Mechanism of the increased ventilatory response to exercise in patients with chronic heart failure.

Minute ventilation, respiratory rate, and metabolic gas exchange were measured continuously during maximal symptom limited treadmill exercise in 30 patients with stable chronic heart failure. The ventilatory response to exercise was assessed by calculation of the slope of the relation between minute ventilation and rate of carbon dioxide production. There was a close correlation between the severity of heart failure, determined as the maximal rate of oxygen consumption, and the ventilatory response to exercise. Reanalysis of the data after correction for ventilation of anatomical dead space did not significantly weaken the correlation but reduced the slope of the relation by approximately one third. These results show that the increased ventilatory response to exercise in patients with chronic heart failure is largely caused by mechanisms other than increased ventilation of anatomical dead space. This finding supports the concept that a significant pulmonary ventilation/perfusion mismatch develops in patients with chronic heart failure and suggests that the magnitude of this abnormality is directly related to the severity of chronic heart failure.     

Anatomical dead space, ventilatory pattern, and exercise capacity in chronic heart failure.

BACKGROUND--Patients with chronic heart failure have an excessive ventilatory response to exercise, characterised by an increase in the slope of the relation between ventilation and carbon dioxide production (VE/VCO2 slope). Patients have an altered respiratory pattern with an increased respiratory rate (f) at a given tidal volume (VT), which may result in increased anatomical dead space ventilation. METHODS--The ventilatory responses in 88 patients with chronic heart failure and 43 age matched controls during maximal incremental treadmill exercise were analysed. Peak oxygen consumption (VO2), VE/VCO2 slope, and the slope of the relation between f and VT were derived. Anatomical dead space was estimated from a standard formula and anatomical dead space ventilation calculated. RESULTS--Peak VO2 was greater (mean (SD)) (33.2 (8.5) v 19.4 (6.7) ml/min/kg; P < 0.001) and the VE/VCO2 slope lower in the controls (25.96 (4.16) v 35.14 (9.80); P < 0.001). During matched submaximal exercise VT was higher (1.97 (0.92) v 1.68 (0.62) 1; P < 0.05) and flower in the controls (18.23 (6.48) v 24.28 (7.58); P < 0.001). At peak exercise there was no difference in f, but VT was higher in the controls (2.66 (0.97) v 1.90 (0.61) 1; P < 0.001). The VT/f slope was the same (0.04 (0.04)) in both groups. The intercept of the relation was greater for the control group (1.31 (1.28) v 0.59 (0.83); P < 0.001). Anatomical dead space ventilation was lower in the controls at submaximal work load (4.17 (1.56) v 5.58 (1.93) l/min; P < 0.001). At peak exercise anatomical dead space ventilation was the same in both groups, but was lower expressed as a percentage of total VE in the control group (9.8 (3.3) v 13.5 (4.0); P < 0.001). There were weak relations within the heart failure group alone between VT/f slope and peak VO2 and VE/VCO2 slope. CONCLUSIONS--The relation between anatomical dead space ventilation and VE/VCO2 slope is expected: as f increases, so do VE/VCO2 slope and anatomical dead space ventilation. The VT/f slope was the same in patients with chronic heart failure and controls, so change in respiratory pattern cannot explain the increase in VE/VCO2 slope. The stimulus causing the increased f has yet to be identified.     

Exercise hyperventilation chronic congestive heart failure, and its relation to functional capacity and hemodynamics.

