Journal of Clinical InvestigationVol. 46, No. 6, 1967

Pulmonary Mechanics during Pregnancy *J. BERNARDL. GEE,t BERNARDS. PACKER4J. EUGENEMILLEN, ANDE. D. ROBIN

(From the Department of Medicine, University of Pittsburgh School of Medicine,Pittsburgh, Pa.)

Summary. Previously reported changes in static lung volumes during preg-nancy have been confirmed.

Measurements of lung compliance (CL) and total pulmonary resistance (RL)were made in 10 women in the last trimester of pregnancy and 2 months post-partum, employing an esophageal balloon and recording spirometer. CL wasunaffected by pregnancy, but RL was 50% below normal during pregnancy.

Measurements of airway conductance (CA) were made, employing the con-stant pressure body plethysmograph on 14 nonpregnant and 13 pregnantwomen. Specific airway conductance was increased during pregnancy.

Serial measurements of CA indicated a progressive increase beginning atabout 6 months of gestation and a return to normal by 2 months postpartum.

The mechanism of the increased CA during pregnancy is not known. It maybe related to changes in bronchial smooth muscle tone and conceivably ex-plains the tolerance of certain patients with lung resections to pregnancy.

Introduction

The mechanical properties of the lungs in preg-nant women are of interest for several reasons.First, there is a conflict between the complaintsof dyspnea made by many women during preg-nancy and the remarkably benign clinical courseshown by women with pulmonary resections dur-ing pregnancy (1). Secondly, detailed spiro-metric studies, notably by Cugell, Frank, Gaensler,and Badger (2), have indicated a progressive re-duction in the functional residual capacity (FRC)and expiratory reserve volume (ERV) as termapproaches. The reduction in the resting lungvolume might be expected to be associated with anincrease in airway resistance (RA), which isknown to be volume dependent (3). This re-duction in FRC is in contrast with the preserva-tion of the vital capacity (VC). The preservation

* Submitted for publication November 7, 1966; acceptedFebruary 17, 1967.

This work was supported in part by grant HE-05059from the National Institutes of Health and in part by agrant from the Tuberculosis League of Pittsburgh.

t Address requests for reprints to Dr. J. Bernard L.Gee, Dept. of Medicine, University of Pittsburgh Schoolof Medicine, Pittsburgh, Pa. 15213.

t Fellow of the Pennsylvania Thoracic Society.

of VC suggests that lung compliance (CL) is notgreatly changed. Third, metabolic changes oc-curring in pregnant women might modify pulmo-nary mechanics. Hypocapnia occurs during preg-nancy (4), and this is known to increase airwayresistance (5). However, hormone-determinedchanges in smooth muscle tone and possibly con-nective tissue elastance might occur during preg-nancy and so could possibly alter the mechanicalproperties of the respiratory system.

Although there are extensive observations ofmany aspects of respiration during pregnancy (6),there are no published studies of the effects ofpregnancy on lung compliance (CL) and only onereport (7) indicating a reduction in total pulmo-nary resistance (RL) demonstrated by the inter-ruptor method.

Methods

Lung volumes were determined on a 9-L Collinsspirometer. FRC was measured by the helium dilutionmethod.

Pulmonary mechanics. Lung compliance was measuredby the method of Neergard and Wirz (8) employing amodel 370 wedge spirometer (Med-Science Electronics)to monitor volume and flow. The wedge spirometer pro-vides electrical calibrations for volume and flow. Thesewere periodically checked with a Collins 9-L spirometer

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GEE, PACKER, MILLEN, AND ROBIN

5

4

3

2

0

* E.R.V.

1MI. C.F.R.C.

SIX SUBJECTS

8 MONTHS POST PARTUM

FIG. 1. A COMPARISONOF THE STATIC LUNG VOLUMES

AT THE EIGHTH MONTHOF PREGNANCYAND POSTPARTUM.

