What is vasopressin used for?

Vasopressin: Uses and Clinical Applications

Vasopressin is primarily indicated to increase blood pressure in adults with vasodilatory shock who remain hypotensive despite fluids and catecholamines, serving as an adjunctive agent to norepinephrine in septic shock management. 1

Mechanism of Action

Vasopressin is a potent nonapeptide vasopressor hormone naturally released by the posterior pituitary gland in response to hypotension and hypernatremia. It acts through several receptor subtypes:

• V1a receptors: Mediates vasoconstriction (primary vascular effect)
• V1b receptors: Regulates ACTH release
• V2 receptors: Controls anti-diuretic effects (water reabsorption)
• Oxytocin receptors: Causes vasodilation
• Purinergic receptors: Limited relevance in septic shock 2

The key advantage of vasopressin is that its V1a-receptor activation produces catecholamine-independent vasoconstriction, making it particularly useful when patients become refractory to traditional catecholamines in septic shock.

Clinical Applications

1. Septic Shock Management

Vasopressin is primarily used in septic shock based on the following rationale:

• Vasopressin deficiency: Patients with prolonged septic shock develop a relative vasopressin deficiency due to depletion of stores and inadequate synthesis 2, 3
• Complementary action: Works through mechanisms independent of catecholamines 2
• Dose range: Low-dose infusion (0.01-0.04 units/min) increases blood pressure and decreases norepinephrine requirements 2, 3

2. FDA-Approved Indication

Vasopressin injection is specifically indicated to increase blood pressure in adults with vasodilatory shock who remain hypotensive despite fluids and catecholamines 1.

Dosing and Administration

According to current guidelines:

• Starting dose: Low-dose vasopressin (0.01-0.04 units/min) 2, 4
• Maximum dose: 0.03-0.04 units/min for standard therapy 2, 4
• Higher doses: Doses exceeding 0.04 units/min should be reserved for salvage therapy only (when other vasopressors have failed) 2
• Administration: Should be given as a continuous infusion with careful monitoring 4

Clinical Evidence and Guidelines

The Surviving Sepsis Campaign guidelines recommend:

1. Norepinephrine as the first-choice vasopressor (Grade 1B) 2
2. Vasopressin (up to 0.03 units/min) can be added to norepinephrine to either:
   • Raise mean arterial pressure (MAP) to target
   • Decrease norepinephrine dosage 2, 4
3. Vasopressin should not be used as the single initial vasopressor for septic shock 2

Clinical Trial Evidence

The VASST trial (Vasopressin versus Norepinephrine Infusion in Patients with Septic Shock) found:

• No significant difference in 28-day mortality between vasopressin and norepinephrine in the overall population (35.4% vs 39.3%) 5
• Potential benefit in the subgroup with less severe septic shock (26.5% vs 35.7% mortality) 5, 6
• The interaction between vasopressin and corticosteroid treatment may improve outcomes 6

Precautions and Adverse Effects

• Cardiac effects: May contribute to vasopressin/NO-induced cardiac depression 2
• Tissue ischemia: Higher doses (>0.04 units/min) have been associated with cardiac, digital, and splanchnic ischemia 2
• Monitoring: Requires continuous arterial blood pressure monitoring 4
• Special populations: Safety and efficacy not established in pediatric patients 4

Algorithm for Vasopressin Use in Septic Shock

1. First-line: Start with norepinephrine as the primary vasopressor
2. When to add vasopressin:
   • When target MAP (≥65 mmHg) cannot be maintained with norepinephrine alone
   • To reduce high-dose norepinephrine requirements
3. Dosing: Start at 0.01 units/min and titrate up to 0.03 units/min maximum
4. Monitoring: Continuously assess MAP, tissue perfusion (lactate, urine output, mental status)
5. Discontinuation: Taper vasopressin only after norepinephrine requirements have significantly decreased

Vasopressin offers a valuable adjunctive therapy for septic shock management, particularly in patients who demonstrate relative vasopressin deficiency and catecholamine resistance.