneous Breathing

Time, percent

Fig. 9. Ensemble averages of interpolated values of mixed venous oxygen saturation (S„oj) during
mechanical ventilation and a trial of spontaneous breathing in patients who succeeded in the trial (open
symbols) and patients who failed the trial (closed symbols). During mechanical ventilation, S^oj was
similar in the two groups (p = 0.28). Between the onset and end of the trial, S^oj decreased in the failure
group (p < 0.01), whereas it remained unchanged in the success group (p = 0.48). Over the course of
the trial, S„oj was lower in the failure group than in the success group (p < 0.02). Bars represent
standard errors. (From Reference 12, with permission.)

value of combining your clinical judgment, which is your
pre-test probability, with a test, in this case the frequency-
to-Vj ratio, and seeing how it alters your post-test prob-
ability.

Weaning Techniques

For the remaining portion of my presentation, I'll focus
on the different methods used for weaning. We have four
approaches. With pressure support and intermittent man-
datory ventilation (IMV), you decrease the support from
the ventilator and force the patient to undertake more of
the work needed for a given minute ventilation. The third
and oldest approach is to perform T-piece trials several
times a day. Dr Egan described how this approach was
being used in 1977: "Some experts advocate removing the
patient from his ventilator for a fixed short period of time
and gradually shorten the intervals between. As an exam-
ple, this might mean letting the patient breathe unassisted
for 2 minutes of an hour, then 2 minutes every half-hour,
quarter-hour, and so on, until mechanical ventilation is
discontinued." That approach involves a huge amount of
work for the intensive care unit staff, and its not hard to

>
o
c
«

£E
"■ «

-I

100

- 80

i 60-

40-

a- 20 H
«

:j#i

« 800

■si -600

"O sg 400
i- 1^200

-'''''*U*#Xl4fi^^

8 12
Minutes

Fig. 10. Breath-by-breath plot of respiratory frequency and tidal
volume (V-r) in a patient who failed a weaning trial. The arrow
indicates the point of resuming spontaneous breathing. Rapid,
shallow breathing developed almost immediately, suggesting the
prompt establishment of a new steady state. (From Reference 1 1 ,
with permission.)

424

Respiratory Care • April 2000 Vol 45 No 4

Weaning from Mechanical Ventilation: What Have We Learned?

B
to

1.0-

^■Hj

§ETr~r^^^71^^B

0.8 -

^Hr

0.6-

^^m /

0.4-

Jv ■

0.2-

/ 1

0.0.

^^^

0.0 0.2 0.4 0.6 0.8

False Positive Rate

1.0

w
o

I-

i.u -
0.8 -

0.6-

0.4-

0.2-

P| max I
0.61 I

0.0,

f^T ilg

■PlJ

0.0

0.2 0.4 0.6 0.8
False Positive Rate

1.0

1.U-

»^--^W

0.8 -

^^^^■L, /

JI^^^^^^^^^^Bf

♦-

^^^^^^^^^^^^^^^^^^K '

^^^^^^^^^^^^^^^^^^K^

a, 0.6-

^^^^^^^^^^^^^^P-

^^^^^^^^^^^^^r^^^^^

<-•

^^^^^K y^

^^^^^K /

^■■■■C: /

°- 0.4.

K^ /

^^v /^ "^rt ' — '*''^-*'"^"5M. 3

^_ / ^^^^gt^tmrnmrn^^mmMt

^B/ ^^^^^^^^^^B

0.2-

iV^ ^l CROP 1

^H ^^B~^ZLJ

0.0.

Hfc^-— fJiVi^Hi

0.0 0.2 0.4 0.6 0.8

False Positive Rate

1.0

0.2 0.4 0.6 0.8
False Positive Rate

Fig. 1 1 . Receiving-operating-characteristic (ROC) curves for frequency-to-tidal volume ratio (f/Vy), CROP
index (acronym for compliance, rate, oxygenation, and pressure, which integrates factors associated
with risk of respiratory failure), maximum inspiratory pressure (P|maJ. and minute ventilation (V^) in
weaning success and weaning failure patients. The ROC curve is generated by plotting the proportion
of true positive results against the proportion of false positive results for each value of a test. The curve
for an arbitrary test that is expected a priori to have no discriminatory value appears as a diagonal line,
whereas a useful test has an ROC curve that rises rapidly and reaches a plateau. The area under the curve
(shaded) is expressed (in box) as a proportion of the total area. (From Reference 7, with permission.)

see why multiple T-piece trials became very unpopular.
The fourth approach, and the one I personally prefer, is to
perform a T-piece trial once a day. If patients are breathing
comfortably after a half hour, they're extubated. Patients
who fail go back on the ventilator for at least 24 hours
before we make another weaning attempt.

Studies from our lab show that WOB is enormous in
patients who fail a weaning trial.'' A major goal of me-
chanical ventilation is to decrease this work.' '' But if the
respiratory muscles get too much rest might they develop
atrophy? Antonio Anzueto'* has shown that 1 1 days of

controlled ventilation in baboons causes a decrease in con-
tractility of the diaphragm, suggesting the development of
muscle atrophy. With mechanical ventilation, we want to
achieve rest without causing muscle atrophy. The ideal
amount of rest needed by a patient has never been studied.
Franco Laghi''* addressed this issue in healthy human vol-
unteers (Figure 13). He induced muscle fatigue by having
the subjects breathe through a resistive load. He stimulated
the phrenic nerves and measured transdiaphragmatic twitch
pressure (Pdj). The subjects started off with a baseline
twitch value in the high 30s, which is normal. When the

Respiratory Care • April 2000 Vol 45 No 4

425

Weaning from Mechanical Ventilation: What Have We Learned?

Pretest
Probability

(%)

0.1 ■

02.

OS-

1000

600'

200
100

/
/

B-

10-

»'

20-

30-

0.5

40-

0.2

50-

""••n^

0.1

00-

— -;

0.06

70-

0.03--.^.

0.01

80-

0.006

0.002

90"

0.001

96-

0.5

OD 4

0.2

A 1

wm *

Lil(e

ihood

^0.1

, f/Vr<80

Posttest
,^ Probability

(%)

'^ f/Vj > 100

Ratio

Fig. 12. The effect of frequency-to-V-r ratio measurements on clin-
ical equipoise, ie, a pre-test probability of 50 per cent. A frequen-
cy-to-Vj ratio of > 100 breaths/min per liter has a likelihood ratio
of 0.04. The post-test probability is obtained by drawing a line
between the pre-test probability, 50 per cent, and the likelihood
ratio, 0.04, and then extending the line; this results in a post-test
probability value of less than 5%. A frequency-to-VT^ ratio of less
than 80, which is known to have a likelihood ratio of 7.5, results in
a post-test probability approaching 95 per cent. (Modified from
Reference 1 5.)

subjects breathed through a resister, the twitch pressure
fell to about 25 cm HjO. Several investigators had previ-
ously shown that twitch pressures fall after resistive load-
ing. What's new here is that Franco measured the change
in the contractile properties of the diaphragm over the
subsequent 24 hours. '** He observed some recovery over
the first 8 hours. Between 8 and 24 hours, there was no
further recovery. Compared with baseline, the twitch pres-
sures at 24 hours were significantly depressed. This ob-
servation tells us that a considerable period of rest is needed
for recovery from diaphragmatic fatigue. That's the reason
I prefer performing a T-piece trial just once a day. When
patients fail, I fear that they may have respiratory muscle

fatigue and it'll require at least 24 hours to recover from
that.

When introduced, IMV looked like the ideal way to
wean patients from the ventilator. It took into account the
need for rest to avoid muscle fatigue and also the idea that
too much rest might cause atrophy.^" By allowing the pa-
tient to take some spontaneous breaths, IMV should pre-
vent muscle atrophy. By resting the patient during the
mandatory breaths, fatigue should be avoided. The balance
between these two factors makes it theoretically possible
to customize the approach for each individual patient.

Unfortunately, IMV doesn't work according to plan.
Figure 14 shows measurements in a single patient.-' Ac-
cording to the theory, we'd expect a decrease in diaphrag-
matic and sternomastoid activity during the assisted breaths.
But we can't tell these tracings from the spontaneous
breaths. That the effort performed by the patient is the
same for the mandatory and spontaneous breaths was first
pointed out by John Marini.-- A patient doesn't know
whether the ventilator is going to provide assistance on the
next breath. As such, the patient fires his respiratory cen-
ters at the onset of the breath. When the ventilator starts to
assist him, he's unable to switch off his respiratory cen-
ters. As a result, the effort he performs is the same for the
ventilator breaths as for the spontaneous breaths.

Pressure support is the other commonly used method of
weaning.-^ Pressure support was popularized as a means
of overcoming the resistance of the endotracheal tube. The
story goes that if patients are able to breathe comfortably
at that level of pressure support, they should be able to
breathe without difficulty following extubation. The prob-
lem is to figure out what's the level of pressure support
that overcomes the resistance of the endotracheal tube.
Various levels, such as 6 or 8 cm HjO, have been sug-
gested.

The people who proposed the addition of pressure sup-
port to overcome the resistance of the endotracheal tube
appear to have forgotten that when a tube is in the airway
for some time it causes inflammation and edema. When
the tube is removed, the resistance of the upper airway will
be higher than normal. This point was nicely shown by
Christian Strauss. ^'i He found that WOB in patients fol-
lowing extubation was virtually identical to what it had
been while they breathed on a T-piece. Any amount of
pressure support causes you to underestimate the work a
patient will have to perform following extubation — which
is what you're trying to forecast.

Another problem arises with pressure support in pa-
tients with chronic obstructive pulmonary disease — the
most challenging group to wean from the ventilator. This
problem relates to the off-cycling of the time of inflation.
Mechanical inflation is switched off when inspiratory flow
falls to some value, such as 25 per cent of the peak value. ^^
Patients with chronic obstructive pulmonary disease have

426

Respiratory Care • April 2000 Vol 45 No 4

E
u

Weaning from Mechanical Ventilation: What Have We Learned?

40-1

30-

25-

-n — I — r-

1 30 60
minutes

hours

Fig. 13. Induction of diaphragmatic fatigue (stippled bar) produced a significant fall in transdiaphrag-
matic twitch pressure (Pj,;) elicited by twitch stimulation of both phrenic nerves. Significant recovery
of twitch pressure was noted in the first 8 hours after completion of the fatigue protocol; no further
change was observed between 8 and 24 hours, and the 24-hour value was significantly lower than
baseline. The delay in reaching the nadir of twitch P^j, probably results from twitch potentiation,
induced by repeated contractions, which was present at the end of the protocol. Values are mean ±
standard error. * Significant difference compared with baseline value, p < 0.01. (From Reference 19,
with permission.)

iiiijMJU^^^

EMGdi

EMG

S ^ A [^°
yrr^ /Ho

Paw (cmHjO)

1 sec
r+8

L-e

Pes (C"1H,0)

Fig. 1 4. Electromyograms of the diaphragm (EMG;ji) and the ster-
nocleidomastoid muscles (EMGjcm) in a patient receiving synchro-
nized intermittent mandatory ventilation. Intensity and duration of
electrical activity is similar during assisted (A) and spontaneous (S)
breaths. P^„ = airway pressure. P^j = esophageal pressure. (From
Reference 21, with permission.)

increases in resistance and compliance. The product of
these two variables is the time constant of the respiratory
system.-'' An increase in the time constant means it'll take
longer for air to move in and out of the bronchi. Specifi-
cally, it'll take longer for flow to drop from its peak down
to 25 per cent of that value. As a result, the expiratory

neurons in the brainstem become impatient. They're say-
ing, "The ventilator is still pumping gas into the lungs, but
we think it's time to breathe out." The expiratory neurons
get switched on, and the patient fights the ventilator. This
is not something you want to do in a patient with preex-
isting weaning difficulties.

Amal Jubran investigated this issue in critically ill pa-
tients. The interrupted tracing in Figure 1 5 represents the
chest wall recoil. -<■ Halfway during the period of mechan-
ical inflation, we see that esophageal pressure was higher
than the chest wall recoil. This means that the patient had
switched on his expiratory muscles while the ventilator
was still pumping gas into the lungs. The measurements in
her study were based on a number of assumptions, partic-
ularly the positioning of the chest wall recoil line. One of
our fellows, Sai Parthasarathy, readdressed the question by
inserting needle electrodes into the transversus abdomi-
nis — the major muscle of expiration.-^ Again, about half-
way during the period of mechanical inflation he found
that the patients recruited their abdominal muscles. This
problem with pressure support arises because of the algo-
rithm used for cycling off the inflation phase. As a result,
most patients with chronic obstructive pulmonary disease
receiving a high level of pressure support will be forced to
fight the ventilator.

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Weaning from Mechanical Ventilation: What Have We Learned?

12-1

CW Recoil Pressure

Time, sec

Fig. 15. Esophageal pressure (continuous line) in a patient with chronic obstructive pulmonary disease
receiving pressure support of 20 cm HjO. The interrupted line represents the estimated recoil pressure
of the chest wall. The tracings have been superimposed so that chest wall recoil pressure is equal to
esophageal pressure at the onset of the rapid fall in esophageal pressure in late expiration (right of
figure). Times at which esophageal pressure is higher than chest wall pressure signify a minimal
estimate (lower bound) of expiratory effort. The expiratory muscles become active about halfway
during the period of mechanical inflation. (From Reference 26, with permission.)

In patients who fail a weaning trial, we want to rest their
respiratory muscles. Clinicians often assume that simply
connecting a patient to a ventilator is sufficient to achieve
rest. But patients can have difficulty even in triggering the
machine (Figure 1 6). One of our fellows, Phil Leung, found
that up to 30 per cent of attempts made by patients fail to
trigger the ventilator.^^ Why do patients have difficulties
in triggering? To understand this phenomenon, Phil looked
at the characteristics of the breaths that immediately pre-
ceded the triggering and nontriggering attempts. The breaths
before nontriggering attempts had a higher Vy and a lower
expiratory time. When you inhale a large Vj, the elastic
recoil pressure at the peak of inspiration will be high. If the
time for exhalation is also shorter, the pressure in your
system — the elastic recoil pressure — will be above normal
when you finish trying to exhale. We quantify this pres-
sure in terms of auto-PEEP. And Phil found that auto-
PEEP was higher before attempts that failed to trigger the
ventilator than for the attempts that triggered the machine.
That is, the real trigger sensitivity — not the set sensitivi-
ty — is much higher in patients who fail to trigger the ma-
chine.

A problem in talking about the subject of weaning is the
word itself. "Weaning" implies a gradual reduction in the

level of ventilator support. In recent randomized, controlled
trials of weaning techniques, however, 70 to 80 per cent of
patients tolerated their first T-piece trial. 2''-'" Patients went
from full ventilator support, consisting of assist-control
ventilation, to a T-piece trial, without a gradual decrease in
the level of support.

A major milestone in weaning research was the first
randomized, controlled trial carried out by Laurent Bro-
chard.-' He compared three different methods: IMV, T-
pieces, and pressure support. Before this study, most com-
mentators said it really didn't matter what technique you
used for weaning — that they're all the same. Laurent
showed it clearly matters. For the first time, he showed
that one technique, IMV, was markedly inferior to the
other weaning approaches. People often misinterpret the
results of Laurent's study, and say that he showed that
pressure support was better than T-pieces. Pressure sup-
port was better than the combination of the T-piece group
and the IMV group. There was no difference between
pressure support and T-pieces, when the T-piece group
was analyzed separately from the IMV group.

The following year we published a randomized con-
trolled trial conducted with collaborators in Spain.'" We
looked at the four approaches I mentioned earlier: single

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Weaning from Mechanical Ventilation: What Have We Learned?

Time, sec

Fig. 16. Recordings of tidal volume, flow, airway pressure (PgJ, and esophageal pressure (PeJ in a
patient with chronic obstructive pulmonary disease receiving pressure support ventilation. Approxi-
mately half of the patient's inspiratory efforts do not succeed in triggering the ventilator. Triggering
occurred only when the patient generated a P^^ more negative than -8 cm H2O (indicated by the
interrupted horizontal line), which was equal in magnitude to the opposing elastic recoil pressure. Each
ineffective triggering attempt is signalled by a braking of expiratory flow, whereby flow returns to zero
due to the action of the inspiratory muscles. Thus, monitoring of expiratory flow provides a more
accurate measurement of the patient's intrinsic respiratory rate than the number of machine cycles
displayed on the bedside monitor. (From Reference 4, with permission.)

daily trials of spontaneous breathing, multiple trials of
spontaneous breathing, pressure support, and IMV. Like
Laurent Brochard, we found that IMV had the worse out-
come. Using a Cox proportional-hazards regression model,
we found that the single daily trial of spontaneous breath-
ing resulted in a three-fold increase in the rate of success-
ful weaning compared with IMV, and a two-fold increase
in the rate of successful weaning compared with pressure
support.

