Chapter 125. Cardioversion
Chapter 125. Cardioversion
Chapter 125. Cardioversion
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Principles and Practice of Hospital Medicine
Chapter 125. Cardioversion
J. Ryan Jordan, MD; B. Robinson Williams, MD
Key Clinical Questions
1. What are the indications for cardioversion?
2. What is the difference between cardioversion and defibrillation?
3. What is the difference between monophasic and biphasic cardioverterdefibrillators?
4. How much energy should be used during cardioversion?
5. What are the indications for anticoagulation prior to cardioversion?
Introduction
Cardioversion is a medical procedure whereby an abnormal heart rhythm (ie, cardiac arrhythmia) is converted back to a normal rhythm using
electricity or drugs. Electrical cardioversion, also referred to as directcurrent or DC cardioversion, involves the delivery of a synchronized (perfectly
timed) electrical shock through the chest wall to the heart to terminate arrhythmias and restore sinus rhythm. Electrical cardioversion is an effective,
rapid, and safe technique that has become a routine procedure in the management of patients with cardiac arrhythmias. Pharmacologic cardioversion,
also called chemical cardioversion, uses antiarrhythmic medication instead of an electrical shock to restore the heart's normal rhythm.
Investigators at Johns Hopkins Hospital were the first to develop techniques of defibrillation by an electrical shock in the 1930s. The first human
defibrillation was performed in the operating room by Claude Beck in 1947, and Paul Zoll introduced defibrillation using alternating current in 1956.
Directcurrent defibrillation was subsequently pioneered and introduced into clinical practice by Bernard Lown in 1962. Subsequent studies in the
early 1960s demonstrated that electrical cardioversion across the closed chest could abolish other cardiac arrhythmias in addition to ventricular
fibrillation (VF). Today, atrial fibrillation (AF) is the most frequent arrhythmia encountered in clinical practice and the most commonly cardioverted
arrhythmia.
Distinguish Cardioversion and Defibrillation
Electrical cardioversion and defibrillation procedures both use a device (eg, cardioverterdefibrillator) to deliver an electrical shock to the heart to treat
abnormal heart rhythms, but they differ in the timing of the shock and energy provided. Electrical cardioversion delivers energy synchronized (ie,
perfectly timed) to the QRS complex and is used to treat arrhythmias such as AF, atrial flutter (AFL), or ventricular tachycardia (VT) with a pulse.
Cardioversion can be performed electively (ie, nonemergently) in stable patients or emergently in situations to correct a rapid abnormal rhythm
associated with faintness, low blood pressure, chest pain, difficulty breathing, or loss of consciousness. Cardioversion is not performed in pulseless
patients.
Defibrillation delivers nonsynchronized (ie, occurs at random timing) energy during the cardiac cycle and is used to treat lifethreatening arrhythmias
such as pulseless VT or VF. Defibrillation is the treatment of choice for the arrhythmias most commonly associated with sudden cardiac arrest. The
electrical shock delivered during cardioversion or defibrillation can be delivered externally to the heart using electrodes (external pads or paddles)
placed on the chest (most common); directly to the heart using internal paddles during an open chest surgery; or through the electrodes of a
permanently implanted cardioverterdefibrillator (ICD).
Mechanism of Cardioversion
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Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 1 / 21
Cardioversion disrupts the abnormal electrical circuit(s) in the heart and restores a normal heartbeat. The shock causes all the heart cells to depolarize
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simultaneously, thereby interrupting and terminating the abnormal electrical rhythm without damaging the heart. This split second interruption of the
abnormal beat allows the heart's electrical system to regain control and restore a normal heartbeat. The delivery of energy during the shock is
such as pulseless VT or VF. Defibrillation is the treatment of choice for the arrhythmias most commonly associated with sudden cardiac arrest. The
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electrical shock delivered during cardioversion or defibrillation can be delivered externally to the heart using electrodes (external pads or paddles)
placed on the chest (most common); directly to the heart using internal paddles during an open chest surgery; or through the electrodes of a
permanently implanted cardioverterdefibrillator (ICD).
Mechanism of Cardioversion
Cardioversion disrupts the abnormal electrical circuit(s) in the heart and restores a normal heartbeat. The shock causes all the heart cells to depolarize
simultaneously, thereby interrupting and terminating the abnormal electrical rhythm without damaging the heart. This split second interruption of the
abnormal beat allows the heart's electrical system to regain control and restore a normal heartbeat. The delivery of energy during the shock is
synchronized to the QRS complex, which represents cardiac depolarization, in order to terminate the arrhythmia safely and allow sinus rhythm to
resume. The accidental delivery of an electrical shock to the T wave, which represents cardiac repolarization, is unsafe and may result in life
threatening ventricular arrhythmias (Figure 1251). For this reason, synchronized cardioversion is used, rather than nonsynchronized defibrillation,
for the abatement of abnormal rhythms with pulse.
Figure 1251
A complication of cardioversion: induction of ventricular fibrillation. The ventricular arrhythmia occurred because the operator failed to enable the
synchronizer, resulting in an inadvertent delivery of the shock on the vulnerable T wave instead of the intended delivery on the R wave. This
complication is preventable by enabling the synchronizer and checking that it is properly functioning before shock delivery. (From Kerber RE.
Transchest cardioversion: optimal techniques. In: Tacker WA, ed. Defibrillation of the Heart: ICDs, AEDs and Manual. St. Louis: MosbyYear Book,
1994:164. With permission.)
Practice Point
The accidental delivery of an electrical shock to the T wave may result in lifethreatening ventricular arrhythmias. For this reason, synchronized
cardioversion is used, rather than nonsynchronized defibrillation, for the abatement of abnormal rhythms with pulse.
Electrical cardioversion appears most effective in terminating arrhythmias that arise from a single reentrant circuit such as AFL, atrioventricular nodal
reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), and monomorphic VT. The highenergy shock depolarizes the
myocardium and the conduction tissue involved in the reentry circuit of the arrhythmia simultaneously. The depolarization of the myocardium is
followed by a period of refractoriness that has the effect of interrupting the reentrant circuit. This interruption breaks the repeating cycle and
terminates the arrhythmia. When the reentrant circuit is broken and the arrhythmia stops, the sinus node begins to fire again and a normal heart
rhythm is restored. This mechanism of action does not explain how electrical cardioversion terminates AF, which arises from multiple reentrant
circuits. As a result of the multiple circuits, successful cardioversion of AF often requires higher energy for termination. The exact mechanism by which
electrical cardioversion terminates AF remains unknown. Other arrhythmias, such as junctional tachycardia and multifocal atrial tachycardia, originate
from ectopic sites (ie, nonpacemaker) in the heart. Cardioversion is not effective for these types of arrhythmias.
Types of Defibrillators
Cardioverterdefibrillators deliver energy in a variety of waveforms, broadly characterized as monophasic or biphasic. Monophasic devices provide a
unidirectional pulse of energy, meaning that electrons flow in a single direction through the heart. Monophasic energy is highly effective, and
monophasic cardioverterdefibrillators remain widely used. Alternatively, biphasic devices deliver a sinusoidal biphasic waveform whereby the initial
phase of energy is positive followed by a phase of opposite polarity, which means that during the shock the polarity and electron flow reverse. Biphasic
cardioverterdefibrillators deliver a more consistent magnitude of current, which terminates arrhythmias more effectively and at lower energies
compared to monophasic devices. As a result, biphasic cardioverterdefibrillators are increasing in use and have now become the standard for trans
chest defibrillation. Clinicians must distinguish which type of cardioverterdefibrillator is available for use, as this will dictate how much energy is
required for successful cardioversion.
