Procainamide
Pronestyl
Class IA antiarrhythmic (Na⁺-channel blocker)
Blocks fast Na⁺ channels (↓ conduction) + K⁺ channels (↑ refractoriness/QT). Slows conduction in accessory pathways.
Indications
- •Stable wide-complex tachycardia / VT
- •Pre-excited AF (WPW — drug of choice over AV-nodal blockers)
- •Conversion of AF
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| Loading | 20–50 mg/min IV (or 100 mg q5 min) until arrhythmia suppressed, hypotension, QRS widens >50%, or max 17 mg/kg | — |
| Maintenance | 1–4 mg/min infusion | — |
Pharmacokinetics
Onset minutes. Metabolized to NAPA (active, class III, renally cleared → accumulates in renal failure). Acetylation rate genetically variable.
Hemodynamic effects
Hypotension (ganglionic blockade + negative inotropy), esp. with fast infusion.
Side effects
- !Hypotension
- !QRS/QT prolongation → torsades
- !Drug-induced lupus (chronic — anti-histone)
- !NAPA accumulation in renal failure
Contraindications
- ×Long QT/torsades
- ×2nd/3rd-degree block without pacer
- ×Systemic lupus
Clinical pearls
- ★Drug of choice for WPW with pre-excited AF — AV-nodal blockers (adenosine, CCB, β-blocker, digoxin) can cause VF.
- ★Stop loading if QRS widens >50%, hypotension, or arrhythmia resolves.
- ★Chronic use → drug-induced lupus (reversible).
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).
Suggested reading
- •Miller's Anesthesia, 9e
- •FDA package insert
- •AHA ACLS guidelines, 2020