Wes Ely-^' subsequently undertook a study that com-
bined two aspects of our previous research: the use of
weaning predictors^ and the use of spontaneous breathing

trials.'" He studied 300 patients who underwent a daily
screen by respiratory therapists. The daily screen consisted
of looking at the patient's oxygenation, the level of PEEP,
the absence of rapid, shallow breathing (a frequency-to-V-j.
ratio of less than 105),'' the presence of a good cough on
suctioning, and lack of infusions of pressors or sedatives.
Patients passing the screen were randomized to an inter-
vention group and a control group. The control group was
managed in the usual manner by the attending physicians,
largely consisting of pressure support or IMV. Patients in
the intervention group underwent a two-hour trial of spon-
taneous breathing,'" without getting permission from the

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Weaning from Mechanical Ventilation: What Have We Learned?

attending physician. The attending physicians of patients
passing the two-hour trial were contacted verbally and a
note to that effect was also written in the chart.

Although the patients in the intervention group were
sicker, with higher acute physiology and chronic health
evaluation and lung injury scores, they were weaned twice
as fast as the control group. That is, a two-step strategy,
consisting of the systematic measurement of weaning pre-
dictors'' combined with a spontaneous breathing trial,'"
achieved a better outcome. Looking at the details, 59 per
cent of the patients tolerated the trial. In general, about 10
to 1 5 per cent of extubated patients require reintubation. If
the investigators had been aggressive and extubated every
patient who passed the spontaneous breathing trial, you'd
expect about 50 per cent of patients to have tolerated ex-
tubation. In contrast, 32 per cent were actually extubated.
Despite this nonaggressive approach, the rate of successful
extubation was more than double that in the control group.

In early 1999, we published a study conducted with
collaborators in Spain to determine if patient outcome was
different for a spontaneous breathing trial lasting a half
hour versus two hours. ^^ Jq emphasize how thinking has
changed about the right length for a T-piece trial, I refer to
what Dr Egan wrote in 1977: "When the patient can breathe
unassisted around the clock, and is moving a reasonable
amount of air without undue effort, and can walk for short
distances consistent with his general physical condition,
and when ventilation is satisfactory and stable by blood
gas values, it is time to consider removal of the endotra-
cheal tube." When we work in a field, we often don't
notice how much it advances. In another 20 years, I expect
people will think some of my statements today as strange —
probably much sooner than 20 years! Returning to our
recent study, patient outcome was the same for spontane-
ous breathing trials lasting for two hours or a half hour."*-
Contrasted with the previous recommendation that T-piece
trials should last 24 hours, being able to make a decision
within a half hour frees up time for staff to take care of
other tasks and simplifies the approach to weaning.

In our recent study, the intensive care unit mortality was
5 per cent in patients who succeeded in a trial and didn't
require reintubation. '^ In contrast, patients who succeeded
in the trial, were extubated, but then required reintubation
had a mortality rate of 33 per cent — a similar experience
has been reported by Scott Epstein.^^ We found that re-
spiratory frequency was high in the patients who failed the
spontaneous breathing trial, but the values were similar in
the patients who were successfully extubated and in those
requiring reintubation. A superficial assessment of these
data might lead you to conclude that weaning indices do
not predict the need for reintubation. The design of our
study, however, was not adequate to reach a conclusion on
this issue. The patients in our study who failed the wean-
ing trial had a much higher frequency, and, if extubated, it

is likely that many of them would have required reintuba-
tion. To properly answer the question, you'd need to take
a group of patients, measure the predictive indices, and
then extubate every patient irrespective of whether or not
they tolerated a weaning trial.

Reintubation represents a major new frontier for re-
search. We need to find out what exactly is going on in
these patients. To date, we don't have a single study prob-
ing the pathophysiology of reintubation.

In summary, the major reason that patients fail weaning
trials is their enormous respiratory work load. We're still
unsure whether these patients develop respiratory muscle
fatigue. We need to answer this question because it has
major implications for patient management. In deciding
the right time to take a patient off the ventilator, we've
learned that the judgment of an experienced clinician is
not enough. You need weaning predictors. And when
they're measured systematically, predictors result in more
effective management. Of the weaning techniques avail-
able, a number of randomized, controlled trials have shown
that one of the most ingrained approaches, IMV, is the
least effective. A single daily trial of spontaneous breath-
ing appears to be the most expeditious weaning technique.
When looking at the story of weaning research over the
last 20 years, one is reminded of the saying of the French
essayist, Michel de Montaigne:

Whenever a new discovery is reported to the sci-
entific world, they say first, "it is probably not true."
Thereafter, when . . . demonstrated beyond ques-
tion, they say "yes, it may be true, but it is not
important." Finally, when a sufficient time has
elapsed, they say "Yes, surely it is important, but it
is no longer new.

That statement was made more than 400 years ago — plus
(a change, plus c'est la meme chose.

I will finish by returning to Dr Egan's book. He pointed
out that weaning is very nearly a pure art. As critical care
shifts increasingly toward a focus on technology, more
than ever is there a need for the personal interaction be-
tween two human beings: the clinician and the patient.
Respiratory therapists play a key role at the bedside of the
patient who's frightened by the process of weaning. This
interplay between one human being and another will re-
main the dominant factor in determining which patients
are successfully weaned from the ventilator.

Thank you.

REFERENCES

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Letters

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decline a letter or edit without changing the author's views. The content of letters as published may simply reflect the author's opinion or
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WX) Ninth Avenue, Suite 702. Seattle WA 98104. Letters may also be submitted electronically at www.rcjournal.com/online_resources.

Are Digital Distance Learners
Learning or Just Distant?

I wish to respond to Shelley Mishoe's
thoughtful editorial (Respir Care 1999
44[12]:1332-1335)on distance education in
respiratory care. That essay clearly expresses
a number of issues that are under intense
scrutiny and investigation in a number of
arenas and by a number of disciplines, where
they are no more resolved than in the field
of respiratory care. I was recently appointed
to an Association for Educational Commu-
nications and Technology committee
charged with developing certification stan-
dards and methods for online courses,

Shelley's hard won experience as an ef-
fective educator is evident in her writing on
distance learning, and although I appreciate
her views and am in general agreement, I
disagree on some points and wish to com-
ment on others.

Degrees of Distance

Most importantly, we must distinguish In-
ternet teaching from its distance learning pre-
decessors, Shelley is correct that distance ed-
ucation is the fastest growing type of education,
nationally and internationally, ' But lumping the
various categories of distance learning into one
and attempting to discuss it as a single entity is
simplistic and misleading. There are 4 basic
categories of group processes^ *"'^ '" ' ' and
these are aseful in differentiating the types of
distance learning;

1 , Same time/same place, such as a tra-
ditional classroom,

2, Different time/different place, such as
a postal or asynchronous on-line
course.

3, Same time/different place, such as a
synchronous audiovisual broadcast
(one-way or two-way),

4, Different time/same place: shared fa-
cilities and resources (not applicable
to distance learning).

A plethora of technologies are avail-
able, ranging from simple printed docu-
ments to videotapes to streaming real-time
video, and the.se can be as.sembled into
nearly infinite combinations in distance
courses. The differences between synchro-
nous, two-way compressed audio-video.

similar to the type Shelley describes from
her own happy experience, and the typi-
cal online course, are as profound as the
differences between mechanical ventila-
tion by iron lung and by high-frequency
jet ventilation. While synchronous (same
time, different place) distance learning
technologies seem to be in decline, Inter-
net course development is exploding.
Some of the attributes of her positive dis-
tance learning experience are not (yet)
technically possible in an Internet course.
The current state of data transmission ca-
pability over the World Wide Web ren-
ders raw audiovisual delivery of digitized
traditional lectures unworkable, even as
postage-stamp-size compressed motion
video images. Arguably, it is the band-
width limitation of today's Internet, rather
than any instructional advantage, that
prompts online application of the exciting
student-centered, collaborative instruc-
tional strategies that Shelley describes.

Pedagogy

There is little agreement on a theory base
for distance learning, which has been de-
scribed in America as chaotic and confused, '
Online teaching, in particular, is so different
from any of the categories of distance learn-
ing that preceded it that it is essentially a
practice without a research foundation. The
literature does not meaningfully guide the
design and development of Internet cours-
es.' More than 9,000 courses in North Amer-
ican higher education have been developed
for Internet delivery,'' but their most distin-
guishing features in common may be an
appalling level of tedium and a vacuum of
judicious instructional design. Shelley is cor-
rect that faculty are pressured (some say
bullied) from within and without to incor-
porate technology,'*'' particularly Internet
technology. But there is a backlash by some
educators who characterize participating in-
stitutions as "digital diploma mills,"-' in a
"climate of Web worship"" and who are
"engaged in a frenzied drive to the Web-
based cliff""

First-generation Internet course develop-
ment tools are criticized for an absence of
sound, underlying pedagogy, and for pro-
mulgating, by design, dubious instructional

strategies,'" Traditional instructional design
models, applied successfully for the devel-
opment of print-based and computer-based
instruction (CBI), do not lend themselves
well to college-level Web-based instruction
or even traditional classroom instruction.
This is because the exhaustive level of de-
tail required of classical instructional design
models is horrifically time-consuming and
expensive, A single hour of commercial cal-
iber Web-based instruction may require
400-500 hours and cost $40,000 (SW Har-
mon, 1 998. personal communication), a cost
too great for a typical college course of more
than 40 hours. The alternative is what prag-
matic online course developers often call
the "good enough" course that, in my esti-
mation, isn't,

A Legacy of Digital Tedium

The low standard of sophistication seen
across the board in commercial CBI for re-
spiratory care is, sadly, also seen through-
out the larger arena of education, ' ' Even
though instructional designers know better,
the dominant instructional strategy in CBI
is ( 1 ) text on screen and (2) ask a few (shal-
low and canned) questions.

There is a tendency to settle for inau-
thentic interactions because they are tech-
nically simple to accommodate, and because
little instructional software in respiratory
care has demonstrated a higher level of so-
phistication for potential buyers to demand.
Although this is the norm in CBI tutorials
for respiratory care, happily, rich examples
of authentic interactions can be found in the
ubiquitous branching-logic clinical simula-
tion, either computer-managed or print-
based,

A similar pattern is seen in Internet cours-
es: (1) text on screen, (2) visit a few links,
and (3) have a chat (threaded on-line bul-
letin board or synchronous on-line chat
riwni).

It is important to note that the Internet is
not the medium — in most online courses
the dominant medium is probably still the
static printed word — the Internet is merely
the delivery technology, Ju.st as the domi-
nant instructional strategy in my experience
in respiratory care education is "talk and
more talk," the dominant strategy in current

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Respiratory Care • April 2000 Vol 45 No 4

Letters

generation online courses is "text and more
text." In examining the actual course con-
tent delivered to the student, few online
courses can be distinguished from postal cor-
respondence lessons, although documents
are disseminated more quickly over the
World Wide Web. In fact, content accuracy
and the level of editing are likely to be su-
perior in refined postal courses, compared
to hasty online courses. Even home-study
postal courses often include conference calls
for questions and interaction, but the qual-
ities Shelley describes in the tone of the in-
structor's voice do not translate to the text of
the online chat room or course bulletin board.
As De Laurentiis" points out, the Inter-
net is but a storage medium, with no inher-
ent capacity for instructional design. This
caution is echoed by Reeves,'- who writes
". . . the World Wide Web does not guar-
antee learning any more than the presence
of a library on campus guarantees learn-
ing." There is nothing magically instructive
about instantaneously transmitting the writ-
ten word across the World Wide Web to be
read by the student on a computer monitor.
However, the level of tedium in this is ar-
guably cruel and unusual punishment.

Does It Work?

Issues of efficacy (Is it as good as tradi-
tional education? Does the learning transfer
to the workplace?) have not been answered.
A recent report by The Institute for Higher
Education*" finds that research on distance
learning is scant and deeply flawed (eg, an-
ecdotal, small sample sizes, confusion of
variables, poor control of extraneous vari-
ables, lack of random sampling, question-
able instruments). The report also notes that
research tends to focus on single courses
rather than outcomes from complete distance
degree programs, and that drof>-out rates are
higher in distance learning courses (possibly
negating any efficacy equivalency finding).
Research specifically on Internet teaching is
thinner still, although some researchers have
found increased reflective thinking in on-
line courses." Head-to-head comparison
of traditional versus online education is sim-
ply not meaningful in most cases, because
online course development involves more
than a mere change in media: it often in-
volves bedrock changes in teaching and
learning philosophy. In other words, the
online course isn't just delivered differently,
it is a different course. This conundrum
moved instructional technology scholars to

abandon media comparison studies altogeth-
er'-* years ago because the almost universal
finding is "no significant difference" (the
NSD phenomenon).'-"^

A highly touted aspect of Internet courses
is the interactive potential of synchronous
chat rooms. As an educator, I agree intu-
itively with Shelley that interaction is surely
essential in an effective course. But the re-
search evidence for the value of interaction
in computer- mediated teaching has been de-
scribed as elusive.'^ My own experience as
an online student revealed that students who
expect to be graded in part on participation
tend to flood the environment with verbiage.
I also did not appreciate reading the fiiis-
trated messages of other students grappling
with a difficult concept — it was simply not
helpful.

Issues of Image

A recent episode of The Simpsons in-
cluded a scene where the medical school
diploma of a quack physician read "Corre-
spondence School." In The Mitppet Movie,
Kermit asks "Fozzie, where did you learn to
drive?" Fozzie Bear responds, "Correspon-
dence school!" The negative correspon-
dence school image persists' and, in my
opinion, has already done incalculable dam-
age to the image of respiratory care. Issues
of efficacy and technology aside, I question
whether respiratory care is well served by
recklessly embracing yet more experiments
in distance learning. A curious reaction I've
noted many times in discussions with respi-
ratory therapists is that the suggestion of
finding oneself in the care of a surgeon
trained by correspondence school brings
laughter. So it is when the correspondence
school hypothetical is posed for anesthesi-
ologists, dentists, nurses, dental hygienists,
and even auto mechanics. That respiratory
therapists are untroubled by the widespread
proliferation of correspondence training in
their own field is puzzling, and suggests
that respiratory therapists, of all health pro-
fessionals, consider their colleagues to be
adequately trained in this way.

To Be (a Respiratory Care Practitioner)
Is To Do

This leads me to my most serious objec-
tion to the prospect of online training in
respiratory care: respiratory care is a doing
vocation. To be sure, there is a great deal of
knowing involved in the safe and effective
practice of respiratory care, but respiratory

therapists are employed to do, under the
direction of physicians. The entry-level
preparation of respiratory therapists is best
classified as training, rather than education.
Reigeluth'^ makes this distinction on the
basis of specificity and immediacy of ap-
plication. Most of what respiratory thera-
pists are taught is highly specific and is in-
tended to be employed immediately.
University System of Georgia's Chancellor,
Stephen Portch,"* emphasizes this by say-
ing ". . . education is. . . 'what's left after
you've forgotten everything you've been
taught.' It's the habits of the mind."

It is my perception that online teaching
has great potential in student-centered, prob-
lem-based education, but less in training. I
would classify some of the instruction in
career ladder programs for therapists to earn
a bachelor's degree as education. Open-
ended online discussion as a primary instruc-
tional technique is better suited to upper di-
vision course topics, such as medical ethics
and management, than to teaching the ba-
sics. More important, we must not forget
that it is the clinical portion of an entry-level
respiratory care program that is of primary
importance — classroom instruction is in
preparation for clinical practice. But the cur-
rent state of distance technology cannot ful-
fill a primary role in clinical training.

