Effects of posture on respiratory mechanics in obesity

J. C. Yap, R. A. Watson, S. Gilbey and N. B. Pride

J Appl Physiol 79:1199-1205, 1995. ; You might find this additional info useful... This article has been cited by 20 other HighWire-hosted articles: http://jap.physiology.org/content/79/4/1199#cited-by Updated information and services including high resolution figures, can be found at: http://jap.physiology.org/content/79/4/1199.full Additional material and information about Journal of Applied Physiology can be found at: http://www.the-aps.org/publications/jappl This information is current as of October 16, 2012.
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Journal of Applied Physiology publishes original papers that deal with diverse area of research in applied physiology, especially those papers emphasizing adaptive and integrative mechanisms. It is published 12 times a year (monthly) by the American Physiological Society, 9650 Rockville Pike, Bethesda MD 20814-3991. Copyright 1995 the American Physiological Society. ISSN: 8750-7587, ESSN: 1522-1601. Visit our website at http://www.the-aps.org/.

Effects of posture

on respiratory

mechanics

in obesity
Hospital,

J. C. H. YAP, R. A. WATSON, S. GILBEY, AND N. B. PRIDE Department of Medicine, Royal Postgraduate Medical School, Hammer-smith London W12 ONN, United Kingdom
Yap, J. C. H., R. A. Watson, S. Gilbey, and N. B. Pride. Effects of posture on respiratory mechanics in obesity. J. AppZ. PhysioZ. 79(4): 1199- 1205, 1995.-Increased abdominal mass in obesity should enhance normal gravitational effects on supine respiratory mechanics. We have examined respiratory impedance (forced oscillation over 4-26 Hz applied at the mouth during tidal breathing), maximum inspiratory and expiratory mouth pressures (MIP and MEP), and maximum effort flow-volume curves seated and supine in seven obese subjects (0) (mean age 51 yr, body mass index 43.6 kg/m2) and seven control subjects (C) (mean age 50 yr, body mass index 21.8 kg/m2). Seated mean total lung capacity was smaller in 0 than in C (82 vs. 100% of predicted); ratio of functional residual capacity (FRC) to total lung capacity averaged 43% in 0 and 61% in C (P < 0.01). Total respiratory resistance (Rrs) at 6 Hz seated was higher in 0 (4.6 cmH20 1-l s) than in C (2.2 cmH20 1-l s; P < 0.001); total respiratory reactance (Xrs) at 6 Hz was lower in 0 than in C. In C, on changing to the supine posture, mean Rrs at 6 Hz rose to 2.9 cmH20 1-l s, FRC fell by 0.68 liter, and Xrs at 6 Hz showed a small fall. In 0, despite no further fall in FRC, supine Rrs at 6 Hz increased to 7.3 cmH20 1-l s, and marked frequency dependency of Rrs and falls in Xrs developed. Seated, MIP and MEP in C and 0 were similar; supine there were small falls in MEP and maximum expiratory flow in 0. The site and mechanism of the increase in supine Rrs and reduction in supine Xrs and the mechanism maintaining supine FRC in obesity all need further investigation.
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in obese and control subjects. In these subjects we have also studied other changes in respiratory mechanics by measuring subdivisions of static lung volumes, maximum expiratory flow-volume curves, and maximum effort inspiratory and expiratory mouth pressures. The results have been compared with the effects of mass loading of the abdomen in the supine posture in normal subjects.
MATERIALS AND METHODS

