Synchronized Electrical Cardioversion

Updated: Sep 22, 2016
  • Author: Sean C Beinart, MD, MSc, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD  more...
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Delivery of direct current (DC) shocks to the heart has long been used successfully to convert abnormal heart rhythms back to normal sinus rhythm. In 1775, Abildgaard reported using electricity to both induce and revive a hen from lifelessness. [1] Beck was the first physician to use DC defibrillation on a human to treat ventricular fibrillation on a 14-year-old during cardiac surgery in 1947. Fifteen years later, Lown applied synchronized DC shocks to the heart to convert atrial fibrillation and ventricular tachycardia to normal sinus rhythm. [2]

Cardioversion is defined as a “synchronized DC discharge, and … does not apply to ventricular defibrillation or to the pharmacologic reversion of arrhythmias.” [3, 4] The DC electrical discharge is synchronized with the R or S wave of the QRS complex. Synchronization in the early part of the QRS complex avoids energy delivery near the apex of the T wave in the surface ECG, which coincides with a vulnerable period for induction of ventricular fibrillation. The peak of the T wave represents the terminal portion of the refractory state when adjacent heart fibers are in differing states of repolarization. Defibrillation refers to an unsynchronized discharge of energy and is only recommended for ventricular fibrillation (VF).

Electrical cardioversion (ECV) use and outcomes in contemporary practice are unknown. Steinberg et al reviewed all nonemergent ECVs for atrial arrhythmias at a tertiary care center (2010 to 2013). They stratified patients by transesophageal echocardiography (TEE) use before ECV, and they compared demographics, history, vitals, and laboratory studies. Outcomes included postprocedural success and complications and repeat cardioversion, rehospitalization, and death within 30 days. Overall, 1,017 patients underwent ECV; 633 underwent TEE before ECV and 384 did not. Within 30 days, 80 patients (7.9%) underwent repeat ECV, 113 (11%) were rehospitalized, and 14 (1.4%) died. ECV success was more common in patients who underwent TEE before ECV, but there were no differences in 30-day death or rehospitalization rates. Multivariate analyses indicated that higher pre-ECV heart rate was associated with increased rehospitalization or death, whereas TEE use was associated with lower rates. Failures, complications, and rehospitalization after nonemergent ECV are common and associated more with patient condition than procedural characteristics. TEE use was associated with better clinical outcomes. [5]

De Vos et al evaluated the relation between mechanical atrial fibrillation cycle length (AFCL-tvi), atrial fibrillatory velocity (AFV-tvi), and success of electrical cardioversion (ECV) in patients with atrial fibrillation (AF). In 133 patients with persistent AF, they performed echocardiography before ECV and measured the AFCL-tvi and AFV-tvi in the right atrium and left atrium. They monitored recurrent AF. Nineteen (14%) patients had failure of ECV, 42 (32%) remained in sinus rhythm after 1-year follow-up, and 72 (54%) had a recurrence of persistent AF. Compared to patients with a successful ECV, patients with immediate ECV failure had a lower median AFV-tvi measured in the right atrium. Compared to patients with recurrence of AF, patients with maintenance of sinus rhythm after 1 year had a longer AFCL-tvi measured in the left atrium and had a higher AFV-tvi in both atria. Multivariate analyses showed that all atrial TVI parameters were independently associated with the maintenance of sinus rhythm after 1 year. Higher atrial fibrillatory wall velocities and longer AFCLs determined by echocardiography are associated with acute and long-term success of ECV. [6]

Basic principles

Transient delivery of electrical current causes a momentary depolarization of most cardiac cells allowing the sinus node to resume normal pacemaker activity. In the presence of reentrant-induced arrhythmia, such as paroxysmal supraventricular tachycardia (PSVT) and ventricular tachycardia (VT), electrical cardioversion interrupts the self-perpetuating circuit and restores a sinus rhythm. Electrical cardioversion is much less effective in treating arrhythmia caused by increased automaticity (eg, digitalis-induced tachycardia, catecholamine-induced arrhythmia) since the mechanism of the arrhythmia remains after the arrhythmia is terminated and therefore is likely to recur. [7]

Two types of defibrillators are in use today for external cardioversion and defibrillation: a monophasic sinusoidal waveform (positive sine wave) and a biphasic truncated waveform. The more recent use of biphasic cardioversion has shown that less energy is required to convert an arrhythmia to a normal sinus rhythm. There are several models available on the market. In 1997, a low-energy, impedance-compensating biphasic waveform was evaluated for atrial and ventricular arrhythmia management. This defibrillator automatically adjusts to the patient's transthoracic impedance.



