PHYSIOLOGICAL EFFECTS OF MECHANICALEXSUFFLATION ON EXPERIMENTALOBSTRUCTIVE BREATHING IN HUMANSUBJECTS

Reuben M. Cherniack, … , Charles A. Gordon, Fred Drimmer

J Clin Invest. 1952;31(12):1028-1035. https://doi.org/10.1172/JCI102695.

Research Article

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PHYSIOLOGICALEFFECTSOF MECHANICALEXSUFFLATIONONEXPERIMENTALOBSTRUCTIVEBREATHINGIN

HUMANSUBJECTS1BY REUBENM. CHERNIACK,2 CHARLESA. GORDON,8AND FRED DRIMMER(From the Department of Medicine, College of Physicians and Surgeons, Columbia University

and the Goldwater Memorial Hospital, Columbia Ditnsion, New York, and thePresbyterian Hospital, New York, N. Y.)

(Submitted for publication June 5, 1952; accepted September 12, 1952)

The increased physical effort necessary tobreathe through a constricted orifice results in aninstantaneous and uncomfortable sensation ofdyspnea. The immediate sensation of difficulty inbreathing is aroused by proprioceptive reflexes.The duration of inspiration and expiration be-comes markedly prolonged, (1, 2) and in spiteof the increased work entailed, the peak volumeflow rates diminish. The minute ventilation hasbeen shown by Cain and Otis (1) to decrease.Haldane and Priestley (3) and others (1, 4) alsonoted that hypoxia and retention of carbon diox-ide develops due to the prolonged duration of therespiratory cycle and reduced alveolar ventilation,resulting from obstructed breathing. Further-more, a lower or more negative intrapleural pres-sure develops during the inspiratory phase whenbreathing against a resistance. The pathologicalconsequences of obstructed breathing, namely pul-monary congestion, have been demonstrated inanimals by Moore and Binger (4, 5) and Barachand his associates (6-8).

During the initial studies on the physiologicaleffects of exsufflation, the principle of which isdescribed in Methods, it was noted that the physi-cal effort required to breathe against a resistanceintroduced at the mouth was markedly diminished(9, 10). Since exsufflation appeared subjectivelyto relieve dyspnea it was of interest to study itsphysiological effect on experimentally producedobstructed breathing in normal human subjects.The purpose of this paper is to show the effect ofexsufflation on 1) inspiratory and expiratory vol-ume flow rates, 2) alveolar pCO2 and PO2, and 3)peripheral venous pressure and intraoral pressureduring obstructed breathing.

I Aided by a grant from the National Foundation forInfantile Paralysis.

2Present address University of Manitoba, Winnipeg,Manitoba, Canada.

a Present address Dalhousie University, Halifax, NovaScotia, Canada.

METHODS

Two mechanical methods of simulating a cough inman were originally devised by Barach and his co-workers (9-11) as a means of eliminating secretions inpatients who are unable to cough effectively. One ofthese methods, exsufflation, i.e., rapid movement of airfrom the lungs, is accomplished by enclosing the body ofthe patient in a conventional tank respirator. A nega-tive intra-tank pressure of 40 mm. Hg, developed overa two-second period by a motor blower unit attached tothe respirator, is followed by a rapid return to atmosphericpressure in 0.06 seconds by means of a swift-openingvalve. The termination of the intra-tank pressure in0.06 seconds removes a force which tends to keep thelungs inflated in other forms of intermittent pressurebreathing where there is a gradually descending expira-tory pressure curve (see Figure 1). The rate of ex-sufflation can be adjusted to produce any desired minuteventilation. This procedure has produced peak expira-tory volume flow rates measuring 60 per cent of those

PRESSURE CURVES WITH

RESPIRATOR AND EXSUFFLATOR

H20 to

A- CONVENTIONAL RESPIRA-TOR 20 cm H20Groduol increase of pressurearound chest during expiro-tion tends to keep lung inflat-ed, and results in low expir-

ltory flow rote.

mm

5- EXSUFFLATOR 40 mmHgSudden increase of pressurearound chest during expirationremoves force *tending to keeplung inflated. and results inhigh expirotary flow rate.

