SUMMARY Muscular work requires the integration of cardiopulmonary mechanisms for gas exchange and 02 delivery. In patients with chronic cardiac failure, the response of these mechanisms may be impaired, and the pattern of 02 utilization (VO2) and gas exchange during exercise would thus provide an objective assessment of the severity of heart failure. Accordingly, rates of air flow, 0, uptake, CO, elimination and minute ventilation were determined during progressive treadmill exercise in 62 patients with stable heart failure. Exercise cardiac output, systemic 0, extraction and lactate production were measured directly in 40 patients with heart failure of varying severity. As the severity of heart failure increased from class A to D, there was a progressive decrease in exercise capacity (from 1157 4 154 to 373 ± 157 seconds) and maximum VO, (23 ± 3.1 to 8.4 ± 1.5 ml/min/kg). These decreases corresponded with the reduced maximum cardiac output and stroke volume during exercise. The appearance of anaerobic metabolism (580 ± 17 to 157 ± 7 seconds of exercise) and the corresponding anaerobic threshold (17 ± 0.34 to 7.1 i 1.5 ml/min/kg), determined noninvasively, were reproducible and correlated with the rise in mixed venous lactate concentration. No apparent untoward effects were experienced during or after the progressive exercise test. We conclude that the measurement of respiratory gas exchange and air flow during exercise is an objective, reproducible and safe noninvasive method for characterizing cardiac reserve and functional status in patients with chronic cardiac failure.AT REST, patients with heart disease often display normal cardiac performance. To elicit an abnormality in ventricular function, a physiologic stress, such as exercise, is required. This concept is well recognized clinically, when the severity of cardiac failure is traditionally evaluated in terms of information that relates levels of exertion with the appearance of breathlessness or fatigue. A more quantitative approach based on the pathophysiologic response to progressive exercise would be valuable for assessing the severity of cardiac disease and the functional capacity.Muscular work elicits a complex interplay of diverse physiologic mechanisms designed to ensure that 02 delivery is commensurate with 02 demand. The heart, lung and 02 carrying capacity of the blood participate in these adjustments. In patients with heart disease, cardiac output may not rise appropriately during exercise. The 02 delivery system is then compromised, and the aerobic capacity is thus reduced. Determination of 02 utilization during exercise, measured by the collection of expired air, provides an objective assessment of functional capacity in normal subjects and in patients with valvular heart disease.1-4 However, enthusiasm for using this method to evaluate patients with chronic failure irrespective of cause and severity is tempered by the relative uncertainty of correlating respiratory gas exchange with cardiac function, the perceived hazards of exposing the pat...