ERV= expiratory reserve volume; IC = inspiratory ca-

pacity; FRC= functional residual capacity.

for volume and a Rotameter flowmeter to provide con-

stant flows of up to 6 L per second, whose values were

predetermined volumetrically. Transpulmonary pres-

sure was obtained by using an esophageal latex rubberballoon, 10 cm in length and 3 cm in circumference, a PE160 catheter, and Sanborn 270 pressure transducer. Re-cordings were made on an Electronics for Medicine re-

corder. The balloon was positioned to obtain the high-est negative end expiratory pressure and contained 1 mlof air. Measurements of CL were obtained during breath-ing by comparing pressure and volume changes at pointsof zero flow. CL was studied during normal quietbreathing at FRC.

Total lung resistance was calculated by the isovolumemethod, which relates changes in pressure to changes inflow at constant volume (8).

Airway resistance was 'measured in a constant pres-

sure body plethysmograph, designed by Mead (9). Vol-ume was measured by a Krogh spirometer and Linearsyntransducer. Flow was measured by a heated wire meshscreen pneumotachograph and Statham PL-5 pressure

transducer. A linear response was obtained up to flowrates of 2.5 L per second. Mouth pressure was obtainedfrom a Sanborn 270 pressure transducer. Flow and vol-ume or pressure and volume were observed on the x-y

screen of an Electronics for Medicine recorder. The re-

sistance of the circuit was 0.2 cm H20 per L per second.The procedures for measuring RA are as follows: Thesubject was comfortably seated in the plethysmographwhile temperature stabilization occurred. Panting res-

pirations at flow rates of about 1.0 L per second werebegun to obtain flow/volume slopes on the x-y recorder.An airway interrupter was then closed while panting con-tinued against the shutter to obtain pressure/volumeslopes. RA and total gas volume (assumed to be intra-thoracic) were calculated by the method of DuBois (3),from the ratio of the two slopes and the appropriatecalibration factors. Six measurements were obtainedat the subject's resting lung volume. Additional measure-ments of RA were obtained at progressively larger vol-umes, and finally at volumes below the resting lungvolumes.

Subjects were nursing and secretarial staff, aged 20 to25 years, who had no history of pulmonary disease andwere free from upper respiratory infections at the timeof testing. No attempt was made to match pregnant andnonpregnant women for body size. All but one of thepregnant women were primigravida.

Types of studies. Four types of comparison were made.(The willingness of some pregnant women to performall the studies proved limited, and, therefore, the com-parative groups are somewhat variable.) 1) Lung vol-ume measurements only were made in 6 separate sub-jects. 2) Lung compliance and total pulmonary resistancewere studied in 10 subjects during pregnancy and afterdelivery. 3) Airway resistance was compared in 14 con-trol and 13 pregnant women. Five of these pregnantsubjects were also studied by comparison 2; the other 8were unwilling to swallow the balloon. 4) The serialchanges in. airway resistance during pregnancy were fol-lowed in 6 subjects. In 5 of these, comparisons 2 and 3were also completed. In the other 1, only data for theserial studies were obtained. Where only 1 techniquewas employed, the procedure outlined for each methodwas followed. Where both balloon and plethysmographywere used, the esophageal pressure method was employedfirst.

Results

Lung volumes. In a separate pilot study, staticlung volumes alone were measured in 6 subjectswho were about 8 months pregnant and then 2months postpartum. The data are indicated inFigure 1, where the average of the 6 subjects isindicated. During late pregnancy, there is a 25%oreduction in FRC and about 40% reduction inERV. Slight and statistically insignificant re-ductions in total lung capacity and VC were alsofound. VC is maintained by the increase in in-spiratory capacity. The changes were consistentin all subjects. These data agree with the moreextensive studies of Cugell and his associates (2)in 19 subjects.

Airway resistance. In clinical practice the termRA is more commonly used than its reciprocal, CA.However, CA bears a near linear relationship to

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(A

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PULMONARYMECHANICSDURING PREGNANCY

the lung volume (3). The use of CA has two ad-vantages. First, comparisons of the relationshipbetween CA and the resting lung volumes withoutreference to the subject's body size may be made.This is accomplished by expressing, the data asCA/L of lung volume, the so-called specific air-way conductance. Anthropometric factors deter-mine CA by their relation to lung volumes (e.g.,FRC). The use of specific CA therefore permitsan estimate of airway conductance adjusted forbody size. Second, direct comparisons may bemade of the rate of rise in CA as the lung is vol-untarily inflated.

