Thirst in critically ill patients: from physiology to sensation

Abstract

Critically ill patients often report distressful episodes of severe thirst, but the complex biochemical, neurohormonal mechanisms that regulate this primal sensation still elude clinicians. The most potent stimuli for thirst are subtle increases in plasma osmolality. These minute changes in osmolality stimulate central osmoreceptors to release vasopressin (also known as antidiuretic hormone). Vasopressin in turn acts on the kidneys to promote the reabsorption of water to correct the increased osmolality. If this compensatory mechanism fails to decrease osmolality, then thirst is triggered to motivate drinking. In contrast, thirst induced by marked volume loss, or hypovolemic thirst, is subject to the tight osmoregulation of the renin-angiotensin aldosterone system and accompanying adrenergic agonists. Understanding the essential role that thirst plays in salt and water regulation can provide clinicians with a better appreciation for the complex physiology that underlies this intense sensation.

Figure

Effect of dehydration on neurohormonal pathways that activate thirst. Dashed lines indicate potential relationship is under investigation. Dotted line indicates atrial natriuretic peptide decreases disinhibition in hypovolemia. ↑ indicates increase; ↓ indicates decrease.