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Practice Point
Biphasic cardioverterdefibrillators deliver a more consistent magnitude of current, which terminates arrhythmias more effectively and at lower
monophasic cardioverterdefibrillators remain widely used. Alternatively, biphasic devices deliver a sinusoidal biphasic waveform whereby the initial
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phase of energy is positive followed by a phase of opposite polarity, which means that during the shock the polarity and electron flow reverse. Biphasic
cardioverterdefibrillators deliver a more consistent magnitude of current, which terminates arrhythmias more effectively and at lower energies
compared to monophasic devices. As a result, biphasic cardioverterdefibrillators are increasing in use and have now become the standard for trans
chest defibrillation. Clinicians must distinguish which type of cardioverterdefibrillator is available for use, as this will dictate how much energy is
required for successful cardioversion.
Practice Point
Biphasic cardioverterdefibrillators deliver a more consistent magnitude of current, which terminates arrhythmias more effectively and at lower
energies compared to monophasic devices.
Indications and Contraindications
Electrical cardioversion has become a routine procedure in the management of cardiac arrhythmias. Indications include patients in whom the rate of
the arrhythmia (eg, AF) cannot be adequately controlled medically or patients who poorly tolerate the arrhythmia (eg, palpitations, angina pectoris,
and heart failure). Multiple cardiac rhythms may bear indications for cardioversion or defibrillation (Tables 1251 and 1252). The most common
reason for the elective cardioversion of atrial arrhythmias is to enhance cardiac performance by restoring sinus rhythm, particularly in patients with
mitral stenosis, left ventricular hypertrophy (aortic stenosis, hypertrophic obstructive cardiomyopathy), and diminished myocardial reserve (heart
failure, myocardial ischemia, and infarction). Urgent cardioversion may be required for patients with atrial or ventricular arrhythmias who have
myocardial ischemia, acute heart failure (pulmonary edema), hypotension, mental status changes, or worsening angina pectoris.
Table 1251 Indications and Contraindications of Cardioversion
Indications Contraindications
AF/AFL Known atrial thrombus
1. Patient with AF/AFL > 48 hours duration and anticoagulation Sinus rhythm or tachycardia
for > 3–4 weeks (INR 2–3) Multifocal atrial tachycardia
2. Acute onset AF/AFL with associated hemodynamic instability Junctional tachycardia
including the following: Accelerated idioventricular rhythm
Angina pectoris Digitalis toxicity (digitalisinduced tachyarrhythmias)
Myocardial ischemia/infarction Severe electrolyte imbalance
Hypotension/shock Hypokalemia
Heart failure Unknown duration of AF/AFL in a stable patient not receiving therapeutic
Pulmonary edema antecedent anticoagulation in the absence of a TEE
Mitral stenosis Patient that cannot be safely sedated
Preexcitation (WPW syndrome)
Left ventricular hypertrophy
AS
HTN
HOCM
3. AF/AFL of unknown duration and absence of thrombus in left
atrium or atrial appendage by TEE
4. AF/AFL < 48hour duration
Atrioventricular nodal reentry tachycardia
Atrioventricular reentry tachycardia
Ventricular tachycardia with a pulse
AF, atrial fibrillation; AFL, atrial flutter; AS, aortic stenosis; HOCM, hypertrophic obstructive cardiomyopathy; HTN, hypertension; TEE, transesophageal echocardiogram; WPW, WolffParkinson
White.
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Table 1252 Indications and Contraindications of Defibrillation
reason for the elective cardioversion of atrial arrhythmias is to enhance cardiac performance by restoring sinus rhythm, particularly in patients with
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mitral stenosis, left ventricular hypertrophy (aortic stenosis, hypertrophic obstructive cardiomyopathy), and diminished myocardial reserve (heart
failure, myocardial ischemia, and infarction). Urgent cardioversion may be required for patients with atrial or ventricular arrhythmias who have
myocardial ischemia, acute heart failure (pulmonary edema), hypotension, mental status changes, or worsening angina pectoris.
Table 1251 Indications and Contraindications of Cardioversion
Indications Contraindications
AF/AFL Known atrial thrombus
1. Patient with AF/AFL > 48 hours duration and anticoagulation Sinus rhythm or tachycardia
for > 3–4 weeks (INR 2–3) Multifocal atrial tachycardia
2. Acute onset AF/AFL with associated hemodynamic instability Junctional tachycardia
including the following: Accelerated idioventricular rhythm
Angina pectoris Digitalis toxicity (digitalisinduced tachyarrhythmias)
Myocardial ischemia/infarction Severe electrolyte imbalance
Hypotension/shock Hypokalemia
Heart failure Unknown duration of AF/AFL in a stable patient not receiving therapeutic
Pulmonary edema antecedent anticoagulation in the absence of a TEE
Mitral stenosis Patient that cannot be safely sedated
Preexcitation (WPW syndrome)
Left ventricular hypertrophy
AS
HTN
HOCM
3. AF/AFL of unknown duration and absence of thrombus in left
atrium or atrial appendage by TEE
4. AF/AFL < 48hour duration
Atrioventricular nodal reentry tachycardia
Atrioventricular reentry tachycardia
Ventricular tachycardia with a pulse
AF, atrial fibrillation; AFL, atrial flutter; AS, aortic stenosis; HOCM, hypertrophic obstructive cardiomyopathy; HTN, hypertension; TEE, transesophageal echocardiogram; WPW, WolffParkinson
White.
Table 1252 Indications and Contraindications of Defibrillation
Indications Contraindications
Pulseless ventricular tachycardia Expressed wishes by patient or patient's surrogate not to be resuscitated
Ventricular fibrillation
Because electrical cardioversion is a lowrisk procedure if properly performed, some authorities believe that every patient deserves one chance to
achieve sinus rhythm by cardioversion, even if the short or longterm prognosis of maintaining sinus rhythm is generally unfavorable. Other experts
suggest that not all patients with newly discovered AF warrant an attempt at restoring sinus rhythm since several large, randomized trials have shown
that the maintenance of sinus rhythm confers no survival (or other outcome) advantage over rate control. Treatment must be determined based on
clinical parameters and patient preferences.
Contraindications to electrical cardioversion include rhythms that do not respond to electrical cardioversion (eg sinus rhythms, multifocal atrial
tachycardia), digitalis toxicity, severe electrolyte imbalance (eg, hypokalemia), and known or suspected atrial thrombus. In AF or AFL, suspicion of atrial
thrombus should be high if the rhythm onset is unknown or not clearly within the prior 48 hours. Transesophageal echo (TEE) evidence that the left
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atrium is free of thrombus may permit cardioversion for AF or AFL with unknown or > 48hour onset.
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Triage/Hospital Admission
that the maintenance of sinus rhythm confers no survival (or other outcome) advantage over rate control. Treatment must be determined based on
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clinical parameters and patient preferences.
