Efficacy of diaphragmatic breathing in persons with chronic obstructive pulmonary disease: a review of the literature

The evidence base for diaphragmatic breathing (DB) as an adjunctive treatment modality for persons with COPD is questionable. This article reviews the literature regarding the efficacy of DB in persons with chronic obstructive pulmonary disease (COPD), and reports on the beneficial and detrimental effects of DB in persons with COPD. Diaphragmatic breathing has been described as breathing predominantly with the diaphragm while minimizing the action of accessory muscles that may assist with inspiration. No single or combined patient characteristic has been identified consistently to help predict which person with COPD may benefit from DB. However, it has been suggested that persons with moderate to severe COPD and marked hyperinflation of the lungs without adequate diaphragmatic movement and increase in tidal volume during DB may be poor candidates for instruction in DB. Conversely, persons with COPD who have elevated respiratory rates, low tidal volumes that increase during DB, and abnormal arterial blood gases with adequate diaphragmatic movement may benefit from DB. Identification of an abdominal paradoxical breathing pattern and worsening dyspnea and fatigue during or after DB are criteria to modify or terminate DB. Persons with COPD demonstrating an abdominal paradox during DB may benefit from a more upright body position or trunk flexion. Several methods to examine diaphragmatic movement and the potential for success with DB will be discussed. Future research is needed to better identify which patients may benefit from DB.     

Immediate effect of respiratory muscle stretch gymnastics and diaphragmatic breathing on respiratory pattern. Respiratory Muscle Conditioning Group

We investigated the immediate effect of respiratory muscle stretch gymnastics (RMSG) and diaphragmatic breathing (DB) on the respiratory pattern in patients with chronic obstructive pulmonary disease (COPD). Sixteen patients with COPD (age, 71.3 +/- 3.9 year) were entered in the study. DB was performed for 10 minutes in supine position. For RMSG, 5 patterns were repeated 10 times each. Respiratory variables were measured in sitting position before and after both RMSG and DB, performed in random order, patient to patient, with a 20-minute washout period in-between. After RMSG, but not after DB, there was a significant overall prolongation in expiratory time. After DB, but not after RMSG, there was an overall decrease in minute ventilation, carbon dioxide output, respiratory gas exchange ratio, end tidal O2 fraction, end tidal CO2 fraction and tidal diaphragmatic volume. The results suggest that RMSG may have a beneficial effect on the respiratory pattern. On the other hand, DB may provoke post-hyperventilation hypoxemia.     

Alteration in breathing pattern with progression of chronic obstructive pulmonary disease

We examined the relationship between breathing pattern and severity of disease in patients with chronic obstructive pulmonary disease (COPD). Resting breathing pattern was recorded for 45 min using the respiratory inductance plethysmograph (RIP) in 22 patients with stable COPD. Six subjects (moderate group) had FEV1 25 to 50% predicted, 8 subjects (severe group) had FEV1 less than 25% predicted, and 8 subjects (respiratory failure group) had FEV1 less than 25% predicted and were hypoxemic. Seven of the subjects with respiratory failure were also hypercapnic. Subjects with respiratory failure were studied with and without supplemental O2. All subjects were studied in the seated position. There were no significant differences in breathing pattern between the moderate and severe groups. Tidal volume (VT) was 120 ml lower in the severe group, but breathing frequency (f) was slightly elevated, allowing minute ventilation (VI) to be maintained. The respiratory failure group demonstrated a significant decrease in VT compared with that in the moderate group and a significant decrease in VT/TI as compared with both moderate and severe groups; TI was unchanged in subjects with respiratory failure, and, as f did not increase significantly, VI was decreased. Acute relief of hypoxemia had no effect on breathing pattern in respiratory failure. Variability was assessed by comparing the coefficients of variation for each timing component. There was no difference in intraindividual variability of breathing pattern between all groups. These results suggest that changes in ventilatory control as reflected by breathing pattern are to some extent independent of mechanical abnormalities.     

