effects position, hyperinflation, blood on respiratoryeffects ofbodyposition, hyperinflation,...

Thorax 1994;49:453-458

Effects of body position, hyperinflation, andblood gas tensions on maximal respiratorypressures in patients with chronic obstructivepulmonary disease

Y F Heijdra, P N R Dekhuijzen, C L A van Herwaarden, H T M Folgering

Department ofPulmonary Diseases,University ofNijmegen, MedicalCentre Dekkerswald,PO Box 9001, 6560 GBGroesbeek,The NetherlandsY F HeijdraP N R DekhuijzenC L A van HerwaardenH T M Folgering

Reprint requests to:Dr Y F Heijdra.

Received 22 March 1993Returned to authors13 August 1993Revised version received20 January 1994Accepted for publication24 January 1994

AbstractBackground - Inspiratory musclestrength in patients with chronic ob-structive pulmonary disease (COPD) can

be affected by mechanical factors whichinfluence the length of the diaphragm,and by non-mechanical factors. The aimof the present study was to evaluatefirstly the effects of body position on res-

piratory pressures and, secondly, to de-termine the relative contribution of age,

body mass index (BMI), lung volumes,and arterial blood gas tensions to respir-atory muscle strength.Methods - Thirty male patients with stableCOPD (mean FEV1 40-4% predicted) parti-

cipated in the study. Maximal inspiratoryand expiratory mouth pressures (Pimax,PEmax) and maximal inspiratory trans-diaphragmatic pressures (PDI) in thesitting and supine position, lung function,and arterial blood gas tensions were

measured.Results - Mean (SD) PImax in the sittingposition was higher than in the supineposition (7-1 (2-3) kPa v 6-4 (2 2) kParespectively). In contrast, PDI in the sit-ting position was lower than in the supineposition (10-0 (3 5) kPa v 108 (3 7) kParespectively). PEmax was higher in thesitting position (9-3 (3 0) kPa) than in thesupine position (8-7 (2 8) kPa). Significantcorrelations were found between inspir-atory muscle strength on the one hand,and lung function parameters, 13MI, andarterial blood gas tensions on the other.Conclusions - Inspiratory musclestrength in patients with COPD isinfluenced by mechanical factors (bodyposition, lung volumes) and non-

mechanical factors (BMI, FEV1, andblood gases). Pimax and PEmax are

lower in the supine position while, incontrast to healthy subjects, PDI is higherin the supine position than in the sittingposition.

(Thorax 1994;49:453-458)

Maximal inspiratory pressures (Pimax) inpatients with chronic obstructive pulmonarydisease (COPD) are frequently reported to belower than in normal adults.'" In some stud-ies, however, taking hyperinflation into ac-

count, Pimax was similar or even increased in

comparison with normal subjects.7-'0 Pressuregeneration by the diaphragm is influenced bythe length of the diaphragm." 12 Theoreticallyit is possible to influence the length of thediaphragm in patients with COPD by chang-ing position from sitting to supine. Theflattened diaphragm will then be displacedupwards by the abdominal contents, and willachieve a more advantageous position on thelength-tension curve. Higher transdiaphrag-matic pressures (PDI) would therefore beexpected in the supine position. This would bein contrast to healthy subjects in whom PDI islower in the supine position.13

Besides mechanical factors, non-mechanicalfactors such as age,' height,3, weight,3'14 sus-tained overload,'5 hypoxaemia,'6 and hypercap-nia,'7 may also influence respiratory pressures.In most studies the influences of these factorshave been analysed separately. The purpose ofthe present study was, firstly, to evaluate theeffects of body position on respiratory pressuresand, secondly, to determine the relativecontribution ofmechanical and non-mechanicalfactors to respiratory muscle strength in stablepatients with COPD.

MethodsSTUDY DESIGNRespiratory muscle strength measurements,lung function tests, and blood gas analyseswere performed in 30 patients with COPD.Informed consent was obtained from all sub-jects. The study was approved by the hospitalethical committee.

