Objective

Implement immediate, guideline-directed interventions for hemodynamically unstable atrial fibrillation, flutter, and supraventricular tachycardia (SVT)—focusing on synchronized cardioversion and the appropriate use of procainamide in pre-excited atrial fibrillation (Wolff-Parkinson-White syndrome).

1. Definitions and Hemodynamic Compromise

Hemodynamic compromise in the context of atrial arrhythmias is defined by clinical signs and symptoms reflecting end-organ hypoperfusion. The presence of such instability mandates urgent rhythm control interventions rather than solely rate control.

Criteria for Hemodynamic Instability:

• Systolic blood pressure (SBP) < 90 mm Hg or a symptomatic drop in perfusion pressure.
• Chest pain suggestive of myocardial ischemia or objective ECG evidence of ongoing ischemia.
• Altered mental status (e.g., confusion, lethargy, syncope) not attributable to other causes.
• Acute pulmonary edema or other signs of acute heart failure.

2. Indications for Synchronized Cardioversion

Synchronized direct current (DC) cardioversion is the first-line therapy for patients with hemodynamically unstable atrial fibrillation (AF), atrial flutter, or supraventricular tachycardia (SVT). The goal is prompt restoration of sinus rhythm to improve cardiac output and perfusion.

Specific Indications:

• Atrial fibrillation with hemodynamic instability (hypotension, ischemia, altered mental status, acute heart failure).
• Atrial flutter with hemodynamic instability.
• Supraventricular tachycardia (SVT) with hemodynamic instability.
• Pre-excited atrial fibrillation (e.g., Wolff-Parkinson-White syndrome) presenting with hemodynamic instability.

Exclusions (Require Unsynchronized Defibrillation):

• Pulseless Ventricular Tachycardia (VT)
• Ventricular Fibrillation (VF)
• Polymorphic VT / Torsades de Pointes (if pulseless or severely unstable)

3. Cardioversion Technique

3.1 Equipment and Synchronization

Proper setup and use of the defibrillator are essential for successful and safe cardioversion. The primary goal of synchronization is to deliver the electrical shock timed with the R-wave of the QRS complex, avoiding the vulnerable T-wave period, which could induce ventricular fibrillation.

• Utilize a biphasic defibrillator, as these are generally more effective at lower energy levels than monophasic devices.
• Ensure the device is set to “SYNC” or “SYNCHRONIZED” mode.
• Visually confirm that the device is detecting and marking the R-wave (often with a dot or arrow above the QRS complex on the monitor display) before each shock delivery. If R-waves are not consistently detected, adjust ECG lead placement or gain.

3.2 Electrode Placement and Energy Selection

Optimal placement of defibrillation pads and appropriate energy selection are crucial for maximizing the chance of successful cardioversion while minimizing potential complications.

Electrode (Pad) Positions:

• Anterior–Lateral (Standard): One pad is placed to the right of the upper sternum, below the clavicle. The other pad is placed on the left mid-axillary line, at the level of the V6 ECG lead (cardiac apex).
• Anterior–Posterior: One pad is placed over the left precordium (anteriorly), and the other is placed on the left posterior chest, inferior to the scapula. This position may be considered for patients with large body habitus or if anterior-lateral placement is unsuccessful.

Energy Selection (Biphasic Defibrillator):

3.3 Sedation and Analgesia

Synchronized cardioversion is a painful procedure; therefore, adequate sedation and analgesia are mandatory in conscious patients. The choice of agent should balance patient comfort with hemodynamic stability and rapid recovery.

• Etomidate (0.1–0.3 mg/kg IV): Offers rapid onset and recovery with minimal cardiovascular depression. Ideal for many unstable patients.
• Ketamine (1–2 mg/kg IV): Provides dissociation, analgesia, and sympathetic stimulation, which can be beneficial if hypotension is a concern. May cause emergence reactions.
• Propofol (0.5–1.5 mg/kg IV, titrated): Potent sedative with rapid onset and offset, but carries a risk of hypotension and respiratory depression. Use cautiously, especially in already hypotensive patients.
• Midazolam or Fentanyl may be used as adjuncts or for lighter sedation if appropriate, but typically a deeper level of sedation is required for cardioversion.

