Assessment of exercise tolerance in chronic congestive heart failure

Abstract

In patients with chronic heart failure, exercise capacity is poorly related to cardiac hemodynamics, and peripheral circulation is an important determinant of exercise tolerance. The ability of the muscle vasculature to dilate is markedly impaired, in part, because of exaggerated neurohumoral activity increasing vascular wall stiffness. For this reason, increasing cardiac output is not sufficient to increase exercise capacity if not accompanied by improving vascular reactivity. The poor reliability and reproducibility of exercise tolerance assessed by maximal exercise duration or maximal attained work load (particularly on a treadmill) has led to widespread measurement of respiratory gas during exercise. Peak oxygen consumption (peak VO2), even if it is symptom-limited, has been shown to be a very reproducible criterion of exercise tolerance; moreover, because VO2 is the product of cardiac output and arteriovenous oxygen difference, it also has a qualitative hemodynamic significance. Ventilatory threshold can be determined before maximal exercise; however, problems of determination limit the practical value of this criterion. Unfortunately, peak VO2 lacks sensitivity to detect minor improvement or impairment of symptoms during daily life, although these are significant to the patient. Submaximal exercises have been proposed for this purpose and are currently being evaluated.