PATIENTSThirty male patients with COPD, accordingto the criteria of the American ThoracicSociety,'8 participated in the study. Age, bodymeasures, and lung function data are shown intable 1. The patients were in a stable con-dition, defined as no change in FEV, duringthe preceding three months. Patients withother pulmonary diseases, a previous thoraco-tomy, diabetes mellitus, and neuromusculardisorders were excluded.

MEASUREMENTSPressure measurementsMaximal inspiratory and expiratory mouthpressures (Pimax, PEmax) were measured witha device based on that used by Black and

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Heijdra, Dekhuijzen, van Herwaarden, Folgering

Table 1 Patient characteristics, lung function data andblood gas values (n = 30)

Mean (SD)

Age (years) 60 7 (6 5)Height (cm) 174-8 (6 9)Weight (kg) 74 0 (10 8)BMI (kg/m2) 24 2 (2 8)FEV, (%pred) 40 4 (19 0)FEVy (1) 1 3 (0 7)FIV (1) 3 1 (0 8)FRd (%pred) 132 4 (29 3)RV (%pred) 146 7 (37 1)TLC (%pred) 107 7 (16 1)RV %TLC (%) 47.4 (9 1)FRC %TLC (%) 63 3 (8 4)Kco (%pred) 57 5 (291)Sao2 (o) 94-0 (2 3)Pao2 (kPa) 9 4 (1 1)Paco2 (kPa) 5 7 (0 7)

BMI = body mass index; FEV, =forced expiratory volume inone second; FIV, =forced inspiratory volume in one second;FRC = functional residual capacity; RV = residual volume;TLC = total lung capacity; Kco = diffusion capacity;Sao2 = arterial oxygen saturation; Pao2 = partial arterial oxygenpressure; Paco2 = partial arterial carbon dioxide tension.

Hyatt. i A metal tube connected a plasticflanged mouthpiece to a wet spirometer (Pul-motest Godart, Bilthoven, The Netherlands).An occluding balloon within the tube could beinflated by the subjects themselves by squeez-

ing a second external balloon. A small leak(internal diameter 1 1 mm, length 40 mm) inthe mouthpiece prevented buccal musclesfrom producing significant pressures and clos-ing the glottis. The pressure inside the mouth-piece was measured with a pressure transducer(Validyne DP103-32, Northridge, California,USA).

Transdiaphragmatic pressure (PDI) was

measured with a flexible double lumencatheter (internal diameter of each lumen1. 1 mm)'920 inserted through the nose. Thecatheter was positioned with the distal openingof the gastric lumen 58 cm from the nares andthe proximal opening of the oesophageallumen 38 cm from the nares. The catheter wasperfused with water at a constant flow of 99 ml/hour. The pressure generated by the waterflow was 12 kPa. The proximal ends of thedouble lumen catheter were connected withtwo pressure transducers (Validyne DP15-32,range ± 40 kPa). The zero reference point was

arbitrarily set as the pressure measured atfunctional residual capacity (FRC). PDI was

calculated by subtracting oesophageal pressure(POES) from gastric pressure (PGA). PImax,PEmax, POES, and PGA were displayed on a

chart recorder (Kipp en Zonen BD 101, Delft,The Netherlands). Pressure measurementswere performed in the sitting and supine posi-tion, with the subjects wearing a noseclip. Ineither position the subjects maintained an

identical posture and had appropriate supportfor their arms throughout the experiment.

Before each static inspiratory effort subjectsinhaled to total lung capacity (TLC) and thenexhaled to residual volume (RV), with visualfeedback on the spirometer. They then closedthe tube by inflating the balloon and per-

formed a maximal inspiratory effort. Maximalinspiratory efforts were maintained for twoseconds separated by at least 60 secondsbetween efforts.PEmax was measured after inhaling to TLC,

followed by inflating the balloon and perform-

ing a maximal static expiratory effort. Theinspiratory manoeuvre at RV and the expira-tory manoeuvre at TLC were repeated untilthree reproducible measurements had beenmade with a maximal variability of 10%."2 Thehighest value was used for analysis. For thesake of convenience, Pimax and POES wereexpressed as positive values. At each measure-ment calibrations were made with a watermanometer.