External cardioversion

Based on advanced cardiac life support (ACLS) guidelines, any patient with narrow or wide QRS complex tachycardia (ventricular rate >150) who is unstable (eg, chest pain, pulmonary edema, lightheadedness, hypotension) should be immediately treated with synchronized electrical cardioversion. [8]  Synchronization to an R or S wave prevents the delivery of a shock during the vulnerable period of cardiac repolarization when VF can be induced. 

Synchronized electrical cardioversion may also be used to treat stable VT that does not respond to a trial of intravenous medications. It is also recommended for the treatment of the following [9] :

  • Supraventricular tachycardia due to reentry

  • Atrial fibrillation

  • Atrial flutter

  • Atrial tachycardia

  • Monomorphic VT with pulses

Internal cardioversion

Internal cardioversion for atrial fibrillation is used in patients who are resistant to external cardioversion or inadvertently induced during an electrophysiologic study. Cardioversion should occur before placement of an atrial defibrillator.



Contraindications include known digitalis toxicity–associated tachycardia, sinus tachycardia caused by various clinical conditions, and multifocal atrial tachycardia.

In addition, because patients with atrial fibrillation are at risk for developing clots in the left atrium, predisposing them to increased stroke risk, patients who are not anticoagulated should not undergo cardioversion without a transesophageal echo that can assess the presence of a left atrial thrombus.

Synchronized cardioversion should also not be used to treat VF, since the cardioverter may not sense a QRS wave and may therefore fail to deliver a shock. Synchronized cardioversion is also not appropriate for the treatment of pulseless VT or polymorphic (irregular) VT, since these require high-energy, unsynchronized shocks (ie, defibrillation doses). In addition, cardioversion is not effective for the treatment of junctional tachycardia. [9]



External cardioversion

ACLS guidelines should be followed as indicated. The key components in preparing the patient are intravenous access, airway management equipment, sedative drugs, and a cardioverter/defibrillator monitoring device. Note the following:

  • The patient should be adequately sedated with a short-acting agent such as midazolam or propofol. In addition, an opioid analgesic, such as fentanyl, is commonly used. Reversal agents, such as flumazenil and naloxone, should be available.
  • The defibrillator should be placed in the synchronized mode, which permits a search for a large R or S wave. The delivered energy is selected. Most monophasic and biphasic models can deliver up to 360 Joules. Manual button depression by the operator causes the defibrillator to discharge an electric current that lasts less than 4 milliseconds and avoids the vulnerable period of cardiac repolarization when VF can be induced. The operator should be aware of this brief delay as the cardioverter searches for a large positive or negative deflection. If deflections are too small for the defibrillator to synchronize, the physician can change the leads or place them closer to the patient's chest or heart. If the patient develops VF, always turn off synchronization to avoid delay in energy delivery.
  • Two options exist for placement of paddles on the chest wall. First is the anterolateral position in which a single paddle is placed on the left fourth or fifth intercostal space on the midaxillary line; the other paddle is placed just to the right of the sternal edge on the second or third intercostal space.
  • The second option is the anteroposterior position. A single paddle is placed to the right of the sternum, as above, and the other paddle is placed between the tip of the left scapula and the spine. Since the skin can conduct away a significant portion of the current, conductive gel or pre-gelled pads are commonly used to ensure good contact. Under ideal circumstances, only 10-30% of the total current reaches the heart.
  • The paddles should be placed firmly against the chest wall to avoid arcing and skin burns. Although there is a risk of receiving a shock if touching the patient or the stretcher, bed, or other equipment in which the patient is in contact, there has been recent evidence that continued contact with the patient is safe during biphasic defibrillation. [10] Pacemakers and ICDs should be at least 10 cm from direct contact with paddles and should eventually be interrogated for any malfunction after cardioversion. The anteroposterior approach is preferred in patients with implantable devices to avoid shunting current to the implantable device and damaging the system.
  • Energy requirements for atrial fibrillation are 100-200 J initially and 360 J for subsequent shocks. A study showed good response to higher energy shocks of 720 J for the treatment of refractory atrial fibrillation. [11] Biphasic shocks require a typical energy level of 75 J for correction of atrial fibrillation. Cardioversion of atrial fibrillation secondary to hyperthyroidism is 90% successful. Only 25% of patients with atrial fibrillation caused by severe mitral regurgitation are successfully treated, and half revert in the first 6 months. Atrial flutter and PSVT require less energy: 50 J initially, then 100 J if needed. Cardioversion of VT involves shocks of 50-100 J initially, then 200 J if unsuccessful.


