ResusDocDrug Monographs

Reference material for UK healthcare professionals. Doses and licensing change — verify against the current SmPC and local policy before use.

Drug monographs / Verapamil

Verapamil

A reliable AV nodal blocker whose reputation is shaped less by what it does than by what happens when it reaches the wrong rhythm or the wrong patient — a broad-complex tachycardia, a pre-excited atrium, or a patient already given an intravenous beta-blocker.

CardiologyArrhythmiaSVTAtrial fibrillationRate controlTachycardia

At a glance

ClassNon-dihydropyridine CCB; Vaughan Williams IV
Adult IV dose5–10 mg over 2 minutes (elderly: over 3 min)
RepeatA further 5 mg after 5–10 minutes if needed
Half-lifeDistribution ~4 min; terminal 2–5 h
Never withIntravenous beta-blockers — contraindicated
Never inBroad-complex tachycardia of uncertain origin
Never inPre-excited AF / WPW — may precipitate VT
InfantsReports of collapse and death — use adenosine

Why this drug is interesting

Verapamil is a good drug with a bad reputation, and the reputation is earned by a small number of specific, catastrophic misuses rather than by anything intrinsic to the molecule. Given to the right rhythm in the right patient it terminates supraventricular tachycardia and controls ventricular rate reliably and cheaply.

Given to a ventricular tachycardia mistaken for SVT with aberrancy, it produces cardiovascular collapse. Given in pre-excited atrial fibrillation, it can precipitate ventricular tachycardia. Given to a patient who has just had an intravenous beta-blocker, it can produce asystole. Each of those is a decision made before the syringe is picked up.

Pharmacology

Mechanism

Verapamil blocks L-type calcium channels. In the sino-atrial and atrioventricular nodes — where the action potential upstroke is calcium- rather than sodium-dependent — this slows conduction and prolongs refractoriness, which is the basis of both its rate-controlling and its SVT-terminating effect.

It also blocks L-type channels in vascular smooth muscle, producing vasodilatation and hypotension, and in cardiac myocytes, producing negative inotropy. Of the non-dihydropyridines, verapamil is the more cardiodepressant and diltiazem the more vasoselective — which is the practical difference between them.

Kinetics

Onset after IV
Within 1–2 minutes
Distribution half-life
About 4 minutes after IV infusion
Terminal half-life
2–5 hours
Metabolism
Extensive hepatic first-pass metabolism — hence the large difference between oral and IV doses
Active metabolite
Norverapamil, contributing to effect

Indications and dosing

The injection is licensed for treatment of paroxysmal supraventricular tachycardia and reduction of ventricular rate in atrial flutter or fibrillation.1

SmPC intravenous dosing
GroupDose
Adults5–10 mg by slow IV injection over 2 minutes, with continuous ECG and BP monitoring. If necessary, a further 5 mg after 5–10 minutes
ElderlySame dose but administered over 3 minutes to minimise adverse effects
Children 1–15 years0.1–0.3 mg/kg (usual single dose 2–5 mg), repeatable after 30 minutes
Children 0–1 year0.1–0.2 mg/kg (usual single dose 0.75–2 mg) — but see the warning below

Rate control in atrial fibrillation

The RCUK 2025 adult tachyarrhythmia algorithm lists verapamil among the rate-control options for probable atrial fibrillation, but conditions it on ventricular function:3

  • EF > 40% — control rate with a beta-blocker, verapamil, diltiazem or digoxin
  • EF < 40% — consider a beta-blocker or digoxin only; verapamil and diltiazem drop off the list
  • Anticoagulate if the arrhythmia has lasted more than 24 hours

The three dangerous errors

1. Verapamil in ventricular tachycardia

2. Verapamil in pre-excited atrial fibrillation

The SmPC states that patients with atrial flutter or fibrillation in the presence of an accessory pathway (e.g. WPW syndrome) may develop increased conduction across the anomalous pathway, and ventricular tachycardia may be precipitated.1

The mechanism is the same as for every AV nodal blocker: remove the node as a competing route and rapid atrial activity is channelled down the accessory pathway. The recognition point is an irregular, broad, very fast tachycardia with varying QRS morphology. The treatment is procainamide or cardioversion — see Adenosine, which carries the same hazard.

