Hyperhidrosis: the neglected sign in heart failure patients.

Abstract

Profuse sweating is a symptom often reported by cardiological patients and could be also an early phenomenon of adaptation or rather cardiac maladaptation in the context of incipient heart failure (HF). By definition, in HF patients the low cardiac output causing reduced renal blood supply and reduced pressure in the arterial baroreceptors activate compensatory mechanisms such as the RAAS and the adrenergic autonomic nervous system. The retention of fluids caused by the decompensation of heart-kidney system could generate a reactive hyperhidrosis and even anticipate an incipient decompensation and might prevent manifest volume overload. Moreover, in HF patients the overactive sympathetic nervous system generates an increase in the reabsorption of fluids in the kidney, on the other hand it generates a signaling to the sweat glands to induce a dispersion of fluids, with loss of sodium and chlorine at the glandular ductal level. Finally sweat gland production physiology during physical activity is also altered in HF patients. This review is focused on sweating and its pathophysiological role in heart failure. Although all the mechanisms underlying this phenomenon are not fully understood, there are interesting connections that might explain this fluid elimination as a wise and sophisticated way to prevent incipient heart failure crisis. Future research could be focused on studying new drugs that selectively would be able to promote fluid elimination by this specific way in patients suffering from heart failure.