Electrical cardioversion and antiarrhythmic drugs

01Purpose and principlesWhat the treatment does and how it fits into care.

Electrical cardioversion is the fastest reliable rhythm treatment for a perfusing tachyarrhythmia causing life-threatening adverse features. Pad position, synchronisation, adequate energy and safe sedation all matter, but the underlying rhythm still determines the initial energy.

Antiarrhythmic drugs can terminate arrhythmia, slow conduction or facilitate a repeat shock, but every drug can also worsen another rhythm. Regularity, QRS width, pre-excitation, QT interval and ventricular function must be checked before selecting one.

Dose context is essential. Resuscitation Council regimens are designed for peri-arrest algorithms and can differ from the general eMC Summary of Product Characteristics; both should be named rather than blended into an invented compromise.

Key points

Synchronised cardioversion times the shock to the R wave to avoid energy delivery during ventricular repolarisation.
A conscious patient needs carefully titrated sedation or anaesthesia, but instability must not be allowed to worsen while waiting.
RCUK 2025 energies: AF at maximum defibrillator output; flutter/regular narrow tachycardia 70-120 J; VT with a pulse 120-150 J.
Re-enable and visually confirm synchronisation before every repeat shock; many defibrillators reset after delivery.
For persistent instability after up to three shocks, RCUK uses procainamide 10-15 mg/kg IV over 20 minutes (maximum 1 g) or amiodarone 300 mg IV over 10-20 minutes, followed by another shock.
For stable regular narrow tachycardia, the March 2026 RCUK adenosine sequence is 6 mg, 12 mg, then 18 mg as rapid IV boluses.
Emergency cardioversion is not delayed for anticoagulation; planned AF/flutter cardioversion requires a thromboembolism strategy when duration exceeds 48 hours or is uncertain.
Amiodarone has important lung, liver, thyroid, ocular, neurological and cardiac toxicity; long-term use needs explicit indication and monitoring.

02Indications, selection and cautionsWho may benefit, who needs urgent treatment and important alternatives.

Unstable tachyarrhythmiaRed flag

Shock, syncope with severe or ongoing hypotension, myocardial ischaemia, severe pulmonary oedema or immediately post-ROSC favours immediate electricity.

Synchronisation markers

The defibrillator should place a marker on each R wave; erratic or T-wave markers require lead/gain adjustment before charging when a pulse is present.

AF versus flutter

AF is irregular without organised atrial activity; flutter may be regular at about 150/min with 2:1 block, and the recommended initial energies differ.

Regular narrow tachycardia

Vagal manoeuvres then rapid-bolus adenosine are appropriate only in stable regular narrow tachycardia when flutter and pre-excitation concerns have been considered.

Broad or irregular warningRed flag

Regular broad tachycardia is VT until proven otherwise; irregular broad tachycardia may be pre-excited AF or polymorphic VT and should not receive routine AV-nodal blockade.

Post-conversion bradycardia

Sinus-node disease, AV block and drug effects can produce significant pauses after cardioversion, so pacing capability and continued monitoring are required.

03Assessment before treatmentTests and checks that guide safe selection.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
12-lead ECGFirst step
Why
Define rhythm, regularity, QRS width, QT, pre-excitation and ischaemia.
Interpretation and limitations
Obtain before treatment when the patient is stable; never delay an urgent shock solely for a diagnostic-quality tracing.
02
Continuous ECG, BP and SpO2
Why
Track deterioration, synchronisation and response to drug or shock.
Interpretation and limitations
Loss of a pulse changes synchronised cardioversion to unsynchronised cardiac-arrest defibrillation.
03
U&Es, magnesium and calcium
Why
Identify pro-arrhythmic deficits and establish safety for antiarrhythmics.
Interpretation and limitations
Correct potassium and magnesium before elective rhythm treatment and urgently in polymorphic ventricular arrhythmia.
04
Renal and liver function
Why
Guide anticoagulant selection and identify risk with hepatically or renally cleared drugs.
Interpretation and limitations
Use Cockcroft-Gault creatinine clearance for DOAC dosing decisions rather than eGFR alone.
05
Echocardiography
Why
Assess LVEF and structural disease when it will alter drug or device decisions.
Interpretation and limitations
Class Ic antiarrhythmics are avoided in important structural/ischaemic heart disease; reduced LVEF limits rate-control choices.
06
TOE for selected planned cardioversion
Why
Exclude atrial thrombus when an imaging-guided early cardioversion strategy is used.
Interpretation and limitations
Atrial thrombus means elective cardioversion is deferred while therapeutic anticoagulation is established.

