Thorax, 1980, 35, 603-610

Analysis of lung volume restriction in patients withrespiratory muscle weaknessANDRE DE TROYER, SAMUEL BORENSTEIN, AND RENE CORDIER

From the Chest Service, Erasme University Hospital, and the Brain Research Unit, Brussels School ofMedicine, Brussels, Belgiumn

ABSTRACT We investigated pulmonary mechanics in 25 patients, 9 to 55 years of age, with a varietyof generalised neuromuscular diseases and variable degrees of respiratory muscle weakness. Theaverage degree of inspiratory muscle force was 39 2% (range 8-83 %) of predicted. The lung volumerestriction far exceeded that expected for the degree of muscle weakness: the observed decrementin respiratory muscle force should, theoretically, decrease vital capacity to 78 % of its control value,while the mean VC in our patients was only 500% of predicted. Analysis of lung pressure-volumecurves indicated that the two principal causes of the disproportionate loss of lung volume were

a reduction in lung distensibility probably caused by widespread microatelectasis, and a decreasein the outward pull of the chest wall. Because it reflects both direct (loss of distending pressure)and secondary (alterations in the elastic properties of the lungs and chest wall) effects of respiratorymuscle weakness on lung function, we conclude that, in these patients, the vital capacity remainsthe most useful measurement to follow evolution of the disease process or response to treatment.

Respiratory muscle weakness is a frequent oc-cu.rrence in many neuromuscular diseases.Although it is well established that weakness ofthe respiratory muscles produces a restrictiveventillatory defect, the precise relationship be-tween the degree of, muscle weakness and thetype of lung dysfuncotion is still unclear. Inparticular, there is disagreement as to whether theresting end-expiratory position decreases,'-4increases,5 or remains unchanged.(-8 Similarly,some inve.stigators have reported no change inresidual volume,2 3 9 while a majority of studieshave found an increase in this volume.5-8 Anadditional proble4m concerns the loss of in-spiratory capacity associated with the impair-ment of inspiratory muscle function. Indeed,because of the shape of the maximal staticpressure-volume curves of the respiratory system,a large degree of respiratory muscle weaknesswould be predicted to have only a moderateeffect on lung volume. However, recent datasuggest that, in patients with respiratory muscleweakness, the relationship between loss ofrespiratory muscle force and loss of lung volumeis not always predictable, in that the decrease

Address for reprint requests: Dr A De Troyer, Chest Service, ErasmeUniversity Hospital, 808 Route de Lennick, 1070 Brussels, Belgium.

in lung volume is often disproportionate to theloss of muscle force.2 10 Similar findings havebeen made in normal volunteers in whom acuteweakness of the respiratory muscles produced bypartial curarisation was accompanied by largechanges in lung volume, changes that far ex-ceeded the predictions of the effects of muscleweakness on lung volume."'We recently investigated pulmonary mechanics

in 25 patients with a variety of generalisedneuromuscular disorders and a wide range ofrespiratory muscle performance. The three mainpurposes of the present report are: (1) todelineate the pattern of pulmonary functionassociated with respiratory muscle weakness; (2)to evaluate the lung volume restriction associatedwith a chronic involvement of the respiratorymuscles, with particular emphasis on the relation-ship between loss of respiratory muscle strengthand loss of lung volume; and (3) to determinethc factors, other than the weakness itself, thatare mainly involved in the lung volumerestriction.

Patients

Twenty-five consecutive patients with generalisedneuromuscular disorders and referred to our

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laboratory for evaluation of respiratory muscleforce form the basis of the report. The groupconsisted of 19 males and six females Who had amean age of 26 years, with a range of 9 to 55years. Eighteen paitients had miscellaneousmyopathies, among which 14 had Duchenne-typemuscular dystrophy, two had limb-gi.rdledystrophy, and two had muscular dystrop.hy ofthe facioscapuilohumeral type. Four patients hadmu-scular wasting associated with dystrophiamyoitonica. The remaining three patients hadres,piratory muscle weakness caused by poly-myositis, previous poliomyelitis, and Guillain-Barre syndrome, respectively. The diagnoseswere based on clinical and appropriate lab-oratory examination including serum enzymes,nerve conduction studies, electromyograms, and,in some cases, muscle biopsies. All patients buttwo were lifelong nonsmokers, but none had ahistory of chronic obsitructive lung disease orclinical evidence of congestive heart failure.Only two patients complained of dyspnoea at restat the time of the study. Four of the 25 patients,all of whom had progressive muscular dystrophy,had radiographic shadowing suggesting partialatelectasis of one lobe on the day of thepulmonary evaluation.

