To compare the effects of posture on bronchial reactivity in 12 patients with mitral valve stenosis (MS) and 10 with bronchial asthma (BA), a methacholine inhalation test was performed 2 h after being in either a supine or sitting position. All patients showed brochial hyperreactivity to inhaled methacholine before the study. In MS patients, logarithmic values of the cumulative dose producing a 35 percent decrease in respiratory conductance (log PD35Grs) were significantly lower 2 h after being in a supine position than in those after being in a sitting position (0.71 [+ or -] 0.78, 1.02 [+ or -! 0.53 log units, respectively, p<0.05). In BA patients, however, log PD35Grs did not show significant changes (0.42 [+ or -] 0.51, 0.58 [+ or -] 0.48 log units, respectively). Variables of pulmonary function tests showed no significant differences between the two positions in both patients with MS and BA. We conclude that the bronchial hyperreactivity in MS is enhanced after the supine position for 2 h and that the supine posture may play an important role in the pathogenesis of cardiac asthma.
(Chest 1994; 106:1391-95)
BA=bronchial asthma;
DCO/VA=diffusion capacity for
carbon monoxide per unit volume;
log PD35Grs=logarith-
mic values of the cumulative dose producing a 35 percent
decrease in respiratory conductance;
MS=mitral valve
stenosis;
PD35Grs=cumulative dose producing a 35 per-
cent decrease in respiratory conductance;
Rrs=respiratory
resistance;
VC=vital capacity;
Vmax25%=maximal expi-
ratory flow at 2 percent of vital capacity
Key words: bronchial asthma; bronchial hyperreactivity; chronic heart failure; pulmonary function test
Cardiac asthma is wheezing due to bronchospasm caused by congestive heart failure.(1) It typically occurs during the night and thus is named as paroxysmal nocturnal dyspnea. Although central blood pooling potentiated by a prolonged supine position at night has long been postulated, the precise pathophysiologic mechanism is still unknown. Nocturnal dyspnea also is one of the well known symptoms of bronchial asthma. With respect to nocturnal dyspnea, clinical distinction between an attack of bronchial asthma (BA) and cardiac asthma usually is not difficult except in cases of chronic lung diseases associated with left heart disease.(2)
We and other investigators recently reported that bronchial hyperreactivity exists in patients with mitral valve diseases.(3)(4)(5) We previously reported that (1) bronchial reactivity was significantly correlated with pulmonary congestion and peripheral airway narrowing in patients with mitral valve disease;(3) and (2) bronchial hyperreactivity to inhaled histamine was closely correlated with pulmonary vascular congestion in the canine model.(6) From these results, we postulated that an increase in central blood pooling may play a role in potentiated bronchial hyperreactivity after lying supine in patients with congestive heart failure.
Bronchial hyperreactivity is a well-known cardinal characteristic of BA.(7) Taken together, these reports point to the fact that both patients with BA and mitral valve diseases develop nocturnal dyspnea and both patients have bronchial hyperreactivity in common. But it is not known whether or not central blood pooling may play a role in nocturnal dyspnea in patients with BA.
To further extend these observations, we studied the effects of a prolonged supine position on bronchial hyperreactivity in patients with mitral valve stenosis (MS) and BA. The purpose of this study was to clarify whether or not the prolonged supine position has a different effect on bronchial hyperreactivity in patients with MS and BA.
METHODS
Study Population
We studied 12 patients with MS (3 males and 9 females; mean age, 47.9 [+ or -] 6.9 [SD] years) and 10 patients with BA (4 males and 6 females; mean age, 41.1 [+ or -] 13.3 years). All patients were confirmed to have bronchial hyperreactivity to inhaled methacholine at time of enrollment in the study. Diagnosis of mitral stenosis was made by physical examination and echocardiography. Range of mitral valve area was 0.65 to 1.22 [cm.sup.2] measured by two-dimensional echocardiography. Illness duration of MS patients ranged from 4 to 26 years. None of the MS patients had a history nor a present status of BA and bronchodilators and steroids were administered. One of the MS patients had mild pulmonary emphysema. Diagnosis of BA was made by criteria of the American Thoracic Society.(8) Each patient was free from recent airway infection and examined in stable condition. Informed consent was obtained.