Predicted values for respiratory musclestrength were calculated according to Wilsonet a13 because these authors also used a flangedmouthpiece.

Lung functionSpirometric tests were performed with a wetspirometer and by a closed circuit heliumdilution method (Pulmonet III, Sensormedics,Bilthoven, The Netherlands). Diffusion capa-city (Kco) was measured by the single breathcarbon monoxide method (Sensormedics2450). Predicted spirometric values were de-rived from ERS standards.22

Blood gas valuesArterial blood samples were taken in thesemirecumbent position at 09.00 hours afterthe patients had been lying down for at least 15minutes. The samples were measured with aCorning Ph 127 blood gas analyser.

DATA ANALYSISData are presented as mean (SD). To analysethe data statistically we performed Spearmancorrelation tests and Wilcoxon signed ranktests. Stepwise multiple regression analysiswas used to assess the relative contributions ofage, body mass index (BMI), FRC %TLC,FEV, (%pred), Sao2, and Paco2 to Pimax, PDI,and PEmax. For all analyses the SAS package(SAS Institute Inc, Cary, North Carolina,USA) was used. p values <005 were con-sidered significant.

ResultsPATIENTSThirty male patients with COPD were in-cluded in the study. There was a wide varia-tion of airway obstruction (FEV, 18-87% pre-dicted) and hyperinflation was modest (meanFRC: 132 (29)% predicted). Four patientswere hypoxaemic (Pao2 < 8 kPa) and onepatient was hypercapnic (Paco2 > 6-5 kPa).

RESPIRATORY MUSCLE FORCE AND EFFECT OFBODY POSITIONSitting Pimax and PEmax were lower thanpredicted, PTmax being 891 (28? 1)% pre-dicted (7-1 (2-3) kPa) and PEmax 74-1 (23-4)%predicted (9-3 (3-0) kPa). The low value forPEmax could be caused by the closing of theglottis when performing a PEmax manoeuvre,so PEmax was also measured at the oesophageallevel. At this level the value was significantly

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14- p<005

12- p < 0O0001

10

6-

4-

.2-

0Pimax Pimax PDI PDI PEmax PEmax

sit sup sit sup sit sup

Figure 1 Maximal inspiratory mouth pressure(Pimax), maximal inspiratory transdiaphragmaticpressure (PDI) and maximal expiratory mouth pressure(PEmax) in sitting (sit) and supine (sup) positions.

higher than at the mouth (10 8 (2 9) kPa v9 3(3 0)kPa (p<001)). The lung volume(expressed as percentage of the predictedTLC) at which maximal inspiratory pressuresin the sitting position were measured was 60 8(14 1)%. The supine maximal inspiratorypressures were measured at a significantlyhigher lung volume (644 (15 3)% of TLCpredicted (p < 0001)). This happened despitepatients being asked to expire to RV in bothpositions. In the supine position the same endexpiratory level was not reached by 24 of the30 patients in comparison with the sittingposition.

PDI could not be measured in three patientsbecause of their inability to swallow the doublelumen catheter. The mean value in the remain-ing 27 patients was 10 0 (3 5) kPa.When changing position from sitting

to supine Pimax decreased by 07 (06) kPa(p<0 0001) and PEmax decreased by06(1 2)kPa (p<0005). In contrast, PDIincreased by 0 9 (1 5) kPa (p < 0 01) (fig 1). Todetermine whether the diaphragm is a betterpressure generator in the supine position thetwo components of PDI (PGA and POES) werestudied. They showed different responses tothe change in body position. PGA increasedfrom 1 8 (1 4) kPa in the sitting positionto 3 0(2 1)kPa in the supine position(p < 0 00001). PoEs decreased from 8 1 (2 8) kPain the sitting position to 7 8 (2 6) kPa in thesupine position, but this change did not reachsignificance. The changes in PGA and POES inrelation to PDI are shown in figs 2 and 3. Themean differences between the sitting andsupine ratios PGA/PDI and POES/PDI were0 11 (0 13) (p<0 0001) and -0 11 (0 13)(p<0-0001), respectively. In the sitting posi-tion the ratio Pimax/POES was 0 07 (0- 11)(p<0-01) higher than in the supine position(fig 4).