FIG. 1

Vertical lines represent 0.2 seconds.

1028

PHYSIOLOGIC EFFECT OF MECHANICALEXSUFFLATION

found in the most vigorous cough obtainable in normalhuman subjects (9, 11).

Young healthy volunteers who exhibited no evidenceof cardio-respiratory disease participated in this study.The subjects were placed in the modified tank respirator,and after the breathing pattern had become regular, con-trol tracings were obtained on a recording spirometer inwhich the resistance was minimal. Immediately afterthe control period, obstructed breathing was produced bythe introduction of a 3 mm. orifice at the mouthpiece for6 minutes. During the latter three minutes of this periodof obstructed breathing exsufflation was applied at a rateof 9 times per minute.

Determinations of inspiratory and expiratory volumeflow rates, alveolar pCO2 and pO2, peripheral venous

pressure, and intraoral pressure were performed duringnormal quiet breathing, after the three minute period ofobstructed breathing, and at the end of the period ofexsufflation.

The spirographic tracings obtained on a high speeddrum during normal breathing and obstructed breathingbefore and after the addition of exsufflation were analyzedin terms of volume of air movement per unit time. Theinspiratory and expiratory volume flow rates were de-rived from these data and plotted graphically.

End expiratory samples of gas were collected andanalyzed by the micro-Scholander method. From thesedata, the alveolar pO2 and pCO2 were calculated.

Peripheral venous pressure was recorded from theantecubital vein through an 18-gauge needle attached toa differential Statham strain gauge which was exposed tothe intra-tank pressure. Intermittent infusion of heparin-ized saline assured the fluidity of the system and pre-

vented clotting at the needle. Mean venous pressure was

determined by planimetric integration of the area underthe pressure curve.

The intraoral pressure tracings were obtained with a

20-gauge needle inserted into the mouthpiece and re-

corded by a Statham strain gauge exposed to the intra-tank pressure in a manner similar to that of the venous

pressure.

The peripheral venous pressure was found to risewith an increase in the mean applied intrapulmonary pres-

sure by Barach and his co-workers (8, 12), Otis, Rahnand Fenn (13) and Barach, Fenn, Ferris and Schmidt(14). Furthermore, Elisberg, Goldberg and Snider (15)noted a positive correlation between intraoral pressures

and intrapleural pressures. Under static conditions atthe end of inspiration or expiration, pleural pressure

equals mouth pressure minus the pressure resulting fromlung elasticity. During inspiration or expiration, theserelationships are altered by the pressures which are re-

quired to overcome the dynamic resistances involved inmoving gas and deforming tissue. The measurements

of the variations in peripheral venous pressure and in-traoral pressure thus served to reflect similar directionalchanges in the intrapleural pressure.

TABLE I

Obstructed breathing: the reversal of altered inspiratory volumeflow rate by exsufilationMaximum volume flow rate

Obstructed breathing andexsufflation

Case Normal ObstructedNo. breathing breathing Change from

obstructedbreathing

cc./sec. cc./sec. cc./sec. per cent1 605 346 951 +1752 649 605 735 + 203 605 519 908 + 754 476 432 692 + 605 843 908 1103 + 216 476 345 692 +1017 476 432 476 + 108 605 435 950 +118

Aver. 592 503 813 + 72

RESULTS

In all subjects the sensation of dyspnea ex-perienced when breathing through a 3 mm. orificewas relieved by exsufflation.

