During in-hospital CPR, vasopressin 40 units IV can be given as an alternative to adrenaline. Vasopressin produces vasoconstriction during CPR through which receptor?

• A V2 receptor (renal collecting duct), causing fluid retention and increased preload
• B Beta-1 adrenoceptor, increasing cardiac contractility during low-flow states
• C Angiotensin II receptor type 1, via renin-angiotensin activation
• D V1 receptor (vascular smooth muscle), causing peripheral vasoconstriction ✓

Explanation

Vasopressin (ADH, AVP) administered during CPR acts on V1 receptors in vascular smooth muscle, causing intense peripheral and splanchnic vasoconstriction, increasing peripheral vascular resistance and coronary perfusion pressure. Unlike adrenaline, vasopressin does not cause beta-adrenergic stimulation and has no direct cardiac effect, but the vasoconstriction improves coronary and cerebral perfusion. V2 receptors are renal and mediate water reabsorption; they are not relevant to CPR. Current AHA 2020 guidelines have removed vasopressin from the ACLS algorithm as it offers no benefit over adrenaline alone.

Reference: Morgan & Mikhail's Clinical Anesthesiology, 6th ed.

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Written and medically reviewed by the StethoPrep medical team.