What are the uses of vasopressin?

Clinical Uses of Vasopressin

Vasopressin is FDA-approved to increase blood pressure in adults with vasodilatory shock who remain hypotensive despite adequate fluid resuscitation and catecholamines, and is also used off-label for bleeding esophageal varices and hemorrhagic shock. 1

Primary Indication: Vasodilatory Shock

Septic Shock

• Vasopressin should be added as a second-line agent when patients with septic shock remain hypotensive despite norepinephrine and adequate fluid resuscitation. 2
• The recommended dose is 0.01 to 0.07 units/minute (up to 0.03 units/minute per most guidelines) to reduce norepinephrine requirements. 2, 1
• Vasopressin works through V1a-receptor mediated vasoconstriction that is catecholamine-independent, making it particularly useful when α-adrenergic receptors are down-regulated in prolonged septic shock. 2, 3
• The VASST trial showed no mortality difference in the overall population, but a subgroup analysis demonstrated survival benefit in patients requiring ≥15 µg/min of norepinephrine at randomization. 2
• Do not use vasopressin as a first-line agent or as monotherapy—it complements norepinephrine but does not replace it. 2

Post-Cardiotomy Shock

• Vasopressin is indicated for post-cardiotomy vasodilatory shock at doses of 0.03 to 0.1 units/minute. 1
• It increases systemic vascular resistance without pulmonary vasoconstriction and may have beneficial effects on right heart function. 2

Other Vasodilatory Shock States

• Vasopressin can be used in cardiogenic shock with persistent hypotension and tachycardia, particularly in afterload-dependent states like aortic or mitral stenosis. 2
• In hemorrhagic shock, vasopressin may transiently improve blood pressure during rapid hemorrhage control without increasing blood loss. 2

Secondary Indication: Bleeding Esophageal Varices

Portal Hypertension Management

• Vasopressin and its analog terlipressin reduce splanchnic blood flow and portal pressure, making them effective for acute bleeding from anorectal and esophageal varices. 2, 4
• Terlipressin is preferred over vasopressin due to its longer half-life and fewer adverse cardiovascular effects. 2
• Vasopressin works through direct vasoconstrictor activity on splanchnic arterioles and precapillary sphincters, secondarily reducing portal venous blood flow and pressure. 4
• These agents should be used as temporizing measures to control bleeding while preparing for definitive endoscopic or surgical intervention—they do not prolong survival from variceal bleeding. 4

Critical Dosing and Safety Considerations

Dose Limitations

• Never exceed 0.04 units/minute in septic shock—higher doses are associated with cardiac, digital, and splanchnic ischemia and should be reserved only when alternative vasopressors have failed. 2, 1
• Doses above 0.04 units/minute may lead to cardiac arrest. 5
• The FDA-approved dosing range is 0.01 to 0.1 units/minute depending on shock type, but clinical guidelines favor the lower end of this range for septic shock. 1

Common Pitfalls

• Vasopressin causes relative vasopressin deficiency in prolonged septic shock (24-48 hours)—levels are initially elevated but then decrease to normal range despite ongoing hypotension. 2
• Bradycardia is an early sign of vasopressin toxicity and requires immediate dose reduction or discontinuation. 4
• The most common adverse reactions include decreased cardiac output, bradycardia, tachyarrhythmias, hyponatremia, and ischemia (coronary, mesenteric, skin, digital). 1
• Monitor for ischemic complications including skin lesions and intestinal ischemia, particularly at higher doses. 5

Drug Interactions

• Pressor effects of catecholamines and vasopressin are additive—expect enhanced blood pressure response when combining agents. 1
• Indomethacin may prolong vasopressin effects. 1
• Ganglionic blockers or drugs causing SIADH may increase the pressor response. 1

Mechanism-Based Advantages

Unique Pharmacologic Properties

• Vasopressin paradoxically induces nitric oxide synthesis, which may preserve renal perfusion while limiting excessive vasoconstriction. 2
• V1a-receptor activation produces vasoconstriction independent of catecholamine pathways, explaining why it complements norepinephrine when α-adrenergic receptors are down-regulated. 2, 3
• Unlike pure α-agonists, vasopressin may improve renal blood flow and urine output at low doses through preferential effects on efferent arterioles. 2, 6

Cardiovascular Effects

• Vasopressin increases systemic vascular resistance without significantly altering cardiac output when used at recommended doses. 2
• At low plasma concentrations, vasopressin mediates vasodilation in coronary, cerebral, and pulmonary arterial circulations. 6
• The risk of supraventricular arrhythmias is significantly lower with vasopressin compared to norepinephrine (RR 7.25 favoring vasopressin). 2