The first comparison of CA between pregnantand nonpregnant women is shown in Figure 2,which indicates the specific airway conductancein 2 groups, namely, 14 control women and 13pregnant women of similar age. The values inthe pregnant women were obtained at a mean of71 months of gestation. When pregnant subjectswere studied serially, the data obtained nearest toterm were employed. These values for specific CAwere obtained from CA and volume data observedat resting lung volumes. The use of such dataobtained near FRC is important to minimize thebetween-groups variations in the regression sloperelating CA to lung volume. The data indicatethat, although there are considerable within-groupvariations, the mean specific CA of pregnant

PREGNANT

2.0h

LO

A

CD

E

0

.2

0.2

O.1L-

A

A

AA

PREGNANT COWROLS

FIG. 2. A COMPARISON OF SPECIFIC AIRWAY CON-DUCTANCE(CA) IN PREGNANTAND NONPREGNANTWOMEN.

V = lung volume. Broken lines indicate the normalrange.

women is 36% higher than the mean specific CAof nonpregnant women (p < 0.05). The meanspecific CA in the control group is within the nor-mal range of 0.20 to 0.28 reported by DuBois (3).

An evaluation of the differences in the regressionrelation between CA and lung inflation in these twogroups is shown in Figure 3. Only those subjectsin both groups whose lung volume ranges duringairway resistance studies exceeded 1.5 L have beenemployed, yielding data on 9 control and 8 preg-

NORMALSUBJECTS

2.0 _ z

LO

I 'I I A2 3 4 5

vI

tow'*- Or' lld f MEANSLOPE - . 30

1 2 3 4 5

vIFIG. 3. A COMPARISONBETWEENTHE REGRESSIONLINES RELATING CA TO VL IN PREGNANTAND NON-

PREGNANTWOMEN. Solid lines represent the regression lines for each subject. Broken lines representthe mean of the slopes in each group.

1

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0. 5 F

0.4 F

11 I

.... - - - - -

GEE, PACKER, MILLEN, AND ROBIN

MONTHS

FIG. 4. TIME COURSE OF SPECIFIC CA DURING PREG-

NANCY IN 5 SUBJECTS. Dotted lines are constructionaland join the last observation during pregnancy to the9-month vertical to permit comparison with the post-partum data.

nant women. This lung volume range requirementwas necessary to permit the calculation by themethod of least squares of the regression coefficientbetween CA and lung volume for each subject.The Figure indicates the calculated regressionlines. The data found in control subjects showeda mean slope of 0.30 0.10, which compares withthe normal range reported by DuBois of 0.13 to0.35 (3). The mean slope of the pregnant women

was 0.44 0.28. These slopes were compared bythe Student t test and were significantly different(p < 0.01). Thus, during pregnancy, there is an

unusually large increase in CA as the lung is pro-gressively inflated.

Time course of the change in airway conduct-ance. In 6 pregnant women, serial observationsof the specific airway conductance were made.These data are shown in Figure 4, which indi-cates the specific CA during pregnancy and post-partum (4 to 6 weeks after delivery). There isa rise in specific CA, particularly in the third tri-mester of pregnancy, with a striking return tonormal by about 5 weeks after delivery. Theexact time course of specific CA after delivery isnot known, since it was not practical to obtainstudies in the immediate postpartum period.