Efficacy of distance learning in respira-
tory care is particularly problematic because
it is possible, even in traditional respiratory
care programs, to statistically demonstrate
efficacy in a program that graduates unsafe
practitioners. That is, it is my perception
that some educators have lost sight over the
years of the core reason for the existence of
programs in respiratory care — to prepare
safe, effective practitioners. This primary
goal seems to have been eroded by a ten-
dency to teach students to pass credential-
ing exams, quite a different undertaking, and
one that serves the needs of programs and
educators rather than students, patients, and
the field of respiratory care. This is pre-
cisely the same dishonesty found occasion-
ally in public schools where teachers pre-
pare students to score well on standardized
tests, rather than actually teaching. As an
experienced respiratory care educator, I
know that there are exemplary practitioners
who struggled to pass credentialing exams
(some never pass!). I also know that there
are frightful pracfitioners who pass the ex-
ams with ease. This concern will be mag-
nified as distance learning programs are ini-
tiated and look to credentialing exam scores

Respiratory Care • April 2000 Vol 45 No 4

433

Letters

for proof of efficacy. I am not convinced
that the doing aspect of respiratory care train-
ing can be accomplished with current dis-
tance technologies, although distance tech-
nologies are probably well suited to
schooling practitioners to pass credentialing
exams. The truly valuable learning that takes
place in a respiratory care program does not
occur in the classroom at all, distant or Ua-
ditional, but in the physical presence of a
master practitioner. What an exemplary clin-
ical instructor possesses can be modeled for
students at the bedside, but probably not
distilled into something digital that can be
transmitted to a far computer monitor, to be
consumed in isolation, or even taught in a
traditional classroom.

My considered recommendation on dis-
tance learning in respiratory care is for mod-
eration. It need not be "whether we want it
or not"; it should be a deliberate, profes-
sional decision. I agree with Shelley and the
American Association for Respiratory Care
Education Consensus Conference that home
study should be eliminated for entry-level
preparation, but expand this to include any
distance learning technology. Shelley's call
for an end to memorizing facts is well taken,
but applies to traditional programs as well
as distance learning. Distance learning tech-
nologies may prove themselves in advanced
training applications where Internet course
tools seem to support the sort of interactive,
open-ended instruction that Shelley de-
scribes. But we must be sure that we un-
derstand that it is the instructional stfategy,
not the technology, that makes the differ-
ence.

Keith B Hopper RRT

Doctoral Candidate

Instructional Technology

Georgia State University

Altanta, Georgia

REFERENCES

1. Mclsaac MS, Gunawardena CN. Distance
education. In: Jona.ssen DH, editor. Hand-
book of research for educational commu-
nications and technology. New York: Si-
mon & Schuster Macmillan; 1996: 403-
437.

2. Johansen R, Martin A, Mittman R, Saffo P.
Leading business teams: how teams can use
technology and group process tools to en-
hance performance. Reading, MA: Addi-
son- Wesley; 1991.

3. Schrum L. On-line education: a study of
emerging pedagogy. In: Cahoon B, editor.

Adult learning and the internet. San Fran-
cisco: Jossey-Bass; 1998: 53-61.
A Innes J. Welcome to the telecampus online
course database. TeleEducation New
Brunswick. Available at http://database.t-
elecampus.com/home/menu.html. Ac-
cessed March 14, 1999.

5. Hopper KB. Mastering the invisible tech-
nologies in education: who are the real tech-
nology prodigies among college teachers?
Educ Technol 1999;39(l):50-56.

6. Phipps R, Merisotis J. What's the differ-
ence? A review of contemporary research
on the effectiveness of distance learning in
higher education. The Institute for Higher
Education Policy, Apr 1999. Available at
http://www.ihep.com/PUB.htm. Accessed
November 5, 1999.

7. Noble DF. Digital diploma mills: the auto-
mation of higher education. First Monday.
Available at http://www.firstmonday.dk/is-
sues/issue3_l/noble/index.html. Accessed
March 1, 1999.

8. Dillon A, Zhu E. Designing web-based in-
struction: a human-computer interaction
perspective. In: Khan BH, editor. Web-
based instruction Englewood Cliffs, NJ: Ed-
ucational Technology Publications; 1997:
221-224.

9. Harmon SW, Jones MG. The five levels of
web use in education: factors to consider in
planning online courses. Educ Technol
1999;39{6):28-32.

10. Firdyiwek Y. Web-based courseware tools:
where is the pedagogy? EducTechnol 1 999;
39(l):29-34.

1 1. De Laurentiis EC. How to recognize excel-
lent educational software. LifeLong Soft-
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.com//Academic World/
ExcelEducSoftware/ExEdSof.html.
Accessed March 1 , 1 999.

12. Reeves TC. A model of the effective di-
mensions of interactive learning on the
world wide web. Available at http://
itechl.coe.uga.edu/Faculty/treeves/Web-
Paper.pdf Accessed April 7, 1999.

13. Holt ME, Kleiber PB, Swenson JD, Rees
EF, Milton J. Facilitating group learning
on the internet. In: Cahoon B, editor. Adult
learning and the internet. San Francisco:
Jossey-Bass; 1998: 43-51.

14. Clark RE. Reconsidering research on learn-
ing from media. Rev Educ Res 1983;53(4):
445-459.

15. Russell TL. The "no significant difference
phenomenon". TeleEducation New Bruns-
wick. Available at http://teleeducation.n-
b.ca/nosignificantdifference/. Accessed
March 14, 1999.

16. Threlkeld, R. Research in distance educa-
tion. In: Willis B, editor. Distance educa-
tion: strategies and tools. Englewood Cliffs,
NJ: Educational Technology Publications;
1994: 41-66.

17. Reigeluth CM. Garfinkle RJ. editors. Sys-
temic change in education. Englewood
Cliffs, NJ: Educational Technology Publi-
cations; 1994.

18. Portch SR. Chancellor responds to Maria
Saporta. University System of Georgia Of-
fice of the Chancellor. 5/20/98. Available
at http://www.peachnet.edu/news/1998/
ajc.html. Accessed April 8, 1999.

The author responds:

I was pleased to read that someone like
Keith, who is immersed in instructional de-
sign and technology, would agree with most
of my major points in my recent editorial.'
It is difficult in a limited space to discuss
such a complex topic. Therefore, I can un-
derstand why Keith would say that a gen-
eral discussion on distance education is sim-
plistic and perhaps misleading. The purpose
of my editorial was not to review the 4 ba-
sic categories of distance education or to
compare synchronous and asynchronous
courses. Rather, my aim was to provoke
thought on how students and professionals
in respiratory care will learn today and into
the future, using the various technology and
methods available. I deliberately avoided the
use of common lingo in distance education,
with the intent of opening up the discussion
to a wider audience within the profession,
not strictly the educator types.

Interaction Between Instructors and
Learners

Although I elaborated on my initial, per-
sonal experience with distance learning via
synchronous audio courses, I have also had
more recent positive experiences with In-
ternet-based courses and CBI. In the Inter-
net-based and CBI courses that I have par-
ticipated in, as well as those of my
colleagues, student feedback indicates that
they can be very satisfied with the quantity
and quality of interaction. I did not wish to
give the impression that my comments about
interaction are limited to face-to-face inter-
action. In addition, I did not base my com-
ments regarding the importance of interac-
tion upon my initial experience with a
synchronous course. The comments I made
regarding the importance of interaction in-
clude all forms of interaction, and are not
limited to synchronous, two-way com-
pressed audio- video courses. 1 disagree that
it is not possible today to have positive in-
teraction among learners and between learn-
ers and teachers via Internet-based courses.

434

Respiratory Care • April 2000 Vol 45 No 4

Letters

It is true that audiovisual delivery of syn-
chronous, traditional lectures via the Inter-
net is not truly workable right now. How-
ever, it is my opinion that this limitation of
technology at the current time is not a bar-
rier to effective interaction or instruction via
Internet-based courses. Even within the lec-
ture method (whether live or delivered via a
synchronous distance education course),
there is wide variation among presenters
with varying degrees of interaction and ef-
fectiveness. If I can use Keith's analogy,
some lectures are like iron lungs whereas
other lectures can be like jet ventilators (or
even liquid oxygen). In general. I am not a
fan of the lecture method for teaching. I
think it is a good thing that it is not practical
to digitally transmit "'talking heads" via the
Internet for the delivery of synchronous, lec-
ture-based courses. However, it is unfortu-
nate that the majority of CBI and Internet-
based courses are often text and more text.-
I am critical of any instruction that places
undue emphasis on the teaching, rather than
the learning, with the typical lecture being a
prime example. Lectures are not my idea of
"interaction" or meaningful learning.

What Can Be Effectively Learned at a
Distance?

The effective teacher must examine and
reflect on the best ways to help students
accomplish course goals, as well as some
personal goals.' True learning occurs when
students, patients, peers, and others come
away from a course or experience with im-
proved understanding, skills, attitudes, and
behaviors. 1 agree that we should question if
we can we teach someone to be a surgeon,
nurse, or auto mechanic via correspondence
school. So what about respiratory care?
Keith presses the point that, since much of
the learning that occurs within professional
preparation is by "doing," how can this be
accomplished if the teacher is at a distance?

I agree that for some types of learning, it
is necessary for the students and teacher to
be in the same place at the same time (like
with the patient in a health care setting). In
addition. 1 agree that the clinical portion of
an entry-level program is of primary impor-
tance and that distance learning cannot ful-
fill the role of clinical training. I would even
say this is important for advanced training,
as well. Therefore, in the distance education
program we have proposed at the Medical
College of Georgia, we have incorporated a

variety of strategies, including synchronous
courses, Intemet-ba.sed courses, and a clin-
ical component with a local faculty mem-
ber. I do not think that we should attempt to
substitute live, clinic-based components of
curriculum with either Internet-based or syn-
chronous audio-video courses.

Although the students in our proposed
distance education program will already
have at least two years of college and the
registered respiratory therapist credential, if
they want to grow in advanced and spe-
cialty areas of practice, they need (and want)
additional clinical training. The targeted
group of students will work with faculty to
gain clinical and professional skills in areas
such as pulmonary rehabilitation, neonatal
respiratory care, sleep-disordered breathing,
and other specialties. They will also have
experiences involving the development of
care plans, patient education materials, car-
diopulmonary protocols/pathways, and re-
search studies. However, incorporating a
clinical component does not exclude teach-
ing other course content from a distance.
Having a clinical component does not mean
that students cannot learn pharmacology,
statistics, concepts of mechanical ventila-
tion, or other content via distance learning.

Students must also observe effective role
models who can interact with patients in
ways that improve patient understanding and
compliance with treatment protocols. Stu-
dents must also work with accomplished
clinicians who interact effectively with phy-
sicians and other colleagues, contributing to
patient outcomes. Role modeling by expe-
rienced, effective clinicians is the most im-
portant part of professional preparation.-*
Keith did a good job further elaborating on
why clinical training is essential for the pro-
fessional preparation of respiratory thera-
pists and why distance learning cannot be a
substitute for these components of our cur-
riculum.

Trancending the "Correspondence
School" Stereotype

Even though the clinical component of
training is essential, 1 still contend that dis-
tance education will have a greater role in
respiratory care, especially for those per-
sons seeking advanced degrees. I also con-
tend that this is whether we want it or not.
but I think we .should want it. I agree with
Keith that the choice should be a deliberate,
professional decision by faculty and stu-
dents. Of course, all things are best in mod-

eration. I further believe that continuing ed-
ucation via the Internet can enhance mean-
ingful learning for professionals beyond the
typical continuing education experience.
With appropriate resources, planning, de-
sign, and implementation, I believe Inter-
net-based courses and other forms of dis-
tance education can provide good to superior
opportunities to further develop our profes-
sion and its professionals. Becker's article^
and our own needs assessment indicate that
re.spiratory therapists want to pursue bacca-
laureate and advanced degrees via distance
education, which includes Internet-based
courses. Furthermore, respiratory therapists
today believe they can experience an even
higher level of interaction via distance ed-
ucation.^

Distance learning via the Internet poses
unique challenges, but also opportunities to
achieve genuine learning and increa.sed re-
flective learning.*" I have seen reserved stu-
dents, who are often dominated in an oral
discussion, write powerful, thoughtful, and
accurate responses to some tough questions.
When these types of examples are shared
within a class (regardless of the technology
used), it can promote confidence within in-
dividual students, as well as mutual appre-
ciation of the talents of others (which are
sometimes hidden). It further builds nov-
ices' abilities to behave as professionals,
which can enhance their effectiveness and
abilities to collaborate in practice.

The teacher of any course should strive
to help learners improve their abilities to
critically read, write, listen, and speak.^ Nei-
ther the traditional lecture, nor the Internet,
nor the clinical rotation can intrinsically
achieve these goals. I believe the teacher
should promote meaningful dialogue within
any course through skillful facilitation, es-
pecially true with distance courses.* I would
clarify again that I did not base my com-
ments about interaction within my editorial
on face-to-face interaction. For Internet-
based courses, I recommend written assign-
ments and the careful use of electronic bul-
letin boards (asynchronous) and other
e-assignments.*""

Suggestions to Promote High-Quality
Interaction

Ground rules for interaction and specific
criteria for evaluating participation are es-
sential, whether the course is live, synchro-
nous, or Internet-based.'" An important
ground rule is that the bulletin board should

Respiratory Care • April 2000 Vol 45 No 4

435

Letters

not be used to post any personal messages
or comments that are unrelated to the as-
signment. For example, students can be re-
quired to post one learning issue related to
each particular patient problem (case) per
class. The ground rules for posting should
be that they focus on their specific issue
related to the case (no personal discussions
or unrelated topics), state reasons for their
opinions and decisions, give recommenda-
tions with supporting documentation, and
cite their resources. Student interaction can
be guided further by requiring them to eval-
uate their sources, using specific criteria pub-
lished with each course. It is also possible
to design Internet-based courses whereby
students are allowed to use tools to link
other learners to their key Internet sources,
thus expanding on all learners' resources. A
real advantage is that many of the links can
give actual clinical data such as an electro-
cardiogram, radiograph, heart sounds, breath
sounds, and other audiovisual data. This type
of experience can be far superior to a typ-
ical lecture.

I agree with Keith that chat rooms are
not helpful, especially when reading the frus-
trated comments of other students or the
mindless verbiage from people's mistaken
notion of participation. In my opinion, chat
rooms are often a waste of time for both
students and teachers. I believe that chat
rooms should be available for those students
who like using them as an adjunct to a course.
Chat rooms are useful to promote social in-
teraction and a sense of belonging for those
students who enjoy this type of experience.
In my opinion, the chat room participation
should be an option, not a requirement. 1
personally avoid chat rooms as either teacher
or learner, depending on my role! Interac-
tion during Internet-based courses should
not be limited to chat rooms, just as the
interaction for other types of distance edu-
cation courses should not be limited to tele-

conferences or two-way compressed audio-
video.

Interaction and Critical Thinking:
Focusing on Instructional Strategy

Our challenge is to use instructional meth-
ods and technology in ways that promote
meaningful learning for both novices and
experts, as well as our patients. I believe
that well designed Internet-based courses
can promote meaningful interaction, critical
thinking, and learning. For thinking to be
critical, our ideas, beliefs, and actions must
be validated through discourse with oth-
ers."'- We cannot think critically in a vac-
uum, whether that vacuum exists during a
"talking head" lecture, or in the form of text
and more text on the Internet. We must have
feedback from others to further evaluate our
thinking.

In closing, Keith nicely summarized a
major point of my editorial in the ending to
his letter: we must "... understand that it is
the instructional strategy, not the technol-
ogy, that makes the difference." I would
reiterate that this statement is true whether
the course is "live" or via distance educa-
tion. I would add that this is also true whether
the course is synchronous or asynchronous,
Internet-based or classroom-based. I think
this dialogue is necessary because too many
people confuse teaching with learning.
Therefore, I believe it is appropriate to dis-
cuss "learning" as a construct, which can
include the various forms of distance learn-
ing. I believe that such dialogue is neither
simplistic nor misleading. I would go as far
as to say that such dialogue is necessary.

I thank Keith for giving his time and
thoughtful reflection to write a letter re-
sponse to my recent editorial. I appreciate
this opportunity to expand, clarify, and fur-
ther state some of my experiences, opin-
ions, and thoughts.

REFERENCES

1. Mishoe SC. Distance education in respiratory
care: whether we want it or not? (editorial) Re-
spirCare 1999:44(1 1):1332-1336.

2. Firdyiwek Y. Web-based courseware tools:
where is the pedagogy? Educ Technol 1999;
39(l):29-34.

3. Brookfield S. Becoming a critically reflective
teacher. San Francisco: Jossey-Bass; 1995.

4. Mishoe SC, Maclntyre NR. Expanding profes-
sional roles for respiratory therapists. Respir
Care 1997:42(l):71-86: discussion 86-91.