The added resistance to breathing resulted in a15 per cent decrease in the peak inspiratory vol-ume flow rate. The use of the exsufflator pro-duced a striking increase in volume flow ratesaveraging 72 per cent above the rate observedduring obstructed breathing. This reversal of al-tered inspiratory volume flow rate is shown inTable I. While breathing against a resistance,the peak expiratory volume flow rate decreased,averaging 28 per cent of that observed during nor-

TABLE II

Obstructed breathing: the reversal of altered expiratory volumeflow rate by exsufflation

Maximum volume flow rate

Obstructed breathing andexsufflation

Case Normal ObstructedNo. breathing breathing Change from

obstructedbreathing

cc./sec. cc./sec. cc./sec. per cent1 605 432 692 + 602 778 432 432 03 519 346 519 + 504 778 432 519 + 205 584 519 1492 +1876 519 432 345 - 207 648 476 385 - 208 519 480 825 + 72

Aver. 619 444 651 + 43

1029

REUBENM. CHERNIACK, CHARLESA. GORDON,AND FRED DRIMMER

900

750

600

450v

( 300

Z)O 150

a: 0

0

ID 300o

450

600

750

A

I:

IhirutIinspiration 8 4

expirationI

I'

I1

it

- obstructed breathing

-- obstructed breathingand emsufflotion

20 3 4 5 6

TIME IN SECONDS

7 8

OBSTRUCTEDBR EATHINGt EFFECT OF EXSUFFLATION ON VOLUMEFLOWRATE

Maximum Volume Flow Rote

Obstructed Breathing

Obstructed BreathingWith Exsufflation

Inspiration ExpIration

435cc 480cc

950 cc 825 cc

cent over that in normal breathing and 121 percent over that during obstructed breathing.

The average minute ventilation of 7,431 cc. fellto 5,328 cc. or by 27 per cent during obstructedbreathing. During exsufflation, minute volumewas 9,644 cc. or 29 per cent higher than duringnormal breathing, and 81 per cent above that dur-ing obstructed breathing. This is shown in TableIV.

TABLE IV

Minute ventilation, cc. /min.

caseNo. Normal Obstructed ObstructedCase No. breathing breathing breathing andexsufflation

cc. man.1 9,555 6,320 13,6172 6,288 4,616 10,8993 8,710 7,920 9,9274 6,165 6,447 7,9745 9,012 7,780 8,5056 6,184 4,182 10,0167 7,488 6,420 8,5598 6,048 4,944 7,884

Aver. 7,431 5,328 9,644

FIG. 2

mal expiration. A rise in expiratory volume flowrate of 43 per cent above the obstructed breathinglevel was induced by exsufflation, as seen in TableII. When the expiratory volume flow rate wasplotted against time, as is demonstrated in Figure2, the maximal increase in flow rate was found tooccur at the onset of expiration.

The average tidal volume during normal breath-ing was 581 cc., and fell to 485 cc. or by 16 per centwhen breathing against a resistance. As is seenin Table III, when exsufflation was added theaverage tidal volume was 1,074 cc., a rise of 85 per

TABLE III

Tidal air volume

Normal Obstructed ObstructedCase No. breathing Obstructed breathing andbreathing breathing exsufflation

cc. cc. cc.1 735 395 1,5132 393 432 1,2113 670 660 1,1034 411 419 8865 751 778 9356 389 246 1,1247 468 535 9518 432 412 876

Aver. 581 485 1,074

In seven subjects the average alveolar pCO2rose 4.8 mm. Hg or 13 per cent (range 5.4 to 29.9per cent) during obstructed breathing. The ad-dition of exsufflation resulted in a reversal of CO2tension toward, and in some instances below, thecontrol level. These findings are illustrated inFigure 3. The average alveolar pCO2 producedby exsufflation was 8.0 mm. Hg or 19 per cent(range 11.2 to 31.4 per cent) below that presentduring obstructed breathing.

During obstructed breathing, the alveolar PO2fell an average of 9.7 mm. Hg or 9.1 per cent

,45x Is

35.

4

25.

I normal breathing

]l obstructed breathing

0 obstructed breathing and nosueflation

Case Cosn 2 Cost CGS, 4 Case 5 Case 6 Case r

OBSTRUCTEDBREATHING: THEEFFECT OF EXSUFFLATION ONELEVATEDALVEOLAR pCOt

FIG. 3

1030

40

PHYSIOLOGIC EFFECT OF MECHANICALEXSUFFLATION

120

110Itx

1

00

E normal breathing

[obstructed breathing

Ca" Cose2 case Coe 7

OBSTRUCTEDBREATHING: EFFECT OF EXSUFFLATION ONLOWEREDALVEOLAR pO0

FIG. 4

(range 3.2 to 17.3 per cent) below the controlvalues in seven subjects. Following 3 minutes ofexsufflation the PO2 increased an average of 12.4mm. Hg or 16.9 per cent (range 7.8 to 34.2 percent) above that observed with obstructed breath-ing. This is graphically illustrated in Figure 4.