Methods

All measurements were carried out with thesubject seated in a constant volume bodyplethysmograph. Lung volumes, maximal ex-piratory and inspiratory flow-volume curves, andspecific airway conductance were obtained bystandard methods described previously.'2

Expiratory pressure-volume (PV) curves wereobtained by a quasi-static method'3 with anoesophageal latex balloon (length 10 cm;perimeter 3 5 cm; air voluTme 0-4 ml) introducedvia the nose into the oesophagus. A marker wasplaced on the polyethylene tubing exactly 42 cmfrom the ballloon tip and balloon adjustmentbegan when this marker a-ppeared at the exter;nalnares. Recording of the curves was preceded bythree full inflations to assure a constant volumehis+ory. Lung volume was plotted versustranspulmonary pressure on a direct-writingX-Y recorder. Several deflational PV curveswere obtained in each patient and a line of bestfit was drawn by eye through at least three setsof PV data that agreed to ± 1 cm HAO. Thestatic recoil pressure of the lung (Pst (1) ) wasmeasured at various percentages of total lungcapacity (TLC) that was calculated by adding toFRC the mean inspiratory capacity measured

during the X-Y recording of the PV curves.Static expiratory lung compliance was measuredas the slope of the PV curve over the 0-5 litreabove functional residual capacity (FRC). Thesame technique was used for obtaining ex-piratory PV curves in the children of the presentstudy, except for the distance between ballon tipand nares.13Minimal (inspiratory) pleural pressures (P pi

min) were oibtained by repeated measurements atvarious lung volumes while the subject attemptedmaximal inspiratory efforts against an obstruc-tion. A conventional mouthpiece and noseclipwere used, and pressures sustained for one secondwere reoorded. At least 15 maximal efforts wererecorded on each patient, and the lowest valuesat each 'lung volume were used to constructcurves of minimal pleural pressure against lungvol.ume.

Predicted values for lung volumes are fromAmrein et al.14 Predicted values for the PVcurves and P p1 min are derived from resultsobtained in 40 healthy children13 and 135 normalsubjects studied in our laboratory.15

Results

In 23 of the 25 patients, the shape of the P plmin-volume curve was similar to that seen innormal subjects-it was curvilinear and the lowestpressures were achieved at or near FRC.Minimal pleural pressure at FRC ranged from-19 to -86 cm H20. However minimal pleuralpressures are highly dependent on the lungvolume at which they are measured, as de-veloped in a previous study.1" Therefore, thelung volume restriction present in our patientshad to be taken into account before comparisonwas made with the normal predicted values.After the correction has been made for the lossof lung volume, the degree of inspiratory muscleforce ranged between 8 and 83 (mean ± SE =39-2 ± 3 6)% of predicted. The mean ourveobtained in our patients is compared to themean predicted one in fig 1.Average values of lung volumes are given in

table 1. The degree of lung volume restrictionvaried from 30 to 101 % of predicted TLC and14 to 93% of predicted VC. The average decreasein VC was 50% and TLC 33%. The FRC wasbelow the normal range in most of the patients:the mean predicted value averaged 2-75 litrescompared to 2-16 litres in the patients, a signi-ficant decrease (p<O0001). A significant positiverelationship was found between FRC and theinspiratory muscle force (fig 2, left panel). The

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Analysis of lung volume restriction in patients with respiratory muscle weakness

1W,

D 80

-o

* 60

40~

20 *

-100Pressu re (cm H20)

0.D

O U0.

I--50

Fig 1 Volume-minimal pleural pressure curvesobtained in 25 patients with respiratory muscleweakness; mean ± SE values are shown. Shaded arearepresents predicted values. Volume expressed as apercentage of predicted TLC. 0 10 20 30

Pst ( I ) (cm H20)

Table 1 Subdivisions of lung volume (mean ± SE)in 25 patients with neuromuscular disorders

Subjects VC (1) FRCS (I) R V (l) TCL (1)

