Receptor Review - The Body's Buttons
| Receptor | Primary Location(s) | Primary Effect |
|---|---|---|
| α1 | Vascular smooth muscle, Pupillary dilator | ↑ Vasoconstriction, ↑ SVR, Mydriasis |
| α2 | Presynaptic nerve terminals, CNS | ↓ Norepinephrine release, ↓ Sympathetic outflow |
| β1 | Heart (SA/AV nodes, myocardium) | ↑ Heart Rate, ↑ Contractility, ↑ Conduction |
| β2 | Lungs, Vascular & Uterine smooth muscle | Bronchodilation, Vasodilation (↓ SVR) |
| D1 | Renal & Mesenteric arteries | Vasodilation, ↑ Renal blood flow |
| V1 | Vascular smooth muscle | Vasoconstriction (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
| Drug | Receptor Activity | Primary Clinical Use | Key Adverse Effect |
|---|---|---|---|
| Norepinephrine | α1 > β1 | Septic shock (1st line) | Peripheral ischemia |
| Epinephrine | β > α (low dose); α > β (high dose) | Anaphylaxis, Cardiac Arrest | Tachyarrhythmias |
| Phenylephrine | α1 only | Neurogenic shock, Anesthesia-induced hypotension | Reflex bradycardia |
| Dopamine | Dose-dependent: D > β1 > α1 | Symptomatic bradycardia, Shock (not 1st line) | Tachyarrhythmias |
| Dobutamine | β1 > β2 | Acute decompensated HF, Cardiogenic shock | Hypotension (β2), Tachyphylaxis |
| Vasopressin | V1 agonist | Septic shock (adjunct), Asystole | Coronary/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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