Contraindications to electrical cardioversion include rhythms that do not respond to electrical cardioversion (eg sinus rhythms, multifocal atrial
tachycardia), digitalis toxicity, severe electrolyte imbalance (eg, hypokalemia), and known or suspected atrial thrombus. In AF or AFL, suspicion of atrial
thrombus should be high if the rhythm onset is unknown or not clearly within the prior 48 hours. Transesophageal echo (TEE) evidence that the left
atrium is free of thrombus may permit cardioversion for AF or AFL with unknown or > 48hour onset.
Triage/Hospital Admission
Cardioversion is routinely performed in most hospitals in a closely monitored setting such as an intensive care unit, an emergency department, or a
specially equipped procedure room. Although patients with atrial arrhythmias are often admitted to the hospital electively for cardioversion,
outpatient cardioversion is a lowrisk, effective, and economical procedure. If performed on an outpatient basis, patients are observed until most of
the effects of sedation have abated (1–2 hours) and require transport home safely after the procedure due to the residual effects of anesthesia.
Overnight hospitalization is seldom required.
Treatment
Preprocedure Checklist
Practice Point
Patients who have an abnormal airway may have increased risk for airway obstruction during sedation and may be difficult to manage if mask
ventilation or intubation becomes necessary. Patients who present with any highrisk features (see Table 1253) should be considered for
anesthesiology consultation prior to cardioversion.
Table 1253 Abnormal Physical Findings on Airway Examination
Habitus
Significant obesity (especially involving the neck and facial structures)
Head and neck
Short neck
Limited neck extension
Cervical spine trauma
Tracheal deviation
Decreased hyoid–mentum distance (<3 cm in an adult)
Mouth
Small mouth opening (<3 cm in an adult)
Edentulous
Protruding incisors
Loose or capped teeth
Higharched palate
Macroglossia
Tonsillar hypertrophy
Nonvisible uvula
Jaw
Micrognathia
Retrognathia
Trismus
Significant malocclusion
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Prior to performing electrical cardioversion, structured measures should be integrated for all patients (Figure 1252) as follows:
1. Informed consent (patient or decision maker)
ventilation or intubation becomes necessary. Patients who present with any highrisk features (see Table 1253) should be considered for
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anesthesiology consultation prior to cardioversion.
Table 1253 Abnormal Physical Findings on Airway Examination
Habitus
Significant obesity (especially involving the neck and facial structures)
Head and neck
Short neck
Limited neck extension
Cervical spine trauma
Tracheal deviation
Decreased hyoid–mentum distance (<3 cm in an adult)
Mouth
Small mouth opening (<3 cm in an adult)
Edentulous
Protruding incisors
Loose or capped teeth
Higharched palate
Macroglossia
Tonsillar hypertrophy
Nonvisible uvula
Jaw
Micrognathia
Retrognathia
Trismus
Significant malocclusion
Prior to performing electrical cardioversion, structured measures should be integrated for all patients (Figure 1252) as follows:
1. Informed consent (patient or decision maker)
2. Fasting (nothing oral) 6–8 hours prior to cardioversion (if elective)
3. History and physical examination
a. History should include current medications, allergies, previous adverse drug reactions or contraindications to sedation, diseases/disorders,
prior hospitalizations, pregnancy status, nothing oral status, and anticoagulation status (if presenting arrhythmia is AF/AFL).
b. Use history to estimate duration of AF/AFL duration and determine need for anticoagulation and/or TEE evaluation.
c. Physical examination should include vital signs, oxygen saturation, pulmonary and cardiovascular examination, and oral cavity and airway
examination. Patients who have an abnormal airway exam should be considered to be at increased risk for airway obstruction during
sedation and may potentially have a difficult airway to manage if mask ventilation or intubation becomes necessary. Patients who present
with any highrisk features (Table 1253) should be considered for anesthesiology consultation prior to the initiation of the procedure.
4. A 12lead electrocardiogram (ECG) is used to confirm rhythm.
5. If any electrolyte abnormality (hypokalemia, hyperkalemia) or drug toxicity (digitalis) is suspected, appropriate blood levels should be checked.
6. Peripheral venous access (for preprocedure sedation and postprocedure medications or fluids if needed) is obtained.
7. Skin preparation includes shaving of the chest hair, if present (with electric clippers rather than a blade) to ensure good contact of the skin and
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electrode pads. Highquality continuous ECG from the cardioverterdefibrillator will confirm proper contact of electrode pads to the skin.
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8. Emergency resuscitation equipment available (Figure 1252).
Figure 1252
4. A 12lead electrocardiogram (ECG) is used to confirm rhythm.
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5. If any electrolyte abnormality (hypokalemia, hyperkalemia) or drug toxicity (digitalis) is suspected, appropriate blood levels should be checked.
6. Peripheral venous access (for preprocedure sedation and postprocedure medications or fluids if needed) is obtained.
7. Skin preparation includes shaving of the chest hair, if present (with electric clippers rather than a blade) to ensure good contact of the skin and
electrode pads. Highquality continuous ECG from the cardioverterdefibrillator will confirm proper contact of electrode pads to the skin.
8. Emergency resuscitation equipment available (Figure 1252).
Figure 1252
Algorithm for external electrical cardioversion (preprocedure preparation and procedure).
Anticoagulation
Practice Point
The 2008 ACCP guidelines recommend that patients undergoing urgent cardioversion be heparinized as soon as possible to prevent thrombi from
forming due to atrial appendage dysfunction after cardioversion.
Cardioversion may be associated with pulmonary or systemic embolization. This complication is more likely to occur in patients with AF/AFL > 48 hours
(ie, highrisk group) who have not been anticoagulated prior to cardioversion. In casecontrol series, the estimated risk of thromboembolism is
between 1% and 5% in (nonanticoagulated patients) with AF/AFL > 48 hours undergoing cardioversion.
In patients with AF/AFL >48 hours, oral anticoagulation with warfarin (International Normalized Ratio (INR) 2.0 to 3.0) for 3–4 weeks prior to
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cardioversion reduces the thromboembolic risk to 0.5–0.8%. Anticoagulation before cardioversion allows time for adherence of any preexisting atrial
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thrombus and for prevention of new thrombus formation. Alternatively, anticoagulation with intravenous unfractionated heparin can be initiated and
a TEE performed to evaluate the left atrium and left atrial appendage for evidence of thrombus. If there is no evidence of thrombus, cardioversion can
safely be performed (thromboembolic risk 0.8%). The 2008 American College of Chest Physicians (ACCP) guidelines recommend that patients
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Cardioversion may be associated with pulmonary or systemic embolization. This complication is more likely to occur in patients with AF/AFL > 48 hours
(ie, highrisk group) who have not been anticoagulated prior to cardioversion. In casecontrol series, the estimated risk of thromboembolism is
between 1% and 5% in (nonanticoagulated patients) with AF/AFL > 48 hours undergoing cardioversion.
