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Thirst in Critically Ill Patients: From Physiology to Sensation

Author(s): Shoshana Arai, PhD, RN, Nancy Stotts, RN, EdD, and Kathleen Puntillo, RN, DNSC

Contact Hours: 1.00

CERP A: 1.00

Expires Jul 01, 2017

Topics: MultiSystem, Neurology

Population: Lifespan

Role: Staff

Member: Free
NonMember: $10.00

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Activity Summary

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 reninangiotensin 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.


  • Discuss ways in which physiologic regulatory controls affect thirst.
  • Describe the similarities and differences between osmotic and hypovolemic thirst.
  • List at least 3 external prompts for fluid intake.

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