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

Abstract

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 (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 produc- (Heart 1997;77:138-146) Keywords: metabolic gas exchange; dead space ventilation; chronic heart failure; exerciseThe cardinal feature of the syndrome of chronic heart failure is exercise limitation. The symptoms causing limitation are most frequently shortness of breath and muscle fatigue. Either symptom can occur in the same patient depending upon the type of exercise undertaken. 12 The syndrome is commonly assessed clinically using incremental exercise protocols to determine ventilation and metabolic gas exchange. Peak exercise capacity is measured as peak oxygen consumption (Vo2), although the reduction in peak Vo2 characteristic of chronic heart failure correlates only poorly with indices of haemodynamic function.134 Many investigators have shown that there is an increase in ventilation,5-7 and this increase in ventilation (VE) expressed as an increase relative to the rate of carbon dioxide production (Vco2), as VEIVCO2 slope, correlates closely with reduction in peak Vo2.89To account for the increased ventilatory response, several investigators have proposed that dead space ventilation is increased,7101 although how this abnormality is sensed is difficult to imagine, given the stability of arterial blood gas tensions during exercise in heart failure. 1213 We have explored the relations between ventilation, blood gas tensions, dead space, and metabolic gas exchange in a large group of patients with chronic heart failure and age matched controls in an attempt to determine the cause of the ventilatory abnormalities. MethodsWe examined the responses of 55 patients (average age 57-9 (SD 13.0) years; five female, 50 male) with documented treated, stable chronic heart failure. The diagnosis was confirmed by the presence of at least the following: (1)

Prognostic Impact of Ventilatory Efficiency in Heart Disease Patients With Preserved Exercise Tolerance

“…Recently, the V • E/V • CO2 slope was proposed as a marker of disease severity in patients with heart failure. [6][7][8] The finding that the V • E/V • CO2 slope is a powerful prognostic marker independent of peak V…”

“…[6][7][8] Increased ventilation/perfusion (V • /Q • ) mismatching is one of the principal mechanisms by which the V…”

Excessive Ventilatory Response During Exercise in Patients With Non-Hypoxic Pulmonary Hypertension.

“…[5][6][7][8][9] Furthermore, SLOPE is an index of ventilatory -perfusion inequality. 6,9 Few studies have investigated the relationship between exercise capacity and SLOPE in patients with pulmonary hypertension (PH), so we examined the relationship between exercise capacity and SLOPE in patients with PH, and the differences in ventilatory response between them and patients with a stable old myocardial infarction (OMI). We also discuss the meaning of the exercise tolerance test in PH patients.…”

Heart rate response to graded exercise correlates with aerobic and ventilatory capacity in patients with heart failure

“…19,30 However, the increased ventilatory drive could be a response to an abnormal stimulus rather than merely a consequence of pulmonary involvement. 31 Increased chemoreflex sensitivity is a common finding in CHF, and activation of chemoreceptors increases ventilation and pulmonic vasoconstriction. 11,13 According to Clark et al, 31 excessive ventilation could be a cause and not a consequence of increased dead space.…”

“…31 Increased chemoreflex sensitivity is a common finding in CHF, and activation of chemoreceptors increases ventilation and pulmonic vasoconstriction. 11,13 According to Clark et al, 31 excessive ventilation could be a cause and not a consequence of increased dead space. The relationship between ventilatory competence, chronotropic response, and aerobic capacity that we observed supports the hypothesis of a unique pathophysiologic model driven by autonomic dysfunction.…”