The ventilatory response to exercise was evaluated in 26 normal sedentary men and 68 patients with chronic heart failure using the slope of the relation between minute ventilation (VE) and carbon dioxide production (VCO2). All subjects underwent maximal upright bicycle cardiopulmonary exercise testing; 33 patients also underwent right-sided cardiac catheterization. The slope of VE/VCO2 was calculated by linear regression analysis using data from all the exercise tests and the first 60% of exercise duration; a high correlation was seen between these results (r = 0.83; p less than 0.001). The slope of VE/VCO2 was significantly, though weakly, related to peak exercise work load, oxygen consumption and ventilatory threshold (r = -0.49, -0.56 and -0.49, respectively), several peak exercise hemodynamic parameters and peak exercise dead space/tidal volume ratio (r = 0.70). With use of multivariate analysis, the only independent determinants of the slope were peak exercise dead space/tidal volume ratio and cardiac index. Thus, in patients with heart failure, exercise hyperventilation can contribute to the impairment of functional capacity and can be considered a compensatory response to abnormal hemodynamics and lung blood distribution in order to keep blood gas concentrations normal.     

Role of respiratory function in exercise limitation in chronic heart failure

OBJECTIVE: To test the hypothesis that respiratory function contributes to limit maximal exercise performance in patients with chronic heart failure by using the technique of dead space loading during exercise. DESIGN: Blinded subjects underwent two maximal incremental exercise tests in random order on an upright bicycle ergometer: one with and one without added dead space. SETTING:: Tertiary-care university teaching hospital. SUBJECTS: Seven patients with stable chronic heart failure (mean +/- SEM left ventricular ejection fraction, 27 +/- 3%). RESULTS: Subjects were able to significantly increase their peak minute ventilation during exercise with added dead space when compared with control exercise (57.4 +/- 5.9 vs 50.0 +/- 5.6 L/min; p < 0.05). Peak oxygen uptake, workload, heart rate, and exercise duration were not significantly different between the added dead space and control tests. Breathing pattern was significantly deeper and slower at matched levels of ventilation during exercise with added dead space. CONCLUSION: Because patients with chronic heart failure had significant ventilatory reserve at the end of exercise and were able to further increase their maximal minute ventilation, we conclude that respiratory function does not contribute to limitation of exercise in patients with chronic heart failure.     

Relation between ventilation and carbon dioxide production in patients with chronic heart failure.

OBJECTIVES. The aim of this study was to analyze the relation between ventilation and carbon dioxide production and the control of ventilation in patients with chronic heart failure. BACKGROUND. Patients with chronic heart failure exhibit an increased ventilatory response to exercise. Ventilation is closely linked to carbon dioxide production, producing a high correlation between the two variables. This relation is nonlinear at high levels of exercise. METHODS. The ventilation/carbon dioxide production ratio during exercise was examined in 29 patients with chronic heart failure and 9 normal volunteers. RESULTS. In the patients with heart failure, there were three patterns: in the least severely affected patients, the pattern was similar to that of the normal subjects, with an initial decrease in the ventilation/carbon dioxide production ratio to a plateau maintained during exercise; in more severely affected patients, there was an increase in the ratio at the end of exercise, and in the most severely affected patients, the ratio increased from the outset of exercise. The ventilation/carbon dioxide relation is not adequately described by a straight line relation. CONCLUSIONS. The ventilation/carbon dioxide ratio is not fixed, and the changes that occur in this ratio reflect either a noncarbon dioxide-driven ventilatory stimulus or an increase in ventilation-perfusion mismatch due to increased dead space ventilation. The different patterns of this ratio may provide clues to the pathophysiologic mechanisms of the excessive ventilation and breathlessness seen during exercise in chronic heart failure.     

Significance of end-tidal P(CO(2)) response to exercise and its relation to functional capacity in patients with chronic heart failure

