Vasostrict (vasopressin)

Antidiuretic Hormone Intravenous Infusion Bottle (ML)

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Last reviewed · Source: First Databank (FDB) drug data

Overview

Vasopressin (antidiuretic hormone (ADH)) is a polypeptide hormone; the primary physiologic role of vasopressin is to maintain serum osmolality within a normal range, but the hormone also causes vasoconstriction.

Commercially available vasopressin injection is an aqueous solution of synthetic arginine vasopressin. Vasopressin is a polypeptide hormone. Vasopressin induces vasoconstriction through activation of V1 receptors on vascular smooth muscle cells.

These receptors are coupled to the Gq/11-phospholipase C-phosphatidylinositol trisphosphate signaling pathway, leading to mobilization of intracellular calcium. Additionally, vasopressin promotes antidiuretic effects through stimulation of V2 receptors coupled to adenyl cyclase.

At therapeutic doses, vasopressin elicits a vasoconstrictive effect in most vascular beds, including the splanchnic, renal, and cutaneous circulation. At pressor doses, vasopressin triggers contraction of smooth muscles in the GI tract mediated by muscular V1 receptors and release of prolactin and adrenocorticotropic hormone (ACTH) via V3 receptors. At lower concentrations typical for its role as an antidiuretic hormone, vasopressin suppresses water diuresis via renal V2 receptors.

Furthermore, vasopressin has been shown to induce vasodilation in multiple vascular beds via mechanisms mediated by V2, V3, oxytocin, and purinergic P2 receptors.

When administered in therapeutic doses to patients with vasodilatory shock, vasopressin increases systemic vascular resistance and mean arterial pressure (MAP). In addition, the medication tends to decrease heart rate and cardiac output. The pressor effect of vasopressin is dose dependent.

No evidence of tachyphylaxis or tolerance to the pressor effect of vasopressin has been observed.

Onset of the pressor effect is rapid, with peak effects occurring within 15 minutes. Plasma concentrations of vasopressin increase linearly with increasing infusion rates from 10-200 microU/kg per minute. Steady state plasma concentrations are achieved after 30 minutes of continuous IV infusion.

Pressor effects fade within 20 minutes following discontinuation of IV infusion.

There is no evidence of plasma protein binding with vasopressin. Vasopressin is cleaved by serine protease, carboxipeptidase, and disulfide oxidoreductase at relevant sites for its pharmacologic activity; resulting metabolites are not expected to be pharmacologically active. When administered by IV infusion at usual rates for vasodilatory shock (e.g., 0.1-1 units/minute), the apparent half-life is 10 minutes or less.

Vasopressin is predominantly metabolized and only about 6% of the dosage is excreted unchanged into urine.

Generic name: vasopressin
Drug class: Antidiuretic Hormone
Therapeutic class: Endocrine

Reference product & biosimilars

No reference, biosimilar or interchangeable associated with this drug.

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Indications

The following indications are listed for Vasostrict:

  • Hypotension Due To Distributive Shock

Dosing

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Drug interactions

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Contraindications

*Known allergy or hypersensitivity to synthetic vasopressin (8-L-arginine vasopressin).

*Known allergy or hypersensitivity to chlorobutanol (a preservative) for the chlorobutanol-containing formulations only.

Adverse reactions

The most common adverse effects of vasopressin include decreased cardiac output, bradycardia, tachyarrhythmias, hyponatremia, and ischemia (coronary, mesenteric, skin, digital).

Precautions

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ICD codes

CodeTypeDescription
Hypotension due to distributive shock
A48.3ICD10CMToxic shock syndrome
E27.2ICD10CMAddisonian crisis
I95ICD10CMHypotension
R65.21ICD10CMSevere sepsis with septic shock
T78.2ICD10CMAnaphylactic shock, unspecified
T78.2xxAICD10CMAnaphylactic shock, unspecified, initial encounter
T81.12ICD10CMPostprocedural septic shock
T81.12xAICD10CMPostprocedural septic shock, initial encounter

ICD code information from First Databank (FDB).

Formulary status

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Last reviewed · Source: First Databank (FDB) drug data