Lung compliance and total pulmonary resistance.The measurement of CL and RL by the esophagealballoon technique depends on the assumption thatduring breathing, the changes in intrapleural and

esophageal pressures are equal. The direct com-parison is clearly impossible in pregnant normalsubjects, but some information may be obtainedfrom a consideration of end expiratory pressures(EEP) during tidal breathing at FRC. Table Iincludes a comparison in 10 women between thevalues of EEP in the third trimester of pregnancyand about 5 weeks postpartum. The postpartumvalues are, in general, negative with a mean of- 2.7 cm H2O. These are within the reportednormal ranges. However, during pregnancy astriking difference is observed. The EEP as mea-sured in the balloon is positive, with a mean of+ 1.7 cm H2O. This positive esophageal pressurecannot equal true transpulmonary pressure at amoment where there is no gas flow. Thus, the as-sumption that changes in esophageal pressure stillreflect changes in transpulmonary pressure is re-quired, if estimates of CL are to be derived. Asomewhat similar assumption is, of course, neededfor the calculation of RL by the isovolume method.The estimates of CL and RL are indicated in TableI and were derived on the basis of these assump-tions. To the extent that such calculations arevalid (see Discussion), our data indicate that, al-though CL does not change, there is a highly sig-nificant change in RL (p < 0.01). The mean RLduring pregnancy is half that observed postpartum.

TABLE I

A comparison of end expiratory pressures (EEP), lungcompliance (CL), and total pulmonary resistance (RL)

in 10 subjects during pregnancy and postpartum

PostpartumPregnant

Subject Predictedno. EEP CL RL EEP CL RL CLt

cm L/cm cmH20/ cm L/cm cm HsO/ L/cmH20 H20 L/sec H20 H20 L/sec H20

1 4.2 0.13 0.2 -3.1 0.13 2.3 0.142 2.7 0.11 1.5 -4.4 0.11 0.8 0.123 1.2 0.12 1.2 -8.6 0.14 1.9 0.174 3.1 0.16 0.5 -3.0 0.19 2.1 0.135 1.5 0.09 0.7 -2.5 0.13 1.7 0.146* 2.2 0.14 0.9 -0.6 0.11 2.0 0.157* -0.8 0.23 1.1 -1.5 0.22 1.8 0.158* 2.2 0.13 0.8 +1.2 0.13 3.2 0.159* -0.1 0.21 0.5 -3.2 0.20 1.0 0.18

10* 0.9 0.09 1.2 -1.2 0.20 1.5 0.16

Mean 1.7 0.14 0.9 -2.7 0.16 1.8 0.15SD 0.047 0.39 0.042 0.47

* Subjects shown in serial studies in Results under "airway resist-ance."

t Predicted CL = (0.00343 X height in centimeters) - 0.425 (10).

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PULMONARYMECHANICSDURING PREGNANCY

Discussion

Esophageal pressure during pregnancy

Before indicating the significance and possiblemechanisms of these findings, we should discussthe validity of the esophageal balloon pressurechanges as measures of changes in transpulmo-nary pressures during pregnancy. The follow-ing technical considerations apply: 1) Everyeffort was made to position the balloon in themidesophagus; 2) cardiac impulses were clearlyvisible in the records; these impulses show theusual amplitude of about 0.5 cm H2O; 3) theballoon was not over distended, since only 1ml of air was introduced into the balloon; 4) intwo subjects (No. 6 and 7) in whom serial stud-ies were performed during pregnancy, progressiverises in EEP occurred from - 4.5 and - 2.5 at 28weeks to values at 36 weeks of - 0.1 and - 0.8cm H2O; 5) no excessive esophageal contractionswere evident in the records; 6) the normal rangeof EEP in the postpartum women argues that bal-loon positioning was correctly performed in thepostpartum state. Thus, it appears that a positiveEEP during pregnancy is not due to the use of animproper technique, but reflects a genuine disparitybetween the esophageal and intrapleural pressuresduring late pregnancy.