Methacholine Inhalation Test
Methacholine inhalation test was performed by the method of Takishima et al(9) with Astograph (TCK-6000M, CHEST MI, Corp, Tokyo, Japan). This apparatus records dose-response curves of respiratory resistance (Rrs) with tidal breathing during continuous inhalation of methacholine in twofold incremental concentration from 0.049 to 25 mg/ml every 1 min. Three indexes were used for the assessment of bronchial hyperreactivity; the baseline value of Rrs (Rrs-cont), the cumulative dose producing a 35 percent decrease in respiratory conductance (PD35Grs), and the minimum cumulative dose required to start to decrease respiratory conductance from the baseline. All subjects were studied between 9:00 and 11:00 AM. Administration of bronchodilators, xanthine derivatives, steroids, and cardiovascular agents, such as diuretics, digitalis derivatives, and vasodilators, was discontinued at least 12 h before the beginning of the study.
Pulmonary Function Test
Vital capacity (VC), [FEV.sub.1], maximal expiratory flow at 25 percent of VC (V max.25%), and diffusion capacity for carbon monoxide per unit volume (DCO/VA) were obtained with a spirometer of computer processing (Autospirometer System-55, Minato Medical Science, Osaka, Japan).
Study Protocol
Two visits to the laboratory were required within 1 week. Measurements were made at the same clock time on two separate days, on one of which days the patients were supine for 2 h and sitting upright on the other. Patients were randomly assigned to either supine posture or sitting upright for each session. They were required to assume the assigned posture for 2 h. At the end of 2 h, pulmonary function tests were performed in the sitting position followed by a methacholine inhalation test in the same position. During the inhalation test, blood pressure and heart rate were carefully monitored every 1 min for avoidance of accidents.
Statistical Analysis
Results are presented as mean values [+ or -] SD. Values of PD35Grs and the minimum cumulative dose required to start to decrease respiratory conductance from the baseline were transformed to logarithmic data because the transformed data show normal distribution. Statistical evaluations were performed by Student's t-test for paired and unpaired data. A probability value of less than 0.05 was considered significant.
RESULTS
Results of anthropometric measurements, pulmonary function tests, and hemodynamic studies are shown in Table 1. There were no significant differences between the two groups. Two MS and two BA patients were smokers, while one MS patient and two BA patients were ex-smokers. The rest, nine MS and four BA patients, had no history of smoking. Pulmonary function tests showed no significant differences between the two groups.
[TABULAR DATA OMITTED]
Tables 2 and 3 show the results of pulmonary function tests 2 h after the patients were in either supine or sitting positions. In both MS and BA patients, the variables of pulmonary function tests showed no significant differences between the two postures.
[TABULAR DATA OMITTED]
Figures 1 and 2 show the results of the methacholine inhalation test. Baseline Rrs in MS was not significantly different between the two postures (4.45 [+ or -] 1.00 vs 4.80 [+ or -] 0.98 cm [H.sub.2]O/L/s, sitting vs supine position, respectively). The log PD35Grs after the supine position, on the other hand, was significantly lower than that after the sitting position (1.02 [+ or -] 0.53 vs 0.71 [+ or -] 0.78 log units, sitting vs supine, respectively, p<0.05). In the patients, baseline airway tone and bronchial reactivity to inhaled methacholine after being in the supine position showed no significant changes as compared with those after being in the sitting position (5.2 [+ or -] 1.4 vs 5.2 [+ or -] 1.5 cm [H.sub.2]O/L/s, 0.51 [+ or -] 0.58 vs 0.42 [+ or -] 0.59 log units, sitting vs supine position, respectively).
[CHART OMITTED]
DISCUSSION
In the present study, we have shown that log PD35Grs significantly decreased 2 h later in the supine position in MS but not in BA patients. These results suggest that bronchial hyperreactivity of the MS patients may be more easily potentiated by supine posture as compared with that of BA.