稳定期中重度慢性阻塞性肺疾病患者运动时胸腹矛盾呼 …

探讨慢性阻塞性肺疾病患者运动时胸腹矛盾呼吸的影响因素并观察氧疗对胸腹矛盾呼吸的影响。方法３０例稳定期中重度ＣＯＰＤ患者,运动前按常规进行功能检查和血气分析,分别在吸空气和３０％氧气态下进行两次递增负荷运动试验,通过呼吸感应性体表描记仪监测运动过程中胸腹呼吸量之和与实际潮气量之比。     

Helium-oxygen breathing in severe chronic obstructive pulmonary disease

The effect of breathing helium-oxygen (He-O2) mixtures was evaluated in 15 patients with severe chronic obstructive pulmonary disease (COPD). Gas exchange was assessed during quiet breathing at rest before and after 15 minutes of breathing 80 percent He-20 percent O2 mixtures in all patients. Functional residual capacity (FRC) determined during argon (Ar) washing studies fell significantly while breathing He-O2, but we did not find significant changes in minute ventilation, tidal volume, respiratory frequency, or inspiratory or expiratory timing. Eleven patients showed decreases in arterial PCO2 and CO2 excretion during resting breathing on He-O2. Expiratory flows were increased at a given lung volume during He-O2 breathing as expected. Apparently, mechanical work of breathing was decreased in patients with severe COPD while breathing He-O2, leading to a reduction in VCO2 and improvement in overall alveolar ventilation. These findings lend support to the therapeutic use of He-O2 under some conditions in patients with severe COPD.     

Accuracy of respiratory inductive plethysmograph over wide range of rib cage and abdominal compartmental contributions to tidal volume in normal subjects and in patients with chronic obstructive pulmonary disease

We assessed the accuracy of the respiratory inductive plethysmograph in the supine position to spirometry by the two-body position, least squares calibration and single-body position, isovolume calibration procedures. The comparison was carried out simultaneously in normal subjects breathing naturally and with voluntarily controlled abdominal or thoracic breathing, and in patients with COPD breathing naturally and with voluntarily controlled abdominal breathing patterns. In both groups, there was no significant difference in estimation of tidal volume between the 2 calibration procedures for the various breathing patterns. There was greater deviation from spirometric tidal volume values for both calibration methods in patients with COPD during abdominal than during natural breathing. In the normal subjects, agreement between the rib cage and abdominal partitioning of tidal volume for both calibration methods was good, but in the patients with COPD there was greater variability. In normal subjects, over a wide range of rib cage and abdominal compartmental contributions to tidal volume, either calibration procedure appears satisfactory. For patients with COPD, if large changes occur in the distribution of rib cage and abdominal contributions to tidal volume, then validation of respiratory inductive plethysmography to spirometry must be rechecked.     

Control of breathing in Duchenne's muscular dystrophy

Duchenne's muscular dystrophy is a progressive degenerative muscular disease which leads to death from respiratory insufficiency in over 80 percent of cases. Recent studies in neuromuscular diseases have suggested that respiratory failure may be of central origin in some of the genetically transmitted neuromuscular diseases. We therefore evaluated the control of breathing in nine patients with advanced Duchenne's muscular dystrophy and compared these patients to nine healthy controls matched on the basis of age, sex and arm span.The purpose of the study was to assess the sensitivity of respiratory centers to hypercapnia, hypoxia and hyperoxia in nine patients with advanced Duchenne's muscular dystrophy. We measured minute ventilation (V?_E), tidal volume (V_T), respiratory frequency (F), mean respiratory flow rate (V_T:T_i) and occlusion pressure (P_0.1) responses as indices of respiratory centers output during hypercapnia (Read's method) and isocarbic hypoxia (Weil's method). We also analysed V?_e during the transient hyperoxia test (Dejours' method). The threshold and magnitude of responses to hypercapnia, hypoxia and hyperoxia were nearly similar in patients and in controls. Patients demonstrated subnormal response of V?_e, V_T:T_i, V_T. Occlusion pressures were nearly the same in normal subjects and in patients with severe muscle weakness. The patterns of responses to those stimuli were markedly different: patients demonstrated a tachypneic pattern of breathing whereas controls preferred to increase their tidal volume.Our study establishes that in patients with advanced Duchenne's muscular dystrophy, the integrity of the carbon dioxide (CO₂) and oxygen (O₂) drive of breathing is well preserved. However in these patients, the pattern of ventilatory response is different from normal. There is a preferential increase in respiratory frequency to hypercapnia and hypoxia stimuli. This tachyphea could well be a clinical manifestation of inspiratory muscle fatigue which resulted in the subnormal ventilatory responses of our patients with Duchenne's muscular dystrophy.     