3. Verapamil with intravenous beta-blockade

Contraindications, adverse effects and interactions

Contraindications

  • Cardiogenic shock
  • Uncompensated heart failure
  • Simultaneous intravenous beta-blockers
  • Hypersensitivity to verapamil
  • Significant sinus bradycardia, second- or third-degree AV block, sick sinus syndrome without a pacemaker
  • Severe hypotension
  • Atrial flutter or fibrillation with an accessory pathway

Adverse effects

  • Hypotension — the commonest acute problem; largely rate-dependent, so give it slowly
  • Bradycardia, AV block, asystole
  • Worsening heart failure from negative inotropy
  • Flushing, headache, dizziness
  • Constipation — the dominant complaint with oral therapy, and a genuine reason patients stop taking it
  • Gum hyperplasia with chronic use

Interactions

  • Beta-blockers — as above; IV combination contraindicated
  • Digoxin — verapamil raises digoxin concentrations; reduce the digoxin dose and monitor
  • Statins — verapamil inhibits CYP3A4, raising simvastatin and atorvastatin exposure and myotoxicity risk
  • Other negative inotropes and antiarrhythmics — additive depression
  • Grapefruit juice raises oral verapamil concentrations

Critical appraisal

  1. Its efficacy in AV nodal re-entrant tachycardia is not in doubt, and there is reasonable evidence it terminates SVT at rates comparable to adenosine, with a longer duration of effect that reduces early recurrence. Its displacement by adenosine owes as much to adenosine's ten-second half-life — and therefore its far greater forgiveness of a wrong diagnosis — as to any efficacy difference.
  2. That forgiveness argument is the strongest case against verapamil in the ED. If the rhythm turns out to be VT, adenosine's error is transient and verapamil's may not be. In a department where broad- and narrow-complex tachycardias are not always distinguished confidently, that asymmetry matters more than conversion rates.
  3. Verapamil versus diltiazem for rate control is decided mostly on inotropy, not on evidence of differing efficacy. Diltiazem is the gentler choice on contractility — but in the UK there is no intravenous diltiazem, which removes the choice acutely. See Diltiazem.
  4. The paediatric labelling is out of step with practice and arguably with safety, and is a reminder that an SmPC dose table is not by itself an endorsement.
  5. Rate versus rhythm control in AF is a wider question this monograph does not settle; verapamil's role sits entirely within the rate-control arm and within a preserved ejection fraction.

References

  1. 1
    Verapamil 2.5 mg/ml Solution for injection — Summary of Product Characteristics. electronic Medicines Compendium. Sections 4.1–4.5, 5.2. Verified 20 Aug 2026.
  2. 2
    Verapamil hydrochloride — dosing and safety monograph. BNF, NICE. bnf.nice.org.uk
  3. 3
    Resuscitation Council UK. Adult tachyarrhythmia algorithm, 2025. resus.org.uk — mirrored at lifesupport.resusdoc.uk. Lists beta-blocker, verapamil, diltiazem or digoxin for rate control where EF > 40%, and beta-blocker or digoxin only where EF < 40%.
  4. 4
    Betaloc 1 mg/ml Solution for Injection (metoprolol tartrate) — Summary of Product Characteristics. electronic Medicines Compendium. Source of the reciprocal warning against intravenous verapamil-type calcium antagonists in beta-blocked patients.
  5. 5
    Epstein ML, Kiel EA, Victorica BE. Cardiac decompensation following verapamil therapy in infants with supraventricular tachycardia. Pediatrics 1985;75(4):737–40.
  6. 6
    TOXBASE — calcium channel blocker poisoning. National Poisons Information Service. toxbase.org (NHS login required.)

Last reviewed 2026-08-20 · Author: Dr Nirmalya Hore