PatientsMean 1-89 2-16 1-48 3 41SE 0-16 0 15 0 11 0-24

PredictedMean 3-80 2 75 1-39 5-10SE 0-22 0-18 0 10 0-31

t value 8-67 5 03 1-15 6 87p value <0 001 <0 001 NS <0 001

The predicted values for lung volumes are those of Amrein et al.14

RV was not significantly altered.The mean deflational PV curve of the lung

obtained in the 25 patients is compared to thepredicted one in fig 3. The graph demonstratesclearly that the PV curve of the patients wasreduced on its volume axis. For any giventranspulmonary pressure there was a markeddecrease in absolute lung volume. Both lungrecoil pressure at full inflation and static ex-

LL

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-looast100

080.

u 60

O 40'

- 20a-

r=062p<0o001

20 40 60 80 100Inspiratory muscle

Fig 3 Static expiratory pressure-volume curve of thelung in patients with neuromuscular disorders andrespiratory muscle weakness; average data of 25patients (open circles). Volume expressed aspercentage of predicted TLC and closed circlesrepresent mean predicted values. Each bar represents+i SEM. Pst (1)= static lung recoil pressure. Theobserved and predicted resting lung volumes are alsoindicated (open squares).

piratory compliance were significantly reduced(,table 2). The average decrease in lung com-plian,ce was 40%. However, when volume wasexpressed !as a fraction of measured, rather thanpredicted, TLC, the mean curve obtained in thepatients was parallel to the predicted one,especially in its linear portion (fig 4). The trans-pulmonary pressure a,t FRC was below normal in23 of the 25 patients and it was very low insome cases. The mean observed value averaged2-8 cm H2O, compared to a mean predictedvalue of 6 6 cm H2O, a significant decrease

Fig 2 Relationships betweeninspiratory muscle force and FRC (leftpanel) and between inspiratory muscleforce and static recoil pressure of thel4ng (Pst (1)) at FRC (right panel) in25 patients with respiratory muscle

r=0 72 weakness. Dashed lines are the lines ofP<0001 regression.

., 0

. "II>

I a. a20 40 60 80 100

strength ('/o predicted )

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Table 2 Data from lung pressume-volume studiesin 25 patients with neuromuscular diseases

Subjects Static expiratory Psi (l) at TLC Pst (1) at FRCcompliance (cm H20) (cm H20)(I/cm H20)

PatientsMean 0 113 19 9 2-8SE 0 017 1-2 0 4

PredictedMean 0188 30-1 6-6SE 0 017 0-6 0 4

t value 6 11 6-27 6-48p value < 0 001 < 0 001 < 0 001

The predicted values are derived from measurements performed in40 healthy children'3 and 120 healthy adults'5 studied in this laboratory

100

80

a

<, 60

10 20 30Pst (1) (cm H20)

Fig 4 Same data as in fig 3, with lung volumeexpressed as a percentage of actual rather thanpredicted TLC.

(p<0 001) (table 2). The Pst (1) at FRC cor-related positively and significantly with the lossof inspiratory muscle force (r=0-72; p<0-001):the weaker the inspiratory muscles, the lowerthe lung recoil pressure at resting lung volume(fig 2, righ.t panel). Finally, in none of thepatients, was there any evidence of airway ob-struction. Specific airway conductance was withinnormal limits or above the normal upper limit of0-371/s/cm H2O in all cases, and the maximumexpiratory flow-static recoil relationship waswithin the normal range in each patient.The four patients who had radiologically

visible atelectasis were among those who hadthe smnallest lung volumes and the lowest valueso-f lung compliance. However, a similar degreeof pulmonary dysfunction was present in somepatients who had clear radiographs, and thefunctional disturbances were qualitativelyidentical in all the patients in this study,regardless of chest radiograph or type of under-lying disease.

Discussion

Weakness of the inspiratory musoles was present,at a variable degree, in most of the 25 patientsstudied here. In 19 of them the minimal pleuralpressures were less than 50% of predicted, whichindicates that severe respi,ratory muscle weaknessis common in patients with generalised neuro-muscular diseases.Our findings confirm that patients with

respiratory muscle weakness have a restrictiveventilatory impairment. In addition, they showthat in these patients, t;he lung volumes arereduced in approximate proportion to thereduction of the pressures developed duringmaximum static inspiratory efforts. The findingof large changes of lung volume was unexpected:because of the shape of the pressure-volumecharacteristic of the relaxed respiratory systemwhich becomes curvilinear only near the ex-tremes of the vital capacity, lung volume shouldbe weJl preserved even in the face of severemuscle weakness. For example, if it is assumedthat the relaxation characteristic of the chestwall in the patients was normal, it can becalculated from our standard maximal staticpressure-volume diagram'15 that a decrement ofinspiratory muscle strength identical to thatobserved here at FRC wouild, theoretically,decrease TLC to only 86-5% of its control value(fig 5). The observed data strongly differ fromthis prediction, since TLC in our patient.s was,on an average, 67% of predicted. The fact that

