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Drug Reference

vasopressin

Vasopressin analog· Brands: Vasostrict, PitressinIMIVSC

Mechanism of action
Vasopressin (argipressin) is the endogenous nonapeptide antidiuretic hormone, and exogenous administration reproduces its actions at three G-protein-coupled receptor subtypes. V1a receptors on vascular smooth muscle couple to Gq and phospholipase C, generating inositol trisphosphate and a rise in cytosolic calcium that causes potent constriction of arterioles, including splanchnic, cutaneous and coronary beds; this V1a effect is the basis of its use in vasodilatory shock and is independent of adrenergic receptors, so it retains activity when catecholamine responsiveness is impaired or downregulated. V2 receptors in the renal collecting duct couple to Gs and adenylyl cyclase, increasing cyclic AMP and inserting aquaporin-2 water channels into the apical membrane, which produces antidiuresis and concentrated urine at low circulating concentrations. V1b (V3) receptors in the anterior pituitary stimulate ACTH release. Weak oxytocin receptor activity may contribute to uterine and other effects. At the higher infusion rates used in shock, V2-mediated water retention can cause hyponatraemia, while V1a-mediated vasoconstriction raises systemic vascular resistance and blood pressure and can reduce cardiac output through increased afterload and reflex bradycardia.
Pharmacokinetics
Vasopressin is a peptide and is destroyed by gastrointestinal peptidases, so it is not active orally and must be given parenterally, usually as a continuous intravenous infusion in critical care and intramuscularly or subcutaneously in endocrine practice. Onset after intravenous administration is within minutes. The plasma half-life is short, roughly 10 to 20 minutes, so the effect wears off quickly when an infusion is stopped and steady state is reached soon after starting or changing a rate. It is metabolised by tissue peptidases in the liver and kidneys, and vasopressinase activity in pregnancy increases clearance; metabolites and a small proportion of unchanged drug are excreted in urine. Plasma protein binding is low and the volume of distribution is small. Clearance may be prolonged in hepatic or renal impairment. Because of the short half-life and rapid titration, response is judged by blood pressure, perfusion markers, urine output and serum sodium rather than by drug concentrations, and regional practices differ in the concentration and rate used.
Indications & dosing

Vasodilatory shock (for example septic shock) refractory to fluids and catecholamines

Start at 0.01 units/min and titrate to effect; usual ceiling 0.04 units/min. Used as an add-on to noradrenaline, not first-line. Extravasation causes local ischaemia; watch for hyponatraemia and digital or gut ischaemia.

  • adult · IV: 0.01–0.04 units/min continuous infusion · Start at 0.01 units/min and titrate to effect; usual ceiling 0.04 units/min. Used as an add-on to noradrenaline, not first-line. Extravasation causes local ischaemia; watch for hyponatraemia and digital or gut ischaemia.

Cardiac arrest (pulseless ventricular fibrillation or tachycardia, asystole, pulseless electrical activity)off-label

Off-label in most formularies and no longer part of current resuscitation algorithms. May be considered only as an alternative where adrenaline is unavailable. Follow the local resuscitation protocol.

  • adult · IV: 40 units single dose · Off-label in most formularies and no longer part of current resuscitation algorithms. May be considered only as an alternative where adrenaline is unavailable. Follow the local resuscitation protocol.

Central diabetes insipidus

Desmopressin is preferred for chronic therapy. Aqueous vasopressin acts for only 2 to 8 hours; titrate against urine output and serum sodium. Route and product availability vary by region.

  • adult · IM/SC: 5–10 units 2-4 times daily · Desmopressin is preferred for chronic therapy. Aqueous vasopressin acts for only 2 to 8 hours; titrate against urine output and serum sodium. Route and product availability vary by region.

Acute variceal bleeding from oesophageal varicesoff-label

Largely replaced by terlipressin or octreotide, which have fewer ischaemic effects. Historically combined with nitroglycerin. Licensing and availability differ between countries; check the local formulary.

  • adult · IV: 0.2–0.4 units/min continuous infusion · Largely replaced by terlipressin or octreotide, which have fewer ischaemic effects. Historically combined with nitroglycerin. Licensing and availability differ between countries; check the local formulary.

Refractory hypotension in paediatric vasodilatory shockoff-label

Evidence is limited to small studies and case series. Start at the lower end of the range and titrate. Risks include hyponatraemia and peripheral or mesenteric ischaemia.

  • pediatric · IV: 0.0001–0.002 units/kg/min continuous infusion · Evidence is limited to small studies and case series. Start at the lower end of the range and titrate. Risks include hyponatraemia and peripheral or mesenteric ischaemia.

Refractory hypotension in the neonateoff-label

Used in some neonatal units after adrenaline and noradrenaline have failed. Evidence is limited and dosing is not standardised. Monitor serum sodium, urine output and peripheral perfusion closely.