In patients with AF/AFL >48 hours, oral anticoagulation with warfarin (International Normalized Ratio (INR) 2.0 to 3.0) for 3–4 weeks prior to
cardioversion reduces the thromboembolic risk to 0.5–0.8%. Anticoagulation before cardioversion allows time for adherence of any preexisting atrial
thrombus and for prevention of new thrombus formation. Alternatively, anticoagulation with intravenous unfractionated heparin can be initiated and
a TEE performed to evaluate the left atrium and left atrial appendage for evidence of thrombus. If there is no evidence of thrombus, cardioversion can
safely be performed (thromboembolic risk 0.8%). The 2008 American College of Chest Physicians (ACCP) guidelines recommend that patients
undergoing urgent cardioversion be heparinized as soon as possible to prevent thrombi from forming due to atrial appendage dysfunction after
cardioversion. Cardioversion in patients who present with acute AF/AFL < 48 hours (ie, lowrisk group) is associated with a low clinical rate of
thrombembolism (0.8%).
Practice Point
Cardioversion in patients who present with acute atrial fibrillation or atrial flutter (AF/AFL) < 48 hours (ie, lowrisk group) is associated with a low
clinical rate of thrombembolism (0.8%). In cardioversion of AF/AFL > 48hour duration (not anticoagulated), the estimated risk for thromboembolism
from a left atrial thrombus is 1–5%. In patients with AF/AFL > 48 hours, oral anticoagulation with warfarin (INR 2.0–3.0) for 3–4 weeks prior to
cardioversion reduces the thromboembolic risk to 0.5–0.8%. Alternatively, if there is no evidence of thrombus on transesophageal echocardiogram
(TEE), anticoagulation may be started, and cardioversion can be safely performed (thromboembolic risk 0.8%).
Late thromboembolic events after cardioversion are probably due to both the development of thrombus as a consequence of atrial stunning and the
delayed recovery of atrial contraction after cardioversion. Pooled data from 32 studies of cardioversioon of AF/AFL suggest that 98% of clinical
thromboembolic events occur within 10 days of cardioversion. Anticoagulation after the procedure prevents thrombus formation from occurring
before normal atrial mechanical activity has resumed, a process that may be delayed for several weeks due to atrial stunning. The American College of
Chest Physicians (ACCP) and American College of Cardiology/American Heart Association, and the European Society of Cardiology (ACC/AHA/ESC)
guidelines therefore recommend continuation of warfarin therapy for at least 4 weeks after cardioversion. This recommendation only addresses
protection from embolic events related to the cardioversion period. Patients with AF at high risk from thromboembolic events based on CHADS2 score
(an acronym for Congestive heart failure, Hypertension, Age > 75, Diabetes mellitus and prior Stroke or transient ischemic attack) may require long
term anticoagulation (see Chapter 126).
Care standards require administration of anticoagulant medications when preparing patients with AF/AFL of > 48 hours for cardioversion. The
ACC/AHA/ESC guidelines for the management of anticoagulation in patients with AF/AFL undergoing cardioversion recommend anticoagulation for at
least 3 weeks prior and 4 weeks following cardioversion if the abnormal rhythm has been present for > 48 hours, with exceptions based on TEE
evaluation (Table 1254).
Table 1254 ACC/AHA/ESC Guideline Summary: Prevention of Thromboembolism in Patients with Atrial Fibrillation Undergoing
Cardioversion
Class I—There is evidence and/or general agreement that the following approaches are effective for the prevention of
thromboembolism in patients with AF undergoing cardioversion
1. AF > 48 h duration, or when the duration of AF is unknown, anticoagulation (INR 2.0–3.0) recommended for at least 3 weeks prior to and 4 weeks after
cardioversion, regardless of the method (electrical or pharmacologic). (Level of evidence: B)
2. AF > 48 h duration requiring immediate cardioversion because of hemodynamic instability; heparin should be administered concurrently (unless
contraindicated) by an initial intravenous bolus injection followed by a continuous infusion in a dose adjusted to prolong the activated partial
thromboplastin time to 1.5 to 2 times the reference control value. Thereafter, oral anticoagulation (INR 2.0–3.0) for at least 4 weeks, as for patients
undergoing elective cardioversion. Limited data support subcutaneous administration of lowmolecularweight heparin in this indication. (Level of
evidence: C)
3. AF < 48 h duration associated with hemodynamic instability (angina pectoris, MI, shock, or pulmonary edema), cardioversion should be performed
immediately without delay for prior initiation of anticoagulation. (Level of evidence: C)
Class IIa—The weight of evidence or opinion is in favor of the usefulness of the following approaches for the prevention of
thrombembolism in patients with AF undergoing cardioversion
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1. During the first 48 hours after onset of AF, the need for anticoagulation before and after cardioversion may be based on the patient's risk of
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thromboembolism. (Level of evidence: C)
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2. As an alternative to anticoagulation prior to cardioversion of AF, it is reasonable to perform TEE in search of thrombus in the LA or LAA. (Level of
evidence: B)
Care standards require administration of anticoagulant medications when preparing patients with AF/AFL of > 48 hours for cardioversion. The
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ACC/AHA/ESC guidelines for the management of anticoagulation in patients with AF/AFL undergoing cardioversion recommend anticoagulation for at
least 3 weeks prior and 4 weeks following cardioversion if the abnormal rhythm has been present for > 48 hours, with exceptions based on TEE
evaluation (Table 1254).
Table 1254 ACC/AHA/ESC Guideline Summary: Prevention of Thromboembolism in Patients with Atrial Fibrillation Undergoing
Cardioversion
Class I—There is evidence and/or general agreement that the following approaches are effective for the prevention of
thromboembolism in patients with AF undergoing cardioversion
1. AF > 48 h duration, or when the duration of AF is unknown, anticoagulation (INR 2.0–3.0) recommended for at least 3 weeks prior to and 4 weeks after
cardioversion, regardless of the method (electrical or pharmacologic). (Level of evidence: B)
2. AF > 48 h duration requiring immediate cardioversion because of hemodynamic instability; heparin should be administered concurrently (unless
contraindicated) by an initial intravenous bolus injection followed by a continuous infusion in a dose adjusted to prolong the activated partial
thromboplastin time to 1.5 to 2 times the reference control value. Thereafter, oral anticoagulation (INR 2.0–3.0) for at least 4 weeks, as for patients
undergoing elective cardioversion. Limited data support subcutaneous administration of lowmolecularweight heparin in this indication. (Level of
evidence: C)
3. AF < 48 h duration associated with hemodynamic instability (angina pectoris, MI, shock, or pulmonary edema), cardioversion should be performed
immediately without delay for prior initiation of anticoagulation. (Level of evidence: C)
Class IIa—The weight of evidence or opinion is in favor of the usefulness of the following approaches for the prevention of
thrombembolism in patients with AF undergoing cardioversion
1. During the first 48 hours after onset of AF, the need for anticoagulation before and after cardioversion may be based on the patient's risk of
thromboembolism. (Level of evidence: C)
2. As an alternative to anticoagulation prior to cardioversion of AF, it is reasonable to perform TEE in search of thrombus in the LA or LAA. (Level of
evidence: B)
a. For patients with no identifiable thrombus, cardioversion is reasonable immediately after anticoagulation with unfractionated heparin (eg,
initiate by intravenous bolus injection and an infusion continued at a dose adjusted to prolong the activated partial thromboplastin time to 1.5
to 2 times the control value until oral anticoagulation has been established with a vitamin K antagonist (eg, warfarin), as evidenced by an INR
equal to or greater than 2.0.). (Level of evidence: B)
i. Thereafter, oral anticoagulation (INR 2.0–3.0) is reasonable for a total anticoagulation period of at least 4 weeks, as for patients undergoing
elective cardioversion. (Level of evidence: B).
ii. Limited data are available to support the subcutaneous administration of a lowmolecularweight heparin in this indication. (Level of
evidence: C)
b. For patients in whom thrombus is identified by TEE, oral anticoagulation (INR 2.0–3.0) is reasonable for at least 3 weeks prior to and 4 weeks
after restoration of sinus rhythm, and a longer period of anticoagulation may be appropriate even after apparently successful cardioversion
because the risk of thromboembolism often remains elevated in such cases. (Level of evidence: C)
3. For patients with atrial flutter undergoing cardioversion, anticoagulation can be beneficial according to the recommendations as for patients with AF.
