Breathless Heart: Final Remarks

Abstract

Whichever the initial noxa damaging the heart is, this elicits a remodeling process, leading to cardiac dysfunction and pump failure, as well as to an increasing arrhythmic burden. The abnormal hemodynamics, accompanied by a decrease in cardiac output, are sensed by visceral feedback systems, modulating autonomic tone. As a consequence, baroreflex is deactivated, while ergoreflex and chemoreflex are stimulated, inducing vagal withdrawal and eliciting adrenergic activation, with a net effect of sympathetic predominance on the neural drive to the heart and vessels. This may be considered an initial compensatory response, because of its effect on vasomotion and mean arterial pressure, on inotropism, and on water–salt retention and plasma volume, further becoming maladaptive, accelerating ventricular remodeling, causing peripheral and pulmonary edema, with accompanying dyspnea, and increasing the risk of sudden death. With time, the combined effect of delayed circulatory time and increased chemoreflex (together with other mechanisms) promotes a delayed robust ventilatory response and blood gas instability, thus favoring the occurrence of periodic breathing (PB) or Cheyne–Stokes respiration (CSR). PB/CSR can be therefore considered as a «marker of clinical severity» of heart failure and has been outlined as a «risk marker», i.e., as predictor of future fatal events.