04Treatment approachPreparation, options, escalation and aftercare.

01unstableImmediate synchronised cardioversionFirst stepA perfusing tachyarrhythmia causes a life-threatening adverse feature.

1Call expert and anaesthetic help, perform ABCDE assessment, attach pads, monitor continuously and obtain IV access.
2Sedate or anaesthetise a conscious patient with careful haemodynamic planning when feasible without dangerous delay.
3EscalationConfirm synchronisation, then use maximum defibrillator output for AF, 70-120 J for flutter/regular narrow tachycardia, or 120-150 J for VT with a pulse; escalate and repeat to three shocks.
4If still unstable, give procainamide 10-15 mg/kg IV over 20 minutes (maximum 1 g) or amiodarone 300 mg IV over 10-20 minutes, then repeat synchronised cardioversion.

02electivePlanned AF or flutter cardioversionRhythm control is chosen without current life-threatening instability.

1Confirm arrhythmia duration, stroke and bleeding risk, adherence and structural disease.
2If duration is more than 48 hours or uncertain, maintain therapeutic anticoagulation for at least 3 weeks before cardioversion, or use a specialist TOE-guided strategy.
3Perform cardioversion with anaesthesia/sedation, rhythm-appropriate energy and uninterrupted monitoring.
4Continue anticoagulation for at least 4 weeks after cardioversion and longer when stroke risk indicates; do not stop solely because sinus rhythm is restored.

03narrowStable regular narrow tachycardiaQRS is under 120 ms, rhythm regular and no adverse feature is present.

1Perform vagal manoeuvres while recording the ECG.
2If ineffective and the rhythm is not flutter and there is no pre-excitation concern, give adenosine 6 mg by very rapid IV bolus and flush.
3If unsuccessful give 12 mg, then 18 mg, each rapidly with continuous ECG recording and resuscitation capability.
4If drug treatment fails, use synchronised cardioversion; consider verapamil or a beta-blocker only after rhythm, ventricular function and contraindications are assessed.

04amiodaroneStarting or continuing amiodaroneA specialist selects amiodarone because safer rhythm-specific options are unsuitable or have failed.

1Document indication, baseline ECG and potassium, thyroid and liver function, and assess pulmonary symptoms and interacting medicines.
2Use the RCUK IV regimen only for the specified peri-arrest context; for general IV prescribing, the SmPC regimen is 5 mg/kg over 20 minutes to 2 hours with up to 1200 mg/24 hours.
3For oral maintenance, use the specialist prescription and lowest effective dose; do not improvise a loading schedule from an emergency IV dose.
4Review thyroid and liver function every 6 months, monitor ECG and investigate new cough, dyspnoea, visual or neurological symptoms promptly.

05Regimens, contraindications and interactionsTreatment details and the circumstances that modify them.

Stable regular narrow tachycardia, and selected regular broad tachycardia suspected to be SVT with aberrancy.

Adenosine

RCUK March 2026: 6 mg, then 12 mg, then 18 mg by very rapid IV bolus, each followed by a rapid flush. This algorithm-specific sequence differs from the cited product SmPC's licensed 3 mg, 6 mg, then 12 mg sequence.

Do not use for irregular broad tachycardia or pre-excited AF. Give with continuous ECG and immediate resuscitation capability. The cited UK SmPC contraindicates bronchospastic chronic lung disease including asthma, long-QT syndrome, severe hypotension, decompensated heart failure, and sick-sinus or second-/third-degree AV block without a functioning pacemaker; avoid concurrent dipyridamole unless an expert-adjusted strategy is essential.

