• • Rapid termination of tachycardia that is either unresponsive to medications or pacing interventions or is hemodynamically compromising, necessitating more urgent intervention.

Cardioversion

• • Tachycardia, either supraventricular or ventricular, with regular ventricular response with mild to moderate hypotension.

  • Mechanisms of supraventricular tachycardia include the following:

  • • Atrial reentry tachycardia.

    • Reciprocating tachycardia utilizing an accessory connection.

    • Atrial flutter.

    • Atrioventricular nodal reentry tachycardia.

Defibrillation

• • The most effective treatment for ventricular fibrillation and pulseless ventricular tachycardia (Table 7–1).

  • Its effectiveness diminishes rapidly over time; therefore, early defibrillation is recommended in patients who have suffered cardiac arrest.

  • Atrial fibrillation.

  • Supraventricular tachycardia with rapid conduction via an accessory connection.

  • Ventricular fibrillation.

  • Torsades de pointes.

Absolute

• • A patient directive regarding resuscitation.

Relative

• • Cardioversion of a rhythm known to be automatic in origin is not indicated.

  • Digoxin toxicity-induced arrhythmia.

  • • With digoxin toxicity, there is a high incidence of post-cardioversion ventricular tachycardia and fibrillation.

  • Elective cardioversion of a hemodynamically stable patient with a known atrial thrombus; however, the likelihood of impending cardiovascular compromise can outweigh the risk of thromboembolism.

  • Repeated cardioversion of a rhythm where the predisposing cause is not eliminated.

• • External defibrillator, either manual or semi-automated (Figure 7–1).

• • Skin electrode patches, wires to connect to defibrillator.

  • Heart rhythm monitor.

  • Equipment to protect the airway as well as resuscitation medications to support blood pressure.

  • Do not delay cardioversion or defibrillation in a hemodynamically unstable patient while waiting for additional monitoring equipment or personnel.

• • Chest wall lesions.

  • Neurologic complications.

  • Arrhythmia complications.

  • Transmitted electrical shock of nonprotected bystanders may occur.

  • Skin burns may result from high-dose energy.

  • Excessive energy delivery may also result in myocardial damage and irreversible cardiomyopathy.

  • Stroke may result from thromboembolism of atrial or ventricular thrombus with energy delivery.

  • Anticoagulation and assessment of risk of thrombus with transesophageal echocardiogram may minimize but not eliminate risk of stroke, which occurs in 1–3% of cardioversions.

  • In very ill patients or patients with longstanding arrhythmia or underlying sinus or junctional node disease, cardioversion may result in asystole or profound bradycardia, which may not respond to medications or temporary pacing.

  • Cardioversion may convert a stable arrhythmia into an unstable tachycardia, particularly with asynchronous cardioversion of a regular tachycardia producing ventricular fibrillation.

  • Immediate defibrillation is necessary in such cases.

• • Most failures of cardioversion relate to any of the following:

  • • Improper lead positioning.

    • Energy selection.

    • Synchronization.

    • Use of cardioversion for an automatic rhythm not responsive to cardioversion (sinus tachycardia, automatic atrial tachycardia).

  • Lead positioning should direct the current of energy across the chamber to be cardioverted.

  • Cardioversion of ventricular tachycardia should direct energy across the ventricle: Position 1 electrode near the cardiac apex.

  • Atrial tachycardia requires the current of energy to be directed across the atria; an anterior-posterior pad configuration may be preferable.

  • Patients with repaired congenital heart disease resulting in dilated atria and atrial tachycardia are candidates for anterior-posterior pad configuration.

  • In dextrocardia, the pads need to positioned across the right chest.

  • Energy selection.

  • • Regular rhythms (atrial flutter, supraventricular tachycardia, ventricular tachycardia) require low-dose energy, up to 1 J/kg.

    • Irregular tachycardias (atrial fibrillation, ventricular fibrillation) require high-dose energy, at least 2 J/kg.

  • Regular rhythms should receive energy synchronized to the QRS.

  • • Check the rhythm monitor to verify that the QRS, not the T wave, is being sensed.

    • Asynchronous energy delivered into a regular rhythm may fire on the T wave and produce ventricular fibrillation.

    • In such cases, immediate asynchronous defibrillation is required.

  • Irregular rhythms require asynchronous cardioversion because the QRS timing cannot be predicted.

  • Remember that the default setting on a defibrillator is asynchronous and must be reset to synchronous if so desired after every discharge.

  • When an arrhythmia is due to a reentrant circuit, a synchronized shock depolarizes all excitable tissue within the circuit, making tissue refractory; therefore, the electrical circuit is no longer able to propagate and terminates.

  • Rhythms due to abnormal accelerated automaticity are not reliant upon a reentrant circuit and do not respond to cardioversion or defibrillation.

  • • Examples of such rhythms are automatic (ectopic) atrial tachycardia or arrhythmias due to drug toxicity or profound metabolic derangement.