OBJECTIVES: The value of end-tidal PCO(2) monitoring during exercise in patients with chronic heart failure has not been elucidated. The present study was designed to examine end-tidal PCO(2) response to exercise and its relation to functional capacity in patients with chronic heart failure. METHODS AND RESULTS: Maximal upright ergometer exercise with respiratory gas analysis and arterial blood gas analysis were performed in 105 patients with chronic heart failure (34 patients in New York Heart Association [NYHA] class I, 38 patients in NYHA class II, and 33 patients in NYHA class III) and 14 normal control subjects. Peak O(2) uptake, excessive exercise ventilation as assessed by the slope of the relation between expired minute ventilation and CO(2) output (VE-VCO(2)), and the ratio of physiologic dead space to tidal volume (VD/VT) were determined. Cardiac output was also measured during exercise in 28 patients with chronic heart failure. Arterial PO(2) or PCO(2) values at rest and during exercise were not different among the four groups. However, end-tidal PCO(2) was significantly lower, and arterial to end-tidal PCO(2) difference and VD/VT were significantly higher in NYHA class III patients than other groups during exercise. The maximal end-tidal PCO(2) during exercise was significantly reduced as the severity of chronic heart failure advanced (45.7 +/- 4.0 mm Hg in normal control subjects, 43.5 +/- 4.8 mm Hg in NYHA class I patients, 39.7 +/- 5.1 mm Hg in NYHA class II patients, and 34.9 +/- 5.3 mm Hg in NYHA class III patients). The maximal end-tidal PCO(2) during exercise was significantly correlated with peak O(2) uptake (r = 0.68; p < 0.001) and maximal cardiac index (r = 0.73; p < 0.001), and inversely related to Ve-VCO(2) (r = - 0.84; p < 0.001) and VD/VT at peak exercise (r = -0.65; p < 0.001). CONCLUSIONS: The decreased end-tidal PCO(2) during exercise, which is caused by high ventilation/perfusion ratio mismatching, reflects both reduced cardiac output response to exercise and increased exercise ventilation due to enlarged physiologic dead space in advanced chronic heart failure. The end-tidal PCO(2) during exercise can be used to evaluate the functional capacity of patients with chronic heart failure.     

The increased ventilatory response to exercise in chronic heart failure: relation to pulmonary pathology.

OBJECTIVE: To assess the exercise limitation of patients with chronic heart failure (CHF) and its relation to possible pulmonary and ventilatory abnormalities. SETTING: A tertiary referral centre for cardiology. METHODS: The metabolic gas exchange responses to maximum incremental treadmill exercise were assessed in 55 patients with CHF (mean (SD) age 57.9 (13.0) years; 5 female, 50 male) and 24 controls (age 53.0 (11.1) years; 4 female, 20 male). Ventilatory response was calculated as the slope of the relation between ventilation and carbon dioxide production (VE/VCO2 slope). RESULTS: Oxygen consumption (VO2) was the same at each stage in each group. Ventilation (VE) was higher in patients at each stage. Patients had a lower peak VO2 and a steeper VE/VCO2 slope than controls. Dead space ventilation as a fraction of tidal volume (VD/VT) was higher in patients at peak exercise, but dead space per breath was greater in controls at peak exercise (0.74 (0.29) v 0.57 (0.17) litres/breath; P = 0.002). End tidal CO2 was lower in patients at all stages, and correlated with peak VO2 (r = 0.58, P < 0.001). Alveolar oxygen tension was higher in patients at each stage than in controls. CONCLUSIONS: Patients with CHF have an increased ventilatory response at all stages of exercise. Although this is accompanied by an increase in VD/VT, there is hyperventilation relative to blood gases. It is more likely that the excessive ventilation is not due to a primary pulmonary pathology, but rather, the increase in dead space is likely to be a response to increased ventilation.     

Cardiopulmonary interaction in heart failure

In heart failure lung dysfunction is frequent and is greater the greater the heart failure severity. It can be evaluated in terms of lung mechanics and gas diffusion. Indeed heart-lung interaction is related to heart dimensions and lung fluid content; furthermore heart-lung interaction is influenced by the body position. Lung diffusion is also altered in patients with chronic heart failure, and a low gas diffusion is associated with a reduced performance. During exercise, heart-lung interaction becomes more evident. Heart failure patients show an abnormal hyperventilation due to a progressively increased respiratory rate, and a lower tidal volume; hyperventilation is due to different causes including enhanced responses from chemo- and metabolo-receptors, increased CO(2) production and increased dead space ventilation. Several drugs affect the ventilatory pattern in heart failure patients: ACE-inhibitors and anti-aldosteronic drugs improve lung diffusion and ventilatory efficiency during exercise; beta-blockers reduce exercise-induced hyperventilation. Furthermore, ultrafiltration improves lung mechanics, both at rest and during exercise, through body fluid content reduction.     