5. Becker EA. Gibson CC. Auiludes among
practicing respiratory therapists in a Mid-
western state toward completing a bacca-
laureate degree and toward distance educa-
tion. Respir Care 1999;44(1 1):1337-1352.

6. Holt ME, Kleiber PB, Swensen JD, Rees
EF, Milton J. Facilitating group learning
on the Internet. In: Cahoon B. editor. Adult
learning and the internet. San Francisco:
Jossey-Bass; 1998.

7. Mishoe SC. Critical thinking, educational
preparation and development of respiratory
therapists. Distinguished Papers Mono-
graph 1993; 1(2): 29^3.

8. Cyrs TE. Teaching and learning at a distance:
new directions for teaching and learning. No
71. San Francisco: Jossey-Bass: 1997.

9. Fristensky R. The use and misuse of elec-
tronic assignments. The Teaching Profes-
sor 1999;13(8):l-3.

10. Hillesheim G. The search for quality stan-
dards in distance learning. Quality in Higher
Education 1998: 7(1 l):l-3.

1 1 . Mishoe SC. Critical thinking in respiratory
care practice. Dissertation Abstracts Inter-
national 1995,55(10): 3066A. (University
Microfilms No. 9507227.)

12. Garrison DR. Critical thinking and self-di-
rected learning in adult education: an anal-
ysis of responsibility and control issues.
Adult Educ Quart 1992;42(3): 136-148.

Shelley C Mishoe PhD RRT FAARC

School of Allied Health Sciences and

School of Graduate Studies

Medical College of Georgia

Augusta, Georgia

436

Respiratory Care • April 2000 Vol 45 No 4

Listing and Reviews of Books and Other Media. Note to publishers: Send review copies of books.
films, tapes, and software to Respiratory Care, 600 Ninth Avenue. Suite 702, Seattle WA 98104.

Books, Films,
Tapes, & Software

Fatal Asthma. Albert L Sheffer, editor.
Lung Biology in Health and Disease Series.
Volume 115. New York: Marcel Dekker.
1998. Hardback, illustrated, 640 pages.
$195.00.

Fatal Asthma, edited by Albert L Shef-
fer, is a scholarly treatment of questions and
issues surrounding asthma-related deaths.
Though asthma mortality is infrequent, it
still occurs in spite of the development of
national and international guidelines for
asthma management. Many of the contrib-
utors to the volume's 34 chapters are na-
tional and international asthma experts and
have been involved in the creation of asthma
practice guidelines. Each of the contribut-
ing authors operates from the premise that
fatal asthma risk can be decreased by iden-
tifying high-risk patients through careful as-
sessment.

The stated purposes of the volume are to
defme and describe: (1) criteria that will
help identify those at risk of succumbing to
asthma and (2) the mechanisms resulting in
fatal asthma episodes. These goals are ac-
complished through insightful review of the
epidemiological characteristics of fatal
asthma, physiologic and pathophysiologic
changes during the development of life-
threatening asthma, and clinical and psy-
chosocial factors associated with fatal and
near-fatal asthma episodes. A common
theme throughout this volume is that the
infrequency of fatal asthma can lead both
patients and health care providers to under-
estimate asthma severity. Inadequate assess-
ment of asthma severity, along with under-
diagnosis and inappropriate treatment, are
key factors leading to increased asthma mor-
bidity and mortality. A strength of this vol-
ume is the way in which each contributor
builds on these common themes, offering
examples, suggestions, and food for thought
from his or her own area of expertise.

The first two chapters set the stage for
the rest of the volume, introducing asthma
mortality as an important problem that is
both real and deserving of specific investi-
gation into its causes and prevention. Chap-
ter 1 discusses the public perception of
asthma and offers a thought provoking per-
spective to clinicians and researchers.
Asthma affects the lives of many people

and is a public health issue. The author un-
derscores the mixed messages the public is
receiving about asthma from researchers and
the medical community. Perhaps one of the
most perplexing mixed messages is that
asthma experts have created guidelines for
optimal management and that new and bet-
ter medications are available, yet asthma
morbidity and mortality are on the rise.
Why? The author concludes that heahh care
researchers and practitioners are responsi-
ble to the public and must continue working
to find answers to their questions. Chapter 2
reviews worldwide trends in asthma mor-
tality over the past century. The authors em-
phasize that the causes of the current in-
crease in asthma mortality worldwide are
unknown and that the factors leading to this
rising trend must be discovered and inves-
tigated fully.

The next 6 chapters introduce and re-
view advances in identifying and under-
standing individual, community, genetic,
and environmental risk factors for fatal
asthma. Chapter 4, about the relationship
between individual and community risk fac-
tors, was particularly interesting and may
provide many clinicians with a new point of
view. Though the literature regarding pov-
erty and access to care is growing, many
clinicians may not realize the extent of the
barriers faced by their patients. This chapter
discusses ways in which limited access to
appropriate medical care and economic dis-
advantage may contribute to increa.sed risk
for asthma mortality. Much of the informa-
tion in this chapter comes from the authors'
own work in socioeconomically disadvan-
taged communities. The authors report un-
derdiagnosed asthma within these commu-
nities, unavailability of spacers and peak
flow meters, and increased over-the-counter
bronchodilator sales as factors that can in-
crease risk for severe or fatal asthma. The
information is pertinent because the current
increase in asthma deaths in the United
States disproportionately affects impover-
ished, urban, African-American and Latino
populations.

There were a few editorial errors, such as
the exclusion of the year of publication in
one reference, and two occurrences of cit-
ing the wrong reference within the text.

Generally, the remainder of the volume was
free of these types of errors. There was
some redundancy in Chapters 6, 7, and 8,
which discuss the relationship between
allergen sensitization and exposure and
asthma morbidity and mortality, especially
in the inner city.

The next 5 chapters consider pathophys-
iological aspects of fatal asthma. Chapter 9
discusses the immunopathology of asthma,
provides an excellent review of the roles
of inflammatory cells and mediators in
asthma, and identifies immunopathologic
features that distinguish fatal asthma from
mild or moderate asthma. Chapter 10 ex-
amines both the macroscopic and micro-
scopic pathology of fatal asthma from the
perspective of the medical examiner. The
majority of the photomicrographs in this
chapter help to illustrate the material dis-
cussed, but the focus of a few of the figures
may not be clear. Nonphysicians may ben-
efit from the arrows in Figures 6 and 7,
which point out important features. Chapter
1 1 discusses physiologic consequences of
fatal asthma and helps explain how pulmo-
nary pathologic changes manifest and lead
to fatal asthma. An error in the references
was noted in this chapter (an incorrect ci-
tation of the title and page numbers in the
article by Paul et al, which should read
"Faul JL, Tormey VJ, Leonard C, Burke
CM, Farmer J, Home SJ, Poulter LW. Lung
immunopathology in cases of sudden
asthma death. Eur Resp J 1997;10(2):301-
307").

Chapters 14 and 15 address the natural
history of asthma. The goals of these chap-
ters are to improve overall knowledge of
asthma and its treatment, and to learn how
to prevent fatal and life-threatening asthma
episodes. Six risk factors for fatal asthma
are noted: a previous episode of near fatal
asthma, severe asthma, lack of regular in-
haled corticosteroid use, poor perception of
airway obstruction, denial of symptoms,
and poor access to acute medical care. The
authors of these chapters emphasize diat
early life events are crucial in determining
asthma severity and that knowledge of the
established risk factors for fatal asthma
should be better disseminated to patients
and health care providers. 1 believe that these
two points are crucial to improved asthma

Respiratory Care • April 2000 Vol 45 No 4

437

Books, Films, Tapes, & Software

management. Many clinicians are still
hesitant to make a diagnosis of asthma in
children and to initiate anti-inflammatory
therapy, despite the literature showing that
early-onset asthma and the associated
chronic inflammation impair airway growth.
Furthermore, when asthma is diagnosed, an-
ti-inflammatory management is still under-
used and few practices routinely assess poor
perception or denial of a.sthma symptoms.
Clinicians must be aware of the established
risk factors and work to identify patients at
ri.sk.

Chapter 1 7 examines the relationship be-
tween socioeconomic status and fatal
asthma. This is a well referenced chapter
that provides evidence that .socioeconomic
.status is a risk factor independent of age,
gender, or ethnic origin. The interactions
among poverty, race, and the health care
system are complex, yet the authors present
a strong case that the United States health
care system is failing asthma patients who
live in poverty. The literature presented in
this chapter suggests that lack of access to
appropriate asthma care that is both contin-
uous and based on national guidelines may
be the primary reason that people of low
socioeconomic status are the highest risk
group for fatal asthma.

Chapter 23 presents an interesting and
important discussion on the relationship be-
tween asthma severity and fatalities. The
literature shows that there is no uniform way
to quantitate asthma severity. Currently,
asthma severity is classified primarily in
terms of patient report of frequency and se-
verity of symptoms, and depends on the pa-
tient" s ability to perceive airway obstruc-
tion. The authors cite retrospective studies
that suggest that up to 30% of a.sthma deaths
occur in patients with mild asthma symp-
toms using this approach. This chapter con-
cludes that estimating asthma severity re-
quires assessment of airway caliber and
reactivity, as well as the patient's percep-
tion of airway ob.struction. I feel that those
two points are key to adequate risk man-
agement with asthma patients. The litera-
ture clearly shows that underappreciation of
asthma severity plays a role in fatal and near-
fatal episodes. Patients who cannot ade-
quately perceive changes in airway caliber
will not reptm adverse symptoms and, thus,
may not be aware of the severity of their
disea.se.

Chapter 28 builds on this theme, discuss-
ing the role of patient adherence in fatal
a.sthma. The authors point out that the in-

frequency of fatal asthma can lead both pa-
tients and health care providers to under-
appreciate the role that inappropriate patient
self-management can play in increasing the
risk of a severe asthma episode. The chap-
ter reviews the prevalence of nonadherence
to asthma therapy, including both prescribed
medications and patient monitoring of peak
expiratory flow rates, and di.scusses the role
of poor perception in limiting patient adher-
ence to therapy and delaying medical care.
The authors conclude that the behavior of
both the patient and the health care provider
may play a greater role in the risk of fatal
asthma than variations in underlying asthma
pathophysiology. Poor adherence to asthma
management plans by patients, undertreat-
ment by health care providers, and inade-
quate perception of asthma severity by both
patients and clinicians are prominent risk
factors for fatal asthma. The authors also
provide a 4-part plan to improve adherence
in the at-risk patient. The plan includes
screening to identify high-risk, nonadherent
patients, encouraging clinician-patient and
clinician-family communication, initiating
an intensive, personalized self-management
plan, and changing clinician behavior from
an authoritarian approach to a more inter-
active approach. The chapter also has an
excellent discussion of different types of
nonadherence and specific strategies that cli-
nicians can use to improve awareness and
open communication to better identify pa-
tients at risk.

Chapter 29 presents an interesting dis-
cussion on the possible link between asthma
mortality and chronic u.se of /3 agonists, and
4 hypotheses are proposed to explain that
association. These hypotheses provide use-
ful information to the clinician as well as
the researcher.

The role of clinician and management
factors in fatal asthma is discussed in the
la.st 4 chapters. Chapter 30, which discusses
outpatient management of asthma, states that
prevention of fatalities in this setting de-
pends on recognizing at-risk patients, un-
derstanding patterns of worsening asthma,
and adjusting tfeatment based on measur-
able outcomes rather than the patient's or
physician's subjective impressions. This
chapter is well referenced, with one notable
exception: the author states that patient in-
ability to perceive airway obstruction is a
rare condition. However, there are numer-
ous reports in the literature suggesting that

poor perception, in both children and adults,
is more common than previously thought
and plays a role in fatal or near-fatal asthma.

Individual chapters are often derived from
the work of the authors and. in general, each
chapter is well referenced. The variety of
sources for individual chapters is both a
strength and a weakness of the book. The
strengths are that each chapter is generally
well developed, contains a complete discus-
sion of the topic covered, and contains cur-
rent references. However, the use of multi-
ple experts also leads to a certain degree of
redundancy and differing writing styles,
which are obvious weaknesses in the vol-
ume. In addition, the chapters are loosely
organized into common themes rather than
specifically grouped. The flow of the vol-
ume might have been improved if the con-
tents were explicitly organized into areas of
study. The tables and figures are, generally,
well laid out. and the majority of the text is
very readable for the health care practitio-
ner. Only Chapter 18. which discuss the
mechanisms of dysfunctional jSj-adrenergic
signaling, is written in a more technical .style,
which stands out from the rest of the chap-
ters. The volume is probably best used as a
reference for specific questions regarding
the relationship of the topics covered to the
understanding or management of severe
asthma.

The primary readership of this volume
will probably be physicians who specialize
in the care of asthma patients, but it con-
tains information valuable to any health care
provider who works with asthma patients.
In fact, primary care physicians, respiratory
therapists, and nurses working in asthma
clinics and specialty practices may derive
more benefit from this volume, since the
emphasis is on early identification of pa-
tients at risk for increased asthma morbidity
or mortality. Prevention of fatal asthma re-
quires eariy asthma diagnosis, careful pa-
tient assessment for risk factors associated
with asthma death, and correction of those
factors. Changes in the United States health
care system have increased the role of pri-
mary care physicians and physician ex-
tenders, including respiratory therapists
and nurses, in screening and educating
asthma patients. Fatal Asthma provides
a guide for identifying patients who may
be more susceptible to life-threatening
a.sthma attacks, as well as strategies for
managing tho.se patients and, therefore, is

438

Respiratory Care • April 2000 Vol 45 No 4

Books, Films, Tapes, & Software

a valuable resource for providers of asthma
care.

Randall Baker PhD RRT

Department of Respiratory Therapy

Medical College of Georgia

Augusta. Georgia

Emergency Asthma. Barry E Brenner, ed-
itor. Clinical Allergy and Immunology. Vol-
ume 13. Michael A Kaliner MD, series ed-
itor. 1999. New York: Marcel Dekker.
Hardback, illustrated. 594 pages. $165.00.

Emergency Asthma presents an exten-
sive review of a wide range of topics per-
taining to the emergency management of
asthma. The book is one of the "Clinical
Allergy and Immunology" series, and its
chapters were written with the goal of being
concise, well-referenced, up-to-date re-
views, with sections covering pathophysi-
ology, epidemiology, clinical manifesta-
tions, and management of acute asthma.
Additional sections cover major inciting fac-
tors of asthma exacerbations and appropri-
ate disposition after emergency department
care. Several chapters have a specific pedi-
atric focus and other chapters have sections
that specifically address pediatric patients.

The book was written primarily for emer-
gency physicians, but other medical person-
nel involved in the management of patients
with acute, severe asthma, such as respira-
tory therapists, nurses, and emergency pre-
hospital personnel will find parts of the book
useful. Although Emergency Asthma cov-
ers a wide range of topics, the focused na-
ture of each chapter makes it easy to find
information about specific topics. As exam-
ples. Chapter 33 covers emergency depart-
ment observation units, which might be use-
ful for emergency department nurses and
nurse managers who want an in-depth re-
view of the literature on observation units.
Chapter 29, which covers out-of-hospital
asthma care, provides a quick review for
emergency personnel who respond to pa-
tients with acute asthma. There are chapters
devoted to asthma during pregnancy, intu-
bation, and ventilation of asthma patients,
all of which have a specific focus but could
be of interest to a broad range of people.

The book is intended to provide a con-
cise, up-to-date guide for clinicians who care
for patients with acute, severe asthma. In
general, the book has met these goals. The
material is organized logically into 7 parts:
Introduction. Pathophysiology. Epidemiol-
ogy, Provocative Factors for Emergency De-

partment Visits. Clinical Manifestations,
Management, and Disposition from the
Emergency Department. Each chapter is
readable (approximately 10-25 pages long)
and many chapters contain more than 100
references. Authors were chosen to write
chapters in their areas of expertise. Three
chapters ("Management of Acute Asthma
in Children," "The Acute Asthmatic Patient
in the Pediatric Emergency Department: To
Admit or Discharge?" and "Follow-Up and
Prevention of Relapse in Children After Dis-
position from the Emergency Department")
are devoted exclusively to pediatric asthma,
whereas other chapters have sections that
address pediatric issues. Chapters about air
pollution, premenstrual asthma, and urban
asthma provide useful information about
these interesting topics. The 1997 National
Asthma Education and Prevention Program
(NAEPP) guidelines are referenced exten-
sively. Chapter 18. "National and Interna-
tional Guidelines for the Emergency Man-
agement of Adult Asthma," not only
references the NAEPP guidelines, but pro-
vide comparisons to other international
asthma management guidelines.

