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OBJECTIVE: To present the physiology of vasopressin, and review published data on its use in critically ill patients. DATA SOURCES: A review of articles on the clinical use of vasopressin in critical care medicine up to 2002 and identified through a MEDLINE search. SUMMARY OF REVIEW: Vasopressin (antidiuretic hormone) acts via vasopressinergic receptors to maintain osmotic and baroreceptor homeostasis. It has complex and varying effects depending on serum levels, coexisting disease states and organs studied. Synthetic vasopressin is available for clinical use. In large doses (e.g. 40 U) it has vasoconstrictor effects comparable to epinephrine during cardiopulmonary resuscitation. The use of much lower "replacement" doses (e.g. 0.04 U/min) may have a marked vasopressor effect in clinical states associated with vasopressin deficiency; for example sepsis, the organ donor and after cardiopulmonary bypass. These doses are much lower than those leading to cardiovascular effects in healthy patients and may avoid the adverse vasoconstrictor effects seen at "pharmacological" doses. The use of vasopressin to reduce portal pressure and bleeding in oesophageal varices is well established. CONCLUSIONS: Vasopressin has widespread effects throughout the body and has several important clinical applications in the critically ill patient.
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Russell et al. (2002) studied this question.
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