Internal cardioversion

The success of internal defibrillation with low-energy shocks to treat VF and VT resulted in further studies of internal cardioversion for the treatment of atrial fibrillation. Note the following:

  • The patient should receive anticoagulation as for external cardioversion, although they should be withheld for safe venous puncture. Various techniques are available; the following is a commonly used procedure.
  • Three temporary catheters are inserted in the venous system and positioned under fluoroscopic guidance. Two catheters of large surface area are used for shock delivery, and a third quadripolar catheter is used for R-wave synchronization and temporary ventricular postshock pacing. The first defibrillation catheter is advanced into the distal coronary sinus; the second is positioned in the right atrium appendix or the lateral wall of the right atrium. These catheters are connected to an external defibrillator that delivers biphasic shocks. The quadripolar catheter is placed in the apex of the right ventricle and is also connected to an external pacemaker. A right atrium-to-coronary sinus cardioversion vector was successfully used with mean of energy of 5.6 +/- 4.7 J (0.4-35) in one study. [12]

Treatment of a specific arrhythmia

Treatment strategies for atrial fibrillation include the following:

  • If the patient is clinically unstable, emergent cardioversion is recommended. Stable patients should have their ventricular rate controlled, and most should be anticoagulated with intravenous heparin and started on warfarin for stroke prevention because of a high risk of thromboembolism. If a high degree of certainty exists that atrial fibrillation is of less than 48 hours' duration, then a patient can proceed to cardioversion.

  • If the arrhythmia is of uncertain duration or of confirmed duration longer than 48 hours, then the patient can proceed to transesophageal echocardiography (TEE) for the evaluation of a thrombus in atrium or appendage (a suggestion of smoke, or stagnant blood flow, is considered positive by some authorities). If TEE findings are negative, the patient can proceed to elective cardioversion. Otherwise, patients should be anticoagulated for 3 weeks before cardioversion with a repeat TEE.

  • All patients should be anticoagulated with warfarin for 4 weeks after cardioversion because mechanical function of the atrium lags by up to 7 days after restoring sinus rhythm. If the foregoing treatment fails, patients can be managed with medical treatment alone, repeat cardioversion after antiarrhythmic (eg, ibutilide) treatment, ablation therapy, or atrial defibrillation. [13]  

Treatment strategies for other SVTs include the following:

  • At present, recurrent atrial flutter is usually permanently cured by radiofrequency catheter ablation. If the patient is unstable, then cardioversion can be used. See the video below.

    The 3-dimensional electroanatomic map of type I atrial flutter. The colors progress from blue to red to white and represent relative conduction time in the right atrium (early to late). An ablation line (red dots) has been created on the tricuspid ridge extending to the inferior vena cava. This interrupts the flutter circuit. RAA: right atrial appendage; CSO: coronary sinus os; IVC: inferior vena cava; TV: tricuspid valve annulus.
  • Anticoagulation is recommended if external cardioversion is used in the treatment of atrial flutter in a similar approach to patients with atrial fibrillation requiring cardioversion. Although atrial flutter was once perceived to be a lower risk for left atrial thrombus than atrial fibrillation, recent data suggest that the risk of clot formation is equivalent.

  • Other patients with SVT rarely require external cardioversion unless they are unstable.

Treatment strategies for other ventricular tachycardia include the following:

  • Patients who do not respond to intravenous medications in treating stable monomorphic VT associated with acute coronary syndrome or acute myocardial infarction should be initially treated with 50- to 100-J synchronized shocks. If no response to low-energy shock is noted, then a 200-J shock should be administered, followed by 300- and 360-J shocks as needed.

  • In unstable VT, unsynchronized shocks should be delivered. Biphasic defibrillators do not require escalating energy, but 3 sequential shocks of 150 J should be used.

Special conditions

In pediatric patients with PSVT or VT who are not hemodynamically stable, an initial synchronized shock of 0.5 J/kg is recommended. In subsequent attempts, the energy is increased.

During pregnancy, recommendations for other adults are applicable.



Complications may affect patients or health care workers. Injury incidence is 1 case per 1700 shocks for paramedics in the field. The patient may become hypoxic or hypoventilate from sedation. Most burns from shocks are superficial partial-thickness burns, but a few are deep. Cardiac complications include dysrhythmia, hypotension, and pulmonary edema.

Inducible arrhythmias include bradycardia, atrioventricular (AV) block, asystole, VT, and VF. In patients with acute coronary syndromes or acute myocardial infarction, bradycardia or AV blocks can be induced, and they may need an external or internal pacemaker. VT and VF commonly occur in patients with prior similar history.

Postcardioversion VF consists of 2 types. The first type occurs immediately after a shock and is related to improper synchronization. This type of VF readily responds to defibrillation (unsynchronized countershock).

The second type is related to digitalis toxicity and manifests within a few minutes of cardioversion. Initially, it can be a junctional or paroxysmal atrial tachycardia, then VF, which can be difficult to convert to a sinus rhythm.

Although some of the complications appear critical, DC synchronized cardioversion is usually safe and effective if performed under the care of well-trained personnel. Troponin I measurements after cardioversion were not elevated in patients with normal and reduced left ventricular function, suggesting lack of myocyte injury. [14]