Ventilatory mechanisms of exercise intolerance in chronic heart failure.

Mechanisms that have been suggested to underlie the abnormal ventilatory response to exercise in patients with chronic congestive heart failure (CHF) include high pulmonary pressures, ventilation-perfusion mismatching, early metabolic acidosis, and abnormal respiratory control. To evaluate the role that ventilation and gas exchange play in limiting exercise capacity in patients with CHF, data from 33 patients with CHF and 34 normal subjects of similar age who underwent maximal exercise testing were analyzed. Maximal oxygen uptake was higher among normal subjects (31.7 +/- 6 ml/kg/min) than among patients with CHF (17.7 +/- 4 ml/kg/min; p less than 0.001). The ventilatory equivalent for oxygen, expressed as a percentage of maximal oxygen uptake, was 25% to 35% higher among patients with CHF compared with normal subjects throughout exercise (p less than 0.01). A steeper component effect of ventilation on maximal oxygen uptake was observed among normal subjects compared with patients with CHF, which suggests that a significant portion of ventilation in CHF is wasted. Maximal oxygen uptake was inversely related to the ratio of maximal estimated ventilatory dead space to maximal tidal volume (VD/VT) in both groups (r = -0.73, p less than 0.001). Any given oxygen uptake at high levels of exercise among patients with CHF was accompanied by a higher VD/VT, lower tidal volume, and higher respiratory rate compared with normal subjects (p less than 0.01). Relative hyperventilation in patients with CHF started at the beginning of exercise and was observed both below and above the ventilatory threshold, which suggests that the excess ventilation was not directly related to earlier than normal metabolic acidosis. Thus abnormal ventilatory mechanisms contribute to exercise intolerance in CHF, and excess ventilation is associated with both a higher physiologic dead space and an abnormal breathing pattern. The high dead space is most likely due to ventilation-perfusion mismatching in the lungs, which is related to poor cardiac output, and the abnormal breathing pattern appears to be an effort to reduce the elevated work of breathing that is caused by high pulmonary pressures and poor lung compliance.     

Ventilatory capacity and exercise tolerance in patients with chronic stable heart failure

BACKGROUND: Patients with chronic heart failure complain of breathlessness. This is associated with an increase in the ventilatory response to carbon dioxide production (VE/VCO(2) slope), yet a reduction in the maximal ventilation achieved at peak exercise. We analysed ventilatory capacity in heart failure in relation to exercise capacity. METHODS: We analysed data from 74 patients with chronic stable heart failure [age (S.D.) 50.6 (8.8) years; left ventricular ejection fraction 30 (15)%] and 36 controls [48.9 (11.5) years]. Subjects undertook maximal incremental exercise testing with metabolic gas exchange measurements to derive peak oxygen consumption (VO(2)), the VE/VCO(2) slope and ventilation. Spirometry was used to measure FEV(1) and FVC. Maximal voluntary ventilation (MVV) was calculated as FEV(1)x 35. RESULTS: Peak VO(2) was lower in patients [20.9 (7.5) ml min(-1) kg(-1) vs. 34.5 (10.1); P<0.001] and VE/VCO(2) greater [33.4 (10.7) vs. 26.0 (4.7); P<0.001]. Ventilation at peak exercise was lower in patients [63.5 (20.4) l/min vs. 86.9 (29.5); P<0.001], as was MVV [110.1 (37.9) l/min vs. 136.2 (53.1); P<0.001], but ventilation at peak as a proportion of MVV was the same in patients [60.0 (19.0)%] as controls [65.7 (12.4)%)]. There was an inverse relation between peak VO(2) and VE/VCO(2) slope (r=-0. 62; P<0.001). Percentage predicted FEV(1) correlated with ventilation at peak (r=0.62; P<0.001) and inversely with VE/VCO(2) slope (r=-0.32; P<0.001). There was no relation between percentage of MVV achieved and peak VO(2), or VE/VCO(2) slope. CONCLUSIONS: Although ventilation at peak exercise is lower in patients with heart failure than normal subjects, ventilation is the same proportion of maximal voluntary ventilation. These findings suggest that ventilatory capacity does not limit exercise capacity in heart failure.     

