Vasopressin
Pitressin · Vasostrict
Antidiuretic hormone analog / V1 vasoconstrictor
Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.
Indications
- •Vasoplegic shock refractory to catecholamines (sepsis, post-CPB, anaphylaxis)
- •Diabetes insipidus (low-dose infusion)
- •Cardiac arrest (historical — removed from ACLS as alternative to epinephrine in 2015 update)
- •Esophageal variceal bleeding
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Vasoplegia rescue (sepsis adjunct to NE) | 0.01–0.04 U/min IV (no titration above 0.04 — myocardial ischemia + skin necrosis risk) | — |
| Bolus during cardiac arrest (legacy) | 40 U IV × 1 (no longer ACLS-preferred; epinephrine is) | — |
| DI replacement | 0.5–10 mU/kg/h IV; or 5–10 U SC q6h aqueous | — |
| Anesthesia-induced hypotension (refractory to phenylephrine + ephedrine) | 0.5–2 U IV bolus | — |
Pharmacokinetics
Onset seconds IV. Half-life 10–20 min. Hepatic + renal metabolism. Receptor-mediated effects independent of adrenergic system — works in catecholamine-resistant shock states (acidosis, sepsis, post-CPB vasoplegia where α-receptor downregulation has occurred).
Hemodynamic effects
Direct vasoconstriction → ↑SVR → ↑MAP. Minimal direct cardiac effect (no inotropy, slight reflex bradycardia possible). Pulmonary vasodilation at low doses (selective splanchnic + skeletal vasoconstriction with relative pulmonary sparing) — useful in RV failure.
Side effects
- !Skin/digital ischemia + necrosis at high doses or peripheral infusion
- !Splanchnic vasoconstriction → mesenteric ischemia
- !Coronary vasoconstriction → angina/MI in CAD
- !Hyponatremia + water intoxication with high V2 effect (low-dose DI replacement)
- !Tachyphylaxis with prolonged use
Contraindications
- ×Severe CAD (relative)
- ×Mesenteric vascular disease
- ×Peripheral vascular disease
Clinical pearls
- ★Anesthesia rescue: vasopressin 1–2 U IV bolus is highly effective for refractory hypotension after spinal or under deep volatile when phenylephrine + ephedrine fail (catecholamine receptor desensitization).
- ★Sepsis: VASST trial (NEJM 2008) showed vasopressin 0.01–0.03 U/min added to norepinephrine improved outcomes in less-severe shock subset.
- ★Post-CPB vasoplegia: vasopressin dramatically improves SVR when α-receptors fail.
- ★ACE-I/ARB patients on chronic therapy may benefit from vasopressin during anesthesia (renin-angiotensin system suppressed; vasopressin pathway preserved).
- ★Always central line for sustained infusion; peripheral OK for emergency boluses with large vein + close inspection.
📊 Related teaching panels
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Other drugs in Cardiac / BP
- Epinephrine
α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.
- Norepinephrine
Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.
- Phenylephrine
Pure α1 agonist → vasoconstriction. No β activity.
- Dexmedetomidine
α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.
- Esmolol
Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.
- Magnesium Sulfate
Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).
- Amiodarone
Multichannel blockade — primarily class III (K+ channel block → prolonged repolarization, increased refractory period), plus class I (Na+ block), class II (β-blocker), class IV (Ca²⁺ block) properties. Treats most supraventricular AND ventricular arrhythmias. Long elimination half-life (weeks–months) limits chronic use.
- Nicardipine
Selective L-type voltage-gated calcium channel blocker, dihydropyridine class (vascular >> cardiac selectivity). Vascular smooth muscle relaxation → arterial vasodilation → afterload reduction. Minimal direct cardiac inotropic or chronotropic effect at clinical doses (vs verapamil/diltiazem which are non-selective).
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