Lung Function and Exercise Gas Exchange in Chronic Heart Failure

Abstract

Background The ventilatory response to exercise in patients with chronic heart failure (HF) is greater than normal for a given metabolic rate. The objective of the present study was to determine the mechanism(s) for the high ventilatory output in patients with chronic HF. Methods and Results Centers in Germany, Italy, Japan, and the United States participated in this study. Each center contributed studies on patients and normal subjects of similar age and sex. One hundred thirty patients with chronic HF and 52 healthy subjects participated. Spirometric and breath-by-breath gas exchange measurements were made during rest and increasing cycle exercise. Arterial blood was sampled for measurement of pH, Pa co 2 , Pa o 2 , and lactate during exercise in 85 patients. Resting forced expiratory volume in 1 second (FEV 1 ) and vital capacity (VC) were proportionately reduced at all levels of impairment. Patients with more severe HF had greater tachypnea and a smaller tidal volume (V t ) at a given exercise expired volume per unit time (V̇ e ). This was associated with an expiratory flow pattern characteristic of lung restriction. V̇ e and V̇ co 2 as a function of V̇ o 2 were increased during exercise in HF patients. The increases were greater the lower the peak V̇ o 2 per kilogram of body weight. The ratio of V d (physiological dead space) to V t and the difference between arterial and end tidal P co 2 at peak V̇ o 2 also increased inversely with peak V̇ o 2 /kg. In contrast, the difference between alveolar and arterial P o 2 and PaCO 2 were both normal, on average, at peak V̇ o 2 regardless of the level of impairment. The more severe the exercise limitation, the higher the lactate and the lower the HCO 3 − at a given V̇ o 2 , although pH was tightly regulated. Conclusions The increase in V̇ e in chronic HF patients is caused by an increase in V d /V t due to high ventilation/perfusion mismatching, an increase in V̇ co 2 relative to V̇ o 2 resulting from HCO 3 − buffering of lactic acid, and a decrease in Pa co 2 due to tight regulation of arterial pH. With regard to the excessive V̇ e in HF patients, the increases in V d /V t and V̇ co 2 relative to V̇ o 2 are more important as the patient becomes more exercise limited. Regional hypoperfusion but not hypoventilation typifies lung gas exchange in HF. This and other mechanisms might account for the restrictive changes leading to exercise tachypnea in HF patients.