As discussed earlier, positive transpulmonarypressures cannot occur at end normal expiration,and, therefore, the measured esophageal EEPvalues cannot reflect the absolute transpulmonarypressures. This raises the problem as to the ef-fect of these EEP values on calculated CL and RL.We cannot directly compare intrapleural andesophageal pressures in pregnant women, butthere is a highly relevant analogy between preg-nancy and the supine posture. The analogy in-cludes a positive resting EEP (11-13) in normalsupine subjects, and, further, the supine postureis associated with an ascent of the diaphragm. Analteration from sitting to supine posture produceschanges in lung volume profile similar to those en-countered in pregnancy, including lowered FRC,increased IC, and a normal VC. More recently,Chiang and Lyons (14) studied the effects of a45 0 tilt towards the supine position. They showedthat esophageal EEP changes from - 3.74 to- 2.71 cm H20 and that FRC falls by 200 ml asa result of this tilt. The full 900 tilt towards a

supine posture was studied by Mead and Gaensler(12), who compared intrapleural and esophagealpressures. They showed that lying supine causesthe directly measured end expiratory intrapleuralpressure to change from - 5.1 to - 1.1 cm H20,while the end expiratory balloon pressure changesfrom - 4.8 to + 2.7 cm H2O. Thus, the supineposture is associated with a lack of agreement be-tween pleural and balloon static pressure differ-ences. These authors concluded that "measure-ments of compliance in the tidal range would befactitiously low as measured from esophageal pres-sure in the supine position" (12). This point wasfurther developed by Knowles, Hong, and Rahn(13) and separately by Ferris, Mead, and Frank(15), who showed differences in the static pres-sure-volume diagram in 2 postures when theesophageal balloon was employed for the measure-ment of transpulmonary pressure. Both groupsindicate that the greatest differences exist in thelower half of lung volume, and agree that the ap-parent supine CL calculated from balloon pressuresat small tidal volumes would appear to be about25%o less than sitting values. The range of thepercentage change in CL between the two posturesis 0 to 40%o (15).

Our data indicate a normal postpartum CL evi-denced by comparing the CL observed and thatpredicted from the subject's height (Table I).The apparent CL during late pregnancy is notstatistically different, but the mean value is lowerby 0.02 U, that is, 12%o lower than postpartum.This change is of similar magnitude to the ap-parent change reported for the supine studies.Thus, if the analogy between pregnancy and thesupine posture is valid, it may be concluded thereis no change in CL. This conclusion is supportedby the preservation of the VCduring pregnancy.

The isovolume method for the calculation of RLrequires less discussion. The method does assume1) that the elastic component of pleural pressure isconstant for any lung volume, irrespective of thephase of respiration (i.e., no significant hystere-sis); 2) that any differences between pleural andesophageal pressures are constant at a given lungvolume; and 3) that the time constants of thelung are sufficiently rapid for pressure equaliza-tion. There are no reasons to question the ap-plicability of assumptions 1 and 2 to pregnantwomen during quiet tidal breathing. The time

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GEE, PACKER, MILLEN, AND ROBIN

constant derives from the product of RL and CL.CL has been shown to be normal, and RA, thelarger component of RL, is, in fact, decreased. Thetime constant of the lungs of pregnant women is,therefore, sufficiently rapid to validate assumption3.

Airway and total pulmonary resistance

Total pulmonary resistance (RL) is known to in-clude 2 components. The larger component is air-way resistance (RA), and the smaller one derivesfrom tissue resistance. Thus, a comparison of RLto RA is pertinent. Two such comparisons are pre-sented in Table II. Section A compares the twomethods on all subjects who were studied by eachmethod. This comparison is, at best, a general onesince these mean data are derived from studies ofRA and RL in groups that included different sub-jects. Section B presents a better comparison sincethese data were obtained on the same subjects.This comparison indicates that approximately 80%of the reduction in RL during pregnancy derivesfrom the reduction in RA. It is not possible tostate whether the tissue-resistive component is al-tered during pregnancy since this component istoo small for precise measurement. A third com-parison between RL and RA is achieved by corre-lating the two measures on the same subjects.This may be shown by comparing the reciprocalof RA, namely CA, and 1/RL. Figure 5 presentsthis comparison. The two methods correlatefairly well (r = 0.61, p < 0.025), and the regres-sion coefficient of CA on 1/RL is 0.77, a value notsignificantly different from 1.0. CA in general ex-ceeds 1/RL as would be required by the presenceof an additional tissue-resistive component in RL.This comparison again can only be approximate,

