Congestive Heart Failure

Abstract

The deleterious consequences of sympathetic activation in chronic heart failure (CHF) have been recognized for nearly 2 decades. 1 The degree of excess neurohormonal activation in this condition correlates with disease severity, is associated with progressive deterioration of cardiac function, accelerates abnormal myocardial remodeling after an infarction, and increases mortality rates. 2-4 In recent years, an interest in beta-adrenergic blocking agents as a therapeutic option in heart failure From the

The ventilatory component of the muscle metaboreflex: catch me if you can!

“…How breathing is regulated during a dynamic exercise to produce an increase in alveolar ventilation commensurate to the change in metabolic rate has long puzzled, if not obsessed, some of the most significant respiratory physiologists (Comroe & Schmidt, 1943;Dejours, 1956Dejours, , 1964Geppert & Zuntz, 1888;Grodins, 1950;Harrison, Harrison, Calhoun, & Marsh, 1932;Zuntz & Geppert, 1886). The ventilatory response to exercise has a very predictable temporal profile: a constant work rate produces an increase in ventilation that always displays an exponential-like pattern (Whipp & Ward, 1980), with an ∼1 min time constant, following an immediate rise whenever exercise is performed from rest (Dejours, 1959).…”

Exchange of Views rebuttal: Reply to White and Bruce

“…As a thought experiment, one could pick the old, yet elegant, theory of Harrison, Harrison, Calhoun, & Marsh (1932) on the role of afferent fibres originating in the right circulation that respond to the load imposed on venous return, a mechanism that has never been disproved (Haouzi, 2009). It is perfectly possible to explain the hyperventilation produced by exercise in patients with cardiac failure through such a mechanism.…”