Cardioversion

Cardioversion is the restoration of a normal sinus rhythm from a tachyarrhythmia by delivering a depolarizing electrical shock or administering antiarrhythmic drugs. It differs from defibrillation in that it is synchronized to the R wave of the QRS complex, which prevents delivering energy during the vulnerable T-wave period (which could precipitate ventricular fibrillation).

Physiology

Cardioversion works by simultaneously depolarizing all myocardial cells, terminating re-entrant circuits that sustain the arrhythmia. Once the entire myocardium is in a uniform refractory state, the SA node can reassert itself as the dominant pacemaker.

Re-entrant arrhythmias (AF, atrial flutter, SVT, VT) are terminated effectively by cardioversion.
Automatic tachycardias (digitalis toxicity rhythms, junctional tachycardia, multifocal atrial tachycardia) are not effectively terminated - homogeneous depolarization already exists, and shocks may worsen the rate.
Roberts and Hedges' Clinical Procedures in Emergency Medicine

Rapid rhythms reduce ventricular filling time, decrease preload, lower cardiac output (CO = HR x SV), raise pulmonary capillary wedge pressure, and can cause lactic acidosis and ventricular ischemia - a downward spiral that cardioversion can interrupt.

Types

1. Synchronized (Elective) Cardioversion

Shock delivered synchronised to the R wave (peak of QRS).
Used for hemodynamically unstable patients with:
- Atrial fibrillation (AF)
- Atrial flutter
- Supraventricular tachycardia (SVT)
- Ventricular tachycardia (VT) with a pulse

2. Unsynchronized Cardioversion (Defibrillation)

Shock delivered without synchronization.
Used for pulseless VT and VF (ventricular fibrillation) - no QRS to synchronize with.
If cardioversion produces VF, most defibrillators automatically revert to unsynchronized mode to allow immediate defibrillation.

3. Pharmacologic Cardioversion

Drug-induced restoration of sinus rhythm.
Best for recent-onset AF (< 48 hours).
Agents: ibutilide, flecainide, propafenone, amiodarone, vernakalant.

Indications

Cardioversion is indicated when a re-entrant tachycardia causes:

Chest pain / ischemia
Pulmonary edema
Hypotension
Altered mental status / syncope

Also indicated when medical therapy has failed in a stable patient (semi-elective cardioversion).

Not indicated for:

Sinus tachycardia (treat the underlying cause)
Digitalis toxicity-induced arrhythmias (risk of ventricular arrhythmia)
Junctional tachycardia, multifocal atrial tachycardia

Energy Levels (Biphasic Device)

Arrhythmia	Starting Energy
Atrial fibrillation	~200 J (biphasic); escalate to 360 J if needed
Atrial flutter / SVT	50-100 J (usually responds at lower energies)
Monomorphic VT (with pulse)	100 J; escalate if needed
Pulseless VT / VF (defibrillation)	120-200 J biphasic; max output if refractory

A recent study showed that starting at 360 J for AF (vs. escalating from 125 J) restored sinus rhythm in 88% vs. 66% of patients (p < 0.001). - Fuster and Hurst's The Heart, 15th ed.

For monophasic devices, use higher energies (~360 J for AF). Biphasic waveforms are now standard and more effective at lower energies.

Procedure (Step-by-Step)

Preparation: Correct metabolic abnormalities (K+, Mg2+, hypoxia) if time allows.
IV access + supplemental oxygen + continuous monitoring (ECG, SpO2, ETCO2).
Sedation of all conscious patients (unless immediately deteriorating).
Electrode placement: Anterior-posterior position is preferred for AF (anterior: over sternum; posterior: left of spine). Anterior-lateral can also be used.
Engage SYNC mode: Confirm that the defibrillator marks R waves correctly on the monitor. Adjust gain if needed.
Select energy level per arrhythmia (see table above).
Charge the defibrillator; announce "Stand clear!"
Deliver shock - press both shock buttons simultaneously (paddles) or shock button (hands-free pads).
Reassess rhythm immediately. If tachycardia persists, escalate energy and repeat.
Re-engage SYNC before each subsequent shock (most devices revert to unsynchronized after each delivery).