Chapter 25, "Medical Management of Se-
vere Acute Asthma," is useful and particu-
larly well-organized. Therapy for acute
asthma is in three tiers: (I) routine care,
including inhaled /3 agonists, corticosteroid
administration, and inhaled anticholinergics,
(2) second-line therapies, including magne-
sium, aminophylline, and systemic cat-
echolamines, and (3) third-line therapies, in-
cluding heliox, ketamine, continuous
positive airway pressure, and bi-level posi-
tive airway pressure. There is also a section
in this chapter on special or unconventional
therapies. This chapter could probably stand
alone as a small guide to the management
of acute asthma.

I would have liked to see a more exten-
sive chapter on inhaled /3 agonists, includ-
ing tables of doses. Aerosol bronchodilator
therapy with /3 agonists is the first line of
therapy for patients with acute asthma, and
a book devoted to emergency management
of asthma should have an extensive chapter
on this topic, including dosing guidelines
for the various ji agonists. ba.sed on deliv-
ery system and patient age. Medication dose
tables in all of the chapters in the manage-
ment section, or grouped into one section
for easy reference, would have been a nice
addition to the book. Chapter 18 presents
some tables with medication doses in the
context of the NAEPP guidelines, but the

only other chapters with dose tables are those
on aminophylline and anticholinergics.

The external appearance of the book is
appealing, and it is the size of most standard
textbooks. All tables and illusn-ations are in
black and white. The tables, diagrams, and
illusu-ations are easy to read. The NAEPP
excerpts and international guidelines for
acute asthma management presented in
Chapter 1 8 are crowded in places, with a lot
of information squeezed on to single pages.
The index provides easy access to topics
covered in the book.

Emergency Asthma would make an im-
f>ortant addition to the references available
in any hospital emergency department that
cares for patients with acute, severe asthma.
The editor has done a nice job of compiling
a group of chapters covering a wide range
of topics pertaining to emergency astbma.

Jay D Eisenberg MD

Department of Pediatrics

Pediatric Pulmonary Division

Doembecher Children's Hospital

Oregon Health Sciences University

Portland, Oregon

Clinical Simulations in Respiratory Care

(CD-ROM). Thomas A Barnes EdD RRT.
1999. Philadelphia: FA Davis. System Re-
quirements: CPU 486 66 MHz (Pentium pre-
ferred). 8 MB of RAM ( 1 6 preferred), SVGA
Color Monitor with 640 X 480 resolution, 2X
CD-ROM (4X or greater preferred), Quick
Time. 8 bit sound card, Windows 3.1, 95/
98, or NT. $49.95 for single-user edition.

Clinical Simulations in Respiratory
Care is an interactive program designed to
test the skills of both the student respiratory
therapist and the seasoned professional alike.
The program consists of 10 clinical simu-
lations. Each of the 10 simulations focuses
on typical scenarios a respiratory therapist
might expect to encounter during his or her
professional practice. The simulations are
also the same type of scenarios graduates of
respiratory therapy programs planning to
take the registered respiratory therapist ex-
aminations will encounter during the Na-
tional Board of Respiratory Care (NBRC)
board examination. The apparent goal of
Clinical Simulations in Respiratory Care
is twofold. First, it allows the user to assess
his or her information-gathering and deci-
sion-making skills. Second, it serves as an
excellent tool for review and preparation
for the NBRC board examination.

Respiratory Care • April 2000 Vol 45 No 4

439

Books, Films, Tapes, & Software

Clinical Simulations in Respiratory
Care comes with very basic, easy to follow
installation instructions. There was no ap-
preciable difference between loading the
program on a Pentium 200MMX (64 MB
RAM, 40 speed CD-ROM, 16MB Diamond
Stealth Video Card. 8 GB hard drive. Cre-
ative Labs Sound Blaster 32 sound card) or
on a Pentium III 500 (128 MB RAM, 6
speed DVD-ROM, 16 MB ATI All-In-
Wonder 128, Creative Labs Sound Blaster
AWE 64 sound card). Both computers were
using the Windows 98 operating system.
During the installation procedure, two ver-
sions of Apple QuickTime (2.1.2 and 3.0)
are installed. If these programs are already
installed, the user is given several options
of how to deal with the existing versions.
Clinical Simulations in Respiratory Care
appears in a screen that fills approximately
one half of the total monitor screen space.
There is no option to maximize or resize the
screen to do away with the wallpaper or
background, which has the potential of be-
ing distracting. On both computers, transi-
tions between screens were rather slow and
a bit choppy. The speed of the processor did
not appear to have any effect on the speed
of the transitions. The quality of each screen
and the colorful illustrations are very good.
The detail of the illustrations (radiographs,
oscilloscope waveforms, patient appear-
ances, etc) enables the user to accurately
visualize the patient condition and diagnos-
tic data in a manner that is much more mean-
ingful. Clinical Simulations in Respira-
tory Care also has audio capabilities. The
user uses the mouse to move the tip of a
stethoscope to the various regions of the
chest to hear high-definition breath and heart
sounds. TTiis is an excellent learning tool in
that it enables and reinforces the user's abil-
ity to associate breath sounds with the cor-
responding pathologies.

Most of the buttons and features of the
program are self-evident. Every screen of-
fers data, score, and help buttons. The data
button leads to a scrolling window with a
complete record of the information gath-
ered up to that point in the simulation. The
score button opens a window with a print-
able score report. The help button opens a
help index that offers "hot text" topics, from
which the user can gather help information.
Once a "hot text," data, or score screen is
opened, however, it is slow to close and
requires a bit of experimenting before the
user learns to click on the screen and wait
for it to close on its own.

When the program is first used, the user
is requested to sign on and enter a pass-
word. From then on, the individual user can
exit and start the program again from where
they left off, or opt to start any simulation
from the beginning.

Clinical Simulations in Respiratory
Care has 3 levels of testing: novice, inter-
mediate, and expert. Each level has specific
features designed to enhance and encourage
the user's learning. As the user moves to the
next level of difficulty, the program offers
less supporting information. In the novice
level, there is no time limit. Scoring for sec-
tions and items can be viewed as the user
progresses through the simulation, explana-
tions of scores are available, "hot text" links
enable the user to acquire additional infor-
mation such as lab values, definitions, and
explanations for text or procedures. The nov-
ice level also allows the user to review the
menu and revisit previous sections.

The intermediate level has similar fea-
tures to the novice level, but in the interme-
diate level the user has the choice of turning
off or on the option of viewing their scores
for sections and items. The intermediate
level does not offer an explanation of the
scores, nor any "hot text." As with the nov-
ice level, the intermediate level responses
are not timed, enabling the student to focus
on critical thinking without having to worry
about time management.

The expert level offers no additional sup-
porting information to provide explanations,
definitions, or normal values to any data
provided. The user must use his or her own
information-gathering and decision-making
skills to progress through the simulations.
The expert level is timed, which requires
effective use of time management skills. The
expert level very closely simulates the ac-
tual clinical examinations respiratory ther-
apy graduates take when pursuing the reg-
istered respiratory therapist credential.

The content of each simulation is very
complete. Each simulation follows a logical
progression from the patient's initial pre-
sentation through discharge. The user is able
to track and review all information they have
gathered on the patient. The choices offered
in both the information-gathering and deci-
sion-making sections contain good distract-
ers, which encourage the user to critically
think about when and why various tests and
priKcdures are appropriate. Should the user
make an incorrect choice, the program of-
fers a detailed explanation of why the choice

was incorrect. No inappropriate or inaccu-
rate information was found.

Overall, Clinical Simulations in Respi-
ratory Care is one of the be,st clinical sim-
ulation programs I have seen for respiratory
care. The content of each simulation is very
concise, and closely, if not exactly, emu-
lates that of the NBRC national examina-
tions. Everything from the installation of
the software to its actual use is very intui-
tive, enabling the user to focus on the exam
rather than on the test-taking process. Clin-
ical Simulations in Respiratory Care is a
valuable learning tool and I would strongly
recommend it to students, educational pro-
grams, and working professionals in respi-
ratory care.

Glen R Kuck MSEd RRT

Department of Cardiopulmonary Sciences
Loma Linda University
Loma Linda, California

Basic Clinical Lab Competencies for Re-
spiratory Care: An Integrated Approach,

3rd edition. Gary C White MEd RRT CPFT.
1998. Albany: Delmar Publishers. Soft-
cover, illustrated. 607 pages. $49.95.

I consider this book to be a link of sorts
between commonly used lecture and labo-
ratory texts in respiratory care and the "clin-
ical world." The author attempts (and is gen-
erally successful) to assist students to make
connections between mechanical pieces of
equipment and their clinical utilization. In
my teaching experience, it has not been un-
common for students to appear to under-
stand facets of equipment selection, assem-
bly, and troubleshooting, but to have
difficulty when they are expected to apply
the information for use with patients. This
book seems to be a potential cure for such
situations.

The book is thoughtfully organized into
chapters that deal with specific types of re-
spiratory care, such as oxygen therapy, de-
livery of aerosolized medications, and me-
chanical ventilation. I was pleasantly
surprised to find chapters on phlebotomy,
intravenous needle insertion and mainte-
nance, and intra-aortic balloon pumping.
Each chapter begins with a brief introduc-
tion, with lists of vocabulary and theory ob-
jectives that serve to organize the reader.
The introduction section is followed by a
brief review of theory related to equipment,
patient conditions, or other pertinent con-
tent. Since the book is intended to facilitate
clinical performance, the next section be-

440

Respiratory Care • April 2000 Vol 45 No 4

Books, Films, Tapes, & Software

gins with proficiency objectives and step-
by-step reviews of clinical performance of
the related skills. Students are encouraged
to review the steps via laboratory simula-
tion with a partner. References and addi-
tional resources are followed by practice ac-
tivities, including step-by-step checklists for
each procedure in that chapter. A short self-
evaluation post-test completes each chap-
ter's content, with answers provided in an
appendix. Last, check sheets are included,
with separate areas for recording scores with
a peer, with an instructor in the lab, and
with patients in the clinical setting. A scor-
ing system is included for each item in the
procedure, with a score for each of 4 objec-
tive levels of performance. A passing score
of 90% is mandated for each skill, which
seems appropriate, since the step-by-step ap-
proach is well laid out, with opportunities
for practice and repeated evaluation. Dili-
gence in practice using this format should
lead most students to mastery of required
skills.

Where appropriate, the author makes ex-
cellent use of the American Association for
Respiratory Care Clinical Practice Guide-
lines by incorporating them into many of
the chapters. In addition, 1 found many help-
ful hints that should assist the astute reader
to rapidly improve clinical performance and
enhance patient care. In my opinion, it might
take a new graduate .several years of expe-
rience to acquire the "clinical wisdom'" so
graciously passed on in these hints.

The general appearance and design of
the book are typical of other paperback texts,
with one exception: each page is perforated
so that score sheets can be turned in to in-
structors for record keeping purposes. 1 find
this to be a thoughtful touch, although this
could also expedite the loss of pages. The

book is replete with photographs and fig-
ures that complement the text, and in some
cases includes simulated clinical applica-
tions of equipment and techniques.

The scope of the book is such that it
could be used in either a technician or a
therapist program, although some chapters
(such as the one on intra-aortic balloon
pumping) may not be as readily utilized in
many programs. The sections on mechani-
cal ventilation include information on older,
as well as current generation mechanical
ventilators, and laboratory practice activi-
ties to accompany each.

There are a substantial number of typo-
graphical errors (beginning with one on the
first page) in this third edition. Most of the
errors involve incorrect spelling, or word
selection that merely makes reading and
comprehension a bit more difficult. Other
errors that could confuse students should be
relatively easily identified by an instructor
who checks the mathematics, carefully reads
the information, and provides students with
a list of errata.

Some content would benefit from using
more current references, although many of
these older references have been considered
"Bibles" for years (such as Respiratory
Pharmacology and Therapeutics, 1978).
Another example of a revered reference in
need of updating is Tlie Adult Respiratory
Distress Syndrome (RDS): Treatment in the
Next Decade (from 1984). It is unlikely that
the majority of information in such older
references is no longer accurate (and prob-
ably valuable from an historical point of
view), although updating references is cer-
tainly part and parcel of writing new edi-
tions of texts.

Another slight problem is misinforma-
tion that has been handed down from gen-

eration to generation and that needs to be
removed from texts and curricula. One ex-
ample of this misinformation is the "old ther-
apist's tale" of decreased drive to breathe as
the mechanism for oxygen-induced hy-
poventilation (mentioned in two sections of
the book). Such misinformation continues
to be passed on by practitioners, and is prob-
ably felt to be justified when it is found in
black and white. Coincidentally, this same
problem was recently identified in another
book review by Sas.soon published in Re-
spiratory Care,' which cites her own 1987
study.-

In summary, I believe that this book
bridges a gap between theory and equip-
ment texts and clinical application. The for-
mat of the book lends itself to use by ded-
icated students who want to perfect the
mechanics of performing procedures in the
laboratory before applying "the art" *at the
patient's bedside. 1 encourage instructors to
do their own reviews of this text to see if it
would be appropriate to add this tool to their
list of required texts, although I would not
substitute it for either a theory text, or an
equipment text.

Jeff Anderson MA RRT

Department of Respiratory Care

College of Health Sciences

Boise State University

Boise, Idaho

REFERENCES

1 . Sassoon C. Review of Mechanical ventila-
tion: physiological and clinical applications,
3rd edition, by Pilbeam S. RespirCare 1999:
44(7):866.

2. Sassoon CSH, Hassell KT, Mahutte CK. Hy-
peroxic-induced hypercapnia in stable
chronic obstructive pulmonary disease. Am
Rev Respir Dis 1987;I35(4):907-91 1.

Respiratory Care • April 2000 Vol 45 No 4

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say that VentNet monitors the status of
each ventilator maintaining a central set-
tings log that is updated whenever a ven-
tilator setting change is made at the bed-
side, and that it also maintains an alarm
log that tracks alarm response times.
According to Mallinckrodt, remote alarm
status notification capabilities can be
added to the system to further enhance
patient safety and provide caregivers
greater flexibility. For more information
from Mallinckrodt, circle number 1 89 on
the reader service card in this issue, or
send your request electronically via
"Advertisers Online" at http://www.
aarc.org/buyers_guide/

RESPIRATORY CARE • APRIL 2000 VOL 45 NO 4

443

Not-for-profit organizations are offered a free advertisement of up to eight lines to appear, on a space-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 the month two months preceding the month in which you wish the ad to run.

Submit copy and insertion orders to Calendar of Events, RESPIRATORY CARE, 1 1030 Abies Lane, Dallas TX 75229-4593.

Calendar
of Events

AARC & AFFILIATES

April 7-9 — Franklin, Tennessee

The TSRC convention will be held at
the Marriott-Cool Springs just outside
of Nashville. Topics include asthma
management, ECMO, nitric oxide
ventilation, a mock trial, fast-track
weaning protocols, and home care
topics. Contact: Patti Joyner, RRT,
CCM, at (901) 725-7100, ext. 3101,
Pjoyner@inmcc-tlc.coin.

April 13-14 — Orange Beach,
Alabama

The ASRC is hosting a clinical
conference at the Hilton Garden Inn.
Topics include therapist-driven
protocols, patient management,
noninvasive positive pressure
ventilation in the acute care setting,
pharmacology, and mechanical
ventilation. Eight CRCE hours have
been requested. Contact: Bill Pruitt at
(334) 434-3405 or wpruitt@jaguarl.
iisouthal.edu.

April 13-14 — King of Prussia,
Pennsylvania

The Pennsylvania Society for
Respiratory Care presents their Third
Annual Eastern Regional Conference
and Exhibition at the Holiday Inn.
"Diversity, Dimension, Design 2000"
will feature speakers Wiliam J.
Malley, MS, RRT, and AARC
President Garry W. Kauffman, MPA,
CHE, RRT. Ten CEUs are pending.
Contact: Angle Herstine at (609)
784-0340, or Ann Cusano at (215)
646-7300, ext. 428.

April 11-19— Bismark, North
Dakota

The North Dakota Society for
Respiratory Care presents their annual
educational symposium at the
Radisson Inn. "On the Horizon of
Respiratory Care" will offer 12 CRCE
hours and will feature speakers Heidi
Heitkamp; North Dakota Attorney
General James Fink, MS, RRT;
George Gaebler, MSEd, RRT; and
Irish Blakely, RRT. Contact: For
more information, contact Mike
Runge at (701) 530-8556.