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Subjects For the main study seven obese subjects without pulmonary disease or spirometric evidence of airway obstruction and with a mean body mass index (BMI) of 43.6 kg/m2 were compared with seven age-matched control subjects with a mean BMI of 21.8 kg/m2 (Table 1). Five of the obese subjects had never smoked; the remaining two were ex-smokers who had smoked for 9 and 1 pack-yr, respectively. One obese man had mild obstructive sleep apnea. All had a normal chest radiograph. In an additional five normal subjects, the effects of mass loading of the abdomen on subdivisions of lung volume and on oscillation mechanics were studied in the supine position. Written consent was obtained from all subjects, and the protocol was approved by the Research Ethics Committee of this medical school. Measurements Forced osciZZation technique. The technique and equipment as described by Landser et al. (14) were used. The subjects supported the cheeks and floor of the mouth with the palms of their hands to minimize dissipation of the applied flow in the upper airway. The head and neck were kept in a neutral to slightly extended position. Oscillation mechanics were measured during tidal breathing via a large-bore mouthpiece and with a noseclip in place. The oscillation apparatus consisted of a loudspeaker that was attached to a tube leading to a screen pneumotachograph. A complex signal of sinusoidal sound-wave oscillation containing all harmonics of 2 Hz up to 26 Hz was applied by the loudspeaker. The signal was presented as preprogrammed pseudorandom noise, the sequence being repeated every 0.5 s for a 16-s period. During oscillation, mouth pressure and airflow were recorded by two identical differential transducers (Validyne MP45) and fed into a Fourier analyzer, ensemble averaged over the measurement period of 16 s, and calculated to give the values of impedance at ~-HZ intervals from 2 Hz up to 26 Hz. The derived values were the mean of both inspiratory and expiratory impedance over the several breaths of the 16-s period. This impedance was further analyzed as the in-phase component [resistance (Rrs)] and the out-of-phase component [reactance (Xrs)] of pressure and flow. The in-phase component of the signal, Rrs, is an index of airflow resistance analogous to resistance derived by other methods such as body plethysmography. The oscillatory frequency at which reactance is zero is resonant frequency (f,). The reliability of the derived values was indicated by a coherence function for measurements at each frequency. Results were only accepted when coherence was >0.95; in some subPhysiological Society 1199

lung volumes;

resistance;

reactance

IN NORMAL

SUBJECTS there is a reduction in functional residual capacity (FRC) and an increase in airway resistance on adopting the supine posture (16); most of the reduction is due to the gravitational effects of the abdominal contents, resulting in the relaxed diaphragm taking up a more expiratory position. In obese subjects the mass load on the chest wall in the supine posture is increased. Because the obese subject already has a reduced FRC and small expiratory reserve volume (ERV) in erect postures (4, 11, 29, 30, 33), any further fall might lead to considerable airway closure and arterial hypoxemia when awake, whereas such changes would augment any tendency to develop severe hypoxemia in obese subjects with obstructive sleep apnea. A few studies have been made of postural changes in subdivisions of lung volume (4, 30) and pulmonary and chest wall compliance (19) in obese subjects, but a major problem in studying the effects of the supine posture on respiratory mechanics in obesity is the difficulty in obtaining reliable esophageal pressure measurements (17). Such measurements are least reliable at small lung volumes in the supine posture and when there is a considerable mass load on the esophagus. In the present study we have used the forced oscillation technique applied at the mouth to estimate airflow resistance and reactance in sitting and supine postures
0161-7567/95 $3.00 Copyright 0

1995 the American

1200
TABLE

POSTURE

AND

RESPIRATORY

MECHANICS

IN

OBESITY

1. Characteristics

of subjects
Obese Control

Male/Female Age, Yr Ht, m w kg Body mass index, kg/m2 Pulmonary function seated TLC, %pred FE&, %pred FEVJFVC, % Raw, cmH,O 1-l s
l l