  • neonatal · IV: 0.0001–0.0005 units/kg/min continuous infusion · Used in some neonatal units after adrenaline and noradrenaline have failed. Evidence is limited and dosing is not standardised. Monitor serum sodium, urine output and peripheral perfusion closely.
Contraindications & precautions
  • Hypersensitivity to vasopressin or any component of the formulation · May cause anaphylaxis. Avoid in patients with known allergy.
  • Severe coronary artery disease · Vasoconstriction may worsen myocardial ischaemia. Use only if benefit outweighs risk, with close monitoring.
  • Peripheral vascular disease · Risk of peripheral ischaemia and gangrene. Monitor peripheral perfusion.
  • Mesenteric ischaemia · May exacerbate intestinal ischaemia. Avoid if suspected.
  • Monitor blood pressure, heart rate, and ECG continuously during intravenous infusion. Adjust rate to maintain target blood pressure and avoid excessive vasoconstriction.
  • Use with caution in patients with coronary artery disease, peripheral vascular disease, or mesenteric ischaemia. Monitor for signs of ischaemia such as chest pain, abdominal pain, or cool extremities.
  • Administer via a central venous catheter when possible to reduce risk of extravasation and skin necrosis. Inspect the infusion site regularly.
  • Monitor serum sodium and osmolality, especially with prolonged infusions, because vasopressin has antidiuretic effects and can cause hyponatraemia.
  • Do not use as a substitute for adequate fluid resuscitation and other vasopressors in septic shock. Follow local protocols for vasopressor selection and titration.
  • In cardiac arrest, vasopressin may be used as an alternative to epinephrine in some protocols, but evidence is limited; follow current resuscitation guidelines.
Adverse effects
  • Hypertension
  • Bradycardiaserious
  • Arrhythmias (atrial fibrillation, ventricular tachycardia)serious
  • Myocardial ischaemia or infarctionserious
  • Mesenteric ischaemiaserious
  • Peripheral ischaemia or gangreneserious
  • Hyponatraemia (water intoxication)serious
  • Nausea, vomiting, abdominal cramps
  • Anaphylaxisserious
Monitoring, pregnancy & toxicity
  • Blood pressure and heart rate · Continuous or every 5-15 minutes during infusion, then as clinically indicated.
  • Serum sodium and osmolality · Baseline and at least daily; more frequently if high dose or prolonged infusion.
  • Urine output and fluid balance · Hourly during infusion; monitor for water intoxication.
  • Signs of ischaemia (peripheral, mesenteric, cardiac) · Regular assessment; ask about abdominal pain, chest pain, and check digits and skin.
  • Infusion site · Check regularly for extravasation, blanching or pain.
  • Pregnancy: Use only if clearly needed. Vasopressin has oxytocic activity and may stimulate uterine contractions. For diabetes insipidus in pregnancy, desmopressin is preferred. In life-threatening vasodilatory shock, the benefits may outweigh the risks. No well-controlled studies in pregnant women.
  • Toxicity: Hypertension and bradycardia · Stop or reduce the infusion. Provide supportive care. If severe, consider short-acting vasodilators and monitor haemodynamics.
  • Toxicity: Myocardial or mesenteric ischaemia (chest pain, abdominal pain, bloody stools, ECG changes) · Stop the infusion. Assess for ischaemia with ECG, cardiac markers and imaging as indicated. Provide supportive care and specialist consultation.
  • Toxicity: Hyponatraemia and water intoxication (confusion, seizures, coma) · Stop the infusion. Restrict fluids. Correct sodium slowly to avoid osmotic demyelination. Treat seizures with appropriate anticonvulsants.
  • Toxicity: Peripheral ischaemia (digital ischaemia, skin necrosis, extravasation) · Stop the infusion. For extravasation, apply local warmth and consider phentolamine infiltration as per local protocol. Monitor for tissue loss.
Clinical notes
Vasopressin is most often used in intensive care as a vasopressor in vasodilatory shock, typically added to noradrenaline in septic shock or used in vasoplegia after cardiac surgery; a common teaching example is a fixed infusion of 0.03 units/min, with ranges of about 0.01 to 0.04 units/min quoted in local protocols, and it is titrated against mean arterial pressure and markers of perfusion. It is not a first-line single agent for most shock states. In endocrine practice it treats central diabetes insipidus, where desmopressin is generally preferred for chronic therapy because of its longer action and greater V2 selectivity, and it has been used for variceal bleeding, although terlipressin, somatostatin analogues or endoscopic therapy are now usual. It is no longer recommended for routine use in cardiac arrest. Adverse effects reflect its pharmacology: digital, mesenteric, cutaneous and coronary ischaemia, reduced cardiac output, reflex bradycardia, hyponatraemia from water retention, bronchoconstriction and rarely hypersensitivity. Extravasation can cause skin necrosis, so peripheral lines need frequent checks and central access is preferred where available. Monitor blood pressure, perfusion, urine output, electrolytes and signs of ischaemia, and review the infusion regularly because benefit falls and harm rises at higher rates. Practice varies by region, formulary and unit protocol.

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BNF or local formulary; current manufacturer prescribing information; local critical care and endocrinology protocols; national resuscitation and sepsis guidance