(Level of evidence: C)
AF, atrial fibrillation; INR, international normalized ratio; LA, left atrium; LAA, left atrial appendage; MI, myocardial infarction; TEE, transesophageal echocardiogram.
Procedure Technique
Following preprocedure preparation, a standardized procedure algorithm for performing electrical cardioversion should be followed (see Figure 125
2), including ECG lead and electrode pad placement, sedation, energy selection, synchronization, shock delivery, postshock patient and ECG
assessment, and postprocedure monitoring.
ECG Lead Placement
Cardioverterdefibrillators provide the option of continuously monitoring the patient's ECG using either external electrode pads or ECG leads. As a
result, the ECG leads (typically three leads) are not required for cardioversion, but it is recommended that the leads be attached to the patient in
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nonemergent situations. Attaching the ECG leads provides additional information about the patient's heart rhythm and allows the operator to switch
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the lead used for monitoring and synchronization by the cardioverterdefibrillator. Using a standard threelead (colorcoded) ECG cable, the white lead
is placed on the right side of the chest just below the right clavicle, the black lead is placed on the left chest just below the left clavicle, and the red lead
is placed in the left midaxillary line near the apex of the heart.
assessment, and postprocedure monitoring.
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ECG Lead Placement
Cardioverterdefibrillators provide the option of continuously monitoring the patient's ECG using either external electrode pads or ECG leads. As a
result, the ECG leads (typically three leads) are not required for cardioversion, but it is recommended that the leads be attached to the patient in
nonemergent situations. Attaching the ECG leads provides additional information about the patient's heart rhythm and allows the operator to switch
the lead used for monitoring and synchronization by the cardioverterdefibrillator. Using a standard threelead (colorcoded) ECG cable, the white lead
is placed on the right side of the chest just below the right clavicle, the black lead is placed on the left chest just below the left clavicle, and the red lead
is placed in the left midaxillary line near the apex of the heart.
Electrode Positioning
Two electrodes (selfadhesive pads or handheld paddles) are placed on the thorax for external cardioversion and determine the transthoracic
current pathway. Electrode positioning on the chest is important to maximize current flow through the heart. The most commonly used electrodes for
external cardioversion are selfadhesive (ie, handsfree), pregelled, lowimpedance, disposablepad electrodes. A variety of anatomic pad placements
can be used. Common electrode positions for transthoracic cardioversion/defibrillation include apexanterior, apexposterior, and anteriorposterior
positions (Figure 1253). Though all positions are effective, several studies have suggested that less energy is required, and the success rate is higher
with the anteriorposterior electrode position in patients cardioverted for AF. More of the atrial mass is placed in the shock vector with anterior
posterior pads compared with apicalanterior pads. Some patients who do not respond to one method occasionally respond to another method.
Therefore, if initial shocks are unsuccessful in terminating the arrhythmia, the pads should be repositioned and cardioversion repeated. Electrode pad
size is an important determinant of transthoracic current flow during cardioversion, and the optimal electrode size for humans is approximately 8–12
cm in diameter.
Figure 1253
Electrode positions commonly used for transthoracic defibrillation and cardioversion. (From Kerber RE. Transchest cardioversion: optimal techniques.
In: Tacker WA, ed. Defibrillation of the Heart: ICDs, AEDs and Manual. St. Louis: MosbyYear Book; 1994:163. With permission.)
While selfadhesive pads are convenient and safe, handheld paddles with manual pressure may be more effective than selfadhesive pads. This was
illustrated in a randomized trial of patients referred for cardioversion for persistent AF, in which success rates were slightly higher for patients
assigned to paddle electrodes (96% vs 88%). Improved electrodetoskin contact and reduced transthoracic impedance with handheld electrodes may
explain the benefit. Handheld paddles require the use of conducting gel to ensure good contact between the paddles and skin.
Practice Point
Anteriorposterior electrode position requires less energy and shows higher cardioversion success rate for AF.
Sedation
External cardioversion under conscious sedation or general anesthesia reduces pain and anxiety related to the procedure, since electrical
cardioversion is an uncomfortable procedure. Prior to the initiation of sedation, the staff must determine and document the availability of a
responsible adult to accompany the patient home at discharge postprocedure. Patent intravenous access must be secured in all patients. All
equipment necessary for emergency resuscitation including oxygen, oxygen equipment/supplies, resuscitation bag and mask, monitoring equipment
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(ECG, pulse oximeter, blood pressure), functioning suction apparatus/catheters, and agents to reverse the effects of drugs administered to produce
Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 10 / 21
the moderate sedation (eg naloxone, flumazenil) must be readily available. Crash cart/defibrillator and emergency airway equipment should be
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immediately accessible. Additionally, a physician skilled in airway management (eg, anesthesiologist) should be present or immediately available.
Shortacting intravenous sedatives and shortacting analgesic agents that produce conscious sedation enable rapid recovery after the procedure
Sedation Access Provided by:
External cardioversion under conscious sedation or general anesthesia reduces pain and anxiety related to the procedure, since electrical
cardioversion is an uncomfortable procedure. Prior to the initiation of sedation, the staff must determine and document the availability of a
responsible adult to accompany the patient home at discharge postprocedure. Patent intravenous access must be secured in all patients. All
equipment necessary for emergency resuscitation including oxygen, oxygen equipment/supplies, resuscitation bag and mask, monitoring equipment
(ECG, pulse oximeter, blood pressure), functioning suction apparatus/catheters, and agents to reverse the effects of drugs administered to produce
the moderate sedation (eg naloxone, flumazenil) must be readily available. Crash cart/defibrillator and emergency airway equipment should be
immediately accessible. Additionally, a physician skilled in airway management (eg, anesthesiologist) should be present or immediately available.
Shortacting intravenous sedatives and shortacting analgesic agents that produce conscious sedation enable rapid recovery after the procedure
(Table 1255). As a result, overnight hospitalization is seldom required. A typical medication combination for conscious sedation would include
intravenous midazolam plus fentanyl.
Table 1255 Dosage and Dose Adjustments of Commonly Used Sedative/Analgesic Drugs
Onset,
Peak
Class and
Dosing Guidelines (IV Effect, Adverse Drug
Drug Mechanism of Reversal
Administration) and Reactions
Action
Duration
of Action
CHF, congestive heart failure; CNS, central nervous system; COPD, chronic obstructive pulmonary disease; GABA, gammaaminobutyric acid.