314 51.1+4.8 1.66t0.03 119.9z8.4 43.622.5 82.122.7 88.424.2 89.32 1.0 4.92 1.0

215 50.125.0 1.7320.03 65.923.9 21.850.7 99.623.7 113.827.1 81.623.6 2.020.4

asked to indicate how breathless they felt on a line that extended from 0 to 10. They were not allowed to refer to previous scoring during each assesssment of VAS when they changed position. Body plethysmography. At the start of the study airway resistance (Raw) (9) and thoracic gas volume and TLC (8) were measured by using a constant-volume body plethysmograph* Mass-loading of anterior chest waZZ. Bags containing lead shot to a total of 25 kg were placed across the lower rib cage and epigastrium of the supine subjects. Measurements of subdivisions of lung volumes and oscillation mechanics were made after the subjects had been breathing quietly for -2 min with the load applied. Protocol The subjects were first familiarized with all the techniques of measurements. TLC and Raw were then measured in the body plethysmograph. Measurements of oscillation mechanics, maximum inspiratory and expiratory flow-volume curves, MIP and MEP, and VAS for dyspnea were recorded. Sao, was monitored continuously. The subject then lay down, and after 5 min a further set of measurements of oscillation mechanics, flow-volume curves, MIP and MEP, and VAS was made. The subject then returned to the sitting posture, and after 5 min a third set of these measurements were obtained. For each of the three sets of measurements, the mean of three successive reproducible measurements were made. Comparisons with predicted values were made by using standard European reference values (22). Statistical Analysis by using paired and unpaired Downloaded from http://jap.physiology.org/ by guest on October 16, 2012

Values are mean lung capacity; FE&, vital capacity; Raw,

t SE for 7 subjects in each group. TLC, total forced expiratory volume in 1 s; FVC, forced airway resistance; %pred, % predicted.

jects, coherence at 2 Hz fell below this value, so we report only results at 4-26 Hz. Three consecutive sets of measurements over 16 s were made while the subject breathed quietly and continuously via the mouthpiece. For measurements in the supine posture, the oscillation apparatus was supported by a gantry over the subject who lay supine on a couch. Care was taken to ensure that a similar slightly extended position of the head and neck was sustained in this position. The two differential pressure transducers were positioned in the perpendicular axis so that their orientation was not altered between sitting and supine postures. We also monitored breathing pattern and changes in lung volume during oscillation measurements by integrating the mouth flow signal to obtain tidal volume. This was displayed on a strip-chart recorder. At the end of each oscillation measurement, a full inspiration was made to relate tidal volume to total lung capacity (TLC), previously determined by constant-volume body plethysmography in the sitting position, and to calculate absolute midtidal lung volume (MTLV) and FRC. In estimating the effects of posture on subdivisions of lung volume, it was assumed TLC was unchanged in both the obese and control groups. Published evidence suggests that although there are small reductions in TLC in the supine posture, these are similar in obese and normal subjects (see DISCUSSION). To allow for postural changes in MTLV and FRC, measurements of Rrs were expressed as specific total Rrs (SRrs) calculated as (Rrs l MTLV). Maximum effort flow-volume curves and spirometry. Forced expiratory volume in 1 s (FE&), forced vital capacity (FVC), and maximum effort expiratory and inspiratory flowvolume curves were recorded by using a lo-liter dry rollingseal spirometer (model 842, Ohio Instruments). The flowvolume curves were displayed on an X-Y storage oscilloscope (model 613, Tektronix, Beaverton, OR), and permanent copies were obtained on a hard-copy thermal Tektronix 4610 printer for later analysis of peak expiratory flow (PEF) and maximum expiratory flow rate at 50 and 25% of the remaining vital capacity (VC) of the first sitting position. To compare sitting with supine values we assumed TLC had fallen by 100 ml in both control and obese subjects in the supine position. Maximum respiratory muscle pressures. Mouth pressures during maximum efforts against a closed airway were recorded with a Validyne pressure transducer. Maximum expiratory pressure (MEP) was recorded during efforts at TLC, and maximum inspiratory pressure (MIP) at was recorded FRC; the best pressures sustained over 1 s were recorded. Oxygen saturation (Sao,). Sao, was measured with an Ohmeda Biox 3740 pulse oximeter. VisuaZ analog scale (VAS) for dyspnea. The subjects were

Mean values were compared t-tests as appropriate.

