Synchronized Electrical Cardioversion 

  • Author: Sean C Beinart, MD, FACC, FHRS; Chief Editor: Jeffrey N Rottman, MD   more...
 
Updated: May 9, 2011
 

Overview

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] 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).

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.

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.

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Indications

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.[4]
  • Synchronized electrical cardioversion may be used to treat stable VT that does not respond to a trial of intravenous medications.
  • In hemodynamically stable patients with atrial fibrillation, atrial flutter, or other supraventricular tachycardia (SVT), synchronized electrical cardioversion can also be used to electively restore sinus rhythm.
  • Because DC delivery is painful, it is usually performed after the patient has received sufficient intravenous sedation from an anesthesiologist or trained nurse to produce an amnestic effect of the procedure.

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.
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Contraindications

  • Contraindications include patients with known digitalis toxicity–associated tachycardia, patients with sinus tachycardia caused by various clinical conditions, or patients with multifocal atrial tachycardia.
  • In addition, patients with atrial fibrillation are at risk for developing clots in the left atrium that predispose to increased stroke risk. As a result, patients who are not anticoagulated should not undergo cardioversion without a transesophageal echo that can assess the presence of left atrial thrombus.
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Technique

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.
  • 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.[5]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.[6] 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.
  • 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.[8]

Treatment of a specific arrhythmia

  • Atrial fibrillation
    • 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.
      The image on the right is a reconstructed 3-dimensional image of the left atrium in a patient undergoing atrial fibrillation ablation. The figure on the left was created with a mapping catheter using Endocardial Solutions mapping technology. It represents the endocardial shell of the left atrium and is used as the template during left atrial ablation procedures.
  • Other SVTs
    • At present, recurrent atrial flutter is usually permanently cured by radiofrequency catheter ablation. If the patient is unstable, then cardioversion can be used.
      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.
  • Ventricular tachycardia
    • 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.
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Complications

  • 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.[7]
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Contributor Information and Disclosures
Author

Sean C Beinart, MD, FACC, FHRS  Electrophysiologist, Cardiac Associates, PC

Sean C Beinart, MD, FACC, FHRS is a member of the following medical societies: Alpha Omega Alpha, American College of Cardiology, American College of Physicians, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Specialty Editor Board

Russell F Kelly, MD  Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College

Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology

Disclosure: Nothing to disclose.

Francisco Talavera, PharmD, PhD  Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy; Senior Pharmacy Editor, eMedicine

Disclosure: eMedicine Salary Employment

Steven J Compton, MD, FACC, FACP  Director of Cardiac Electrophysiology, Alaska Heart Institute, Providence and Alaska Regional Hospitals

Steven J Compton, MD, FACC, FACP is a member of the following medical societies: Alaska State Medical Association, American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Heart Rhythm Society

Disclosure: Nothing to disclose.

Amer Suleman, MD  Private Practice

Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions

Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD  Professor of Medicine and Pharmacology, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center

Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)

Disclosure: Nothing to disclose.

References
  1. Abilgard CP. Tentamina electrica in animalibus instituta. Societatis Medicae Havniensis Colectanea. 1775;2:157.

  2. Lown B, Amarasingham R, Neuman J. New method for terminating cardiac arrhythmias. Use of synchronized capacitor discharge. JAMA. Nov 3 1962;182:548-55. [Medline].

  3. Lown B. Defibrillation and cardioversion. Cardiovasc Res. Aug 1 2002;55(2):220-4. [Medline].

  4. Part 5: Electrical Therapies. Automated External Defibrillators, Defibrillation, Cardioversion, and Pacing. Circulation. 2005;112:IV-35-IV-46.

  5. Lloyd MS, Heeke B, Paul F. Walter and Jonathan J. Langberg; Rescuers in Direct Contact With Patients During Biphasic External Hands-On Defibrillation. An Analysis of Electrical Current Flow Through Defibrillation Circulation. Circulation. 2008.

  6. Saliba W, Juratli N, Chung MK, et al. Higher energy synchronized external direct current cardioversion for refractory atrial fibrillation. J Am Coll Cardiol. Dec 1999;34(7):2031-4. [Medline].

  7. Cemin R, Rauhe W, Marini M, Pescoller F, Pitscheider W. Serum troponin I level after external electrical direct current synchronized cardioversion in patients with normal or reduced ejection fraction: no evidence of myocytes injury. Clin Cardiol. Oct 2005;28(10):467-70. [Medline].

  8. Levy S, Ricard P, Gueunoun M, et al. Low-energy cardioversion of spontaneous atrial fibrillation. Immediate and long-term results. Circulation. Jul 1 1997;96(1):253-9. [Medline].

  9. Bellotti P, Spirito P, Lupi G, Vecchio C. Left atrial appendage function assessed by transesophageal echocardiography before and on the day after elective cardioversion for nonvalvular atrial fibrillation. Am J Cardiol. May 15 1998;81(10):1199-202. [Medline].

  10. Burdick W. Carotid Sinus Massage and Cardioversion. In: Clinical Procedures in Emergency Medicine. 3rd ed. 1998:178-185.

  11. Ewy GA. The optimal technique for electrical cardioversion of atrial fibrillation. Clin Cardiol. Feb 1994;17(2):79-84. [Medline].

  12. Lüderitz B, Pfeiffer D, Tebbenjohanns J, Jung W. Nonpharmacologic strategies for treating atrial fibrillation. Am J Cardiol. Jan 25 1996;77(3):45A-52A. [Medline].

  13. Oral H, Souza JJ, Michaud GF, et al. Facilitating transthoracic cardioversion of atrial fibrillation with ibutilide pretreatment. N Engl J Med. Jun 17 1999;340(24):1849-54. [Medline].

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The image on the right is a reconstructed 3-dimensional image of the left atrium in a patient undergoing atrial fibrillation ablation. The figure on the left was created with a mapping catheter using Endocardial Solutions mapping technology. It represents the endocardial shell of the left atrium and is used as the template during left atrial ablation procedures.
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.
 
 
 
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