Increased exercise capacity after digoxin administration in patients with heart failure

Failure to objectively assess the effect of digitalis on exercise capacity has resulted in controversy regarding its use in patients with chronic congestive heart failure. To clarify this situation, maximal treadmill testing with respiratory gas exchange analysis was performed on 11 patients (mean age 57 +/- 9 years) with chronic congestive heart failure with and without digoxin therapy. Ten of the 11 had a consistent third sound gallop, and the mean ejection fraction of the group was 24 +/- 10%. Rest heart rate was significantly higher (91 +/- 16 versus 102 +/- 16 beats/min; p less than 0.05) and rest systolic blood pressure was significantly reduced in the absence of digoxin (130 +/- 23 versus 121 +/- 15 mm Hg; p less than 0.05). No differences in heart rate or blood pressure were observed during exercise. Significant increases in ventilatory oxygen uptake were observed with digoxin submaximally (3.0 mph, 0% grade), at the gas exchange anaerobic threshold and at maximal exercise (mean increase of 2.6 ml/kg per min; p less than 0.02). An improvement in the estimated ratio of ventilatory dead space to tidal volume (VD/VT), an index of physiologic efficiency, occurred throughout exercise during digoxin therapy, and there was a significant negative correlation between the change in maximal oxygen uptake and change in maximal estimated VD/VT (r = -0.63; p less than 0.05). Thus, digoxin therapy is associated with a significant improvement in exercise capacity in patients with chronic heart failure, most likely due to an improved matching of ventilation to perfusion.     

Perfusion/ventilation mismatch during exercise in chronic heart failure: an investigation of circulatory determinants.

BACKGROUND--The ventilatory cost of carbon dioxide (CO2) elimination on exercise (VE/VCO2) is increased in chronic heart failure (CHF). This reflects increased physiological dead space ventilation secondary to mismatching between perfusion and ventilation during exercise. The objectives of this study were to investigate the relation of this increased VE/VCO2 slope to the syndrome of CHF or to limitation of the exercise related increase of pulmonary blood flow, or both. PATIENTS AND METHODS--Maximal treadmill exercise tests with respiratory gas analysis were performed in 45 patients with CHF (defined as resting left ventricular ejection fraction < 40% on radionuclide scan); 15 normal controls; 23 patients with coronary artery disease and normal resting left ventricular function; and 13 pacemaker dependent patients (six with and seven without CHF) directly comparing exercise responses in rate responsive and fixed rate mode. RESULTS--Patients with CHF had a steeper VE/VCO2 slope than normal controls: this was related inversely to peak VO2 below 20 mol/min/kg. In patients with coronary artery disease in whom peak VO2 (at respiratory exchange ratio > 1) was as limited as in the patients with CHF but resting left ventricular function was normal, the VE/VCO2 slope was normal. In pacemaker dependent patients fixed rate pacing resulted in lower exercise capacity and peak VO2 than rate responsive pacing; the VE/VCO2 slope was normal in patients without CHF but steeper than normal in patients with CHF; the VE/VCO2 slope was steeper during fixed rate than during rate responsive pacing in these patients with CHF. CONCLUSIONS--These findings suggest that the perfusion/ventilation mismatch during exercise in CHF is related to the chronic consequences of the syndrome and not directly to limitation of exercise related pulmonary flow. Only when the syndrome of CHF is present can matching between perfusion and ventilation be acutely influenced by changes in pulmonary flow.     