RESULTS

There were no systematic differences in the two sets of sitting measurements made before and after lying supine; the results presented and used for statistical analysis are those seated before adoption of the supine position. Static Lung Volumes Even after correction for the slightly smaller height in the obese subjects, values of TLC and its subdivisions in the sitting position were smaller in the obese subjects than in the control subjects. In addition to these absolute changes, FRCITLC was considerably smaller in the obese than in the control subjects (P < 0.001; Fig. 1). On adoption of the supine posture, mean FRC increasd by 0.04 liter in the obese subjects but fell by 0.65 liter in the control subjects. Oscillation Mechanics Results at 6 Hz (Table 2). SITTING POSITION. Mean Rrs in the obesesubjects was more than twice the mean value in the control subjects (P < 0.001). When values were corrected for differences in volume at which the measurement was made (by using SRrs), these differences were

POSTURE

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MECHANICS
A g-

IN

OBESITY

1201

TLC

z7. I - . .
Onl I E

8765-

A M

n=7

sitting supine

4-

FRC RV sitting supine Obese sitting supine Control

: 2

32l-

o!,,,,,,,,,,.,.,
0
4 8 12 16 20 Frequency (Hz)

24

28

FIG. 1. Mean values for subdivisions of total lung capacity (TLC) in obese and control subjects in sitting and supine postures. FRC, functional residual capacity; RV, residual volume; ERV, expiratory reserve volume. TLC is assumed not to change significantly on adoption of supine posture (see text).

B
zFI. d Icu E -5% 2

9. 81
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not significant. Reactance was considerably lower in the obese than in the normal subjects (P < 0.04).
CHANGES BETWEEN SUPINE AND SITTING POSTURES.

5432loi 0

The absolute and proportional increase in sitting Rrs at 6 Hz was considerably greater in the obese (P < 0.001) than in the control subjects (P < 0.02). Changes in MTLV mirrored those in FRC, showing a small increase in obese subjects (mean +0.03 liter) but a mean fall of 0.61 liter in the control subjects; as a consequence, increases in SRrs were much greater in obese (P < 0.002) th an in control subjects (in whom the small increase did not reach statistical significance). There were decreases in Xrs in both groups in the supine posture, but these were significant (P < 0.002) only in the obese group. Changes in Rrs and Xrs With Oscillation Frequency In control subjects there was little variation of Rrs with frequency in either the sitting or the supine position (Fig. 2). In the obese subjects there was a small decline in Rrs with increasing oscillation frequency between 4 and 16 Hz in the sitting position, which was exaggerated when supine. In control subjects there was 2. Forced oscillation mechanics in sitting and supine positions
TABLE
Obese Control

, 4

, , , , , , , , , , , 8 12 16 20 24 28 Frequency (Hz)

FIG. 2. Total respiratory resistance (Rrs) at different oscillation frequencies in control subjects (A) and obese subjects (B). Results obtained during tidal breathing in sitting and supine positions are compared. All values are means + SE for 7 subjects in each group.

a slight and similar fall in Xrs at all frequencies in the supine posture without change in the slope of the curve (Fig. 3); this resulted in a small rise in mean fR from 7.8 to 10.0 Hz (P = 0.02 for paired t-test). In the obese subjects, Xrs was lower than in control subjects at all frequencies when seated and there were large falls in Xrs in the supine posture with a much steeper Xrsfrequency slope; this resulted in a rise in mean fR from 17.0 to 22.6 Hz (P = 0.03). FVC Maneuvers (Table 3) In the sitting position, FE& and FVC were significantly smaller both in absolute volumes (P < 0.005 and < 0.001, respectively) and as percent predicted, and FEVJFVC was greater [not significant (NS)] in the obese than in the control subjects. All the obese subjects had seated FEVJFVC > 85%. On adoption of the supine posture, there were small reductions (NS) in FVC and FE& in both groups, but falls in peak expiratory flow were larger in the obese subjects (P < 0.01). Maximum Respiratory Pressures (Table 4)

