Cardioversion

Reading File

Cardioversion is the process of restoring a normal heart rhythm - either electrically (synchronized DC shock) or pharmacologically (antiarrhythmic drugs). It's used for atrial fibrillation, atrial flutter, SVT, and hemodynamically unstable VT/VF.

Searching sources...

Finding Sources

Searching PubMed

cardioversion atrial fibrillation

Good sources found. Let me read the main cardioversion sections now in parallel.

Reading File

Good content found. Let me now read the detailed cardioversion procedure section from Roberts & Hedges and Fuster's Heart for energy levels, indications, and pharmacologic cardioversion details.

Reading File

Excellent - rich content. Let me now get the pharmacologic cardioversion details and energy level table from Roberts & Hedges.

Reading File

I have comprehensive content. Let me compile the full, detailed answer now.

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)

This is a shared conversation. Sign in to Orris to start your own chat.