Pulmonary hemodynamics during mild exercise in COPD

The effects of mild exercise on pulmonary hemodynamics and ventilatory responses in COPD were studied. Six patients with FEV1% less than 70% received 20 watt exercise tests by cycle ergometers for 5 minutes. Changes in hemodynamics and ventilation were observed before and during exercise. Nine patients with an FEV1% of more than 70% also received exercise tests as controls. There were no different in changes in respiratory frequency, tidal volume and minute ventilation between control and COPD group. However, the mean pulmonary arterial pressure were higher in the COPD group than in the control group before exercise. Moreover increments of mean pulmonary arterial pressure by exercise were also greater in COPD group. It was concluded that hemodynamics in COPD are much more influenced by mild exercise than in healthy subjects.     

Clinical manifestations of inspiratory muscle fatigue

Twelve patients exhibiting difficulties during discontinuation of artificial ventilation permitted us to investigate physical examination techniques used in diagnosing inspiratory muscle fatigue. Diaphragmatic and intercostal electromyographic tracings, arterial blood gases, rate and depth of ventilation, and thoracoabdominal motion were monitored during spontaneous breathing. Six patients showed electromyographic evidence of inspiratory muscle fatigue. A sequence of events leading to respiratory acidemia emerged--namely electromyographic evidence of fatigue, accompanied or followed by an increased respiratory rate, in turn followed by alternation between abdominal and rib cage breathing (respiratory alternans), paradoxical inward abdominal motion during inspiration (abdominal paradox), and finally an increase in PaCO2 associated with a fall in minute ventilation and respiratory rate, and worsening of respiratory acidemia. The abnormalities of respiratory movements may be reliable clinical signs of inspiratory muscle fatigue, particularly when accompanied by tachypnea and hypercapnia.     

Low-dose acetazolamide does affect respiratory muscle function in spontaneously breathing anesthetized rabbits

Patients with chronic obstructive pulmonary diseases (COPD) and/or central sleep apnea are sometimes treated with the carbonic anhydrase inhibitor acteazolamide to improve blood gas values. Studies have shown that this agent may have a complicated effect on lung ventilation, because carbonic anhydrase has a widespread distribution within the body, particularly in tissues involved in the control of breathing. To investigate whether acetazolamide may have (neuro)muscular effects on respiration, we measured the responses of ventilation, phrenic nerve activity, and transpulmonary pressure to changes in arterial PCO2 before and after intravenous administration of a low-dose (4.6 +/- 0.2 mg x kg(-1), mean +/- SEM) of this inhibitor in anesthetized spontaneously breathing rabbits. The agent decreased the mean resting end-tidal PCO2 by 1 kPa and increased ventilation from 258 +/- 15 to 292 +/- 14 ml x min(-1) x kg(-1) (p < or = 0.05). The ventilatory and tidal volume responses to CO2 were reduced, and the response curves were shifted to lower PCO2 values. At the level of phrenic activity, however, the response was shifted leftward without altering CO2 sensitivity. With an unchanged lung compliance, the slopes of the relationships between tidal volume and phrenic activity and that between the tidal change in transpulmonary pressure and phrenic amplitude were both reduced by about 40%, indicating an action of acetazolamide on (neuro)muscular level. The results raise the suggestion that treatment of some hypercapnic COPD patients with acetazolamide may have undesired clinical implications, particularly in those with already weakened respiratory muscles.     

Assessment of asynchronous and paradoxic motion between rib cage and abdomen in normal subjects and in patients with chronic obstructive pulmonary disease

Both scalar tracings and XY plots of rib cage (RC) and abdominal (AB) excursions were analyzed to detect asynchronous and/or paradoxic motion of one compartment with respect to the other in an effort to distinguish differences between normal subjects and patients with chronic obstructive pulmonary disease (COPD). An inspiratory asynchrony index (IAI) was obtained by connecting a straight line from beginning inspiration to end inspiration of the RC-AB loop, and dividing the area enclosed by the inspiratory portion by the tidal volume. In like manner, an expiratory asynchrony index (EAI) was computed. Values of IAI and EAI in the supine posture were greater in patients with COPD than in normal subjects, and such differences were consistently demonstrated during natural and voluntarily controlled abdominal breathing. Paradoxic motion as percent of volume or time period of inspiratory and expiratory compartmental excursions was indicated when RC or AB compartments moved in an opposite direction to the sum of the two. During natural breathing, paradoxic motion was almost absent in normal subjects and variably present in patients with COPD. Voluntarily controlled breathing patterns produced increased IAI, EAI, and paradoxic motion. Passive tilting from supine to the upright posture did not affect indexes in normal subjects but reduced asynchronous and paradoxic motion of the RC in patients with COPD. Other indexes of loop analysis, such as phase angle and maximal compartment amplitude/tidal volume, were not as consistent in distinguishing between normal subjects and patients with COPD during natural and voluntarily controlled breathing patterns.(ABSTRACT TRUNCATED AT 250 WORDS)     