Rrs (6 Hz), cmH20 Sitting Supine SRrs (6 Hz), cmH20 Sitting Supine Xrs (6 Hz), cmH20 Sitting Supine Resonant frequency, Sitting Supine Values respiratory Xrs, total

1-l

s 4.59+0.41 7.3250.63 2.1620.17 2.9350.16 9.2820.97 10.56+0.61

s 11.0351.17 17.745 1.56

1-l

s - 1.2050.34 -3.4850.46

Hz 17.Ok2.68 22.621.46 + SE of 7 subjects in each group. SRrs, specific total respiratory reactance. 7.8kO.42 10.050.79 Rrs, total resistance;

are means resistance; respiratory

MIP and MEP were similar in the two groups seated, but there was a small fall in MEP in obese subjects in the supine position (mean sitting, 99 cmH20; supine, 87 cmH,O; paired t-test, P = 0.09).

1202 A 3
2

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OBESITY

4. Oxygen saturation and maximum effort mouth pressures in sitting and supine positions
TABLE
Obese Control P Value

-a

sitting supine

12 16 20 Frequency (Hz)

24

28

Oxygen saturation, % Sitting Supine Maximum inspiratory pressure, cmH20 Sitting Supine Maximum expiratory pressure, cmH20 Sitting Supine Values cant. are mean

96.3kO.42 94.720.92

97.320.57 97.320.64

0.18 0.04

94217 90218

95510 94217

NS NS

99+15 87~16

93+13 95216 in each group.

NS NS NS, not signifi-

6
F

32lO -I-2-3: -4-5

n=7 -

+ SE of 7 subjects

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T o ; ,o s!! x

the supine posture, but there was a small fall from 96.3 to 94.7% in the obese subjects (paired t-test, sitting vs. supine, P = 0.052). In the supine posture mean Sao2 was lower in the obese than in the control subjects (unpaired t-test, P = 0.04). Mass Loading in Normal Subjects In the five additional normal subjects there was a small fall in VC on adopting the supine posture (mean 5.0-4.7 liters), and ERV fell from a mean of 2.3 liters to 0.9 liter. Changes in oscillation mechanics between sitting and supine positions were similar to those in the main control group, with Rrs rising and Xrs falling at all frequencies in the supine position (Fig. 4). Mean Rrs at 6 Hz was 1.75 cmHzO? s sitting and 2.70 cmHzO 01-l s supine; mean Xrs at 6 Hz was -0.07 cmH20 1-l s sitting and -0.58 cmH20 1-l s supine; and mean fR was 6.1 Hz sitting and 9.7 Hz supine (P < 0.009 for paired t-test in all cases). After the application of the mass load in the supine position, there was no further change in ERV (mean value 1.0 liter) or Rrs at 6 Hz (mean value 2.48 cmHzO 1-l s) but there was a further reduction in XIX, the value at 6 Hz falling from -0.58 to -1.39 cmHsO 1-l s (paired t-test, P = 0.001) and increase in fR from 9.7 to 12.1 Hz (paired t-test, P = 0.007). The changes in Xrs were similar in direction to those noted in supine obese subjects, with a trend to an increase in Xxx-frequency slope, but they were considerably smaller in magnitude.
l l l l l l l l l l

, , , , , , . , I , 9 , 1 28 4 8 12 16 20 24 0 Frequency (Hz)

FIG. 3. Total respiratory reactance (Xrs) at different oscillation frequencies in control subjects (A) and obese subjects (B). Results obtained during tidal breathing in sitting and supine positions are compared. Resonant frequency is frequency at which Xrs is zero, indicated by position at which Xrs frequency curve crosses horizontal dotted line. AI1 values are mean + SE for 7 subjects in each group.