Morgan and Mikhail's Clinical Anesthesiology, 7e | Roberts and Hedges'

Sedation Agents

Drug	Dose	Notes
Midazolam	0.15 mg/kg	Most commonly used; ~2 min onset; flumazenil reversal available
Etomidate	0.15 mg/kg	Hemodynamically neutral; preferred in hypotensive patients
Propofol	1.5 mg/kg	Small BP drop; can be painful IV
Ketamine	1.5 mg/kg	No hypotension; can combine with low-dose propofol
Fentanyl	1.5 μg/kg	Opioid adjunct; monitor for respiratory depression

Roberts and Hedges'

Anticoagulation for AF Cardioversion

This is a key safety consideration:

AF duration < 48 hours:

Risk of thromboembolism is lower but not zero (especially with elevated CHA2DS2-VASc score).
Start anticoagulation as soon as possible and continue for at least 4 weeks after cardioversion.
Recent data (FinCV study) suggest that even short-duration AF carries embolic risk in patients with comorbidities.

AF duration > 48 hours (or unknown duration):

Option 1: Anticoagulate with warfarin (INR ≥ 2.0 for ≥ 3 consecutive weeks) or DOAC before cardioversion, then continue for ≥ 4 weeks after.
Option 2: Transesophageal echocardiography (TEE) to exclude left atrial thrombus, then cardiovert with heparin/DOAC bridge.
- If thrombus is found: postpone cardioversion, treat with anticoagulation for ≥ 3 weeks, then repeat TEE.
CHA2DS2-VASc ≥ 2 (men) or ≥ 3 (women): TEE recommended even if uncertain about duration.

Post-cardioversion "stunning": Atrial mechanical function may be impaired for up to 4 weeks after cardioversion even when sinus rhythm is restored - the reason anticoagulation continues post-procedure regardless of apparent success.

Fuster and Hurst's The Heart, 15th ed.

Complications

Thromboembolism (stroke) - mitigated by anticoagulation protocol above
Skin burns - from electrode contact
Transient arrhythmias post-shock (bradycardia, AV block, PVCs) - usually self-limiting
Precipitation of VF if shock falls on T wave (prevented by synchronization)
Myocardial injury - rare with modern biphasic devices
Failed cardioversion / early recurrence - more common in persistent AF, large left atrium, or no antiarrhythmic preloading

Pharmacologic Cardioversion (for Recent-Onset AF)

When stable and AF onset < 48 hours, pharmacologic cardioversion can be attempted:

Flecainide / Propafenone - high efficacy for recent-onset AF; avoid in structural heart disease
Ibutilide - IV; can also facilitate electrical cardioversion when shocks alone fail
Amiodarone - slower conversion but useful when structural heart disease is present
Vernakalant - atrial-selective; rapid IV conversion

A 2024 Cochrane network meta-analysis (PMID 38828867) comparing electrical and pharmacological cardioversion found that electrical cardioversion has higher immediate success rates, while pharmacologic agents vary in speed and safety profile. A 2025 Bayesian network meta-analysis (PMID 38324103) confirmed flecainide and propafenone as most effective for pharmacologic conversion of recent-onset AF.

Pediatric Cardioversion

Synchronized cardioversion dose: 0.5-1 J/kg (initial), escalate to 2 J/kg if needed.
Defibrillation (pulseless arrest): 2 J/kg initial, escalate to 4 J/kg or max 10 J/kg.

Key Reminders

Always re-engage SYNC mode between shocks (devices default to unsynchronized after each delivery).
Do not use synchronized cardioversion for pulseless VT or VF - use unsynchronized defibrillation.
In Wolff-Parkinson-White (WPW) with AF: avoid AV nodal blockers (adenosine, verapamil, digoxin); electrical cardioversion is preferred.
Lowering thoracic impedance (applying firm pressure to electrodes, using gel pads) improves shock efficacy.

Sources: Roberts and Hedges' Clinical Procedures in Emergency Medicine | Fuster and Hurst's The Heart, 15th ed. | Morgan and Mikhail's Clinical Anesthesiology, 7e | Braunwald's Heart Disease | 2024 Cochrane meta-analysis (PMID 38828867) | 2025 Pharmacologic cardioversion meta-analysis (PMID 38324103)

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