Pathogenesis of respiratory insufficiency in myotonic dystrophy: the mechanical factors

We have previously shown that the chemosensitivity of the respiratory centers is well preserved in myotonic dystrophy but that the ventilatory output is reduced. The present study was designed to determine at which degree of ventilatory performance weakness and fatigability of the respiratory muscles are interfering with ventilation and which mechanical factors contribute to the tachypnea of patients with myotonic dystrophy at rest and during low ventilatory output. We studied 10 patients with the disease and 10 normal control subjects. The strength of respiratory muscles was assessed by measurements of maximal pressure-volume diagrams generated against airway occlusion. Performance was evaluated during 1-min maximal voluntary ventilation (1-min MVV) test, during 7-min 7% CO2 breathing and during quiet breathing. Occlusion pressure (P0.1) in patients at rest was slightly higher than in control subjects, and during CO2 breathing, it was similar to that of control subjects. Maximal static pressure was reduced in patients to an average of 35% of that of control subjects. During the 1-min MVV test, there was a 50% reduction in esophageal and transdiaphragmatic pressure output (Pes, Pdi) in patients, resulting in similar reduction in ventilation (VE) and patients had rapid cycles of alternating dominant thoracic and abdominal volume displacements (Vrc/Vabd) suggesting respiratory muscle fatigue. During the 3- to 4-fold increase in breathing drive induced by hypercapnia, pressure output and the Vrc/Vabd were identical in both groups. However, ventilation was reduced in patients who had tachypneic respiration. In patients, tachypnea was also observed during quiet breathing. This tachypnea was associated with higher impedance of the respiratory system (Zrs) in patients and identical impedance of the lung (ZL) in both groups. In addition, Pdi during tidal volume was significantly higher in patients. These data demonstrate that the ventilatory output in out patients was altered predominantly by weakness and fatigability of the respiratory muscles during high ventilatory performance and by increased impedance of the respiratory system at lower degrees of ventilation.     

Exercise dyspnea in patients with COPD

Dyspnea, a symptom limiting exercise capacity in patients with COPD, is associated with central perception of an overall increase in central respiratory motor output directed preferentially to the rib cage muscles. On the other hand, disparity between respiratory motor output, mechanical and ventilatory response of the system is also thought to play an important role on the increased perception of exercise in these patients. Both inspiratory and expiratory muscles and operational lung volumes are important contributors to exercise dyspnea. However, the potential link between dyspnea, abnormal mechanics of breathing and impaired exercise performance via the circulation rather than a malfunctioning ventilatory pump per se should not be disregarded. Change in arterial blood gas content may affect dyspnea via direct or indirect effects. An increase in carbon dioxide arterial tension seems to be the most important stimulus overriding all other inputs from dyspnea in hypercapnic COPD patients. Hypoxia may act indirectly by increasing ventilation and indirectly independent of changes in ventilation. A greater treatment effect is often achieved after the addition of pulmonary rehabilitation with pharmacological treatment.     

Hyperinflation and its management in COPD

Chronic obstructive pulmonary disease (COPD) is characterized by poorly reversible airflow limitation. The pathological hallmarks of COPD are inflammation of the peripheral airways and destruction of lung parenchyma or emphysema. The functional consequences of these abnormalities are expiratory airflow limitation and dynamic hyperinflation, which then increase the elastic load of the respiratory system and decrease the performance of the respiratory muscles. These pathophysiologic features contribute significantly to the development of dyspnea, exercise intolerance and ventilatory failure. Several treatments may palliate flow limitation, including interventions that modify the respiratory pattern (deeper, slower) such as pursed lip breathing, exercise training, oxygen, and some drugs. Other therapies are aimed at its amelioration, such as bronchodilators, lung volume reduction surgery or breathing mixtures of helium and oxygen. Finally some interventions, such as inspiratory pressure support, alleviate the threshold load associated to flow limitation. The degree of flow limitation can be assessed by certain spirometry indexes, such as vital capacity and inspiratory capacity, or by other more complexes indexes such as residual volume/total lung capacity or functional residual capacity/total lung capacity. Two of the best methods to measure flow limitation are to superimpose a flow–volume loop of a tidal breath within a maximum flow–volume curve, or to use negative expiratory pressure technique. Likely this method is more accurate and can be used during spontaneous breathing. A definitive definition of dynamic hyperinflation is lacking in the literature, but serial measurements of inspiratory capacity during exercise will document the trend of end-expiratory lung volume and allow establishing relationships with other measurements such as dyspnea, respiratory pattern, exercise tolerance, and gas exchange.     

