What Are Vasopressors?
Vasopressors are medications that cause vasoconstriction to increase blood pressure and restore adequate tissue perfusion in patients with shock states, primarily by activating receptors on vascular smooth muscle. 1
Classification and Mechanisms of Action
Vasopressors are categorized into three main classes based on their mechanism 1:
Sympathomimetic Agents (Catecholamines)
- Act by stimulating α and β adrenergic receptors on vascular smooth muscle and cardiac tissue, causing vasoconstriction and increased cardiac contractility 1, 2
- Direct-acting catecholamines include:
- Norepinephrine: Predominantly α1-adrenergic effects with some β1 activity, causing both arterial and venous vasoconstriction 1
- Epinephrine: Non-selective α and β receptor stimulation 1
- Dopamine: Dose-dependent effects on dopamine, β, and α receptors 1
- Phenylephrine: Pure α1-agonist with no β activity 1
Vasopressin Analogues
- Vasopressin is a nonapeptide hormone released by the posterior pituitary that acts on V1a receptors to cause vasoconstriction through a catecholamine-independent mechanism 1
- This mechanism explains why vasopressin complements norepinephrine in septic shock when α-adrenergic receptors are down-regulated 1
- Typical dosing is 0.01-0.04 units/min for hemodynamic support 1
Angiotensin II
- Acts on AG1 and AG2 receptors to cause vasoconstriction 3
- May be useful for rapid resuscitation in profoundly hypotensive patients refractory to other vasopressors 3, 4
Physiological Effects Beyond Vasoconstriction
Vasopressors have multiple systemic effects that clinicians must understand 1:
- Cardiovascular: Increase arterial resistance and cardiac afterload; β-stimulation increases inotropy and heart rate 1
- Venous effects: Norepinephrine causes splanchnic venoconstriction, actively shifting blood volume to systemic circulation 1
- Metabolic: Stimulate glycogenolysis in liver, free fatty acid release from adipose tissue, and modulate insulin release 1, 2
- Renal: Can affect renal perfusion, though vasopressin may preserve renal blood flow through nitric oxide synthesis 1
Clinical Indications
Vasopressors are primarily indicated for vasodilatory shock states after adequate fluid resuscitation 1, 3:
- Septic shock: Norepinephrine is the first-line agent 1, 3
- Cardiogenic shock: Used cautiously, often combined with inotropes like dobutamine 1, 5
- Hemorrhagic shock: Should only be used transiently for life-threatening hypotension (systolic BP <80 mmHg) after volume replacement, as they may worsen organ perfusion if used prematurely 1, 6
- Anesthesia-induced hypotension: For perioperative blood pressure management 7
Critical Safety Considerations
Vasopressors have a narrow therapeutic window and expose patients to potentially lethal complications 6:
- Adverse effects include: Excessive vasoconstriction causing organ ischemia/infarction, hyperglycemia, hyperlactatemia, tachycardia, and tachyarrhythmias 3, 4
- Require precise hemodynamic targets: Typically mean arterial pressure ≥65 mmHg, though this may need individualization based on baseline blood pressure and comorbidities 6
- Demand close monitoring: Urine output (>0.5 mL/kg/hour), lactate clearance, and cardiac function assessment 6
- Should be withdrawn as soon as possible once the underlying shock state resolves 6
Common Pitfalls
A critical caveat in hemorrhagic shock: early vasopressor use before adequate volume resuscitation may be harmful 1. The European trauma guidelines emphasize that vasopressors should only be used transiently when systolic blood pressure remains <80 mmHg despite restricted volume replacement, as premature vasoconstriction can worsen tissue perfusion and increase mortality 1, 6. This contrasts with septic shock, where norepinephrine is started earlier alongside fluid resuscitation 3.
Vasopressors increase cardiac afterload, which can be detrimental in patients with myocardial dysfunction 1. In such cases, assessment of cardiac function is essential, and inotropic agents like dobutamine or epinephrine should be added 1.