TABLE IIA comparison of total pulmonary resistance (RL) and airway

resistance (RA)*

No. of Post-subjects Pregnant partum

cm H20/L/secA RL 10 0.9 1.8

RA 13 0.9 1.1B RL 5 0.9 1.9

RA 5 0.7 1.5

* Group A = unmatched subjects; group B = matchedsubjects. (For explanation see text.)

| L/sec/cm H 0RL 2

FIG. 5. COMPARISONBETWEENCA AND 1/RL (TOTALPULMONARYRESISTANCE) FOR THE SAME SUBJECTS. A =

pregnant; * =postpartum. Solid line is the line ofidentity. Broken line is the calculated regression line ofCA on 1/RL.

since the flow rates and the lung volumes wereonly approximately similar during the applicationsof the 2 methods.

Mechanism of changes in airway conductance

The rise in CA at a constant flow during preg-nancy clearly indicates an increase in airway cross-sectional area. The effects of pregnancy on cer-tain factors known to modify airway size may nowbe considered.

Lung volume and elastic recoil. It has beendemonstrated by Caro, Butler, and DuBois (16)that temporary restriction of thoracic or abdominalmobility by external straps results in an increasein specific CA. This increase in specific CA wasshown to depend on a diminished CL. The analogybetween external strapping of the abdomen withpossible restriction of the diaphragm and re-striction by the enlarging uterus suggests a com-mon mechanism for an increased specific CA.However, our data do not indicate any change inCL during pregnancy. Further, in spite of ahigher end normal expiration position of the dia-phragm, there can be no true restriction of dia-phragm movement since the VC is preserved dur-ing pregnancy.

Effects of lung inflation. The volume historyof the lung before the measurement of its mechani-cal properties has been shown to influence bothCL and RA. Since the lung during pregnancy hasa reduced resting volume, this effect might be

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PULMONARYMECHANICSDURING PREGNANCY

potentiated. However, the sequence of our stud-ies, and particularly the change in RL shown af-ter a rest period in the laboratory, do not supportthis explanation.

Metabolic factors. One important metabolicchange during pregnancy is the increased levelsof various hormones. These might reduce airwayresistance. Three possible hormones might beconsidered. Progesterone levels rise progressivelyduring pregnancy, and the decreased tone in cer-tain smooth muscles, namely in the ureters, hasbeen attributed to progesterone (17). This effectalso occurs at the sixth to seventh month of preg-nancy. Thus, progesterone might reduce normalbronchomotor tone.

The production of cortisone and related steroidsis also well known to be increased during preg-nancy. One may speculate that these steroidsalso modify normal bronchomotor tone.

Relaxin is known to mobilize cartilaginousstructures in pregnant lower mammals (18), andit is conceivable that similar effects occur in preg-nant women. However, too little is known aboutrelaxin to permit further discussion of this point.

The possible relationship between hormonalchanges during pregnancy and decreased RA isintriguing but speculative.

Dyspnea and work of breathing during pregnancy

Bader, Bader, and Rose (19) demonstrated aprogressive increase in the °2 cost of breathingunder standardized patterns of respiration duringthe last 4 months of pregnancy. These authorssuggested that these increased 02 costs of breath-ing were not related to altered lung mechanics,but rather to increased diaphragmatic work. Ourdata indicating an unchanged CL and reduction inboth RL and RA support their view.

The demonstrated reduction in RA during preg-nancy cannot account for the "dyspnea of preg-.nancy." The reduced RA is, however, probablyrelevant to the failure of pregnancy to cause re-spiratory embarrassment in patients with lungresections. Gaensler, Patton, Verstraeten, andBadger (1) studied 7 such patients in whom thevital capacities were reduced to a mean of 1.4 L.The alterations in the static lung volumes duringpregnancy were similar to those of normal women.It is reasonable, therefore, to presume that RA

was reduced in such patients. Gaensler and as-sociates specifically indicate that these patients didnot complain of dyspnea during pregnancy. Inthese patients, the increased ventilatory demandsof pregnancy must be met by rises in the respira-tory rate. Thus, a reduced RA assumes some im-portance in minimizing the increase in total re-spiratory work and might possibly relate to theabsence of dyspnea.