-100 +50-50 0Pressure ( cm H20 )

Fig 5 Comparison between observed (open circles)and theoretically predicted (dashed line) maximalstatic inspiratory pressure-volume relationship ofthe respiratory system in patients with chronicrespiratory muscle weakness. The normal curve(closed circles) is drawn from the data obtained in135 healthy subjects.'5 The predicted relationshipwas constructed assuming a decrement in musclepressure at all lung volumes proportional to thatmeasured at FRC. Dotted line is the normalrelaxation PV relationship of the respiratory system.

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.4nalysis of lung volume restriction in patients with respiratory muscle weakness

the loss of lung volume was out of proportion tothat anticipated for the degree of musclewe.akness is also illustrated in fig 6. The solidcurve in this graph is the theoretical relationbetween VC and respiratory muscle strength,calculated from the standard maximal staticpressure-volume diagram, and assuming againthat respiratory system recoil for patients withchronic weakness of the respiratory muscles isthe same as that measured in normal subjects,and that there is a uniform involvement of theinspiratory and expiratory muscles. Based onthese theoretical considerations, a 61 % decreasein respiratory muscle strength would be as-sociated with a VC of 78%. The graph shows alsothe individual values obtained in our patientsand the logarithmic regression calculated fromthese values. As expected, the VC was highlyand positively correlated with the inspiratorymuscle strength (r=0 88; p<0001), but therelationship was shifted downwards when com-pared to the theoretical one-that is, the VCin the patients was clearly lower, at any levelof respiratory muscle force, than would be pre-dicted on the basis of normal respiratory systemrecoil. These considerations show that the loss oflung volume in patients with a chronic involve-

100

80-'a-

a 60

a40.

0._

a

0

L' 20-5

Theoretical

I

0 /

14 Ow

./0~ 0

/O

A.0

r= 0 88p<0.001

0 20 40 60 80 100Inspiratory muscle strength (o/o predicted )

Fig 6 The solid curve indicates the theoretical effectof respiratory muscle weakness on vital capacityconstructed by assuming (1) that the relaxation PVcharacteristic of the chest wall is normal, and(2) that the inspiratory and expiratory muscles are

involved uniformly. The dashed curve is thelogarithmic regression calculated from the dataobtained in the 25 patients with various neuro-muscular diseases (closed circles).

ment of the respiratory muscles is dispropor-tionate to the loss of respiratory muscle forceand thus suggest that factors other than weaknessitself are implicated in the lung volume restric-tion. We believe these discrepancies betweentheoretical considerations and experimentalfindings are explained by changes in lungelasticity and by alterations in the passive recoilof the chest wall.

Statilc expiratory 'lung icompliance wasmarkedly decreased in our patients. Most clearly,this reduction far exceeded the effects that couldresult from the only difference in lung volumehistory, and values o-f compliance obtainedduring inflation were also reduced. This impliesthat patients with a longstanding involvement ofthe respiratory muscles have alterations in theelastic properties of the lung. Indeed, if the lossof distending pressure were the only effect ofmuscle weakness, the PV curve of the lung wouldbe truncated but compliance measured over thetidal range should be close to normal. Con-sequently there exists in these patients aparenchymal involvement that must contribute tothe loss of lung volume. That the change in lungdistensibility is an important determinant of thedegree of lung volume restriction is suggested bythe finding tha.t there was a clear relationshipbetween TLC and the compliance at FRC (fig 7),as well as between VC and compliance(r=079; p<0-001). A close relationship betweencompliance and TLC has already been reportedin such patients.16

120

100

', 80LIa0

I.-260

() 40.

20

4,'-. pc~~~0001

Static lung compliance80 100

( 0/4 predicted )120

Fig 7 Relationship betwen static lung compliance(CL) and total lung capacity (TLC) in 25 patients withrespiratory muscle weakness. Dashed line is the line ofregression.