April 26-28 — Indianapolis, Indiana

Region II for Respiratory Care will
holds its 27th annual program at the
Hyatt Convention Center. The

conference will feature psychiatrist
Dr. Clifford Kuhn (alias "The Laugh
Doctor"), Dr. James Stoller, Dr. Neil
Maclntyre, and Vijay Deshpande.
Topics on pediatrics, home care, and
management will be included; and an
exhibit hall will feature the latest
respiratory care technology and
resources. Contact: For information,
call (800) 69 1 -304 1 , Mailbox # 1 , or
www.bright.net/~dsibb/reg2rc.htm,

April 28 — Erie, Pennsylvania

The Pennsylvania Society for
Respiratory Care presents their 19th
annual Northwest District Educational
Seminar and Equipment Exhibition at
the Quality Inn, Contact: Sue
Sheakley at (814) 452-5406 or
ssheakle@svhs.org for more
information.

May 5 — San Antonio, Texas

The University of Texas Health
Science Center at San Antonio, in
conjunction with the TSRC (Alamo
District) and Wilford Hall Medical
Center, announce the 5th Annual
Respiratory Care Symposium to be
held at The University of Texas
Health Science Center at San
Antonio, Topics include the state of
the profession, newer modes of
mechanical ventilation, care of the
adult asthmatic, pediatric
assessment, COPD, mechanical
ventilation of the neonate,
shock/trauma, and pediatric asthma.
Six CRCE credits provided.
Contact: UTHSCSA, Department
of Respiratory Care-MSC 6248,
7703 Floyd Curl Dr„ San Antonio,
TX 78229-3900, (210) 567-8850,

May 9-12 — Grand Rapids,

Michigan

The Michigan Society for Respiratory
Care will host their Annual Spring
Conference at the Grand Center/Amway
Grand Plaza Hotel, Contact: For more
information, call (517) 336-7570 or
visit their web site at www.
MichiganRC.com.

May 15-17 — Southerington,
Connecticut

The CTSRC and the Connecticut
Thoracic Society will co-host their
spring conference, "Branching Forth,
Reaching Up, Speaking Out," at the
Aqua Turf Club, Speakers include
Richard Branson, Dr, James Stoller,
and AARC President-Elect Carl

Wiezalis. Sessions will cover topics
on pulmonary rehab, sleep disorders,
and critical care. CRCE credits for
RTs, CE credits for physicians, and
CEU credits for nurses are being
applied for. Contact: Frank
Salvatore for more information at
(860) 827-1958, ext. 5706, or access
www.ctsrc.org.

May 19 — Brainerd, Minnesota
The Minnesota Society for
Respiratory Care host their Spring
Fling — "Rev It Up" at the Breezy
Point Resort. Five CRCEs will be
requested. Contact: For more
information, contact Laurie
Tomaszewski at (651 ) 232-1922,
Carolyn Dunow at dunowc@
fhpcare.com, or Carl Mottram at
mottram.carl@mayo.edu.

May 21-22 — Spokane, Washington

The Respiratory Care Society of
Washgton will hold its 27th Annual
Pacific Northwest Regional
Respiratory Care Conference at
Cavanaugh's Inn at the Park. Topics
will include current government
issues and respiratory care, high
frequency, and open lung strategies.
Contact: For more information,
contact Larry Knisley at (509) 921-
6560, Garth Arkell at (509) 924-1 197
or e-mail arkell4@gateway.net.

September 20-22 — Rochester,
Minnesota

The Minnesota Society for
Respiratory Care host their 3 1 st
Annual Fall State Conference — "Too
Hot to Handle." Contact: For more
information, contact Laurie
Tomaszewski at (651) 232-1922.
Carolyn Dunow at dunowc@
fhpcare.com, or Carl Mottram at
mottram.carl @ mayo.edu.

Other Meetings

May 19-21 — Atlanta, Georgia

Children's Healthcare of Atlanta-
Egleston will sponsor "Moving
ECMO into the New Millennium" —
SEECMO 2000, the 10th Annual
Southeastern ECMO Conference, at
the Grand Hyatt Buckhead.
Presentations will cover adult ECMO,
ECMO flow direction, CVVH
techniques, and hands-on water drills.
Contact: Micheal Heard, RN, at
(404) 315-2593 or
micheal.heard@choa.org.

444

RESPIRATORY CARE • APRIL 2000 VOL 45 NO 4

Respiratory Care • Open Forum 2000

The American Asscx;iation 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 invited
to present posters at the OPEN FORUM during the AARC In-
ternational Respiratory Congress in Cincinnati, Ohio, October
7-10, 2000. Accepted abstracts will be published in the Au-
gust 2000 issue of RESPIRATORY Care. Membership in the
AARC is not required for participation. All accepted abstracts
are automatically considered for ARCF research grants.

SPECIFICATIONS— READ CAREFULLY!

An abstract may report (1) an original study, (2) the eval-
uation of a method, device or protocol, or (3) a case or case
series. Topics may be aspects of adult acute care, continuing
care/rehabilitation, perinatology/pediatrics, cardiopulmonary
technology, or health care delivery. The abstract may have been
presented previously at a local or regional — but not nation-
al — meeting and should not have been published previously
in a national journal. The abstract will be the only evidence
by which the reviewers can decide whether the author should
be invited to present a poster at the Open FORUM. Therefore,
the abstract must provide all important data, findings, and con-
clusions. Give specific information. Do not write such gen-
eral statements as "Results will be presented" or "Significance
will be discussed."

FORMAT AND TYPING INSTRUCTIONS

Accepted abstracts will be photographed and reduced by
40%; therefore, the size of the original text should be at least
10 points. A font like Helvetica or Times makes the clearest
reproduction. The first line of the abstract should be the title
in all capital letters. Title should explain content. Follow title
with names of all authors (including credentials), institution(s),
and location; underline presenter's name. Type or electron-
ically print the abstract single spaced in one paragraph on a
clean sheet of paper, using margins set so that the abstract
will fit into a box no bigger than 18.8 cm (7.4") by 13.9 cm
(5.5"), as shown on the reverse of this page. Insert only one
letter space between sentences. Text submission on diskette
is allowed but must be accompanied by a hard copy. Data may
be submitted in table form, and simple figures may be included
provided they fit within the space allotted No figure, illustration,
or table is to be attached to the abstract form. Provide all au-
thor information requested. Standard abbreviations may be em-
ployed without explanation; new or infrequently used ab-
breviations should be spelled out on first use. Any recurring
phrase or expression may be abbreviated, if it is first explained.
Check the abstract for ( 1 ) errors in spelling, grammar, facts,
and figures; (2) clarity of language; and (3) conformance to
these specifications. An abstract not prepared as requested may
not be reviewed. Questions about abstract preparation may be
telephoned to Linda Barcus at (972) 406-4667.

ESSENTIAL CONTENT ELEMENTS

Original study. Abstract nuist include ( 1 ) Background: state-
ment of research problem, question, or hypothesis; (2) Method:
description of research design and conduct in sufficient de-
tail to permit judgment of validity; (3) Results: statement of
research findings with quantitative data and statistical anal-
ysis; (4) Conclusions: interpretation of the meaning of the re-
sults.

Method, device, or protocal valuation. Abstract must in-
clude ( 1 ) Background: identification of the method, device,
or protocol 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-
tation of the evaluation and experience. Cost comparisons should
be included where possible and appropriate.

Case report Abstract must report a case that is uncommon
or of exceptional educational value and must include (1) In-
troduction: relevant basic information important to understanding
the case. (2) Case Summary: patient data and response, de-
tails of interventions. (3) Discussion: content should reflect
results of literature review. The author(s) should have been
actively involved in the case and a case-managing physician
must be a co-author or must approve the report.

Early Deadline Allowing Revision. Authors may choose
to submit abstracts early. Abstracts postmarked by February
29, 2000 will be reviewed and the authors notified by letter
only to be mailed by March 31, 2000. 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 Deadline (April 28, 2000).

Final Deadline. The mandatory Final Deadline is April 28,
2000 (postmark). Authors will be notified of acceptance or re-
jection by letter only. These letters will be mailed by July 12,
2000.

Mailing Instructions. Mail (Do not fax!) 2 clear copies
of the completed abstract form, diskette (if possible), and a
stamped, self-addressed postcard (for notice of receipt) to:

2000 Respiratory Care Open Forum

11030 Abies Lane

Dallas TX 75229-4593

submit your Open Forum abstract electronically

I visitwww.rcjournai.com ,

Respiratory Care Open Forum 2000 Abstract Form

E
o

13.9 cm or 5.5"

1. Title must be in all
upper case (capital)
letters, authors' full
names and text in
upfier and lower case.

2. Follow title with all
authors' names
including credentials
(underline presenter's
name), institution, and
location.

3. Do not justify (ie,
leave a 'ragged' right
margin).

4. Do not use type size
less than 10 points.

5. All text and the table,
or figure, must fit into
the rectangle shown.
(Use only 1 clear, con-
cise table or figure.)

6. Submit 2 clean copies.

Mail original & 1
photocopy (along with
postage-paid postcard) to

2000 respiratory
Care Open Forum

11030 Abies Lane
Dallas TX 75229-4593

Earlv deadline is
February 28, 2000
(postmark)

Final deadline is
April 28, 2000
(postmark)

Electronic
Submission Is Now

Available. Visit
www.rcjournal.com

to find out more

Name & Credentials

Mailing Address

Voice Phone & Fax

■TJJ Name & Credentials

Mailing Address

Voice Phone & Fax

American Association for Respiratory Care

_7V_

/ \

Please read the eligibility requirements for each of tfie classifications in ftie
right-tiand column, tfien complete tfie applicable section. All information
requested below must be provided, except where indicated as optional.
See other side for more information and fee schedule. Please sign and date
application on reverse side and type or print clearly. Processing of applica-
tion takes approximately 1 5 days.

D Active
Associate

D Foreign

D Physician

D Industrial
D Special
n Student

Lost Nome _
First Name

Social Security No.

Home Address

City

State

.Zip

Phone No.

Primary Job Responsibility fcfieck one only)

D Technical Director

D Assistant Technical Director

D Pulmonary Function Specialist

n Instructor/Educator

n Supervisor

D Staff Therapist

n Staff Technician

D Rehabilitation/Home Core

n Medical Director

D Sales

n Student

□ Other, specify

lyp* of Business

□ Hospital

n Skilled Nursing Facility

D DME/HME

D Home Health Agency

D Educational Institution

n Manufacturer or supplier

n Other, specify

Date of Birth (optional)

Sex (optional) .

U.S. Citizen?

Yes

Have you ever been a member of the AARC?

If so, when? From to

Preferred mailing address: n Home D Business

For office use only

FOK ACTIVE MEMBER

An individual is eligible if he/she lives in the U.S. or its territories or was an Active Member
prior to moving outside its borders or territories, and meets ONE of the following criteria; (1 ) is
legally credentialed as a respiratory core professional if employed in a state thot mandates
such, OR (21 is a groduate of on accredited educational progrom in respirotory core, OR (31
holds credential issued by the NBRC. An individual who is on AARC Active Member in gooa
standing on December 8, T994, will continue as such provided his/her membership remoms in
good standing.

PLEASE USE THE ADDRESS OF THE LOCATION WHERE YOU PERFORM YOUR JOB, NOT
THE CORPORATE HEADQUARTERS IF IT IS LOCATED ELSEWHERE.

Place of Employment

Address ^

City

State

-Zip

Phone No.

Medical Director/Medical Sponsor

FOR ASSOCIATE OR SPECIAL MEMBER

Individuals who hold a position related to respiratory core but do not meet the requirements of
Active Member shall be Associate Members. They have all the rights and benefits of the Asso-
ciation except to hold office, vote, or serve as chair of a standing committee. The following sub-
classes of Associate Membership ore available; Foreign, Physician, and Industrial (individuols
whose primary occupation is directly or indirectly devoted to the monufocture, sale, or distribu-
tion of respiratory care eouipmenf or supplies). Special Members ore those not working in o
respiratory carew^elated field.

PLEASE USE THE ADDRESS OF THE LCXTATION WHERE YOU PERFORM YOUR JOB, NOT
THE CORPORATE HEADQUARTERS IF IT IS LOCATED ELSEWHERE.

Place of Employment

Address

City

Stote

-Zip

Phone No.

FOR STUDENT MEMBER

Individuals will be classified as Student Members if they meet all the requirements for Associate
Membership and are enrolled in an educational program in respiratory core accredited by, or
in the process of seeking accreditation from, an AARC -recognized agency.

SPECIAL NOTICE — Student Members do not receive Continuing Respiratory Care Education
(CRCE) transcripts. Upon completion of your respiratory core education, continuing education
credits may be pursued upon your rectassificaNon to Active or Associate Memtier.

School/RC Program

Address

City_
State

-Zip

Phone No.

Length of program

D 1 year
12 2 years

Expected Date of Graduation (REQUIRED
INFORMATION)

n 4 years

12 Other, specify

Month

Year

Amerkan Association for Respirotory Core « 1 1030 Abies Lone » Polios, TX 75229-4593 » [972] 243-2272 « fax [972] 484-2720

merican Association for Respiratory Care

EMBERSHIP APPLICATION

Demographic Questions

We request that you answer these questions in order to help us
design services and programs to meet your needs.

Cfiecit the Highest Degree Earned

D High School

D RC Graduate Technician

D Associate Degree

n Bachelor's Degree

D Master's Degree

D Doctorate Degree

Number of Years in Respiratory Care

ZZ 0-2 years O 11-15 Years

n 3-5 years D 1 6 years or more

n 6-10 years

Job Status

Full Time

Part Time

Credentials

RRT

CRT

Physician

CRNA

Salary

Less than $10,000

□

$10,001 -$20,000

$20,001 -$30,000

$30,001 -$40,000

$40,000 or more

n LVN/LPN

n CPFT

n RPFT

n Perinotal/Pediatric

PLEASE SIGN

I hereby apply for membership in the American Association for Respiratory Core
and hove enclosed my dues. If approved for membership in the AARC, I will abide
by its bylaws and professional code of ethics. I authorize investigation of all state-
ments contained herein and understand that misrepresentations or omissions of
facts called for is cause for re|ection or expulsion.

A yearly subscription to RESPIRATORY CARE iournal and AARC Times magazine
includes an allocation of $1 1 .50 from my dues for each of these publications.

NOTE: Contributions or gifts to the AARC are not tax deductible as charitable con-
tributions for income tax purposes. However, they may be tax deductible as ordi-
nary and necessary business expenses subject to restrictions imposed as a result of
association lobbying activities. The AARC estimates that the nondeductible portion
of your dues — the portion which is allocable to lobbying — is 26%.

Dofa

Membership Fees

Payment must accompany your application to tfie AARC. Fees are for 12
months. (NOTE: Renewal fees are $75.00 Active, Associate-Industrial or Associ-
ate-Pfiysician, or Special status; $90.00 for Associate-Foreign status; and
$45.00 for Student status).

n Active

$ 87.50

D Associate (Industrial or Physician)

$ 87.50

D Associate (Foreign)

$102.50

n Special

$ 87.50

D Student

$ 45.00

TOTAL

Spetialty Settions

Established to recognize the specialty areas of respiratory care, these sections
publish a bi-monthly newsletter that focuses on issues of specific concern to that
specialty. The sections also design the specialty programming at the national
AARC meetings.

D Adult Acute Care Section $ 1 5.00
D Education Section $20.00
D Perinotal-Pediatric Section $15.00
n Diagnostics Section $15.00
D Continuing Care-
Rehabilitation Section $15.00
D Management Section $20.00
n Transport Section $15.00
D Home Core Section $15.00
D Subacute Care Section $15.00

TOTAL $

ORAND TOTAL = Membership Fee

plus optional sections $

D Total Amount Enclosed/Charged $_
D Please charge my dues (see below)

To charge your dues, complete the following:
D MasterCard
D Visa

Card Number

Card Expires /_

Signature

Mail application and appropriate fees to:
American Association for Respiratory Core • 1 1030 Abies Lane • Dallas, TX 75229-4593

[9721 243-2272 • Fax [972] 484-2720

RE/PIRATORy QVRE

Manuscript Preparation Guide

Respiratory Care welcomes original manuscripts related to the sci-
ence and technology of respiratory care and prepared according to the
following instructions and the Uniform Requirements for Manuscripts
Submitted to Biomedical Journals (available at http://www.acpon-
line.org/joumals/resource/unifreqr.htm). Manuscripts are blinded and
reviewed by professionals who are experts in their fields. Authors
are responsible for obtaining written permission to publish previ-
ously-published figures and tables from the original copyright hold-
er. Accepted manuscripts are copyedited for clarity, concision, and
consistency with RESPIRATORY Care format. Before publication,
authors receive page proofs for minor correction. Published papers
are copyrighted by Daedalus Inc and may not be published elsewhere
without permission. Editorial consultation is available at any stage
of planning or writing for any submission; contact the Editorial Office.

