Thirst in Critically Ill Patients: From Physiology to Sensation

Abstract

Critically ill patients often have distressful episodes of severe thirst, but the underlying complex biochemical, neurohormonal regulatory controls that regulate this primal sensation have rarely been addressed by clinicians. Subtle changes in plasma osmolality are the most potent stimulus for thirst. In response to increases in osmolality, osmoreceptors activate release of the neurohormone vasopressin (also known as antidiuretic hormone). The released vasopressin acts on the kidneys to conserve water to correct the hyperosmolar state. If this compensatory mechanism is unsuccessful, thirst arises to promote drinking. Thirst induced by marked volume loss, in contrast, is more closely related to the volemic and pressure changes regulated by the renin-angiotensin aldosterone system. Understanding the physiological mechanisms of thirst will help in understanding the pathophysiological consequences of underlying thirst-related disease and treatments in critically ill patients. Further clinical research is needed to elucidate the multiple inhibitory and excitatory neurohormonal stimuli that motivate patients’ intense desire for water.

Perioperative thirst: an analysis from the perspective of the Symptom Management Theory

“…Besides fear, anxiety and tracheal intubation, use of drugs that reduce the production and secretion of saliva decreasing the moistness of the oral cavity, resulting in stimulating thirst (9) .…”

“…With regards to the physiological aspects of thirst in humans, it is determined by osmotic and blood volume changes that almost always occur after the loss of solute and water, denominated respectively as osmotic thirst and hypovolemic thirst (9) .…”

“…The massive blood changes activate a neuro-hormone complex that release ADH, corticotropin and glucocorticoids, activating the renin-angiotensin-aldosterone system and adrenergic agonists epinephrine and norepinephrine, in order to restore blood volume (9) .…”

“…Osmotic thirst, or intracellular dehydration, results in response to an imbalance between increased cell tone and failure of compensatory mechanisms to conserve body fluids (9) . These changes in osmolarity are easily detected by osmoreceptors in the brain's circumventricular organs (10) and cells from the same brain region, which synthesize two important neuro-pituitary peptides in the thirst adjustment mechanism: ADH and natriuretic hormone (11) .…”

“…The surgical patient is exposed to a confluence of factors which cause them to feel thirsty, such as the need for preoperative fasting maintenance, intraoperative bleeding and heat loss from breathing and sweating (1,9,(11)(12) .…”