The peripheral venous pressure was determinedin eight subjects and recorded relative to thetank pressure. The average mean venous pressurefell 7 mm. H20 when a resistance to breathing was

introduced. The addition of exsufflation resultedin an average rise of 20 mm. H20 above this leveland 13 mm. H20 above the normal breathing level,as seen in Table V. During the inspiratory phasean average drop of 6 mm. H20 (range 3 to 16mm.) was noted when the obstruction to breath-ing was added. The minimal level recorded dur-ing exsufflation was 12 mm. H20 above thevalue obtained during obstructed breathing and 6mm. H20 above the normal breathing value. A

TABLE V

Obstructed breathing: the reversal of altered mean venouspressure by exsufflation

Mean venous pressure(mm. HO)

Normal Obstructed ObstructedCase No. breathing breathing breathing andexsufflation

1 83 77 8772 69 79

2 106 100 11281 72 101

3 98 79 9099 91 99

4 97 92 1135 70 63 78

64 52 646 78 73 1107 74 72 848 68 62 106

78 71 108Aver. 82 75 95

e f ltio M_sedtOIM _g~

OBSTRUCTEDBREATHING: EFFECT OF EXSUFFLATEIN ONVENOUSPRESSURE

Minimum Mi

Normal Breathinq

Obstructed BrealtiN

Obstructed BreathinqWith Exsufraflon

87mm 108mm

78mm 113 mm

90mm 123mm

FIG. 5

The lowering of the inspiratory venous pressure produced by obstructivebreathing is abolished during exsufflation.

1031

904-i0

49

0z S~

Ia 120.

as0

LL 30

80J

REUBENM. CHERNIACK, CHARLESA. GORDON,AND FRED DRIMMER

TABLE VI

Obstruted breaing: the rersal of altered intraoral pressure by exsufflation

Intraoral pressure(mm. H20)

Case No. Minimal level recorded Maximal level recorded

Normal Obstructed Obstructed Normal Obstructed

breathing breathing eatfliatkng breathing breathing exsufaation

1 -6 -43 +4 0 +58 +1122 -2 -84 +4 +1 +66 +1393 -3 -36 +6 0 +36 +1434 -2 -45 +3 +1 +31 +1495 -5 -52 +2 +2 +35 +1436 -5 -87 +1 0 +53 +124

Aver. -4 -58 +3 +0.6 +47 +135

representative venous pressure tracing, shown inFigure 5, reveals that the lowered negative pres-sure during inspiration is no longer present whenexsufflation is added.

An average negative intraoral pressure of 58mm. H20 relative to the tank pressure was re-corded when breathing through a 3 mm. orifice.The addition of exsufflation resulted in a strik-ing reversal of this negative intraoral pres-sure. From data presented in Table VI andFigure 6 the lowest pressure observed with ex-sufflation was plus 1 mm. H20.

,t40

4100

+500

+60

+40w

itO

I0

0

V40

-f0

___ _ __ _ _ __0-

NORMLBRATIN

OIRUGMDOWFHNGAtND EXSUFFLATION

OBSTRUCTEDBREWATH

OBSTRUCTEDBRE SING: EFFECT OF EXSUFFLfflONOR INTRA-ORAL PRESURE

FIG. 6

The lowering of the inspiratory intraoral pressure pro-

duced by obstructed breathing is abolished during ex-

sufflation.

DISCUSSION

An attempt has been made in this study to simu-late as much as possible the obstructive com-ponent present in clinical conditions which con-strict the larynx, trachea or bronchi, includingtumor mass, foreign body, or the thick viscidbronchial secretions associated with bronchialasthma, bronchiectasis and the bronchospastictype of pulmonary emphysema. In normal res-piration the bronchial tree lengthens and dilatesduring inspiration and less resistance or obstruc-tion to breathing is therefore present in this phaseof breathing than in the expiratory cycle. Inthe present study the added resistance to breathingremained constant during both phases of respira-tion and therefore a pathologic intrabronchial ob-struction to breathing is not entirely reproduced.