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The present observations of markedlydecreased lung compliance and increased lungrecoil pressure in patien,ts with respiratorymuscle weakness are consistent with those ofGibson et al.2 These workers pointed out thatthese changes were similar to those seen innormal subjects in whom expansion is preventedby strapping of the chest wall.'7 18 Because ofthis similarity and although they felt atelectasiswas the most likely explanation, they discussedthe possibility that some alterations in thesurface properties of the alveolar lining layer,related to the low volume breathing, was respon-sible for these changes. This possibility is notsupported by the observation that the mean PVcurve in our patients was quite parallel to thepredicted normal when lung volume wasrelated to the measured TLC. The value of relat-ing volume to the measured rather than predictedTLC has been recently discussed by Gibson andPride'9 in their study of patients with severefibrosing alveolitis. They reasoned that in theselungs, the loss of gas-containing alveoli wasresponsible for most of the changes in the PVcurve, and suggested that expressing volume as apercentage of measured TLC would reflect theelastic properties of the surviving ventilatedalveoli. This view has been supported by recentmeasurements obtained in dog lungs wi,th diffusegranulomatous disease.20 Therefore the presentobservation that the slope of the PV curve(AV/AP) was normal when lung volume wasrelated to the measured TLC would suggest that,in patients with longstanding respiratory muscleweakness, the largest number of functioningalveoli retain normal elastic properties. Resultsof recent studies in this laboratory on normalvolunteers during submaximal neuromuscularblockade are also compatible with the conceptthat weakness of the respiratory muscles, despitethe associated low volume breathing, is notassociated with alterations in surface forces anddoes not directly influence the elastic propertiesof the lung.'2The theoretical considerations discussed above

between the degree of muscle weakness and thedegree of lung volume restriction were based onthe assumption that the PV relationship of therelaxed chest wall was normal in patients withrespiratory muscle dysfunction. However, analysisof lung pressure-volume data obtained in theregion of resting ventilation suggests that theelastic behaviour of the chest wall is altered inthese patients. Indeed the FRC was decreased inmost cases. Inasmuch as FRC is determined by thebalance between lung and chest wall forces, the

observed fall in FRC could have resulted fromthe increase in the inward pull of the lung, orfrom a decrease in the tendency of the chest wallto recoil outward, or from a combination of thetwo. The first possibility is unlikely. Figure 8illustrates the theoretical relationship betweenFRC and transpulmonary pressure at FRC whenthe PV characteristic of the chest wall remainsunchanged (solid curve): when an increase inlung recoil pressure is the only cause of adecreased FRC, the Pst (1) at FRC must increase.By contrast, in most of our patients, thedecrease in FRC was assoiciated with a decrease,not an increase, in Pst (1) at FRC (fig 8). This isstrong evidence that the fall in FRC in thesepatients is caused primarily by a decrease in the(outward) pull of the chest wall. This observationis consistent with other studies that demonstratedthat the ability of the chest wall to recoil out-wards decreased in normal volunteers when acuteweakness of the respiratory muscles was pro-duced by partial curarisation.12 Moreover, in ourpatients, a close relationship existed between theinspiratory muscle force and the decrease of bothFRC and Pst (1) at FRC (fig 2), fu-rther suggestingthat the reduction of the chest wall force is

'a,-

. _

;o

,C)

.0.r.r ~~~~~~~~~~~~~~~~~~~I0 'l * 0

.0 0

0

0 100Pst (1l) at FRC

200(1/o predicted )

300

Fig 8 The solid curve indicates the theoreticalrelationship between FRC and lung static recoilpressure (Pst (1)) at FRC when the elastic recoil ofthe relaxed chest wall remains normal. The individualvalues obtained in 25 patients with respiratorymuscle weakness are also shown.

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related to the degree of involvement of theinspiratory muscles. Such a decrease in the out-ward pull of the chest wall would contribute tothe disproportionate loss of lung volume observedin our patients.The finding of a normal RV in our patien,ts

despite a severe muscle weakness may beexplained by at least two factors. Firstly, somepatients had radiologically visible atelectasis and,as discussed above, it is likely that atelectasis ofa more focal nature, undetectable by chestradiographs, was present in the other cases.Secondly, preservation of RV in the face ofdecreased expiratory muscle strength may beexplained if one considers the determinants ofRV. It is well established that the recoil force ofthe chest wall has a major determining effect onRV in younger healthy people.21 Accordingly,the lack of increase in RV in our patients mightbe caused by the fact that the decreased expira-tory muscle force is counterbalanced by a lesserresistance of the chest wall during expiration.From these data it would appear that character-

