[Ergospirometry in the evaluation of cardiovascular drugs]

In the evaluation of drugs intended to alleviate symptomatology and to improve exercise capacity in congestive heart failure, various pathophysiologic mechanisms including impairment of cardiac output, oxygenation of blood, muscle blood flow, and muscle metabolism have to be considered. In various forms of acute and chronic heart failure these mechanisms contribute more or less to impaired oxygen uptake. In acute forms of heart failure pulmonary congestion and its effects on airway resistance and lung capacity might be the predominating mechanisms of symptoms, while in chronic heart failure impedement of muscle blood flow and metabolic changes, comparable with deconditioning, are additional pathomechanisms. The increase in cardiac output and in muscle blood flow provided by some positive inotropic agents and by vasodilators after acute administration is often paralleled by a decrease in arteriovenous oxygen difference and does not lead to an improvement of oxygen uptake. However, chronic therapy with some vasodilators can lead to improvement in oxygen uptake, either due to training effects or due to flow dependent or direct effects on muscle metabolism. In pulmonary congestion a decrease of elevated filling pressures can acutely lead to some improvement of exercise capacity. Furthermore, chronic decrease in filling pressures by administration of diuretics, nitrates, ACE-inhibitors or dopaminergic drugs leads to long-term improvement in oxygen uptake. By comparing hemodynamic effects of acute and chronic drug therapy in CHF with their effects on exercise capacity, the chronic decrease of filling pressures seems to be the major hemodynamic variable leading to improvement of exercise capacity.(ABSTRACT TRUNCATED AT 250 WORDS)