FACTORS INFLUENCING RESPIRATORY MUSCLEFORCESpearman correlation coefficients betweenmaximal respiratory pressures on the one handand age, BMI, lung function parameters, andblood gas values on the other are shown in

060110-60 ~~p< 0.00010*50-

0-40

0-30-<020-

0-10-0000-

-0 10

-0 20PGA/PDI PGA/PDIsitting supine

Figure 2 PGA /PDI in sitting and supine positions(> and < indicate mean values).

table 2. The highest correlation coefficientswere found between maximal inspiratorypressures and FRC %TLC (%) and arterialoxygen saturation (tension). PEmax was notcorrelated with any of these parameters, andwas only significantly correlated with Pimaxand PDI; both correlation coefficients were 0 60(p<0O00l).

POES/PDI POES/PDIsitting supine

Figure 3 POEs/PDI in sitting and supine positions(> and < indicate mean values).

1*10

Pimax/PoEs Pimax/PoEssitting supine

Figure 4 PimaxlPOES in sitting and supine positions( > and < indicate mean values).

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Table 2 Spearman correlation coefficients between maximal inspiratory (Pimax) andexpiratory (PEmax) pressures and maximal inspiratory transdiaphragmatic pressure(PDI) and age, BMI, lung function parameters, and blood gas values

Pimax Pimax PDI PEmax PEmax(kPa) (0%pred) (kPa) (kPa) (0%pred}

Age (years) - 0-32 0 05 - 0 36 - 0 35 -0-21BMI (kg/M2) 0 30 0.39* 0-34 006 006FRC %TLC(%) -059*** -0 61*** -0 54** - 0 09 - 0 05RV %TLC (%) -048** -044* -045* -005 000FEV, (%pred) 049** 060*** 0.43* 008 008FIVl, (1) 048** 0 51** 0.48* 025 023Sao2 (%) 0 62*** 0.55** 0 64*** 0 27 0.19Pao2(kPa) 0 58*** 0 51** 0 67*** 0 30 0 24Paco2 (kPa) 0.41* 0 27 0 30 -0-25 -0 15

For definition of abbreviations see footnote to table 1.* p< 0-05; ** p< 001; *** p<0001.

Table 3 Stepwise multiple regression analyses, r2, andp values to predict maximal inspiratory (Pimax),expiratory (PEmax), and transdiaphragmatic (PDI)pressures

Step Variable r2 p

Pimax (kPa) 1 FRC %TLC 0 34 00012 Sao2 043 0004

Pimax (%pred) 1 FRC %TLC 0 30 0002PDI (kPa) 1 Sao2 0 33 0 002PEmax 1 Age 0 14 0004PEmax (%pred) - - -

For definition of abbreviations see footnote to table 1.

Stepwise multiple regression analysisshowed that Pimax (kPa) could be predictedfrom a combination of Sao2 and FRC %TLC:Pimax (kPa) = -17 8-0.12 Sao2 + 0 34 FRC

%TLC (r2= 0-44).PDI (kPa) could be predicted only by Sao2:

PDI= -70 2+0 85 Sao2 (r2=0 33).PEmax (kPa) was predicted by age:

PEmax = 20-1 -0-18 age (r2 =0-14).Table 3 shows the complete data with values

of p and r2.