RCUK option after failed cardioversion in persistent instability and preferred drug for stable monomorphic VT when sedation/anaesthesia risk is high.

Procainamide

10-15 mg/kg IV over 20 minutes, maximum 1 g.

Continuous ECG and BP monitoring; stop or slow for hypotension, QRS widening or QT prolongation.

Conditional peri-arrest antiarrhythmic and specialist long-term rhythm drug when other treatment is unsuitable.

Amiodarone

RCUK after failed shock: 300 mg IV over 10-20 minutes; stable broad-tachycardia alternative: 300 mg IV over 10-60 minutes then 900 mg/24 h. General eMC SmPC: 5 mg/kg IV over 20 minutes to 2 hours, with repeat infusion up to 1200 mg/24 h.

Avoid in torsades and pre-excited AF. IV administration requires ECG/BP monitoring; chronic therapy can injure lung, liver, thyroid, eye, skin and nerves and has many interactions.

One anticoagulant option for stroke prevention and planned cardioversion where appropriate. The SmPC cardioversion regimen is for NVAF; isolated-flutter anticoagulation follows the NICE AF/flutter stroke-risk framework and may be off-label for the product.

Apixaban

5 mg by mouth twice daily for eligible NVAF; reduce to 2.5 mg twice daily when at least two apply: age 80 years or older, weight 60 kg or less, serum creatinine at least 133 micromol/L. For NVAF, also use 2.5 mg twice daily when Cockcroft-Gault creatinine clearance is 15-29 mL/min regardless of the two-of-three rule.

Not for mechanical valves or moderate-to-severe rheumatic mitral stenosis; assess Cockcroft-Gault renal function, bleeding and adherence. The cited SmPC does not recommend apixaban when creatinine clearance is below 15 mL/min or during dialysis.

06Complications, monitoring and follow-upAdverse effects, response and longer-term review.

Before every shock, confirm rhythm, pulse, synchronisation markers, energy, pad contact and that oxygen is safely managed away from the chest.
After cardioversion, monitor rhythm, blood pressure, airway, oxygenation and sedation recovery, including post-conversion pauses.
Record pre- and post-treatment 12-lead ECGs and all drug doses, shock energies and responses.
With procainamide or IV amiodarone, continuously monitor QRS/QT, heart rate and blood pressure.
On long-term amiodarone, check thyroid and liver function before treatment and every 6 months; continue thyroid surveillance for months after stopping.
For anticoagulants, review haemoglobin, renal function, bleeding, interacting drugs and missed doses.

07Special situationsVariants, exceptions and circumstances that change the usual approach.

Synchronisation can reset

Many defibrillators revert to an unsynchronised mode after a shock. Check the R-wave markers again before pressing for the next shock.

AF now starts high

RCUK 2025 considers maximum defibrillator output a reasonable initial synchronised strategy for AF rather than an escalating low-energy sequence.

Adenosine needs speed

Its extremely short half-life means a rapid proximal bolus and immediate flush are essential; a slow infusion is ineffective.

Electricity does not remove clot risk

A successful shock restores rhythm but can mobilise pre-existing atrial thrombus; anticoagulation timing remains a separate safety step.

Drug labels and resuscitation algorithms differ

The amiodarone SmPC provides a weight-based general infusion, while RCUK specifies fixed peri-arrest doses. State which authority and scenario is being used.

Sedation can destabilise

A conscious unstable patient needs anaesthetic expertise because induction can worsen hypotension; this reinforces preparation but should not create a dangerous delay.

08Common pitfallsFrequent interpretation and management errors.

01
Delivering an unsynchronised shock to a patient with a pulse and organised QRS complexes.
02
Failing to re-enable synchronisation after the first shock.
03
Using the same initial energy for AF, flutter and VT despite current rhythm-specific RCUK guidance.
04
Mixing the RCUK amiodarone regimen with the SmPC regimen without naming the clinical context.
05
Stopping anticoagulation immediately after successful AF/flutter cardioversion.