In animal experiments it has been shown byMoore and Binger (4, 5) and Barach (6-8) thatobstructed breathing either during inspiration orboth phases of respiration results in pulmonarycongestion and intra-alveolar edema. Thesechanges were not found when a comparable re-sistance to breathing was maintained during ex-piration only. The pathological consequences ofobstructive breathing were therefore attributed tothe abnormally lowered pressure exerted on thelungs during inspiration. The sequelae of ob-structive respiration appear to be traced to the ef-fect of increased negative pressure on pulmonarycapillaries, production of mucus from the bronchialmucous membrane, an increased output of theright heart, and a diminished output from the leftheart. In cases of severe bronchial asthma, a

EL-I

1032

PHYSIOLOGIC EFFECT OF MECHANICALEXSUFFLATION

pathologically lowered negative intrapleural pres-sure during inspiration has also been demonstratedby Barach (16).

Maloney and Whittenberger (17) and Beck,Seanor and Barach (18) have shown that thephysiological effects of negative pressure sur-rounding the body in a tank respirator are com-parable to those produced by positive pressure ap-plied at the mouth and nose. This relationshiphad already been pointed out by Henderson (19).The mechanism of exsufflation, therefore, in-cludes inspiratory positive pressure breathing,which is mainly comparable to positive pressurebreathing produced in other ways. In studies byMotley and his co-workers (20, 21) on intermit-tent positive pressure breathing it was found thatthe type III curve with a low mean pressure anda rather rapid return to atmospheric pressure inexpiration was the respirator of choice. How-ever, in the type III curve expiration lasts 1.11seconds and the return to atmosphere takes placein approximately 0.5 seconds. In exsufflation themean applied pressure is 5.5 cm. H2Oand expira-tion, except for the first 0.06 seconds, takes placeat atmospheric pressure. The relaxation pres-sure of the lungs, therefore, operates more effec-tively during the greater part of the expiratorycycle. Furthermore, the relative absence of in-creased intrapulmonary pressure during the ex-piratory cycle of exsufflation permits the use ofhigh ventilatory pressures with minimal effect onthe circulation. Since the effect on cardiac outputhas been shown to depend on the mean appliedintrapulmonary pressure (14) and rapidity ofdrop of expiration pressure (20, 21), exsufflationwith its low mean pressure and rapid drop of pres-sure at the beginning of expiration probably haslittle effect on the mean output of the heart.

The introduction of a resistance to breathing,resulting in increased inspiratory and expiratoryeffort produces physiological effects comparableto negative pressure breathing in inspiration andpositive pressure breathing in expiration. Theaddition of inspiratory positive pressure by ex-sufflation more than compensates for the inspira-tory negative pressure breathing, and inspirationnow takes place under positive pressure. Sincewith exsufflation expiration (except for the first0.06 seconds) takes place at atmospheric pressure,the relaxation pressure of the lungs during this

procedure overcomes the effect of resistance toair flow during the expiratory cycle. Thus, ex-sufflation during obstructed breathing results inpositive pressure breathing during both phases ofrespiration.

It has been demonstrated (1, 2) that the in-spiratory flow rate is less frequently disturbed inobstructed breathing than is that of expiration.In our studies, peak volume flow rate decreased15 per cent during inspiration and 29 per centduring expiration. The alteration of volume flowrate produced by exsufflation was most strikinglymanifested in inspiration. The expiratory vol-ume flow rate was increased particularly at theonset of expiration. The major action of exsuffla-tion on the volume flow rate during inspiration isexplained by the fact that air is being introducedinto the lungs under positive pressure. The in-creased flow rate at the onset of expiration can beattributed to the rapid elimination of the negativepressure surrounding the chest, allowing the re-laxation pressure of the lungs and surrounding tis-sues to operate promptly and at its fullest extent.