Categories of Articles

Research Article: A report of an original investigation (a study).
Must include Title Page, Abstract, Key Words, Background,
Methods. Results, Discussion, Conclusions, and References. May
also include Tables, Figures (if so, must include Figure Legends),
Acknowledgments, and Appendices.

Review Article: A comprehensive, critical review of the literature
and state-of-the-art summary of a topic that has been the subject of
at least 40 published research articles. Must include: Title Page, Out-
line, Key Words, Introduction, Review of the Literature, Summa-
ry, and References. May also include: Tables, Figures (if so, must
include Figure Legends), and Acknowledgments.

Overview: A critical review of a pertinent topic that has fewer than
40 published research articles. Same structure as Review Article.

Update: A report of subsequent developments in a topic that has
been critically reviewed in RESPIRATORY Care or elsewhere. Same
structure as a Review Article.

Special Article: A pertinent paper not fitting one of the other categories.
Consult with the Editor before writing or submitting such a paper.

Editorial: A paper addressing an issue in the practice or adminis-
tration of respiratory care. It may present an opposing opinion, clar-
ify a position, or bring a problem into focus.

Letter: A brief, signed communication responding to an item pub-
lished in Respiratory Care or about other pertinent topics. Tables,
Figures, and References may be included. The letter should be marked
"For Publication."

Case Report: Report of an uncommon clinical case or a new or
improved method of management or treatment. A case-manag-

ing physician must either be an author or furnish a letter
approving the manuscript. Must include: Title Page, Abstract, Intro-
duction, Case Summary, Discussion, and References. May also
include: Tables, Figures (if so, must include Figure Legends), and
Acknowledgments.

Point-of-View Paper: A paper expressing personal but substanti-
ated opinions on a pertinent topic. Must include: Title Page, Text,
and References. May also include Tables and Figures (if so, must
include Figure Legends).

Drug Capsule: A miniature review paper about a drug or class of
drugs that includes discussions of pharmacology, pharmacokinet-
ics, or pharmacotherapy.

Graphics Corner: A brief case report discussing and illustrating
waveforms for monitoring or diagnosis. Should include Questions,
Answers, and Discussion sections.

Kittredge's Comer: A brief description of the operation of respiratory
care equipment. Should include information from manufacturers and
editorial comments and suggestions.

PFT Comer: A brief, instructive case report including pul-
monary function testing, accompanied by a review of the relevant
physiology and appropriate references to the literature.

Test Your Radiologic Skill: A brief, insttuctive case report involv-
ing pulmonary medicine radiography and including one or more radio-
graphs. May involve imaging techniques other than conventional
chest radiography.

Review of a Book, Film, Tape, or Software: A balanced, critical
review of a recent release. RESPIRATORY Care does not accept unso-
licited book reviews; please contact the Editor if you have a sug-
gestion for a book review.

Preparing the Manuscript

Print on one side of white 8.5 xl 1 inch paper, with margins of at
least 1 inch on all sides. Double-space the text and number the pages.
Do not include author names, author institutional affiliations, or allu-
sions to institutional affiliations anywhere except on the title page.
On the Abstract page include the tide but do not include author names.
Begin each of the following on a new page: Title Page, Abstract,
Text, Acknowledgments, References, each Table, each Figure, and
each Appendix. Use standard English in the first person and active
voice. Type all headings in initial-capital letters (eg. Background,
Methods, Patients, Equipment, Statistical Analysis, Results, Dis-
cussion). Center the main section headings and place second-level
headings on the left margin.

Respiratory Care Manuscript Preparation Guide, Revised 12/99

Manuscript Preparation Guide

Abstract. Please ensure that the abstract does not contain any facts
or conclusions that do not also appear in the body text. Limit the
abstract to no more than 400 words.

Key Words. Research, Review, Overview, and Special Articles
require Key Words. On the Abstract or Outline page, include a list
of 6 to 10 key words or two-word phrases.

References. Assign reference numbers in the order that articles are
cited in your manuscript. At the end of your manuscript, list the cited
works in numerical order. Abbreviate journal names as in Index Medi-
cus. List all authors. The following examples show RESPIRATORY
Care's style for references.

Article in a journal carrying pagination throughout the volume:

Rau JL, Harwood RJ. Comparison of nebulizer delivery meth-
ods through a neonatal endotracheal tube; a bench study. Respir
Care 1992;37(1 1):1233-1240.

Article in a publication that numbers each issue beginning with Page 1 :

Bunch D. Estabhshing a national database for home care. AARC
Times 1991 ;15(Mar):61, 62,64.

Corporate author journal article:

American Association for Respiratory Care. Criteria for estab-
lishing units for chronic ventilator-dependent patients in hospitals.
Respir Care 1988;33(1 1):1044-1046.

Article in journal supplement: (Journals differ in numbering and iden-
tifying supplements. Supply information sufficient to allow
retrieval.)

Reynolds HY. Idiopathic interstitial pulmonary fibrosis. Chest
1 986; 89(3 Suppl): 1 39S- 1 43S.

Abstract in journal: (Abstracts citations are to be avoided, and those
more than 3 years old should not be cited.)

Stevens DP. Scavenging ribavirin from an oxygen hood to reduce
environmental exposure (abstract). Respir Care 1990;35(1 1): 1087-
1088.

Editorial in a journal:

Enright P. Can we relax during spiromeu^? (editorial). Am Rev
Respir Dis I993;148(2):274.

Editorial with no author given:

Negative-pressure ventilation for chronic obstructive pul-
monary disease (editorial). Lancet 1992;340(8833):1440-1441.

Letter in journal:

Aelony Y. Ethnic norms for pulmonary function tests (letter).
Chest 1991;99(4):1051.

Corporate author book:

American Medical Association Department of Drugs. AMA drug
evaluations, 3rd ed. Littleton CO: Publishing Sciences Group; 1977.

Book: (For any book, specific pages should be cited whenever ref-
erence is made to specific statements or other content.)

DeRemee RA. Clinical profiles of diffuse interstitial pul-
monary disease. New York: Futura; 1990:76-85.

Chapter in book with editor(s):

Pierce AK. Acute respiratory failure. In: Guenter CA, Welch MH,
editors. Pulmonary medicine. Philadelphia: JB Lippincott;
1977:26-42.

Paper accepted but not yet published:

Hess D. New therapies for asthma. Respir Care (year, in press).

Personal communication of unpublished data not yet accepted for
publication: You must obtain written permission to cite unpublished
data received via personal communication. Do not number such ref-
erences, but instead make parenthetical reference in the body text
of your manuscript. Example: "Recently, Jones found this treatment
effective in 45 of 83 patients (Jones HI, University of the Cascades,
1999, personal communication)."

Tables. Tables should be consecutively numbered. Start each table
on a separate page. Number and tide the table and give each column
a brief heading. Place explanations in footnotes, including all non-
standard abbreviations and symbols. Key the footnotes with die fol-
lowing symbols, superscripted, in the table body, and in the following
order:*, t, t, §, II, 1, **, tt- Do not use horizontal or vertical
rules or borders. Do not submit tables as photographs, reduced in
size, or on oversize paper.

Figures (illustrations). Figures include graphs, line drawings, pho-
tographs, and radiographs. Use only illustrations that clarify and aug-
ment the text. Number figures consecutively as Figure 1, Figure 2,
etc. All the figures must be mentioned in the text. Every figure should
have a legend (a title and/or description explaining the figure). Fig-
ure legends should appear as separate paragraphs at the end of the
manuscript (after the References section), in the same computer file
as the manuscript (not in a separate file, as with the tables and fig-
ures). Do not create scanned versions of figures borrowed from other
publications; clear photocopies are preferable. To include figures
previously published in other publications, you must obtain permission
from the original copyright holder (see below). Figures must be of
professional quality and a copy of the article from which the figure
came should be available. If color is essential to die figure, consult
the Editor for more information. In reports of animal experiments,
use schematic drawings, not photographs. A letter of consent must
accompany any photograph of an identifiable person. If possible,
submit radiographs as prints and full-size copies of film.

Drugs. Precisely identify all drugs and chemicals used, giving gener-
ic names, doses, and methods of administration. Brand names may
be given in parentheses after generic names.

Commercial Products. In the text, parenthetically identify com-
mercial products only on first mention, giving the manufacturer's
name, city, and state or country. Example: "We performed spirom-

RE-SPIRATORY Care Manuscript Preparation Guide, Revised 12/99

Manuscript Preparation Guide

eiry (1085 System, Medical Graphics, Minneapolis, Minnesota)."
Provide model numbers if available, and manufacturer's suggest-
ed price, if the study has cost implications.

Permissions: You must obtain written permission to use pictures
of identifiable individuals or to name individuals in the Acknowl-
edgments section. You must obtain written permission from the orig-
inal copyright holder to use figures and tables from other publica-
tions. Copies of all applicable permissions must be on file at
Respiratory Care before a manuscript goes to press. Copyright
is most often held by the journal or book in which the figure or table
originally appeared and applies to the creativity, style, and form in
which the facts/data are presented to the reader; the facts themselves
are not copyright-protectable. Therefore, if you were asking per-
mission to reproduce a table or figure direcdy from a journal or book,
or with minor adaptations, permission would be necessary. How-
ever, if you intend to extract some data from text or illustrations and
present them in an entirely new form, permission would not be need-
ed. Simply cite the source of the data using the following statement;
"Figure adapted from data published in ..."

Ethics. When reporting experiments on human subjects, indicate
that procedures were conducted in accordance with the ethical stan-
dards of the World Medical Association Declaration of Helsinki (see
Respir Care I997;42(6);635-636) or of the institution's committee
on human experimentation. State that informed consent was
obtained. Do not use patient's names, initials, or hospital numbers
in text or illustrations. When reporting experiments on animals, indi-
cate that the institution's policy, a national guideline, or a law on
the care and use of laboratory animals was followed.

Statistics. Identify the statistical tests used in analyzing the data and
give the prospectively determined level of significance in the Meth-
ods section. Report actual p values in the Resuhs section. Cite only
textbook and published article references to support choices of tests.
As with commercial products (see above), parenthetically identi-
fy any general-use or commercial computer programs used.

Units of Measurement. Express measurements of length, height,
weight, and volume in metric units appropriately abbreviated; tem-
peratures in degrees Celsius; and blood pressures in millimeters of
mercury (mm Hg). Report hematologic and clinical-chemistry mea-
surements in conventional metric and in SI (Systeme Internationale)
units (units and conversion factors listed at Respir Care
1997;42(6);640). Show gas pressures (including blood gas tensions)
in millimeters of mercury (mm Hg).

abbreviations. Do not use abbreviations in the title, in section head-
ings, and do not use unusual abbreviations in the abstract Use an abbre-
viation only if the term occurs 4 or more times in the paper. Define
all abbreviations (ie, write out the full term on first mention, followed
by the abbreviation in parentheses) and thereafter use only the abbre-
viation. Standard units of measurement and scientific terms can be
abbreviated without explanation (eg, L/min, mm Hg, pH, O2).
Please use the following forms: cm H2O (not cmH20), f (not bpm),
L (not I), L/min (not LPM, l/min, or Ipm), mL (not ml), mm Hg
(not mmHg), pH (not Ph or PH), p > 0.001 (not p>0.001 ), s (not sec),
Spo, (arterial oxygen saturation measured via pulse-oximetry).

Prior and Duplicate Publication. In general, do not submit work
that has been published or accepted elsewhere, though in special
instances the Editor may consider such material if the original pub-
lisher grants permission. Please consult the Editor before submit-
ting such work.

Autliorship. All persons listed as authors should have participat-
ed in the reported work and in the shaping of the manuscript all must
have proofread the submitted manuscript, and all should be able to
publicly discuss and defend the paper's content. A paper of corporate
authorship must specify the key persons responsible for the article.
Attribution of authorship is not based solely on solicitation of fund-
ing, collection or analysis of data, provision of advice, or similar ser-
vices. Persons who provide such ancillary services may be recog-
nized in an Acknowledgments section.

Reviewers: Please supply the names, credentials, affiliations, address-
es, and phone/fax numbers of 3 professionals whom you consider
expert on the topic of your paper. Your manuscript may be sent to
one or more of them for blind peer review.

Submitting the Manuscript

Submit three printed copies and one (3.5-inch) computer diskette.
The printed copies should each include photocopies of all of the Fig-
ures, Tables, and Appendixes. On the diskette, the manuscript should
be in one file and the tables in a separate file. If soft copies of the fig-
ures are available, they should also be in a separate file. However,
do not create scanned versions of figures borrowed from other pub-
lications; clear photocopies are preferable. Include the completed
Cover Letter and Checklist (see next page) and permission letters.
Mail to Respiratory Care, 600 Ninth Avenue, Suite 702, Seat-
tle WA 98 1 04. Do not fax manuscripts. Receipt will be acknowledged.

Conflict of Interest. On the cover page, authors must disclose any
liaison or financial arrangement they have with a manufacturer or
distributor whose product is addressed in the manuscript or with the
manufacturer or distributor of a competing product. Such arrange-
ments do not disqualify a paper from consideration and are not dis-
closed to reviewers. Reviewers are screened for possible conflict
of interest.

Abbreviations and Symbols. Use standard abbreviations and sym-
bols, listed at Respir Care 1997;42(6):637-642. Do not create new

Respiratory Care
Editorial Office:

600 Ninth Avenue, Suite 702
Seattle W A 98104

(206) 223-0558 (voice)

(206) 223-0563 (fax)

rcjoumal @ aarc.org

rcjkk@oz.net

Respiratory Care Manuscript Preparation Guide, Revised 12/99

Cover Letter & Checklist

A copy of this completed form must accompany all manuscripts submitted for publication.

Title of Paper:

Publication Category: _
Corresponding Authior:
Mailing Address:

Reprints: □ Yes □ No

_Phone:

FAX:

E-mail Address:

"We, the undersigned, have all participated in the work reported, proofread the accompanying manuscript, and approve its sub-
mission for publication." Please print and include credentials, title, institution, academic appointments, city and state. If more
than 4 authors, please use another copy of this form.*

•First Author:

'Second Author:

*Third Author:

Author Signature/Date,

Author Signature/Date_

•Fourth Author:

Author Signature/Date,

Has this research been presented in any public forum? □ Yes □ No
If yes, where, when and by whom?

Has this research received any awards? □ Yes □ No
If yes, please describe.

Has this research received any grants or other support, financial or material? □ Yes □ No
If yes, please describe. .

Do any of the authors of this manuscript have a financial interest in (or a commercial or consulting relationship to) any of the
products or manufacturers mentioned in this paper or any competing products or manufacturers? □ Yes □ No

If yes, please describe.

□ Have you enclosed a copy of the manuscript on diskette?

□ Is double-spacing used throughout entire manuscript?

□ Are all pages numbered in upper-right corners?

□ Are all references, figures, and tables cited in the text?

□ Has the accuracy of the references been checked, and are they correctly formatted?

□ Have SI values been provided?

□ Has all arithmetic been checked?

□ Have generic names of drugs been provided?

□ Have necessary written permissions been provided?

□ Have authors' names been omitted from text and figure labels?

□ Have copies of 'in press' references been provided?

□ Has the manuscript been proofread by all the authors?

□ Have the manufacturers and their locations been provided for all devices and equipment used?

Respiratory Care Manuscript Preparation Guide, Revised 1 2/99

MEI^^TCH

For VOLUNTARY reporting

by health professionals of adverse

events and product problems

FDA Use Onty (Resp Care)

Triage unit
sequence a

B. Adverse event or product problem

1, Q Adverse event and/or Q Product problem (eg, defects/malfunctions)

2 Outcomes attributed to adverse event

(check all that apply)

□ death

I I life-threatening

I I hospitalization - initial or prolonged LJ o^^'

I I disability

I I congenital anomaly

I I required intervention to prevent
permanent impairment/damage

3 Date of
event

(fnoday y

4 Date of
this report

5. Describe event or problem

6 Relevant tests/laboratory data, including dates

7 Other relevant history, including preexisting medical conditions (e.g.. allergies,
race, pregnancy. smol<ing and alcohol use, hepatic/renal dysfunction, etc.)