Oxygen Saturation

(Table 4)

In the sitting position mean Sao, was slightly lower in the obese subjects than in the control subjects. In the control subjects there was no change on adopting
TABLE 3. FVC maneuvers in sitting and supine positions
Obese Control

FE&, liters Sitting Supine FVC, liters Sitting Supine FEVJFVC, Sitting Supine PEF, I/s Sitting Supine MEF 50% vc, Sitting Supine MEF 25% vc, Sitting Supine

2.3920.14 2.1750.13 2.6920.17 2.50+0.15 % 89.321.04 86.820.91 8.7220.95 6.9720.68

l/S

3.58t0.18 3.4250.19 4.3120.22 4.11kO.24 81.623.59 81.623.94 8.9OkO.62 8.6420.61 3.8520.42 3.6050.39 1.4350.25 1.19+0.18

DISCUSSION

3.28t0.38 2.7120.39
l/S

1.2050.16 0.8650.15

Values are means + SE of 7 subjects in each group. PEF, peak expiratory flow; MEFSO% vc and MEF25% vc, maximum expiratory flow when 50 and 25% of vital capacity remains to be expired, respectively.

The present results confirm that when normal subjects move from the sitting to the supine position there is a rise in Rrs that can largely be attributed to the fall in MTLV and FRC. In contrast, in obese subjects, who had reduced FRC and ERV when seated, there was no further fall in these volumes when supine; nevertheless, Rrs, which was already increased seated, increased further in the supine posture and there were also large falls in Xrs. Parallel experiments in supine normal subjects showed that mass loading of the anterior chest wall did not further reduce FRC.

POSTURE

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1203

n=5

-h

sitting supine loaded

obesity much of the mass load is intra-abdominal and the supine contour of the abdominal wall is protuberant. Although the applied mass load was built up over a few minutes in our normal subjects, contraction of abdominal muscles was obviously induced. The relevance of this experiment in untrained alert subjects to long-term mass loading, as present in obesity, is therefore uncertain. Changes in TLC and Subdivisions

12 16 20 Frequency (Hz)

24

28

3,

12 16 20 Frequency (Hz)

24

28
oscillation studied sitchest wall

FIG. 4. Mean values of Rrs (A) and Xrs (B) at different frequencies during tid .a1 breathing in 5 normal subjects ting, supine unloaded, and supine with an added anterior

Technical Factors We did not measure FRC in the supine posture in these studies but derived change in FRC and residual volume (RV) by measuring VC and its subdivisions in the supine posture and assuming changes in TLC were small and similar in normal and obese subjects. Measured reductions in VC and FVC in the supine position averaged 200 ml in both control and obese subjects in the present study. Two previous studies of TLC on changing posture have shown mean falls of 140 ml in normal and of 200 ml in obese subjects (30) and of 137 ml in normal and of 115 ml in obese subjects (4), respectively. Changes in RV with posture are agreed to be small (4, 30), so these previous studies of TLC agree closely with our observed changes in VC. In a further study in our laboratory of 12 obese subjects in whom FRC was measured by multibreath helium dilution in both postures, mean values were 2.36 liters seated and 2.29 liters supine, confirming the implied lack of fall in FRC found in the present study. Previous studies of mass loading of thorax and/or abdominal wall have produced large changes in the pressure-volume characteristics of the relaxed respiratory system in both conscious and anesthetized normal subjects (26). Nevertheless, mass loading in normal subjects does not simulate the load of obesity fully because it is applied acutely, is entirely external to the abdominal wall and is associated with a normal scaphoid contour of the ventral abdominal wall, whereas in