References

1. Gaensler, E .A., W. E. Patton, J. M. Verstraeten, andT. L. Badger. Pulmonary function in pregnancy.III. Serial observations in patients with pulmo-nary insufficiency. Amer. Rev. Tuberc. 1953, 67,779.

2. Cugell, D. W., N. R. Frank, E. A. Gaensler, andT. L. Badger. Pulmonary function in pregnancy.I. Serial observations in normal women. Amer.Rev. Tuberc. 1953, 67, 568.

3. DuBois, A. B. Resistance to breathing in Hand-book of Physiology, sect. 3, vol. 1, Respiration,W. 0. Fenn and H. Rahn, Eds. Baltimore,Waverly, 1964, p. 451.

4. Gaensler, E. A. Lung displacement: abdominal en-largement, pleural space disorders, deformities ofthe thoracic cage in Handbook of Physiology, sect.3, vol. 2, Respiration, W. 0. Fenn and H. Rahn,Eds. Baltimore, Waverly, 1964, p. 1623.

5. Newhouse, M. T., M. R. Becklake, P. T. Macklem,and M. McGregor. Effect of alterations in end-tidal C02 tension on flow resistance. J. appl.Physiol. 1964, 19, 745.

6. Prowse, C. M., and E. A. Gaensler. Respiratory andacid-base changes during pregnancy. Anesthesi-ology 1965, 26, 381.

7. Rubin, A., N. Russo, and D. Goucher. The effectof pregnancy upon pulmonary function in normalwomen. Amer. J. Obstet. Gynec. 1956, 72, 963.

S. Marshall, R. Objective tests of respiratory me-chanics in Handbook of Physiology, sect. 3, vol. 2,Respiration, W. 0. Fenn and H. Rahn, Eds.Baltimore, Waverly, 1964, p. 1399.

9. Mead, J. Volume displacement body plethysmographfor respiratory measurements in human subjects.J. appl. Physiol. 1960, 15, 736.

10. Frank, N. R., J. Mead, A. A. Siebens, and C. F.Storey. Measurements of pulmonary compliancein seventy healthy young adults. J. appl. Physiol.1956, 9, 38.

11. Attinger, E. O., R. G. Monroe, and M. S. Segal.The mechanics of breathing in different body posi-tions. I. In normal subjects. J. clin. Invest. 1956,35, 904.

12. Mead, J., and E. A. Gaensler. Esophageal andpleural pressures in man, upright and supine. J.appl. Physiol. 1959, 14, 81.

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13. Knowles, J. H., S. K. Hong, and H. Rahn. Possibleerrors using esophageal balloon in determination ofpressure-volume characteristics of the lung andthoracic cage. J. appl. Physiol. 1959, 14, 525.

14. Chiang, S. T., and H. A. Lyons. The effect of pos-

tural change on pulmonary compliance. Resp.Physiol. 1966, 1, 99.

15. Ferris, B. G., Jr., J. Mead, and N. R. Frank. Effectof body position on esophageal pressure and mea-

surement of pulmonary compliance. J. appl. Phys-iol. 1959, 14, 521.

16. Caro, C. G., J. Butler, and A. B. DuBois. Some ef-fects of restriction of chest cage expansion on pul-

monary function in man: an experimental study.J. dlin. Invest. 1960, 39, 573.

17. Daly, D. F. Maternal physiology in Textbook ofObstetrics, J. C. Ullery and Z. S. R. Hollenbeck,Eds. St. Louis, C. V. Mosby, 1965, p. 56.

18. Bisca, B. V. Medication during labor and deliveryin Textbook of Obstetrics, J. C. Ullery, and Z. S.R. Hollenbeck, Eds. St. Louis, C. V. Mosby, 1965,p. 397.

19. Bader, R. A., M. E. Bader, and D. J. Rose. Theoxygen cost of breathing in dyspnoeic subjectsas studied in normal pregnant women. Clin. Sci.1959, 18, 223.

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