3.4 Post-Shock Monitoring and Troubleshooting

Immediate reassessment after each shock is critical to determine success and guide further interventions.

• Immediate Post-Shock Assessment: Check the ECG rhythm and patient’s vital signs (pulse, blood pressure, oxygen saturation) immediately.
• If Shock Fails to Convert Rhythm:
  • Reconfirm proper synchronization if another shock is planned.
  • Ensure good pad-to-skin contact; consider repositioning pads (e.g., to anterior-posterior).
  • Escalate the energy level for the next synchronized shock.
  • Administer additional sedation as needed, ensuring the patient remains adequately sedated.
• Monitor for Complications:
  • Bradyarrhythmias or asystole (be prepared for pacing).
  • Skin burns (less common with modern pads and proper technique).
  • Recurrence of the tachyarrhythmia.
  • Embolic events (especially if anticoagulation status is unknown or inadequate for AF >48h).

4. Management of Pre-Excited Atrial Fibrillation (WPW)

Pre-excited atrial fibrillation (AF) occurs in patients with Wolff-Parkinson-White (WPW) syndrome, where an accessory pathway allows rapid conduction of atrial impulses to the ventricles, bypassing the AV node. This can lead to extremely rapid ventricular rates and degenerate into ventricular fibrillation (VF).

Pathophysiology:

In WPW, the accessory pathway does not have the same rate-slowing properties as the AV node. During AF, if conduction predominantly occurs via the accessory pathway, ventricular rates can exceed 250-300 bpm, leading to hemodynamic collapse and VF.

Contraindicated Drugs:

AV nodal blocking agents are contraindicated in pre-excited AF because they can block the AV node, thereby preferentially shunting impulses down the accessory pathway, potentially increasing the ventricular rate and risk of VF. These include:

• Adenosine
• Beta-blockers (e.g., metoprolol, esmolol)
• Calcium-channel blockers (non-dihydropyridine, e.g., verapamil, diltiazem)
• Digoxin
• Amiodarone (IV amiodarone has some AV nodal blocking properties and its use is controversial and generally avoided in acute unstable pre-excited AF).

5. Procainamide Pharmacotherapy

5.1 Mechanism and Indication

Procainamide is a Class IA antiarrhythmic agent that blocks sodium channels. It slows conduction velocity and prolongs refractory periods in atrial tissue, ventricular tissue, and, importantly, accessory pathways. This makes it effective in managing pre-excited atrial fibrillation.

• Indication: Hemodynamically stable pre-excited atrial fibrillation (WPW with AF) when immediate DC cardioversion is not performed or is deferred. It can also be used for other stable supraventricular and ventricular tachycardias.

5.2 Dosing and Administration

Careful, slow infusion and monitoring are essential to reduce the risk of hypotension and proarrhythmia.

• Loading Dose: 15–18 mg/kg administered intravenously at a rate of 20–50 mg/minute. Some protocols suggest a maximum rate of 30 mg/min.
• Maximum Dose/Endpoints: The infusion should be stopped if the arrhythmia terminates, the patient develops hypotension, the QRS complex widens by more than 50% from baseline, or a total dose of 17 mg/kg (or up to 1-1.5 grams in some guidelines) has been administered.
• Maintenance Infusion (if needed after conversion): 1–4 mg/minute.

5.3 Monitoring During Procainamide Infusion

• Continuous ECG Monitoring: Closely watch for changes in rhythm, QRS duration (stop if >50% widening from baseline or QRS >120-140 ms), and QT interval prolongation.
• Blood Pressure: Monitor frequently (e.g., every 2-5 minutes during loading dose) via noninvasive cuff or invasive arterial line if available. Slow or stop infusion if significant hypotension develops.
• Laboratory Parameters: Baseline and periodic monitoring of electrolytes (especially potassium and magnesium, as hypokalemia and hypomagnesemia can potentiate proarrhythmia) and renal function (as procainamide and its active metabolite NAPA are renally cleared).

