Vasopressors & Inotropes

Explore shock physiology and circulatory failure that disrupts tissue and organ perfusion, causing cellular injury and progression to organ dysfunction, with microvascular, endothelial derangements and clotting and inflammatory cascades.

Learn how blood pressure and mean arterial pressure rise with vascular resistance and cardiac output, as vasopressors and inotropes alter vessel constriction and total peripheral resistance.

Vasopressors and inotropes raise cardiac output by increasing heart rate (chronotherapy) and contractility. They enhance stroke volume via preload and reduce afterload, boosting mean arterial pressure.

Explore hypovolemic, distributive, cardiogenic, and obstructive shock with examples like hemorrhagic, septic, neurogenic, anaphylactic, inflammatory, and mechanical or pulmonary vascular causes.

Identify alpha 1 on vascular walls, beta 1 on the heart, beta 2 on vessels, and dopamine receptors on renal, coronary, and cerebral beds, with vasoconstriction, increased contractility, and vasodilation.

Epinephrine is a beta-1 agonist that increases cardiac output; at low doses beta-2 effects overlap with alpha-1 vasoconstriction, while at high doses alpha-1 dominates, raising vascular resistance and blood pressure.

Norepinephrine acts on alpha and beta-1 receptors to raise vascular resistance and cardiac contractility, increasing stroke volume and mean arterial pressure, used in vasodilatory or septic shock.

Dobutamine stimulates beta-1 receptors to raise cardiac output with only mild effects on vascular resistance, making it useful in refractory heart failure and cardiogenic shock.

Dopamine acts as a vasopressor and inotrope, producing renal vasodilation at low doses, beta-1 receptor effects at intermediate doses, and alpha receptor vasoconstriction at high doses; start low and titrate.

Phenylephrine is a pure alpha agonist that constricts vessels via alpha-1 receptors, increasing vascular resistance and blood pressure, with cardiac output typically maintained.