Ibutilide
Corvert
Class III antiarrhythmic (K⁺-channel effect; also activates slow Na⁺ current)
Prolongs action potential/repolarization → chemical cardioversion of atrial fibrillation/flutter.
Indications
- •Acute chemical cardioversion of recent-onset AF/atrial flutter
- •Facilitating DC cardioversion
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Cardioversion | 1 mg IV over 10 min (0.01 mg/kg if <60 kg); may repeat once after 10 min | — |
Pharmacokinetics
Onset ~30 min (most convert during/soon after infusion). Half-life ~6 h. Hepatic.
Hemodynamic effects
Minimal BP effect (unlike other antiarrhythmics).
Side effects
- !Torsades de pointes (~2–4% — the key risk)
- !QT prolongation
Contraindications
- ×Long QT / hypokalemia / hypomagnesemia
- ×Concomitant QT-prolonging drugs
Clinical pearls
- ★Pre-treat/co-treat with magnesium and correct K⁺/Mg²⁺ to reduce torsades risk.
- ★Monitor on telemetry for ≥4 h after (or until QTc normalizes) — torsades is the danger.
- ★More effective for atrial FLUTTER than fibrillation.
Other drugs in Cardiac / BP
- Epinephrine
α1 (vasoconstriction), α2, β1 (inotropy + chronotropy), β2 (bronchodilation, vasodilation in skeletal muscle). Dose-dependent receptor preference: low-dose β-predominant, high-dose α-predominant.
- 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.
Browse all classes: /reference/drugs
Suggested reading
- •Stoelting & Hines, Pharmacology & Physiology in Anesthetic Practice, 6e
- •Miller's Anesthesia, 9e
- •FDA package insert
