vasopressin

Brand: Pitressin, Vasostrict

ISMP High Alert Prototype Drug
Drug Class: vasopressor
Drug Family: vasopressor
Subclass: ADH (antidiuretic hormone) analog
Organ Systems: cardiovascularrenal

Mechanism of Action

V1a receptor activation causes vasoconstriction; V2 receptor increases water reabsorption (antidiuretic effect); does not cause tachycardia unlike catecholamines.

V1a vasopressin receptor (vascular smooth muscle)V2 vasopressin receptor (renal tubule)

Indications

  • septic shock (vasodilatory — adjunct to NE)
  • vasodilatory shock (post-cardiac surgery)
  • esophageal varices bleeding (IV)
  • diabetes insipidus (central)
  • cardiac arrest (no longer in ACLS 2010)

Contraindications

  • anaphylaxis (relative)
  • coronary artery disease (relative — vasoconstriction)

Adverse Effects

Common

  • oliguria
  • ischemia
  • nausea
  • abdominal cramping

Serious

  • severe ischemia (mesenteric, coronary)
  • hyponatremia (SIADH-like)

Pharmacokinetics (ADME)

Absorption IV/IM/SQ
Distribution wide
Metabolism hepatic and renal
Excretion renal
Half-life 10-35 min (vasopressor context)
Onset immediate IV
Peak 1-2 hours IM
Duration 20-120 min
Protein Binding very low
Vd 0.1-0.14 L/kg

Drug Interactions

Drug / Agent Mechanism Severity
other vasopressors additive vasoconstriction moderate

Nursing Considerations

  1. VASST trial: vasopressin 0.03-0.04 units/min as catecholamine-sparing agent in septic shock
  2. Fixed dose (0.03-0.04 U/min) in septic shock — do NOT titrate
  3. Monitor for signs of ischemia (fingers, toes, mesenteric)
  4. Do not abruptly discontinue (rebound vasodilation) in vasopressor-dependent patients

Clinical Pearls

  • VASST/VANISH trials: vasopressin reduces NE requirements in septic shock but does not reduce mortality
  • Septic shock: endogenous vasopressin levels fall — physiologic replacement rationale

Safety Profile

Pregnancy use-with-caution
Lactation use-with-caution
Renal Adjustment Not required
Hepatic Adjustment Not required
TDM Not required