5.4 Contraindications and Interactions

• Contraindications:
  • Significant hypotension (unless due to the arrhythmia itself and expected to improve with conversion).
  • Second- or third-degree AV block without a functioning pacemaker.
  • Baseline prolongation of the QT interval or history of torsades de pointes.
  • Known hypersensitivity to procainamide.
  • Myasthenia gravis (can exacerbate weakness).
• Interactions: Avoid coadministration with other agents that prolong the QT interval (e.g., certain antipsychotics, macrolide antibiotics, other antiarrhythmics) due to increased risk of torsades de pointes.

5.5 Pharmacokinetic/Pharmacodynamic Considerations

• Volume of Distribution (Vd): Approximately 2.5–4 L/kg.
• Half-life (t½): Procainamide: 2.5–5 hours. Its active metabolite, N-acetylprocainamide (NAPA), has a longer half-life (6–8 hours). Both are prolonged in renal dysfunction.
• Metabolism and Excretion: Procainamide is acetylated in the liver to NAPA (which has Class III antiarrhythmic properties). Both procainamide and NAPA are primarily excreted by the kidneys. Dose adjustments are necessary in renal impairment.

5.6 Advantages and Disadvantages

• Advantages:
  • Effective in slowing conduction over accessory pathways in WPW.
  • Avoids the unopposed AV nodal blockade seen with other agents in pre-excited AF.
  • Can be used for both supraventricular and ventricular tachycardias.
• Disadvantages:
  • Risk of hypotension, particularly with rapid infusion.
  • Proarrhythmic potential, including torsades de pointes (especially if QT prolongs significantly).
  • Requires slow infusion and intensive hemodynamic and ECG monitoring.
  • Infusion site reactions can occur.
  • Long-term use associated with drug-induced lupus syndrome (not relevant for acute IV use).

6. Integrated Decision Algorithm for Unstable Atrial Arrhythmias

A stepwise approach ensures rapid, guideline-concordant care for patients presenting with atrial tachyarrhythmias, particularly when hemodynamic instability or pre-excitation is present.

7. Post-Intervention Care

Following successful cardioversion or termination of the arrhythmia with procainamide, vigilant observation and proactive management are essential to prevent recurrence, manage complications, and plan long-term care.

• Monitoring:
  • Continuous telemetry to monitor for arrhythmia recurrence, bradyarrhythmias, or proarrhythmic events.
  • Frequent vital signs assessment (blood pressure, heart rate, oxygen saturation, respiratory rate).
  • Serial ECGs as clinically indicated, especially if antiarrhythmic medications are continued or initiated.
• Anticoagulation:
  • Assess the need for anticoagulation based on the CHA₂DS₂-VASc score for patients with atrial fibrillation or atrial flutter.
  • For AF/flutter of duration >48 hours or unknown duration, anticoagulation is generally recommended for at least 4 weeks post-cardioversion, or long-term based on CHA₂DS₂-VASc score.
  • If cardioversion was emergent for AF/flutter <48 hours duration in a low-risk patient, the decision for anticoagulation is individualized but often initiated.
• Long-Term Management:
  • Identify and address underlying causes or precipitating factors (e.g., electrolyte imbalances, ischemia, thyroid dysfunction, substance use).
  • Consider referral to an electrophysiologist for further evaluation, risk stratification, and discussion of long-term rhythm control strategies, including catheter ablation (especially for WPW or recurrent symptomatic arrhythmias).
  • Optimize medical therapy for any underlying heart disease.
• Documentation:
  • Thoroughly document the event, including pre-procedure rhythm, vital signs, sedation agents and doses used.
  • Record details of cardioversion attempts: energy levels, synchronization status, pad placement, and rhythm outcomes.
  • Note any complications encountered and their management.
  • Document post-procedure rhythm, vital signs, and the plan for ongoing care.