Epinephrine
Adrenalin
Endogenous catecholamine, α + β agonist
α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.
Indications
- •Anaphylaxis
- •Cardiac arrest
- •Hemodynamic support / inotropy
- •Bronchospasm
- •Local anesthetic vasoconstrictor
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Anaphylaxis IM | 0.3–0.5 mg IM (1:1000) | 0.01 mg/kg IM |
| Anaphylaxis IV titrated | 10–100 mcg IV q1–2 min | — |
| Cardiac arrest | 1 mg IV q3–5 min | 0.01 mg/kg IV q3–5 min |
| Inotrope infusion | 0.02–0.5 mcg/kg/min | — |
| Local anesthetic adjunct | 1:200,000 (5 mcg/mL) — max 7 mg/kg lido + epi | — |
Pharmacokinetics
Onset seconds. Duration 5–10 min. Catecholamine reuptake + COMT/MAO degradation.
Hemodynamic effects
↑HR, ↑contractility, ↑CO. SVR ↑ at high dose, ↓ at low dose (β2). Can paradoxically ↓BP at very low doses.
Respiratory effects
Bronchodilation. Decongestant (mucosal vasoconstriction).
Side effects
- !Tachyarrhythmias
- !Hyperglycemia
- !Lactic acidosis
- !Tissue ischemia at extravasation site (treat with phentolamine local infiltration)
- !Pulmonary edema (high-dose, prolonged)
Contraindications
- ×None for life-threatening indications
Clinical pearls
- ★Anaphylaxis: IM lateral thigh fastest absorption; IV in resuscitation only.
- ★LAST: drop epi to ≤1 mcg/kg (≤100 mcg).
- ★Caution: with halothane ('sensitized myocardium' — but halothane is rarely used in 2026).
📊 Related teaching panels
Standalone diagrams matched to this topic.
Other drugs in Cardiac / BP
- Norepinephrine
Strong α1 → vasoconstriction. Mild β1 → modest inotropy. Minimal β2.
- Phenylephrine
Pure α1 agonist → vasoconstriction. No β activity.
- Dexmedetomidine
α2 agonist (locus coeruleus) → sedation + analgesia + anxiolysis without significant respiratory depression.
- Vasopressin
Endogenous nonapeptide hormone. V1 receptor agonist on vascular smooth muscle (Gq → IP3 → Ca²⁺ → vasoconstriction). V2 on renal collecting ducts (Gs → cAMP → aquaporin insertion → water reabsorption). At pressor doses (0.01–0.04 U/min), V1 effects dominate.
- Esmolol
Selective β1-adrenergic receptor antagonist. Decreases HR, contractility, conduction velocity, and AV node refractoriness. Selectivity for β1 over β2 reduces (does not eliminate) bronchospasm risk vs non-selective beta-blockers.
- Magnesium Sulfate
Multiple mechanisms: (1) NMDA receptor antagonism (anticonvulsant, analgesic); (2) Voltage-gated calcium channel blockade in vascular + uterine smooth muscle (vasodilation, tocolysis); (3) Decreased ACh release at neuromuscular junction (NMB potentiation); (4) Membrane stabilization (antiarrhythmic, especially torsades).
- Amiodarone
Multichannel blockade — primarily class III (K+ channel block → prolonged repolarization, increased refractory period), plus class I (Na+ block), class II (β-blocker), class IV (Ca²⁺ block) properties. Treats most supraventricular AND ventricular arrhythmias. Long elimination half-life (weeks–months) limits chronic use.
- Nicardipine
Selective L-type voltage-gated calcium channel blocker, dihydropyridine class (vascular >> cardiac selectivity). Vascular smooth muscle relaxation → arterial vasodilation → afterload reduction. Minimal direct cardiac inotropic or chronotropic effect at clinical doses (vs verapamil/diltiazem which are non-selective).
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