istic alterations in lung volumes and respiratorymechanics develop in patients with respiratorymuscle weakness. These alterations include reduc-tion in vital capacity, decreased functionalresidual capacity, normal residual volume, anddecreased lung compliance with low lung recoilat resting lung volume. Moreover, it is quite clearfrom these studies that the change in vitalcapacity in these patients reflects both direct (lossof distending pressure) and secondary (changesin the passive characteristics of the lungs andchest wall) effects of respiratory muscle weaknesson pulmonary function. Measurements of maxi-mal static pressures, in contrast, explore only alimited part of these effects. We conclude,therefore, in disagreement with Braun andRochester,'0 that vital capacity, in addition tobeing the easiest measurement, is the most usefulone to perform in these patients to followevolution of the disease process or response totreatment.

We are indebted to Dr Renoirte for his co-operation in this study, to Miss M Lebrun fortechnical assistance, and to Miss Douillet for thepreparation of the manuscript.

References

1 Faerber I, Liebert PB, Suskind M. Loss of func-tional residual capacity in poliomyelitis. J ApplPhysiol 1962; 17:289-92.

2 Gibson GJ, Pride NB, Davis JN, Loh LC. Pul-monary mechanics in patients with respiratory

muscle weakness. Am Rev Respir Dis 1977; 115:389-95.

3 Hapke EJ, Meek JC, Jacobs J. Pulmonary func-tion in progressive muscular dystrophy. Chest1972; 61:41-7.

4 Vallbona C, Spencer WA. The total lung capacityand its subdivisions in respiratory poliomyelitis.J Chronic Dis 1959; 9:617-35.

5 Inkley SR, Oldenburg FC, Vignos PJ. Pulmonaryfunction in Duchenne muscular dystrophy relatedto stage of disease. Am J Med 1974; 56:297-306.

6 Affeldt JE, Whittenberger JL, Mead J, FerrisBG. Pulmonary function in convalescent polio-myelitic patients. II. The pressure-volume rela-tions of the thorax and lungs of chronic respira-tory patients. N Engl J Med 1952; 247:43-7.

7 Ferris BG, Whittenberger JL, Affeldt JE. Pul-monary function in convalescent poliomyeliticpatients. I. Pulmonary subdivisions and maximumbreathing capacity. N Engl J Med 1952; 246:919-23.

8 Kreitzer SM, Saunders NA, Tyler HR, IngramRH Jr. Respiratory muscle function in amyo-trophic lateral sclerosis. Am Rev Respir Dis 1978;117:437-47.

9 Kilburn KH, Eagan JT, Sieker HO, Heyman A.Cardiopulmonary insufficiency in myotonic andprogressive muscular dystrophy. N Engl J Med1959; 261:1089-96.

10 Braun NMT, Rochester DF. Muscular weaknessand respiratory failure. Am Rev Respir Dis 1979;119:123-5.

11 Saunders NA, Rigg JRA, Pengelly LD, CampbellEJM. Effect of curare on maximum static PVrelationships of the respiratory system. J ApplPhysiol 1978; 44:589-95.

12 De Troyer A, Bastenier-Geens J. Effects of neuro-muscular blockade on respiratory mechanics inconscious man. J Appl Physiol 1979; 47:1162-8.

13 De Troyer A, Yernault JC, Englert M, Baran D,Paiva M. Evolution of intrathoracic airwaymechanics during lung growth. J A ppl Physiol1978; 44:521-7.

14 Amrein R, Keller R, Joos H. Herzog H. Valeurstheoriques nouvelles de l'exploration de lafonction ventilatoire du poumon. Bull Physio-pathol Respir 1970; 6:317-49.

15 De Troyer A, Yemault JC. Inspiratory muscleforce in normal subjects and patients with inter-stitial lung disease. Thorax 1980; 35:92-100.

16 Gibson GJ, Pride NB. Lung mechanics in dia-phragmatic paralysis. Am Rev Respir Dis 1979;119:119-20.

17 Stubbs SE, Hyatt RE. Effect of increased lungrecoil pressure on maximal expiratory flow innormal subiects. J Appl Physiol 1972; 32:325-31.

18 Sybrecht GW, Garret L, Anthonisen NP. Effectof chest strapping on regional lung function.J Appl Physiol 1975; 39:707-13.

19 Gibson GJ, Pride NB. Pulmonary mechanics in

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21 Leith DE, Mead J. Mechanisms determiningresidual volume of the lungs in normal subjects.J Appl Physiol 1967; 23:221-7.

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