DiscussionThe purpose of this study was to evaluate theeffects of body position on respiratory pres-

sures and to determine the relative contribu-tion of mechanical and non-mechanical factorsto respiratory muscle strength in patients withCOPD. Firstly, we found that body positioninfluences respiratory pressures. Pimax andPEmax were higher in the sitting position thanin the supine position, while PDI, in contrast tohealthy subjects, was higher in the supineposition than in the sitting position (fig 1).Secondly, mechanical and non-mechanicalfactors indeed contributed to respiratorymuscle strength. This was indicated by signi-ficant correlations between inspiratory musclestrength and static lung volumes (mechanicalfactors), and between inspiratory musclestrength and BMI, FEV,, Sao2, and Paco2(non-mechanical factors).The diaphragm appeared to be a better

pressure generator in the supine position inthese patients with COPD. In this positionhigher PDI values were caused by an increasein the ratio PGA/PDI combined with a decreasein the ratio POES/PDI (figs 2 and 3). Thedifference between the ratio Pimax/PoEs in thesitting and supine positions was - 0 07 (fig 4),

since Pimax decreased more than POES in thesupine position. The reason why POES did notdecrease significantly in contrast to Pimaxmight be the elastic recoil pressure of the lungswhich influences Pimax but not POES. Thesupine inspiratory pressures were measured at64-4 (15-3)% of TLC predicted, while thesitting inspiratory pressures were measured at60-8 (14-1)% of TLC predicted, although thepatients were asked to expire as far as possiblebefore they performed a maximal inspiratorymanoeuvre in both positions. At higher lungvolumes the elastic recoil pressure of the lungsincreases, and thus the difference between in-spiratory mouth pressures and inspiratoryoesophageal pressures will increase.6 This isconfirmed by the findings in the present study:the mean difference between Pimax and POESin the sitting position was 10 kPa, while themean difference in the supine position was1 4 kPa.In healthy subjects both Pimax and PDI

were lower in the supine position.'3 The effectof postural changes on maximal respiratorypressures in patients with COPD has not pre-viously been described. Swings in PDI duringtidal breathing in the supine position weresignificantly higher than in the sitting posi-tion.23 This is in line with the findings in thepresent study. An explanation might be that inthe supine position the abdominal contentsdisplace the flattened diaphragm upwardsleading to a more favourable position on thelength-tension curve. However, the increasedforce generated by the diaphragm apparentlycannot compensate for the decreased phasicand tonic activity of the scalene, sternocleido-mastoid, and parasternal-intercostal musclesand the decreased compliance of the rib cage inthe supine position.2425 This may explain whyin our patients Pimax in the supine positionwas significantly lower than Pimax in the sit-ting position.Pimax values were lower than predicted (89 1

(28-1)%), but these pressures were measured at60 8 (14 1)% predicted TLC. Rochester26 sug-gested that the observed values of Pimax inpatients with COPD should be compared withthe values that normal subjects would achieve atsimilar lung volumes. For normal subjects weexpected 80-90% of the predicted Pimax at60% TLC.627 This means that Pimax, aftercorrection for lung volume, was not lower thanin normal subjects as was suggested in previousstudies.7"'0 Also, in a postmortem studydiaphragm dimensions of patients with andwithout COPD did not differ significantly.28Pimax values in our patients (7-1 (2 3) kPa)were within the same range as Pimax values inpatients with COPD described in previousstudies (7-1 (2-4) kPa,'0 5 6 (2 5) kPa,4 60(1 9) kPa,5 and 8-0 (2 7) kPa29). These differentresults may be explained by differences inpatient characteristics. The relation betweenPimax and FEV, (% predicted) in these studiesseems linear (fig 5).For PDI no predicted values are available.

Mean PDI in normal subjects varied from9 1 kPa to 15 0 kPa and in patients with COPDfrom 3-7 kPa to 9 8 kPa.2' We measured a mean

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10 -

0-

x

0-

8-

6-

4-

2-

r2= 0-89p < 0.05

II

0 10 20 30 40FEV, (% pred)

Figure 5 Correlation between Pimax and FEV in

different studies. M, ref 4; A, ref 7; *, ref 5; *,

ref 29; *, present study.

PDI of 10 0 (3 5) kPa. The observed differencebetween healthy subjects and patients withCOPD may be explained by a differentposition on the length-tension curve due tochanges in lung volumes.' 20- 2 This may

explain the correlation between maximalinspiratory pressures and FRC and RV aspercentages of TLC in the present study.