Thoracoabdominal motion in chronic obstructive pulmonary disease.

Studies of thoracoabdominal motion using the respiratory magnetometer were performed in 30 patients with chronic obstructive pulmonary disease. Volume equivalency of thoracic and abdominal deflections was established by using the concepts and methods developed by Konno and Mead. Twenty patients were ambulatory, although disabled, and 10 were in acute respiratory failure and were studied in a respiratory intensive care unit. Five of 20 ambulatory patients and 8 of 10 patients in acute respiratory failure showed inward abdominal motion coincident with outward rib cage motion during inspiration, suggesting ineffective diaphragmatic function. This pattern of thoracoabdominal motion was identical to that seen in 2 high quadriplegics with diaphragmatic paralysis when they were breathing entirely with their neck muscles. Inspiratory ascent of the diaphragm was confirmed fluoroscopically in 3 of the 5 ambulatory patients. Patients showing this pattern were generally severely disabled and had the largest residual volumes. Two abnormal patterns of thoracoabdominal motion were observed during the performance of maximal voluntary ventilation in the ambulatory patients. The first, seen in 9 of 20 patients, was characterized by reciprocal or paradoxical motion of rib cage and abdomen, with increase in rib cage volume associated with decrease in abdominal volume during inspiration. The second pattern, seen in 5 of 20 patients, showed complete disorganization of rib cage and abdominal motion, with no consistent or reproducible pattern. Thus, a significant proportion of patients with disabling chronic obstructive pulmonary disease show abnormalities in thoracoabdominal motion that are observable with the respiratory magnetometer and ofter by simple inspection. Most of these abnormalities suggest malfunction of respiratory muscles, particularly the diaphragm.     

Efficacy of positive vs negative pressure ventilation in unloading the respiratory muscles

We compared the efficacy of positive pressure ventilation (PPV) vs negative pressure ventilation (NPV) in providing ventilatory muscle rest for five normal subjects and six patients with chronic obstructive pulmonary disease (COPD). All participants underwent measurement of transdiaphragmatic pressure (Pdi), pressure time integral of the diaphragm (PTI), integrated diaphragmatic electromyogram (iEMG), minute ventilation (Ve), tidal volume (Vt), and end-tidal CO2 (etCO2) during 15 minutes of PPV and NPV. For each subject, ventilator adjustments were made to obtain Ve similar to levels measured during quiet breathing (QB). We found that the iEMG, Pdi, PTI, and average coefficient of variation of the tidal volume (CV-Vt) were consistently lower during PPV as compared with NPV (p = 0.01). The iEMG normalized for Ve and Vt was also significantly lower during PPV (p = 0.01). During PPV, subjects were mildly hyperventilated (lower etCO2 and higher Ve) compared with QB and NPV, but no significant correlation was noted between the change in etCO2 and the change in iEMG. The change in PTI was significantly correlated with the change in iEMG (p less than 0.01). We conclude that in the short term, PPV is more effective than NPV in reducing diaphragmatic activity. Positive pressure ventilation may be the preferred method of assisted ventilation in future studies of ventilatory muscle rest therapy.     

Effect of naloxone on the respiratory responses to hypoxia in chronic obstructive pulmonary disease

Ventilatory and airway occlusion pressure responses to hypoxia were measured in 7 subjects with chronic obstructive pulmonary disease (COPD). Paired responses were obtained after the administration of saline or naloxone and, on separate days, in 5 of the 7 subjects, after 2 saline injections. Naloxone increased (p less than 0.05) the mean inspiratory flow and the ventilatory and airway occlusion pressure responses to hypoxia when compared with the saline responses. Resting ventilation and tidal volume also increased, but not significantly. Involvement of endogenously generated opioid substances in the control of breathing of patients with COPD is further suggested by this study.     