Conscious sedation is assessed by lack of response to tactile and verbal stimuli. The patient's ability to communicate should be preserved. Heart rate
and rhythm, blood pressure, oxygen saturation, respiratory rate, and response to verbal stimuli (level of consciousness) should be continuously
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monitored until the patient regains consciousness and makes a full recovery. The patient usually awakens 5–10 minutes after the cardioversion. The
Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 11 / 21
patient should be monitored until full consciousness is restored and at least 1 hour (preferably several hours) after the last dosing of a sedative or an
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analgesic.
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CHF, congestive heart failure; CNS, central nervous system; COPD, chronic obstructive pulmonary disease; GABA, gammaaminobutyric acid.
Conscious sedation is assessed by lack of response to tactile and verbal stimuli. The patient's ability to communicate should be preserved. Heart rate
and rhythm, blood pressure, oxygen saturation, respiratory rate, and response to verbal stimuli (level of consciousness) should be continuously
monitored until the patient regains consciousness and makes a full recovery. The patient usually awakens 5–10 minutes after the cardioversion. The
patient should be monitored until full consciousness is restored and at least 1 hour (preferably several hours) after the last dosing of a sedative or an
analgesic.
Energy Selection and Transthoracic Impedance
Practice Point
Obesity and severe obstructive lung disease increase thoracic impedance, which reduces the efficacy of cardioversion.
Successful cardioversion depends on the adequate delivery of energy to the heart, determined by the amount of energy provided by the cardioverter
defibrillator and the patient's transthoracic impedance. The amount of energy provided by the cardioverterdefibrillator is adjustable and selected at
the time of cardioversion. The amount of energy selected for initial attempts of cardioversiondefibrillation has been controversial. More organized
arrhythmias, such as AFL and VT, terminate with lower energy compared to AF and VF. In urgent settings, such as hemodynamic collapse associated
with VT or VF, highenergy defibrillation (ie, 200 J max with a biphasic defibrillator; 360 J max with a monophasic defibrillator) may be used, but lower
energy may be considered in this situation, with monophasic defibrillators based on manufacturer recommendation (starting dose of 120 J is
acceptable). There is no benefit to using greater than 360 joules. For cardioversion, lower energies effectively convert to sinus rhythm in most
hemodynamically stable patients. In cardioversion, the minimum effective energy dose for shocks should be administered initially, and energy dose
can be titrated up for additional shocks when the clinical situation permits (Table 1256).
Table 1256 Energy Selection for Cardioversion of Commonly Encountered Arrhythmias
AF, atrial fibrillation; AFL, atrial flutter; AT, atrial tachycardia; AVNRT, atrioventricular nodal reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia; VT, ventricular tachycardia.
Practice Point
Measures to reduce impedance and improve success during cardioversion include applying pressure to the pads, shocking during endexpiration,
improving skinelectrode interface, and using conducting gels.
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High transthoracic impedance, defined as the resistance of the chest to the flow of electrical current, degrades current flow through the heart. During
transthoracic cardioversion, a considerably larger current must be delivered to compensate for transthoracic impedance. In animal studies, 82% of the
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AF, atrial fibrillation; AFL, atrial flutter; AT, atrial tachycardia; AVNRT, atrioventricular nodal reciprocating tachycardia; AVRT, atrioventricular reciprocating tachycardia; VT, ventricular tachycardia.
Practice Point
Measures to reduce impedance and improve success during cardioversion include applying pressure to the pads, shocking during endexpiration,
improving skinelectrode interface, and using conducting gels.
High transthoracic impedance, defined as the resistance of the chest to the flow of electrical current, degrades current flow through the heart. During
transthoracic cardioversion, a considerably larger current must be delivered to compensate for transthoracic impedance. In animal studies, 82% of the
transthoracic current was shunted to the thoracic cage, 14% to the lungs, and only 4% passed through to the heart during cardioversion. Obesity and
severe obstructive lung disease increase impedance, which reduces the efficacy of cardioversion. Measures to reduce impedance should be
undertaken, which include applying pressure to the pads, shocking during endexpiration, improving skin–electrode interface, and the use of
conducting gels. The repeat administration of shocks also lowers impedance and improves efficacy of cardioversion. Conversely, increasing the
distance between electrodes or increasing the amount of tissue or lung parenchyma between the electrodes increases impedance.
Practice Point
In cardioversion, the minimum effective energy dose for shocks should be administered initially, and energy dose can be titrated up for additional
shocks when the clinical situation permits.
Synchronization
Once the ECG leads and electrode pads are attached to the patient and the cardioverterdefibrillator is powered on, a good quality rhythm strip should
be obtained to confirm the rhythm. The synchronize mode should be switched on, and confirmation of synchronization with the QRS complex should
be confirmed on the monitor and on a telemetry printout. If the QRS is low amplitude or synchronization occurs with the T wave, the lead used for
monitoring and synchronization on the cardioverterdefibrillator should be switched until a satisfactory QRS is seen and appropriate synchronization
with each QRS complex is confirmed. Synchronization is essential to avoid delivery of a shock during the vulnerable repolarization period, which can
result in VF (see Figure 1251). If defibrillation is intended, the mode must be switched to asynchronous as the lack of an identifiable QRS complex will
prevent the cardioverterdefibrillator from discharging in the synchronous mode.
Shock Delivery
A continuous rhythm strip should be obtained during the electroshock. Once the electrode pads are positioned and the appropriate energy and mode
(synchronized or nonsynchronized) are selected, the adequacy of patient sedation should be confirmed. Next, the cardioverterdefibrillator capacitors
are charged, the staff is warned to stay clear of the patient, and the shock is delivered to the patient. The patient is subsequently examined for
adequacy of airway, breathing, and circulation, and the rhythm is confirmed by ECG. If the first attempt is unsuccessful, the procedure can be repeated
as necessary with higherenergy shocks and/or changing the electrode pad position. This can be repeated until the arrhythmia terminates or a
decision is made to abandon electrical cardioversion.
Efficacy of Cardioversion
The overall immediate success rate of electrical cardioversion with AF is 75–94% and is inversely proportional to the duration of AF and size of the left
atrium (Table 1256). Although sinus rhythm can be restored in a substantial proportion of patients, the rate of relapse is high without concomitant
antiarrhythmic drug therapy. After electrical cardioversion only 20–40% of patients maintain sinus rhythm for the first year compared to 29–53% in
patients treated with antiarrhythmic drugs before electrical cardioversion and throughout followup. Most recurrences of AF occur within the first
month after electrical cardioversion. Pretreatment with antiarrhythmic drugs (eg, amiodarone, flecanide, ibutilide, propafenone, or sotalol),
recommended by the ACC/AHA/ESC, can enhance the success of electrical cardioversion and prevent recurrent AF. Pretreatment with pharmacological
agents may have the greatest efficacy in patients who fail to respond to cardioversion and in those who develop acute or subacute recurrence of AF. In
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addition, prophylactic antiarrhythmic drug therapy may obviate the need for electrical cardioversion or reduce the energy required for the procedure
Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 13 / 21
by lowering the cardioversion threshold. In randomized trials of electrical cardioversion, patients pretreated with intravenous ibutilide were more
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often converted to sinus rhythm compared to untreated controls, and patients in whom cardioversion initially failed could more often be converted
when the procedure was repeated after treatment with ibutilide.
atrium (Table 1256). Although sinus rhythm can be restored in a substantial proportion of patients, the rate of relapse is high without concomitant
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antiarrhythmic drug therapy. After electrical cardioversion only 20–40% of patients maintain sinus rhythm for the first year compared to 29–53% in
patients treated with antiarrhythmic drugs before electrical cardioversion and throughout followup. Most recurrences of AF occur within the first
month after electrical cardioversion. Pretreatment with antiarrhythmic drugs (eg, amiodarone, flecanide, ibutilide, propafenone, or sotalol),
recommended by the ACC/AHA/ESC, can enhance the success of electrical cardioversion and prevent recurrent AF. Pretreatment with pharmacological
agents may have the greatest efficacy in patients who fail to respond to cardioversion and in those who develop acute or subacute recurrence of AF. In
addition, prophylactic antiarrhythmic drug therapy may obviate the need for electrical cardioversion or reduce the energy required for the procedure
by lowering the cardioversion threshold. In randomized trials of electrical cardioversion, patients pretreated with intravenous ibutilide were more
often converted to sinus rhythm compared to untreated controls, and patients in whom cardioversion initially failed could more often be converted
when the procedure was repeated after treatment with ibutilide.