How supine posture potentiated bronchial hyperreactivity in our MS patients is not known from the present study. But we strongly suspect that central blood pooling potentiated by the supine position may be most responsible. Since the two major pulmonary changes associated with central blood pooling are (1) an increase in pulmonary vascular congestion and (2) bronchial wall edema, we speculate that the latter may be most responsible for augumented bronchial hyperreactivity in the MS patients. Bronchial wall edema is well known to augment bronchial hyperreactivity.(7) Hogg et al(10) showed that pulmonary congestion mainly increased resistance in the peripheral airway rather than that in the central airway, probably because of the passive effect of vascular engorgement. Gray et al(11) also reported that dynamic compliance decreased in pulmonary congestion of the canine model while total pulmonary resistance did not, suggesting that pulmonary congestion increases peripheral airway resistance. We reported in canine experimental models that peribronchovascular edema was prominent around bronchioles and small vessels of the lung 60 min after pulmonary congestion.(12) Therefore, we strongly suspect that peripheral airway edema which developed in MS patients during the supine position played an important role in the decrease of PD35Grs. The reason why we failed to detect a decrease in [FEV.sub.1] is not known from the present study. It may be that [FEV.sub.1] reflects central rather than peripheral airway caliber or detection limit was well higher than rather small changes of airway caliber, or both.
Another possible explanation of our results would be that a reduction of lung volume in the supine position caused supine bronchial hyperreactivity. Close association of bronchial responsiveness with lung volume has been reported by several laboratories.(13)(14) Bronchial response, however, was not altered by either posture. Since our MS and BA patients showed no significant changes in the variables of pulmonary function between the supine and sitting positions, it is unlikely that the loss of lung volume played a significant role in bronchial hyperreactivity after being in the supine position in this study. A decrease in plasma catecholamine level after the supine position is another possibility that cannot be completely ruled out.(15) Jonsson and Mossberg(16) suggested that the catecholamine level might be one of the factors responsible for bronchial hyperreactivity after lying supine in asthmatic subjects. In addition, they considered a decrease in mucociliary clearance as a possible mechanism of bronchial hyperreactivity after lying supine.(17)
The reason why patients with mitral valve disease demonstrated augmented bronchial hyperreactivity after being in the supine position while BA patients did not is not known from the present study. We speculate that central blood pooling to a much lesser degree actually occurred in BA patients, in a much more heterogeneous manner, or both, or 2 h in the supine position was not long enough to change bronchial hyperreactivity. Jonsson and Mossberg(16) showed forced vital capacity and peak flow rate decreased 4 h after being in the supine position. Moreover, it may be that there is a difference in parasympathetic tone between patients with MS and BA. We previously reported that parasympathetic overactivity was observed in patients with BA but not in patients with chronic heart failure.(18)
The limitations of the present study need to be mentioned. First, with this small sample size, we could not exclude a type 2 error. But we suspect this is not likely because, while all of the MS patients showed a decrease in PD35Grs after lying in the supine position, only half of the BA patients exhibited a decrease. These results strongly suggest that there exists a qualitative difference in the effects of the postures between the two groups. Second, since our BA patients had normal spirometry test results, more severe asthmatic patients may show changes uniformly. This is, however, less likely because the changes in PD35Grs did not significantly correlate with the spirometric data in BA group. Third, the position of the patients was set to a sitting posture in the present study when pulmonary function and metacholine inhalation tests were performed. It could be argued that the results might be different if the tests were performed in a different posture.(19) Last, although there was a slight difference in smoking history between MS and BA patients, we speculate that it did not affect our results much because (1) none of the BA patients had COPD and (2) as shown in both Figures 1 and 2, smoking history was not significantly correlated with bronchial reactivity to inhaled methacholine in both patient groups.
In summary, we have shown an augmentation of bronchial reactivity to inhaled methacholine after 2 h of being in the supine position in MS but not in BA patients. We conclude that the posture may play an important role in the pathogenesis of cardiac asthma. Further experimental studies are needed to confirm the relationship between bronchial hyperreactivity and airway edema associated with vascular congestion in patients with congestive heart failure.
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