Relationship between ventilatory expired gas and cardiac parameters during symptom-limited exercise testing in patients with heart failure.

PURPOSE: This study investigates the relationship between ventilatory expired gas and cardiac parameters measured during exercise testing in patients with heart failure. METHODS: Twenty-five subjects (12 male, 13 female) diagnosed with compensated heart failure underwent symptom-limited exercise testing with ventilatory expired gas analysis. Metabolic and cardiac measures of interest were collected during testing. RESULTS: Mean peak oxygen consumption (VO2), minute ventilation/carbon dioxide production (VE/VCO2) slope, percentage of age predicted maximal heart rate achieved during exercise testing (%APMHR), and peak respiratory exchange ratio were 14.7 +/- 4.7 mL O2/kg/min-1, 33.8 +/- 9.8, 76% +/- 15%, and 1.1 +/- 0.11, respectively. The VE/VCO2 slope was significantly correlated with the following: %APMHR (r = -0.81, P < 0.001), peak VO2 (r = -0.83, P < 0.001), VO2 at ventilatory threshold (r = -0.70, P < 0.001), and the dead space to tidal volume ratio (VD/Vt) (r = 0.65, P < 0.001). The ability of peak VO2 and %APMHR to predict the VE/VCO2 slope was significant (r = 0.86, r2 = 0.72, P < 0.0001). CONCLUSION: This study demonstrates the importance of analyzing multiple exercise test parameters, including metabolic measures, in patients with heart failure.     

A critical threshold of exercise capacity in the ventilatory response to exercise in heart failure.

During exercise patients with chronic left heart failure ventilate more than normal individuals at the same workload; the ratio of minute ventilation to minute production of carbon dioxide (VE/VCO2) is increased. The relation between increased VE/VCO2, severity of heart failure, and exercise capacity has not been defined. VE/VCO2 was measured in 47 patients with chronic left heart failure (New York Heart Association grades II and III) and in 1009 healthy controls. Exercise capacity was assessed by peak oxygen consumption (VO2max) during progressive exercise. In the controls VO2max ranged from 25 to 93 ml/kg/min; VE/VCO2 was 17-36 and did not correlate with VO2max. In chronic left heart failure the VO2max ranged from 9 to 29 ml/kg/min; VE/VCO2 was 22-42 and correlated strongly with VO2max. End tidal carbon dioxide and respiratory rate at peak exercise were similar in the controls and patients with chronic left heart failure. The increase in VE/VCO2 on exercise in chronic left heart failure indicates increased physiological dead space, presumably caused by a ventilation-perfusion mismatch. In the controls and patients with chronic left heart failure the relation of VE/VCO2 to VO2max was curvilinear with a threshold of VO2max below which VE/VCO2 started to rise above the normal range. This point of inflection may be explained by the existence of a critical level of cardiac function necessary to perfuse adequately all lung zones on exercise.     

A critical threshold of exercise capacity in the ventilatory response to exercise in heart failure

During exercise patients with chronic left heart failure ventilate more than normal individuals at the same workload; the ratio of minute ventilation to minute production of carbon dioxide (VE/VCO2) is increased. The relation between increased VE/VCO2, severity of heart failure, and exercise capacity has not been defined. VE/VCO2 was measured in 47 patients with chronic left heart failure (New York Heart Association grades II and III) and in 1009 healthy controls. Exercise capacity was assessed by peak oxygen consumption (VO2max) during progressive exercise. In the controls VO2max ranged from 25 to 93 ml/kg/min; VE/VCO2 was 17-36 and did not correlate with VO2max. In chronic left heart failure the VO2max ranged from 9 to 29 ml/kg/min; VE/VCO2 was 22-42 and correlated strongly with VO2max. End tidal carbon dioxide and respiratory rate at peak exercise were similar in the controls and patients with chronic left heart failure. The increase in VE/VCO2 on exercise in chronic left heart failure indicates increased physiological dead space, presumably caused by a ventilation-perfusion mismatch. In the controls and patients with chronic left heart failure the relation of VE/VCO2 to VO2max was curvilinear with a threshold of VO2max below which VE/VCO2 started to rise above the normal range. This point of inflection may be explained by the existence of a critical level of cardiac function necessary to perfuse adequately all lung zones on exercise.     