Pharmacologic Cardioversion
The development of new drugs has increased the popularity of pharmacologic cardioversion. Although pharmacologic and electrical cardioversion
have not been directly compared, pharmacologic approaches appear simpler but are less effective. Unlike electrical cardioversion, pharmacologic
cardioversion does not require conscious sedation or anesthesia. The major risk is related to the toxicity of antiarrhythmic drugs such as druginduced
torsades de pointes. Medications indicated for the pharmacologic cardioversion of AF less than or equal to 7 days’ duration include flecanide,
dofetilide, propafenone, ibutilide, or amiodarone. Pharmacologic cardioversion of AF present for more than 7 days includes dofetilide, amiodarone,
or ibutilide.
Ibutilide is a class III antiarrhythmic drug (potassiumchannel blocker) that prolongs the time for repolarization in atrial and ventricular myocardium. It
is only available for intravenous use and is approved for the acute termination of AF/AFL of recent onset, but more effective for conversion of AFL. The
2006 practice guidelines from ACC/AHA/ESC recommend intravenous ibutilide for the pharmacologic cardioversion of AF/AFL ≤ 7 days’ duration (class
I recommendation) and for cardioversion of AF/AFL of more than 7 days duration (class IIA recommendation). In most patients who respond to
ibutilide, arrhythmia termination is seen within 40 to 60 minutes after initiating the infusion. Ibutilide has a conversion rate of up to 75% to 80% in
recentonset atrial fibrillation and flutter; the conversion rate is higher for atrial flutter than for atrial fibrillation. Ibutilide has a 4% risk of torsades de
pointes and should be avoided in patients with heart failure or prolonged QT interval.
Serum potassium and magnesium should be measured and electrolyte disturbances, especially hypokalemia or hypomagnesemia, corrected prior to
use and throughout therapy with ibutilide. Ibutilide should be administered with continuous ECG monitoring at a dose of 0.01 mg/kg infused over 10
minutes for patients weighing less than 60 kg and at a dose of 1 mg over 10 minutes for patients weighing more than 60 kg. If the arrhythmia does not
terminate 10 minutes after the end of the infusion, a second bolus (same dose over 10 minutes) can be given. The infusion should be stopped when the
presenting arrhythmia is terminated or the patient develops sustained or nonsustained VT or marked prolongation of the QT interval. Because of the
risk of QT prolongation and arrhythmias, patients treated with ibutilide should be observed with continuous ECG monitoring for at least 4 hours after
the infusion or until the QTC interval has returned to baseline. There is no evidence that the risk of thromboembolism with pharmacologic
cardioversion differs from electrical cardioversion. Recommendations for anticoagulation are therefore the same for both methods.
Practice Point
Ibutilide has a 4% risk of torsades de pointes and should be avoided in patients with depressed heart failure or prolonged QT interval.
Complications
Complications after electrical cardioversion are uncommon but can be serious and are mainly related to thromboembolism and arrhythmias (Table
1257).
Table 1257 Complications (and Incidence When Known) of Electrical Cardioversion
Electrocardiographic changes
ST segment depression (35%)
ST segment elevation (15–19%)
T wave changes
Arrhythmia and conduction abnormalities
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Premature atrial contractions
Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 14 / 21
Premature ventricular contractions
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SVT (primarily sinus tachycardia) (30%)
Bradycardia (25%)
Complications Access Provided by:
Complications after electrical cardioversion are uncommon but can be serious and are mainly related to thromboembolism and arrhythmias (Table
1257).
Table 1257 Complications (and Incidence When Known) of Electrical Cardioversion
Electrocardiographic changes
ST segment depression (35%)
ST segment elevation (15–19%)
T wave changes
Arrhythmia and conduction abnormalities
Premature atrial contractions
Premature ventricular contractions
SVT (primarily sinus tachycardia) (30%)
Bradycardia (25%)
Left bundle branch block
Sinus arrest
Highdegree atrioventricular heart block (15%)
NSVT (5%)
VT
VF (usually the result of an asynchronous shock)
Embolization (pulmonary and systemic)
1–5% nonanticoagulated patients
0.5–0.8% anticoagulated patients
Myocardial necrosis
Myocardial dysfunction
Atrial stunning
Left ventricular dysfunction
Transient hypotension
Pulmonary edema rare
Airway compromise
Painful skin burns (20–25%)
Physical trauma rare
NSVT, nonsustained ventricular tachycardia; SVT, supraventricular tachycardia; VF, ventricular fibrillation; VT, ventricular tachycardia.
Thromboembolism
Practice Point
Risk of thromboembolism with pharmacological cardioversion is similar to that with electrical cardioversion. Recommendations for anticoagulation
are the same for both methods.
Thrombi can form within the atria (especially the left atrial appendage) due to stagnant blood flow that exists with AF/AFL. As a result, pulmonary and
systemic embolization can occur after cardioversion (spontaneous, pharmacologic, or electrical) if an embolus becomes dislodged from the atria as
the heart begins to contract normally. Such emboli in the systemic circulation could lead to stroke, myocardial infarction, bowel ischemia or infarction,
or limb ischemia. Emboli occur less frequently in patients who have had AF/AFL < 48 hours (thromboembolic risk 0.8%). If patients with AF/AFL are
appropriately anticoagulated for 3–4 weeks before cardioversion, the incidence of thromboembolism is 0.5–0.8%. The incidence is approximately 0.8%
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Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 15 / 21
in TEEguided cardioversion. The incidence of embolism in AF/AFL without precardioversion anticoagulation ranges from 1 to 5%. Patients with a
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previous embolism do not have an increased risk of embolization if anticoagulation is adequate. The risk of thromboembolism is highest in patients
with rheumatic (or other) mitral stenosis, large left atrium, chronic AF, diabetes, hypertension, and prior cardiac embolic stroke.