Reductions in FRC and ERV in normal subjects moving from the sitting to the supine posture were similar to those previously described in this (32) and other laboratories (16, 20) and presumably reflect changes in relaxation volume of the respiratory system (Vr) due to alteration of the pressure-volume characteristics of the chest wall and increases in intrathoracic blood volume with posture (1). The reductions in TLC, VC, FRC, and ERV found in seated obese subjects were also similar to those found by previous authors (4, 19, 26, 30, 33). The reduction in FRC and ERV, which is a function of increasing weight (23), has been assumed to be due to a reduction in Vr caused by a shift to smaller volumes of the pressure-volume curve of the relaxed chest wall. In contrast, RV is not reduced, at least in middle-aged obese subjects (4, 29, 30), probably because in such subjects RV is limited by airway closure rather than the chest wall (15). The mechanism of the reduction in TLC is uncertain but presumably reflects a change in extrapulmonary structures; conceivably, inspiratory descent of the diaphragm is impeded by restriction of anterior movement of the abdominal wall. The strength of the inspiratory muscles in our obese subjects was normal at FRC, but we are not aware of studies of pleural and abdominal pressure at full inflation that would help to analyze the cause of the reduction in TLC. Because of the increased mass of the abdomen in obese subjects, gravitational forces in the supine position would be expected to enhance the cranial movement of the diaphragm; the striking feature of our results is our failure to find any further fall in FRC in obese subjects when they adopt the supine posture. Two previous studies (4,30) have shown that the mean fall in ERV in obese subjects adopting the supine position was -0.5 liter less than the fall in control subjects of normal weight. RV presents an absolute lower limit to end-tidal volume, and published data imply that Vr could fall below RV in obese subjects (19,26). Very low values of ERV (<0.4 liter) are associated with reduced ventilation of basal regions (7, 11). Conceivably obese subjects may be breathing tidally above Vr even when seated; our results imply that, when supine, respiratory muscle activity sustains dynamic hyperinflation above Vr. Compared with patients with severe airway obstruction, the pressure load on the inspiratory muscles would be much less and their ability to sustain this load larger because of their greater length and greater force-generating capacity. Favorable consequences of breathing at larger lung volumes are a reduction in airway closure, less hypoxemia (in the pres-

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ent obese subjects Sa o2 was only slightly lower in the supine posture), and a larger lung O2 store should obstructive apnea develop. The failure of anterior chest wall mass loading to further reduce FRC and ERV in supine normal subjects also implies alteration in respiratory muscle activity. Abdominal muscle contraction was obviously induced as the load was increased, attenuating the increase in abdominal pressure. Conceivably, tonic diaphragm activity was also induced, opposing the deflationary effect of the increase in abdominal pressure. Changes in Respiratory Mechanics With Posture

The changes found in normal subjects with recumbency (increase in Rrs, fall in MTLV and FRC, reduction in Xrs, and increase in fR) were all of similar direction and magnitude to those found in previous studies (16, 20, 32). Most of th e increase in Rrs can be accounted for by the reduction in MTLV as shown by earlier detailed studies of airway resistance vs. lung volume (16) and as indicated by the small change in SRrs with change in posture in the present studies. Seated Rrs was considerably higher in the obese than the normal subjects, but as shown by the smaller differences in SRrs (Table 2), a large part of the increase in Rrs was due to the smaller lung volume at which the measurement was made. Differences between Raw (measured at slightly smaller lung volume) and Rrs were small, confirming that the increased Rrs was not due to increased resistance of the chest wall. These results are similar to those of another recent study (33). The supine rise in Rrs in the obese subjects cannot be attributed to a further reduction in midtidal lung volume. The serial site of the supine increase in Rrs could be the intra- or extrathoracic airways or a change in chest wall properties. Mass loading of the supralaryngeal airway by fat in the supine posture could increase its resistance (2, 13). In obesity there is an enhanced increase in intrapulmonary blood volume when supine (24), and this conceivably could lead to intrapulmonary airway narrowing, either directly or by stimulating - reflex bronchoconstriction, as postulated in the orthopnea of heart failure. The shape of maximum expiratory flow-volume curves in our supine obese subjects favored an extrathoracic airway narrowing because they showed a disproportionate fall in PEF with only small changes in the later part of the curve, which might be expected if the rise in Rrs was due to intrapulmonary changes. Unfortunately, interpretation is complicated by the accompanying fall in MEP, which also might account for the disproportionate reduction in PEF. The enhanced frequency dependence of Rrs is equally inconclusive; whereas it might be due to increased inequalities of intrapulmonary time constants and airway closure at small lung volume, it may simply reflect an effect of upper airway shunt that develops whenever Rrs is increased and is not completely removed by the external support of the cheeks and floor of the mouth used in this study (21,31). Clearly, further studies are needed to establish the serial site of the increase in supine Rrs.