Cardiopulmonary exercise testing in congestive heart failure

Cardiopulmonary exercise testing includes the monitoring of respiratory gases and airflow to determine oxygen uptake, carbon dioxide (CO2) production, respiratory rate, tidal volume, and minute ventilation during a graded maximal exercise test. A plateau in oxygen uptake, which occurs despite an increase in work load, and which is termed maximal oxygen uptake (VO2 max), correlates with the maximal exercise cardiac output and can therefore be used to grade the severity of heart failure. The anaerobic threshold occurs at 60 to 70% of VO2 max and is another indicator of the severity of heart failure and, when attained, indicates that the patient is close to performing a maximal test. We have found VO2 max and anaerobic threshold to be objective measures of efficacy of both investigational and noninvestigational therapy in patients with heart failure. A pulmonary limitation to exercise can be identified by the failure to attain anaerobic threshold or VO2 max, as well as exhaustion of the ventilatory reserve, as estimated by maximal voluntary ventilation. Thus, cardiopulmonary exercise testing can be used to (1) grade the severity of heart failure, (2) objectively follow the response to therapy, and (3) differentiate a cardiac from a pulmonary limitation to exercise.     

吸入异丙托溴胺对慢性阻塞性肺疾病患者运动肺功能的影响

目的 评价吸入异丙托溴胺(ipratropium bromide,IPB)是否改善慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)患者的静态肺功能,运动通气功能和运动耐量.方法 随机抽取稳定期COPD患者12例,吸入IPB溶液2 mg,吸人前后分别进行静态肺功能和运动肺功能测定.结果 吸入IPB后,COPD患者最大运动功率(Wmax)、最大耗氧量(VO2max)、最大运动时每分钟通气量(Vemax)和比潮气量(Vtmax/IC),较吸人前均有显著增加;死腔通气(VD/VT)和二氧化碳通气当量(Vemax/VCO2max)无明显改变.Vtmax/IC的变化(⊿Vtmax/IC)与VO2max的变化(⊿VO2max)有显著相关性(r=0.598,P＜0.05);⊿Vtmax/IC与最大运动功率的变化(⊿Wmax)也存在显著相关性(r=0.743,P＜0.05).结论 吸入IPB能够增加COPD患者的运动耐量,COPD患者吸入IPB后,⊿Vtmax/IC可能是运动耐量增加机制中的一个重要环节.     

Response in oxygen uptake and ventilation during stair climbing in patients with chronic heart failure

To examine the level of muscular work and ventilatory response to stair climbing (mobile Stairmaster staircase, 1 step/2.5 s), respiratory gas exchange, ventilation, heart rate and arterial pressure were monitored in patients with chronic heart failure and their response compared with that of normal individuals. Aerobic capacity (maximal oxygen uptake) and anaerobic threshold during treadmill exercise were also determined and used to ascertain the metabolic cost of stair climbing. No differences were observed in the response of mean arterial blood pressure between the 12 patients and 10 normal subjects during exercise or recovery. However, the heart rate and oxygen consumption obtained during exercise were significantly lower in the patients with chronic heart failure than in the normal subjects (p less than 0.05). All patients with a maximal oxygen uptake less than 20 ml/min/kg during treadmill exercise had an oxygen uptake during stair climbing that exceeded their anaerobic threshold and, consequently, they attained a significantly (p less than 0.01) higher level of ventilation during exercise and recovery. This was not the case for those patients with greater aerobic capacity. Therefore, it is concluded that stair climbing for the 12 patients with heart failure and moderate to moderately severe impairment in aerobic capacity represents strenuous anaerobic exercise. The resultant excess ventilation may explain the limiting sensation of dyspnea that is frequently experienced by these patients during and after stair climbing.     

