Verapamil
Calan · Isoptin
Non-dihydropyridine calcium channel blocker (class IV antiarrhythmic)
Blocks L-type Ca²⁺ channels — strong AV-nodal + myocardial effect (more cardiac than diltiazem), less vascular. Negative inotrope/chronotrope/dromotrope.
Indications
- •SVT (AV-nodal re-entry)
- •Rate control in AF/flutter
- •Angina
- •HTN
Dosing
| Context | Adult | Pediatric |
|---|---|---|
| SVT/rate control | 2.5–5 mg IV over 2 min, repeat 5–10 mg q15–30 min (max ~20 mg) | — |
Pharmacokinetics
Onset 1–5 min IV. Hepatic CYP3A4 metabolism.
Hemodynamic effects
Hypotension + bradycardia + negative inotropy — more myocardial depression than diltiazem.
Side effects
- !Bradycardia, heart block, hypotension
- !Worsens heart failure (negative inotrope)
- !Constipation
- !Raises digoxin levels
Contraindications
- ×WPW with pre-excited AF (→ VF)
- ×2nd/3rd-degree block
- ×HFrEF
- ×Wide-complex tachycardia of uncertain origin
- ×With IV β-blocker (additive block)
Clinical pearls
- ★Treat verapamil-induced hypotension/bradycardia with IV CALCIUM (calcium chloride/gluconate) ± glucagon.
- ★More negative inotropy than diltiazem — avoid in reduced EF.
- ★AV-nodal blocker → contraindicated in pre-excited AF (WPW).
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