Xrs depends on the balance between effective respiratory system compliance (Crs) and inertance (Irs). Various models have been used to derive Crs and Irs from forced oscillation data (18, 20); it has been estimated that the larger part of the postural change in normal subjects was caused by a fall in Crs (20), which might be explained by stiffening of the lung (16,20) and possibly the chest wall (16, 19), related to breathing at a smaller lung volume. However, values of effective Crs estimated from impedance measurements (20) are much lower than static measurements of Crs obtained with the weighted spirometer technique. Furthermore, by using the latter technique, total Crs has not changed between sitting and supine positions in normal subjects (6, 10, 19>, although there are changes in its components with reductions in compliance of the rib cage and increases in compliance of the diaphragm-abdomen compartment in supine subjects (10). Obese subjects had lower sitting values of Xrs and higher fR than did control subjects and showed further striking reductions in Xrs and increase in fR in the supine position. There are few studies of Crs in obese subjects. Naimark and Cherniack (19) found a reduced Crs in seated obese subjects and a small further fall when supine. The major component appeared to be stiffening of the chest wall. The differences in ventral abdominal wall contours between the seated and supine position, which are thought to account for the increase in supine abdominal compliance in normal subjects (27), clearly might not apply in grossly obese subjects. Other authors have failed to find any abnormality in Crs (28), whereas increases in the tissue component of Irs have also been described (25). Alternatively, the decrease in total reactance might be due to an increased contribution from the low compliance of the upper airway, a further effect of an increased upper airway shunt. Precise interpretation of the changes in Xrs will require more invasive investigations combining direct measurements of pleural and gastric pressures with movements of the abdominal wall. In contrast to the large falls in supine Xrs in obesity, mass loading of the anterior thorax and abdominal wall only produced a small fall in Xrs in supine normal subjects. This fall was presumably due to a reduction in anterior abdominal wall compliance induced by muscle contraction in response to the load; compliance of the rib cage and lateral abdominal wall may not have been affected, thereby reducing the effect on total Crs (5). Mouth pressures on maximum inspiratory and expiratory efforts were similar in control and obese subjects when seated, as described before (3, 12). The only significant change when supine was a small fall in MEP in obese subjects that may reflect less effective abdominal muscle contraction. In summary, despite the increased gravitational load in the supine position in obese subjects, FRC did not fall below seated values. This lack of further gravitational effect on FRC aids tidal expiratory flow and avoids excessive airway closure and further hypoxemia. Despite the lack of fall in FRC, Rrs increased and Xrs decreased. The mechanical load on the inspiratory muscles, therefore, was increased in the supine posture because of

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POSTURE

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RESPIRATORY

MECHANICS

IN

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both worsening of respiratory plied need to sustain end-tidal

mechanics and the imvolume above Vr.

15.

This work was supported by a Commonwealth fellowship and by a grant from the British Lung Foundation. Present address of J. C. H. Yap: Dept. of Medicine III, Tan Tack Seng Hospital, Singapore. Address for reprint requests: N. B. Pride, Dept. of Medicine, Royal Postgraduate Medical School, Hammersmith Hospital, London W12 ONN, UK. Received 27 January 1995; accepted in final form 27 April 1995.

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