In current studies by Bickerman, Beck andBarach (22) the diameters of medium-sizedbronchi of dogs are increased two-fold at the peakof the 40 mm. Hg pressure. With the abrupttermination of this pressure there is a rapid con-traction and shortening of the entire bronchialtree, which is a factor in the production of the highvolume flow rate seen especially at the onset ofexpiration.

The advantageous effect of exsufflation in re-lieving the hypercapnia and hypoxia which de-velop during obstructed breathing is clearly dem-onstrated. Exsufflation would appear to be ofspecial value in patients with pulmonary emphy-sema who have developed respiratory acidosis,since it would provide an effective method of re-storing to normal the altered CO2 and 02 ten-sions present in this syndrome.

Cain and Otis (1) have shown that the totalventilation decreases while breathing against anadded resistance. In our studies the fall in tidalvolume and minute ventilation during obstructivebreathing was markedly reversed by the additionof exsufflation. The rise in oxygen tension duringexsufflation despite a rate of only nine times aminute must be due to a more effective alveolarventilation. Since the rate of exsufflation can be

1033

REUBENM. CHERNIACK, CHARLESA. GORDON,AND FRED DRIMMER

controlled, any desired increase in minute ventila-tion can easily be achieved without the high meanintrapulmonary pressures produced by conven-tional forms of pressure breathing, where there isventilation with a gradually descending expiratorypressure curve.

The marked drop in peripheral venous pressureand intraoral pressure during the inspiratoryphase of obstructed breathing is overcome by ex-sufflation and there is at no time the developmentof lowered intraoral or peripheral venous pressure.Assuming that intraoral- and peripheral venouspressure are reflections of intrathoracic pressures,an abnormally lowered negative intrapleural pres-sure is present during the inspiratory phase of ob-structed breathing, and a reversal of this statetakes place with the addition of exsufflation. Areduction in the height of negative intrapleuralpressure by the application of pressure breathinghas also been shown by Barach (7) in experi-mentally induced obstructive dyspnea in dogs andin a patient with severe bronchial asthma. Healso showed that as the intrapleural pressure be-came more negative, pulmonary congestion devel-oped, and that anything that decreased the nega-tive intrapleural pressure would tend to decreasethe likelihood of development of congestion. Sinceobstructed breathing over a prolonged period oftime will result in pulmonary congestion, thephysiologic action of exsufflation in reversing thelowered venous pressure and presumably thelowered intrapleural pressure would appear toprevent the consequences of obstructive dyspneaand thus be useful in clinical entities characterizedby obstructive lesions in the respiratory tract.

SUMMARY

Obstructive respiration was produced in nor-mal human subjects by breathing through a 3 mm.orifice. Marked subjective dyspnea was accom-panied by the following pathophysiological con-sequences: 1) A diminution of inspiratory and ex-piratory volume flow rates; 2) An elevation of al-veolar pCO2 and lowering of PO2; 3) A loweringof peripheral venous pressure; and 4) A markeddecrease in inspiratory intraoral pressure.

Exsufflation consists of inflation of the lungswith a 40 mm. Hg pressure and a rapid termina-tion of the pressure at the onset of the expiratorycycle. When this mechanism was applied during

obstructed breathing, subjective dyspnea was re-lieved and the physiological alterations noted werereversed towards normal levels. The beneficialeffect of exsufflation can be attributed to (a) in-spiratory positive pressure breathing, and (b)the prompt and effective use of the increased re-laxation pressure of the lungs.

The restoration towards normal of physiologicconsequences of experimentally induced ob-structed breathing suggests that the use of themechanism of exsufflation would be of thera-peutic value in those clinical conditions character-ized by obstructive lesions in the respiratory tract.

REFERENCES

1. Cain, C. C., and Otis, A. B., Some physiological ef-fects resulting from added resistance to respira-tion. J. Aviation Med., 1949, 20, 149.

2. Proctor, D. F., Hardy, J. B., and McLean, R., Stud-ies of respiratory air flow. II. Observations onpatients with pulmonary disease. Bull. JohnsHopkins Hosp., 1950, 87, 255.