FDA Form 3500 1/96)

Mall to: MEdWaTCH or FAX to:

5600 Fishers Lane 1-800-FDA-0178

Rockville, MD 20852-9787

C. Suspect medication(s)

1. Name (give labeled strength & mfr/labeler, if known)
#1

2 Dose, frequency & route used

3 Therapy dates (if unknown, give duration)

lfom,'io lor best estimate)
#1

4 Diagnosis for use (indication)

5 Event abated after use
stopped or dose reduced

*1 Dyes Dno ngggPy"'
#2 Dyes n no Dgg^Fy"'

6. Lot # (If known)

7. Exp. date (if known)
#1

8 Event reappeared after

#1 Dyes Dno ngg^Fy"'

#2 Dyes Dno Dgg^fy"'

9. NDC # (for product problems only)

10. Concomitant medical products and therapy dates (exclude treatment of event)

D. Suspect medical device

3 Manufacturer name & address

1 Brand name

2 Type of device

6.
model #

catalog #

serial #

lot#

other #

4. Operator of device

I I health professional
I I lay user/patient
□ other;

5 Expiration date

(mo/day/yr|

7. If implanted, give date

ItDorcJay/yr)

8. If explanted, give date

|mo^day/yr}

9 Device available for evaluation? (Do not send to FDA)

I I yes CD no Q returned to manufacturer on

10 Concomitant medical products and therapy dates (exclude treatment of event)

E. Reporter (see confidentiality section on bacit)

1. Name & address

phone #

2 Health professional?

□ yes □ no

3. Occupation

5 If you do NOT want your identity disclosed to
the manufacturer, place an " X " in this box. LJ

4 Also reported to
I I manufacturer
I I user facility
I I distributor

Submission of a report does not constitute an admission that medical personnel or the product caused or contributed to the event.

ADVICE ABOUT VOLUNTARY REPORTING

Report experiences with:

• medications (drugs or biologies)

• medical devices (including in-vitro diagnostics)

• special nutritional products (dietary
supplements, medical foods, infant formulas)

• other products regulated by FDA

Report SERIOUS adverse events. An event
is serious when the patient outcome is:

• death

• life-threatening (real risk of dying)

• hospitalization (initial or prolonged)

• disability (significant, persistent or permanent)

• congenital anomaly

• required intervention to prevent permanent
impairment or damage

Report even if:

• you're not certain the product caused the
event

• you don't have all the details

Report product problems - quality, performance
or safety concerns such as:

• suspected contamination

• questionable stability

• defective components

• poor packaging or labeling

• therapeutic failures

How to report:

• just fill in the sections that apply to your report

• use section C for all products except
medical devices

• attach additional blank pages if needed

• use a separate form for each patient

• report either to FDA or the manufacturer
(or both)

Important numbers:

• 1-800-FDA-0178

• 1-800-FDA-7737

• 1-800-FDA-1088

1-800-822-7967

to FAX report

to report by modem

to report by phone or for

more information

for a VAERS form

for vaccines

If your report involves a serious adverse event
with a device and it occurred in a facility outside a doc-
tor's office, thiat facility may be legally required to report to
FDA and/or ttie manufacturer. Please notify the person in
that facility who would handle such reporting.

Confidentiality: The patient's identity is held in strict
confidence by FDA and protected to the fullest extent of
the law. The reporter's identity, including the identity of a
self-reporter, may be shared with the manufacturer unless
requested otherwise. However, FDA will not disclose the
reporter's identity in response to a request from the
public, pursuant to the Freedom of Information Act.

The public reporting burden for this collection of information
has been estimated to average 30 minutes per response,
including the time for reviewing instructions, searching exist-
ing data sources, gathering and maintaining the data needed,
and completing and reviewing the collection of information.
Send comments regarding this burden estimate or any other
aspect of this collection of information, including suggestions
for reducing this burden to:

DHHS Reports Clearance Office
Paperwork Reduction Project (0910-0291)
Hubert H. Humphrey Building, Room 531 -H
200 Independence Avenue. S.W.
Washington. DC 20201

"An agency may not conduct or sponsor,
and a person is not required to respond to.
a collection of information unless it displays
a currently valid 0MB control number."

Please do NOT
return this form
to either of these
addresses.

U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES
Public Health Service • Food and Drug Administration

FDA Form 3500-back

Please Use Address Provided Below - Just Fold In Thirds, Tape and Mail

Department of

Health and Human Services

Public Health Service

Food and Drug Administration

Rockville, tyiD 20857

Official Business

Penalty for Private Use $300

NO POSTAGE

NECESSARY

IFt^AILED

IN THE

UNITED STATES

OR APO/FPO

BUSINESS REPLY MAIL

FIRST CLASS MAIL PERMIT NO. 946 ROCKVILLE, MD

POSTAGE WILL BE PAID BY FOOD AND DRUG ADMINISTRATION

MEE^J^TCH

The FDA Medical Products Reporting Program
Food and Drug Administration
5600 Fishers Lane
Rockville, MD 20852-9787

|,,l,lll..,li.l..l,l...l.ll.l..l...lll.l.lM,lMl.ll

Notices

Notices of competitions, scholarships, fellowships, examination dates, new educational programs,

and the like will be listed here free of charge, hems 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.

Sciitduled Pto^fe^.^O't'^. ^o-uttd^- 2000

Pulmonary Rehabilitation: What You Need to Know — Julien M Roy
RRT; Host, Richard Branson RRT— Video March 7; Audio April 4

Pediatric Asthma in the ER — Tim Myers RRT; Host, Richard Branson
RRT— Video March 28; Audio April 18

Drugs, Medications and Delivery Devices of Importance in Respiratory

Care— Jim Finl. MS RRT; Host, David Pierson MD— Video April 25;
Audio May 16

Cost Effective Respiratory Care: You've Got to Change — Kevin Slirake
MA RRT FACHE; Host, Sam P Giordano MBA RRT— Video May 23;
Audio June 20

Pediatric Ventilation: Kids Are Different — Marie Heulitt MD; Host,
Richard Branson RRT — Video July 25; Audio August 15

What Matters in Respiratory Monitoring: What Goes and What

Stays— Dean Hess PhD RRT FAARC; Host, Richard Branson RRT—
Video August 22; Audio September 26

Managing Asthma: An Update — Patti Joyner RRT CCM; Host, Man
Jones MSN RN RRT— Video September 19; Audio October 17

Routine Pulmonary Function Testing: Doing It Right — Carl D Mottram
RRT RPFT; Host, David Pierson MD— Video November 7; Audio
December 5

MARK YOUR CALENDARS!
FUTURE AARC CONGRESSES

October 7-10, 2000
Cincinnati, Ohio

December 1-4, 2001
San Antonio, Texas

October 5-8, 2002
Tampa, Florida

December 8-11, 2003
Las Vegas, Nevada

December 4-7, 2004
New Orleans, Louisiana

Helpful UJeb.Sltes

American Association for Respiratory Care

http://www.aarc.org

— Current job listings

— American Respiratory Care Foundation
feiiowsiiips, grants, & awards

— Clinical Practice Guidelines

National Board for Respiratory Care

http://www.nbrc.org

RESPIRATORY CARE online

http://www.rcjournal.conn

— Subject and Author Indexes

— Contact the editorial staff

— Open Forum; subnnit your abstract online

Asthma Management
Model System

http://www.nhlbi.nih.gov

Keys to Professional Excellence

http://www.aarc.org/keys/

The National Board for Respiratory Care —
Examination Dates and Fees for 2000

Examination Fees

$190 (new applicant)
$150(reapplicant)

$250 (new applicant)
$220 (reapplicant)

$200 (new applicant)
$170 (reapplicant)

$250 (new applicant)
$170 (reapplicant)

$190 (new - written only)

$200 (new - CSE only)

$390 (new - both)

For information about other services or fees, write to

the National Board for Respiratory Care,

8310 Nieman Road, Lenexa KS 66214, or call

(913) 599-4200, FAX (913) 541-0156,

ore-mail: nbrc-info@nbrc.org

Examination

CRT

Perinatal/Pediatric

CPFT

RPFT

RRT
(Written & CSE)

RESPIRATORY CARE • APRIL 2000 VOL 45 NO 4

455

Authors
in This Issue

Adams, Alexander B 390

Anderson, Jeff 440

Baker, Randy 437

Bliss, Peter L 390

Chan, Theodore C 407

Clausen, Jack L 407

Eisenberg, Jay D 439

Hopper, Keith B 432

Hotchkiss, John 390

Kuck, Glen R 439

Mishoe, Shelley C 434

Neuman, Tom 407

Oba, Yuji 401

Pierson, David J 388

Salzman, Gary A 401

Sarodia, Bipin D 411

Stoller, James K 411

Tobin, Martin J 417

Vilke, Gary M 407

Willsie, Sandra K 401

Advertisers
in This Issue

To advertise in RESPIRATORY CARE, contact Tim Goldsbury, 20 Tradewinds Circle, Tequesta FL 33469
at (561) 745-6793, Fax (561) 745-6795, e-mail: goldsbury@aarc.org, for rates and media liits. For recruitment/
classified advertising contact Beth Binkley, Marketing Assistant for RESPIRATORY CARE, at (972) 243-2272,
Fax (972) 484-6010. Dale Grifflths is the Marketing Director for RESPIRATORY CARE.

Company

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Copyright information. Respiratory Care is copyrighted by
Daedalus Enterprises Inc. Reproduction in whole or in part without the express
written permission of Daedalus Enterprises Inc is prohibited. Permission to
photocopy a single article in this Journal for noncommercial purposes of
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RATORY Care. Anyone may, without permission, quote up to 500 words of
material in this journal provided the quotation is for noncommercial use and
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authors. Reprints for commercial use may be purchased from Daedalus En-
terprises Inc. For more information and prices call (972) 243-2272.

Disclaimer. The opinions expressed in any article or editorial are those
of the author and do not necessarily reflect the views of the Editors, the
American Ass(x;iation for Respiratory Care (AARC), or Daedalus Enter-
prises Inc. Neither are the Editors, the AARC, or the Publisher responsible
for the consequences of the clinical applications or use of any methods or de-
vices described in any article or advertisement.

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Subscription Rates for Associations. Basic annual subscrip-
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Change of address. Notify the AARC at (972) 243-2272 as soon as pos-
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Manuscripts. The Journal publishes clinical studies, method/device
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PIRATORY Care, 600 Ninth Avenue, Suite 702, Seattle WA 98104. In-
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the Instructions is available from the editorial office.

456

RESPIRATORY CARE • APRIL 2000 VOL 45 NO 4

GAUCEO

Receive FREE information on the
products and services mentioned in this
issue, by circling the corresponding
advertiser's number. Fill in your name
and address and mail this postage-paid
card. Information will be sent directly to
you from the manufacturer. IrKomplete
forms will not be processed.

Product
Information^

Fof AABC rn*mb*fih^

^^^^^BB7 108 109 110 111 II^BI^^^HH

I^HJI

119 120 121

122 123 124 125 126 127 128 129 130 131 132 133 134

135 136

155 156 157

158 159 160 161 162 163 164 165 166 167 168 169 170

171 172

191 192 193

194 195 196 197 198 199 200

ptMM cMb no mon Itunis Itafm.

Name

TWc

FadMyName

Mdms

at,

StaK Zip Co* Countiy

liHcphone

Aoril2000 ExDires 7/15/00

ifmnAiyMMi ^*ne

mm m(B-^MMk.

.EG, the most
tern. Advanced

■■^

naximum in patient

^^^

into the future.

1 TYreofNsrnuiw W

6 D Diagnostics/

OR PRACTICE

Pulmonary Function

1 D Hospital

7 D Management

■ring the clinician a

2 D Skilled Nursing

8 D Home Care

Facility

9 D Rehabilitation

3 D Subacute Care Facility

10 D Education

4 n Home Care Practice

5 n School

IV POSITION

lEDICALat

6 D Distfibutof

A D Department Head
B D Chief Therapist

1 DEMRTMENT

C D Supervisor

A n Respiratory Care
B O Cardiopulmonary
C D Subacute Care

D D Staff Therapist/

Technician
E D Medical Director

i/IILTON

D D Home Care

F D Educator/Instructor
C D Sales

■ SPECIALTY

H a Other (please specify)

>IOLOGY SERVE MANKIND

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2 D Perinatal/ Pediatrics

3 D Critical Care

V AREVOOANAARC

4 D Research

5 D Subacute Care

MEMBER?

1 D Yes 2 D No

1-641 9008, Fax 0181-641 9054
17 33

Authors
in This Issue

Adams, Alexander B 390

Anderson, Jeff 440

Baker, Randy 437

Bliss, Peter L 390

Chan, Theodore C 407

Clausen, Jack L 407

Eisenberg, Jay D 439

Hopper, Keith B 432

Hotchkiss, John 390

Kuck, Glen R 439

Mishoe, Shelley C 434

Neuman, Tom 407

Oba, Yuji 401

Pierson, David J 388

Salzman, Gary A 401

Sarodia, Bipin D 411

Stoller, James K 411

Tobin, Martin J 417

Vilke, Gary M 407

WiUsie, Sandra K 401

Advertij
in This Is

Company

Bird Products
Dale Medical Product
DEY

DHD Healthcare
Fisher & Paykel
Hamilton Medical
Hans Rudolph, inc
Hospitalhub.com
IngMar Medical
Instrumentation Indus
Mallinckrodt
Masimo Corp
Pulmonetic Systems
Respironics Health Sc
SIMS Portex Inc
Symphony Respirator
VersaMed

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456

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The new view of Ventilation

Derived from years of advanced research and prartical clinical experience, HAMILTON MEDICAL introduces GALILEO, the most
advanced ventilator in the world. GALILEO combines the newest innovative technology in an easy to operate system. Advanced
Rules Based Strategic Modes combined (Adaptive Support Ventilation ASV) with Virtual Controls provides the maximum in patient
care flexibility. GALILEO defines a new dimension in the ventilator management of critically ill patients today and into the future.

GALILEO is the ventilator of choice to implement comprehensive clinical pathways for all ventilator patients. Offering the clinician a
new dimension in respiratory care. Ventilation without Limitations.

GALILEO is available from your local HAMILTON MEDICAL partner. For further information, contact HAMILTON MEDICAL at
www.hamilton-medical.ch, phone +41-81-641-2627, fax +41-81-641-2689 or call our local representative.

Circle 119 on product info card

HAMILTON
MEDICAL

MAKING TECHNOLOGY SERVE MANKIND

International: HAMILTON MEDICAL AG, Via Nova, CH-7403 Rhaziins/Switzerland, Telephone (+41) 81-641 26 27, Fax (+41) 81- 641 26 89

USA: HAMILTON MEDICAL Inc., P.O.Box 30008, Reno, NV 89520, Telephone (702) 858-3201, (800) HAM-MED-1, Fax (702) 856-5621

Great Britain: HAMILTON MEDICAL (G.B.) Limited, Kimpton Business Centre, Kimpton Road, Sutton, Surrey SM3 9QR, Telephone 0181-641 9008, Fax 0181-641 9054

Germany: HAMILTON Deutschland GmbH, Abt. MEDICAL Daimlerweg 5a, D-64293 Darmstadt, Tel. (06151) 98020, Fax (06151) 89 17 33

New EZ-PAPr The EASY option for atele(fasis.

|DHD

Healthcare

Innovations for respiratory care

125 Rjsbucb Smet, Cinaacu. NY 13032 USA
(800)847-8000 (3I5)»97-222I FAX: (315) W7-5191
www.dbd.com

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When incentive spirometry alone won't open patients' airways, expand your
options with new EZ-PAP. It maices provi(Jing positive airway pressure
positively easy. Simply connect to a flow meter (wail air or Ot for
enhanced Fi02 ). adjust to 5 - 15 Ipm. and instruct the patient to breathe
diaphragmatically through the mouthpiece or mask.
No equipment to roll around. No labor-intensive
CPT. No extensive training. Just a few minutes of
therapy, once an hour — not for hours at a time.

EZ-PAP features a pressure port for connection to a gauge (recommended
for initial use with each patient), and standard 22-mm OD fitting to
accommodate a mouthpiece or 3 mask options. For more information,
call DHD Healthcare toll-free today: 1 ■800-847-8(100.
Circle 1 16 on reader service card