慢性阻塞性肺疾病急性发作期患者对比例辅助通气的生理反应

目的　探讨比例辅助通气 (PAV)不同辅助水平对慢性阻塞性肺疾病 (COPD)急性发作期患者生理反应的影响。方法　 9例COPD急性发作期患者接受三个不同比例辅助水平的PAV通气 ,观察患者吸气肌肉用力情况和呼吸方式的变化。结果　 (1)与自主呼吸 (SB)相比 ,PAV各辅助水平时的潮气量 (VT)、分钟通气量 (V·E)和呼吸频率 (RR)均稍增高 (P >0 0 5 )。各比例辅助水平之间的VT、V·E 和RR比较差异无显著性 (P >0 0 5 )。 (2 )与SB相比 ,各比例辅助水平时的跨膈压 (Pdi)、压力时间乘积 (PTP)和患者呼吸做功均明显减少 (P >0 0 1) ,Pdi、PTP和患者呼吸做功分别平均减少 8 36cmH2 O、11 4 9cmH2 O·s-1·L-1和 0 5 3J/L。随比例辅助水平的升高 ,Pdi、PTP和患者呼吸功无明显变化(P >0 0 5 )。 (3)PAV可减轻患者呼吸困难 (P <0 0 5 )。结论　本试验证实了无创PAV在COPD急性发作期患者中应用的可行性。患者感觉最舒适的PAV辅助比例水平是 (5 7± 11) %。根据患者感觉舒适情况而设定比例辅助水平的无创PAV可减轻患者的呼吸肌肉负担 ,最舒适水平时呼吸功减少5 7% ,Pdi减少 72 % ,PTP减少 6 5 % ;并改善患者的呼吸方式和呼吸困难     

Breathing pattern during and after maximal exercise in patients with chronic obstructive lung disease, interstitial lung disease, and cardiac disease, and in normal subjects

Inspiratory muscle fatigue and pulmonary edema are both known to cause rapid shallow breathing. It has been suggested that exercise tolerance in patients with pulmonary disease and cardiac disease may be limited by the development of inspiratory muscle fatigue and pulmonary edema, respectively, at maximal exercise. If these hypotheses are correct, breathing pattern during recovery from maximal exercise in these patients should be rapid and shallow compared with that during exercise. This study was performed to test these hypotheses. Seven patients with chronic obstructive pulmonary disease (COPD), 8 patients with interstitial lung disease (ILD), 7 patients with cardiac disease (CD) (mitral valve disease or left ventricular dysfunction) and 8 normal (NR) subjects each performed maximal incremental exercise on a cycle ergometer. Exercise breathing pattern was compared with that during recovery by calculating the mean difference in tidal volume (at the same levels of minute ventilation) between exercise and recovery for each subject. Recovery breathing pattern was similar to that during exercise for the COPD, ILD, and NR subjects. In contrast, breathing pattern during recovery was rapid and shallow compared with that during exercise for the CD patients; recovery tidal volume was less than that during exercise for the same level of minute ventilation. The fact that rapid shallow breathing does not develop during recovery from maximal exercise in patients with COPD or ILD suggests that inspiratory muscle fatigue does not limit their exercise tolerance. The relative rapid shallow breathing during recovery from maximal exercise in patients with CD is probably due to the development of pulmonary edema at maximal exercise, but further studies are needed to confirm this.(ABSTRACT TRUNCATED AT 250 WORDS)     

The effects of acute bronchoconstriction on respiratory activity in patients with chronic obstructive pulmonary disease

Attacks of acute airway obstruction often complicate the course of chronic obstructive pulmonary disease (COPD). In asthmatic subjects, bronchospasm triggers an increase in respiratory drive, which results in hyperventilation and hypocapnia. In the present study, we assessed the effects of acute bronchoconstriction induced by aerosolized methacholine on breathing and lung mechanics in 12 patients with stable COPD. Even low doses of methacholine markedly increased airway resistance and caused hyperinflation and decreased inspiratory muscle performance in the patients. Increasing airway obstruction produced a progressive rise in PCO2 despite an increase in minute ventilation. Breathing frequency and average inspiratory flow were greater, but tidal volume decreased because of shortening of the inspiratory duration. The magnitude of CO2 retention during acute bronchoconstriction was inversely related to the changes in tidal volume and inspiratory time (p less than 0.01 for each). In subjects with COPD, the occlusion pressure response to progressive hypercapnia failed to increase during bronchoconstriction. These results show that patients with COPD retain CO2 during acutely increasing airway obstruction induced by bronchoconstriction partly because of a rapid shallow breathing pattern that reduces alveolar ventilation.