3. Haldane, J. S., and Priestley, J. G., Respiration, Newed. New Haven, Yale University Press, 1935, p.311.

4. Moore, R. L., and Binger, C. A. L., Observations onresistance to the flow of blood to and from thelungs. J. Exper. Med., 1927, 45, 655.

5. Moore, R. L., Ind Binger, C. A. L., The response torespiratory resistance: A comparison of the ef-fects produced by partial obstruction in the inspira-tory and expiratory phases of respiration. J. Ex-per. Med., 1927, 45, 1065.

6. Barach, A. L., The effects of inhalation of heliummixed with oxygen on the mechanics of respira-tion. J. Clin. Invest., 1936, 15, 47.

7. Barach, A. L., The therapeutic use of helium. J.A.M.A., 1936, 107, 1273.

8. Barach, A. L., Martin, J., and Eckman, M., Positivepressure respiration and its application to thetreatment of acute pulmonary edema. Ann. Int.Med., 1938, 12, 754.

9. Barach, A. L., Beck, G. J., Bickerman, H. A., andSeanor, H. E., Mechanical coughing: Studies onphysical methods of producing high velocity flowrates during the expiratory cycle. Tr. A. Am.Physicians., 1951, 64, 360.

10. Barach, A. L., Beck, G. J., Bickerman, H. A., andSeanor, H. E., Physical methods of simulating ahuman cough. To be published.

11. Barach, A. L., Bickerman, H. A., and Beck, G. J.,Advances in the treatment of non-tuberculous pul-monary disease. Bull. New York Acad. Med.,1952, 28, 353.

12. Barach, A. L., Eckman, M., Ginsburg, E., Rumsey,C. C., Korr, I., Eckman, I., and Besson G., Stud-ies on positive pressure respiration. I. General

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PHYSIOLOGIC EFFECT OF MECHANICALEXSUFFLATION

aspects and types of pressure breathing. II. Ef-fects on respiration and circulation at sea level.J. Aviation Med., 1946, 17, 290.

13. Otis, A. B., Rahn, H., and Fenn, W. O., Venous pres-sure changes associated with positive intrapul-monary pressures; their relationship to the dis-tensibility of the lung. Am. J. Physiol., 1946, 146,307.

14. -Barach, A. L., Fenn, W. O., Ferris, E. B., andSchmidt, C. F., The physiology of pressure breath-ing. J. Aviation Med., 1947, 18, 73.

15. Elisberg, E. I., Goldberg, H., and Snider, G. L.,Value of intraoral pressure as a measure of intra-pleural pressure. J. Appl. Physiol., 1951, 4, 171.

16. Barach, A. L., Physiologic Therapy in RespiratoryDiseases, 2d ed., Philadelphia, J. B. Lippincott,1948, p. 122.

17. Maloney, J. V., and Whittenberger, J. L., Clinicalimplications of pressures used in the body res-

pirator. Am. J. M. Sc., 1951, 221, 425.

18. Beck, G. J., Seanor, H. E., and Barach, A. L., Ef-fects of pressure breathing on venous pressure;A comparative study of positive pressure ap-plied to the upper respiratory passageway andnegative pressure to the body of normal individuals.Am. J. M. Sc., 1952, 224, 169.

19. Henderson, Y., Adventures in Respiration, Baltimore,Williams & Wilkins Co., 1938, p. 272.

20. Motley, H. L., Werko, L., Cournand, A., andRichards, D. W., Jr., Observations on the clini-cal use of intermittent positive pressure. J. Avia-tion Med., 1947, 18, 417.

21. Motley, H. L., Cournand, A., Werko, L., Dresdale,D. T., Himmelstein, A., and Richards, D. W., Jr.,Intermittent positive pressure breathing. A means

of administering artificial respiration in man. J.A.M.A., 1948, 137, 370.

22. Bickerman, H. A., Beck, G. J., and Barach, A. L.,Physical methods of eliminating radiopaque materialfrom the bronchi of dogs. To be published.

1035