Differential contribution of dead space ventilation and low arterial pCO2 to exercise hyperpnea in patients with chronic heart failure secondary to ischemic or idiopathic dilated cardiomyopathy

In chronic heart failure (CHF), the abnormally large ventilatory response to exercise (VE/VCO(2) slope) has 2 conceptual elements: the requirement of restraining arterial partial pressure of carbon dioxide (pCO(2)) from increasing (because of an increased ratio between increased physiologic dead space and tidal volume [VD/VT]) and the depression of arterial pCO(2) by further increased ventilation, which necessarily implies an important non-carbon dioxide stimulus to ventilation. We aimed to assess the contribution of these 2 factors in determining the elevated VE/VCO(2) slope in CHF. Thirty patients with CHF underwent cardiopulmonary exercise testing (age 65 +/- 11 years, left ventricular ejection fraction 34 +/- 15%, peak oxygen uptake 15.2 +/- 4 ml/kg/min, VE/VCO(2) slope 36.4). At rest and during exercise, arterial pCO(2) was measured and VD was calculated and separated into serial and alveolar components. VD/VT decreased from 0.57 at rest to 0.44 at peak exercise (p <0.01). VE/VCO(2) slope was correlated with peak exercise VD/VT (r = 0.67), the serial VD/VT ratio (r = 0.64), and alveolar VD/VT ratio (r = 0.51) at peak exercise (all p <0.01). VE/VCO(2) slope was also correlated with arterial pCO(2) (r = -0.75, p <0.001). Despite this, arterial pCO(2) was not related to peak oxygen uptake (r = 0.2) or to arterial lactate (r = -0.25) and only weakly to New York Heart Association functional class (F = 3.7). First, the increased VE/VCO(2) slope was caused by both the high VD/VT ratio and by other mechanisms, as shown by low arterial pCO(2) during exercise. Second, this latter component (depression of arterial pCO(2)) was not related to conventional measures of heart failure severity.     

Ventilation in chronic heart failure: effects of physical training.

OBJECTIVE--To assess the effects of exercise training on ventilatory function in chronic heart failure. DESIGN--Observer blinded random allocation crossover training and detraining trial. SETTING--Assessment in hospital based clinical laboratory; training home based. PATIENTS--22 patients with chronic heart failure (New York Heart Association (NYHA) class II or III) recruited from a tertiary referral centre. All finished the study. INTERVENTION--Bicycle ergometer exercise for 20 minutes a day, five days a week for eight weeks at 70%-80% of maximum heart rate. MAIN OUTCOME MEASURES--Exercise capacity on graded incremental exercise test, minute ventilation, oxygen consumption and carbon dioxide output. RESULTS--Peak work load increased from 96 W to 112 W and peak oxygen consumption from 14.1 ml/kg/min to 15.4 ml/kg/min (p < 0.01). At submaximal workloads carbon dioxide excretion (VCO2) and minute ventilation (Vi) decreased significantly (p < 0.05) though oxygen consumption was unchanged. The relation between Vi and carbon dioxide excretion changed: the slope of the Vi to VCO2 plot decreased from 38.6 to 35.3, indicating an improvement in overall ventilary efficiency. The instantaneous carbon dioxide ventilatory equivalent (Vi/VCO2) decreased at submaximal workloads, and reached a lower minimum value after training, indicating that optimum ventilatory performance improved. The exercise capacity of patients was related to the optimum ventilatory performance. It is suggested that this may in part be mediated through changes in skeletal muscles. CONCLUSION--Exercise training reduces the ventilatory abnormalities in chronic heart failure; thus some of these changes may be due to physical deconditioning.