In previous studies the variability of PEmaxin patients with COPD was larger than thatof Pimax (20 6 (4 1) kPa,'0 13 7 (4 8) kPa,413 8 (6 5) kPa,5 and 10-0 kPa6), whereas in our

study PEmax was 9 3 (3 0) kPa. PEmax in thepresent study was rather low in comparisonwith the other studies. An explanation mightbe the closing of the glottis by some patientswhen performing a PEmax manoeuvre becausePEmax measured in the oesophagus was signi-ficantly higher than PEmax measured in themouth (10 8 (2 9) kPa v 9-3 (3 0) kPa, respect-ively (p<0 01)). Decramer et a16 suggestedthat minor variations in the technique contrib-uted to high variations in PEmax values.Another explanation for the low PEmax valuesin the present study could be generalisedmuscle weakness. This was probably not thecase, since Pimax (% predicted) was less de-creased than PEmax (% predicted). Pimax isinfluenced by hyperinflation and generalisedmuscle weakness, while PEmax is influencedby generalised muscle weakness alone.4 More-over, malnutrition may be responsible forlower PEmax values,33 but this was unlikelysince BMI was within the normal range. Inview of these considerations it is most likelythat the low PEmax values in the present studywere due to the technique used.

Besides mechanical factors (body position,static lung volumes), non-mechanical factorsmay influence respiratory muscle strength.Significant correlation coefficients were foundbetween inspiratory pressures and BMI,FEV,, Sao2, and Paco2 (table 2).The effect of BMI on inspiratory pressures

is known. Undernourished patients withCOPD have lower inspiratory muscle strengththan well nourished patients.33The relation between FEVI and Pimax

might suggest that the impaired muscle func-tion results in lower FEVI values. It is alsopossible, however, that a decrease in FEV,

contributes to the impairment of inspiratorymuscle function because of a sustained over-load.'5 Indeed, the diameters of the type I andtype II fibres of the diaphragm in normalsubjects were significantly higher than inpatients with COPD.34 Moreover, there was alinear relation between FEV, and diaphrag-matic fibre diameters in these patients.

Little is known about the consequences ofchronic hypoxaemia on respiratory muscles, asis present in patients with chronic respiratoryfailure, or about the influence of respiratorymuscle dysfunction on Pao2. It has been sug-gested that impairment of the respiratorymuscles causes microatelectasis resulting in adecrease of Pao2.35 36 The consequences ofacute hypoxaemia on respiratory muscles innormal persons have been investigated. Onestudy showed that the respiratory musclesfailed more quickly during low oxygen breath-ing,'6 but this was not confirmed in a laterstudy.37A negative correlation between Pimax and

Paco, has been found in previous studies.4 1738Rochester et al4 showed a correlation of - 066in 18 patients with COPD with Pimax< 5-5 kPa. Braun et al38 studied the correlationbetween Pimax and Paco2 in patients withproximal myopathies and found a correlationcoefficient of - 059 when respiratory musclestrength was less than 50V/o predicted. Dia-phragmatic contractility was reduced whenend tidal Fco2 was raised above 7 5%°.17

Multiple regression analysis was used todetermine the relative contribution ofinfluencing factors such as age, BMI, bloodgas tensions, and lung function to respiratorymuscle strength (table 3). Only low predictivevalues were obtained. This suggests that otherindividual features such as elastic recoil pres-sure of the respiratory system and physicalfitness also influence maximal respiratory pres-sures.

In conclusion, this study shows that respira-tory pressures in patients with COPD areinfluenced by body position. Pimax andPEmax are lower in the supine position while,in contrast to healthy subjects, PDI is higher inthe supine position than in the sitting position.In addition, significant correlations have beenfound between maximal respiratory pressuresand mechanical and non-mechanical factors,although the value of these factors in predict-ing maximal respiratory pressures is low.The authors thank Th M de Boo and W J G M Lemmens ofthe Medical Statistical Department for their statistical advice.The study was supported by a grant of the Dutch AsthmaFoundation (no. 90-27).

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