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Vasopressors and inotropes

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Receptor Review - The Body's Buttons

ReceptorPrimary Location(s)Primary Effect
α1Vascular smooth muscle, Pupillary dilator↑ Vasoconstriction, ↑ SVR, Mydriasis
α2Presynaptic nerve terminals, CNS↓ Norepinephrine release, ↓ Sympathetic outflow
β1Heart (SA/AV nodes, myocardium)↑ Heart Rate, ↑ Contractility, ↑ Conduction
β2Lungs, Vascular & Uterine smooth muscleBronchodilation, Vasodilation (↓ SVR)
D1Renal & Mesenteric arteriesVasodilation, ↑ Renal blood flow
V1Vascular smooth muscleVasoconstriction (via $G_q$ pathway)

Exam Favorite: Dopamine's effects are dose-dependent: low doses target D1 (renal vasodilation), moderate doses β1 (↑ contractility), and high doses α1 (vasoconstriction).

The Pressure Crew - Meet the Agents

DrugReceptor ActivityPrimary Clinical UseKey Adverse Effect
Norepinephrineα1 > β1Septic shock (1st line)Peripheral ischemia
Epinephrineβ > α (low dose); α > β (high dose)Anaphylaxis, Cardiac ArrestTachyarrhythmias
Phenylephrineα1 onlyNeurogenic shock, Anesthesia-induced hypotensionReflex bradycardia
DopamineDose-dependent: D > β1 > α1Symptomatic bradycardia, Shock (not 1st line)Tachyarrhythmias
Dobutamineβ1 > β2Acute decompensated HF, Cardiogenic shockHypotension (β2), Tachyphylaxis
VasopressinV1 agonistSeptic shock (adjunct), AsystoleCoronary/mesenteric ischemia

⭐ In patients with cardiogenic shock, dobutamine can paradoxically cause hypotension if the patient is hypovolemic, as its β2-mediated vasodilation may outweigh its β1-mediated increase in cardiac output.

Shock Scenarios - The Right Drug, Right Time

Clinical decision-making for shock requires rapid identification of the underlying cause to guide pharmacotherapy. The primary goal is to restore tissue perfusion by targeting mean arterial pressure (MAP) > 65 mmHg.

⭐ In early, hyperdynamic septic shock ("warm shock"), cardiac output is paradoxically high due to peripheral vasodilation and a compensatory ↑ heart rate. As shock progresses, cardiac function deteriorates.

High‑Yield Points - ⚡ Biggest Takeaways

  • Phenylephrine, a pure α1 agonist, causes potent vasoconstriction and can lead to reflex bradycardia.
  • Norepinephrine is the first-line vasopressor for septic shock, with strong α1 and moderate β1 activity.
  • Epinephrine has dose-dependent effects: β-receptor effects dominate at low doses, while α-receptor effects dominate at high doses. It is the drug of choice for anaphylaxis.
  • Dobutamine is a primary β1 agonist that increases inotropy and is used in cardiogenic shock.
  • Milrinone, a PDE-3 inhibitor, increases intracellular cAMP, leading to increased inotropy and vasodilation.

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