Increased exercise ventilation in patients with chronic heart failure: intact ventilatory control despite hemodynamic and pulmonary abnormalities.

Abstract

This study was designed to determine the pathophysiologic basis of increased exercise ventilation in the presence of chronic heart failure. Sixty-four ambulatory patients with chronic heart failure and 38 age-matched normal control subjects performed exercise according to identical staged, symptom-limited bicycle exercise protocols with measurement of hemodynamic, ventilatory, and metabolic responses. Compared with normal subjects, ventilation and the ratio of ventilation to CO2 production (Ve/VC02), and pulmonary capillary wedge pressure were elevated in patients at rest and during exercise. The ratio of pulmonary dead space to tidal volume (Vd/Vt) also was elevated in the heart failure group at rest and during exercise and was closely related to Ve/VC02 (all r > .72, p < .001). Rest and exercise arterial PCO2 regulation was normal in patients. Peak exercise Ve!VC02 did not correlate with pulmonary vascular pressures, but was inversely related to cardiac output (r = -.49, p < .001). Thus, neurohumoral ventilatory control mechanisms are intact in patients with chronic heart failure and act to maintain normal PacO2 levels in the face of increased pulmonary dead space. Activation of abnormal reflexes due to hemodynamic derangements during exercise are not important in determining ventilation in the presence of chronic heart failure. The demonstration of a correlation between decreased cardiac output and increased ventilation in the patient group suggests that attenuated pulmonary perfusion may play a role in causing exercise hyperpnea in the presence of chronic heart failure by producing ventilation perfusion abnormalities and thereby increasing physiologic pulmonary dead space. Circulation 77, No. 3, 552-559, 1988. IN PATIENTS who present with acute pulmonary edema, a rapid elevation in pulmonary capillary wedge pressure leads to interstitial fluid accumulation, decreased lung compliance, and obstructive airway physiology,"1 2 and is the primary factor causing dyspnea. However, the role of increased intrapulmonary vascular pressures in causing ventilatory abnormalities and dyspnea in stable ambulatory patients with chronic heart failure has not been clearly defined. Studies in patients with mainly valvular heart disease have emphasized the importance of elevated pulmonary capillary wedge pressures during exercise in causing dysp-

Exercise Tolerance, Exercise Hyperpnea and Central Chemosensitivity to Carbon Dioxide in Sleep Apnea Syndrome in Heart Failure Patients

“…Exercise hyperpnea correlates with ventilatory perfusion abnormalities and increasing physiological pulmonary dead space. 29 Because of left ventricular end-diastolic volume and pulmonary capillary wedge pressure are associated with CHF-CSAS, 26,27 and because of the presence of increased ventilatory perfusion abnormalities and physiological pulmonary dead space, the V…”

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

“…[9][10][11] Because deteriorated alveolar hypoventilation rarely occurs in patients with heart failure, the cause of the augmented V…”

Diaphragmatic function after intense exercise in congestive heart failure patients

“…Studies have found respiratory muscle weakness [3] and reduced respiratory muscle endurance [4] in patients with CHF. In addition, patients with heart failure show an increased ventilatory response to exercise [5], further exacerbating the imbalance between inspiratory muscle capacity and load. Therefore, it is reasonable to hypothesise that diaphragmatic fatigue may occur in patients with CHF when stressed by exercise.…”