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Thrombi can form within the atria (especially the left atrial appendage) due to stagnant blood flow that exists with AF/AFL. As a result, pulmonary and
systemic embolization can occur after cardioversion (spontaneous, pharmacologic, or electrical) if an embolus becomes dislodged from the atria as
the heart begins to contract normally. Such emboli in the systemic circulation could lead to stroke, myocardial infarction, bowel ischemia or infarction,
or limb ischemia. Emboli occur less frequently in patients who have had AF/AFL < 48 hours (thromboembolic risk 0.8%). If patients with AF/AFL are
appropriately anticoagulated for 3–4 weeks before cardioversion, the incidence of thromboembolism is 0.5–0.8%. The incidence is approximately 0.8%
in TEEguided cardioversion. The incidence of embolism in AF/AFL without precardioversion anticoagulation ranges from 1 to 5%. Patients with a
previous embolism do not have an increased risk of embolization if anticoagulation is adequate. The risk of thromboembolism is highest in patients
with rheumatic (or other) mitral stenosis, large left atrium, chronic AF, diabetes, hypertension, and prior cardiac embolic stroke.
Arrhythmias
Practice Point
Premature atrial or ventricular beats occur commonly after cardioversion, and atrial arrhythmias—primarily sinus tachycardia—occur in up to 30% of
patients. Bradycardia occurs in up to 25% of patients immediately after cardioversion. Nonsustained VT is seen in up to 5%, even without structural
heart disease. Ventricular arrhythmias occur rarely, are not related to the number of shocks, and cannot be prevented by antiarrhythmic therapy.
Arrhythmias are occasionally observed after cardioversion. Premature atrial or ventricular beats are not uncommon after cardioversion, and atrial
arrhythmias, primarily sinus tachycardia, are seen in up to 30% of patients. Alternatively, bradycardia is seen in up to 25% of patients immediately after
cardioversion since cardioversion increases vagal tone. In one study of 75 patients undergoing cardioversion, sinus bradycardia occurred in 18
patients (24%), highdegree atrioventricular block occurred in 11 (15%), and temporary pacing was required in 10 (13%). Nonsustained VT is seen in up
to 5% of patients and can occur in patients without structural heart disease. Patients receiving antiarrhythmic drugs are more prone to develop
bradycardia and asystole postcardioversion. Temporary transthoracic pacing should be readily available at the time of cardioversion. Lifethreatening
arrhythmias are infrequent and may occur if the device is not properly synchronized. The occurrence of ventricular arrhythmias does not appear to be
related to the number of shocks and cannot be prevented by antiarrhythmic therapy. Electrolyte imbalances, such as hypokalemia, and digitalis toxicity
increase the risk of ventricular tachyarrhythmias.
Airway Compromise
Oversedation occurs most frequently in the elderly and in patients with renal and hepatic impairment and can cause respiratory depression. Dose
adjustment should be considered in those populations. The patient's airway and oxygenation should be monitored carefully until complete recovery.
Reversal agents for opiates and benzodiazepines (naloxone and flumazenil, respectively) should be readily available during the procedure. If the
patient has identifiable highrisk airway features (described earlier) consultation with an anesthesiologist may be valuable.
Chest Wall Injury and Skin Burns
Practice Point
In order to reduce the frequency and severity of burns, proper skin–electrode interface should be confirmed, liberal conductive gel should be utilized,
and the lowest effective amount of energy should be used.
Firstdegree skin burns of the chest wall, which can be painful, have been described with electrical cardioversion. These burns can be moderate to
severe in up to 20–25% of patients undergoing cardioversion. In order to reduce the frequency and severity of burns, good skin–electrode interface
should be confirmed, liberal conductive gel utilized (when using handheld paddles), and the lowest effective amount of energy should be used. Skin
burns are more likely with improper technique and placement of electrodes. Though not performed routinely, the pretreatment of the skin with topical
ibuprofen or steroid cream can reduce the pain and inflammation. The incidence of skin burns has been substantially reduced with the use of pre
gelled pads and biphasic defibrillators.
Electrocardiographic Changes and Myocardial Injury
Electrocardiographic changes, including ST segment and T wave changes, can occur immediately after cardioversion. The frequency and extent of ST
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segment changes are lower with biphasic defibrillators. The QRS and QT intervals are not altered. Electrocardiogram findings are nonspecific, typically
Chapter 125. Cardioversion, J. Ryan Jordan, MD; B. Robinson Williams, MD Page 16 / 21
resolve within 5 minutes, and should not be used as the sole criteria for identifying an acute ischemic event. The pathogenesis of ST elevation is
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uncertain since elevations in creatine kinase MB isoenzyme or troponin are uncommon and are usually minimal when they occur. Some myocardial
tissue damage or stunning may occur as a result of highenergy shocks or repeated shocks. Significant damage is uncommon, and there are generally
ibuprofen or steroid cream can reduce the pain and inflammation. The incidence of skin burns has been substantially reduced with the use of pre
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gelled pads and biphasic defibrillators.
Electrocardiographic Changes and Myocardial Injury
Electrocardiographic changes, including ST segment and T wave changes, can occur immediately after cardioversion. The frequency and extent of ST
segment changes are lower with biphasic defibrillators. The QRS and QT intervals are not altered. Electrocardiogram findings are nonspecific, typically
resolve within 5 minutes, and should not be used as the sole criteria for identifying an acute ischemic event. The pathogenesis of ST elevation is
uncertain since elevations in creatine kinase MB isoenzyme or troponin are uncommon and are usually minimal when they occur. Some myocardial
tissue damage or stunning may occur as a result of highenergy shocks or repeated shocks. Significant damage is uncommon, and there are generally
no short or longterm complications. Any decline in cardiac function after cardioversion is typically temporary and does not produce symptoms.
Practice Point
ECG ST or Twave changes following cardioversion are nonspecific, typically resolve within 5 minutes, and should not be used as the sole criteria for
identifying an acute ischemic event.
Injuries to the Operator
Operator injuries during cardioversion occur very rarely, with an incidence of less than 1 in 1700. Cases of major electrocution have been described in
extremely rare instances and have all been associated with equipment failure.
Physical Trauma to the Patient
Physical trauma to the patient is a rare complication and results from vigorous body movements during the delivery of the electric shock.
Troubleshooting
Failure of the monitor to work properly typically reflects a mechanical problem. The power source, lead connections, ECG leads, and electrode pads
should be checked and confirmed. If the timing artifact during synchronization mode falls on the T wave, the monitoring lead should be changed until
the correct position of the timing artifact is confirmed on the QRS complex. If the capacitor fails to discharge, this probably represents a failure to
identify a QRS complex while in synchronized mode. The monitoring lead should be switched, synchronization on the QRS complex confirmed, and
cardioversion reattempted.
Cardioversion Unsuccessful
Important factors that determine the immediate and longterm success of cardioversion of atrial arrhythmias include the duration of the arrhythmia,
the extent of atrial fibrosis, the size of the left atrium, and underlying structural heart disease (Table 1258). If cardioversion is unsuccessful, a repeat
ECG should be obtained to confirm the underlying rhythm. Next, the cardioversion telemetry strips should be carefully examined to distinguish
between true failure to cardiovert and successful cardioversion that is followed by recurrence of arrhythmia. Patients with recurrence of arrhythmia
might benefit from antiarrhythmic therapy before repeat attempts at cardioversion. For patients who truly fail to cardiovert, a higher level of energy, an
alternate electrode pad configuration, or a biphasic device can be used on repeat attempts. In patients in whom AF recurs acutely or cardioversion
fails, the combination of AV nodal blocker plus intravenous loading with amiodarone, procainamide, or ibutilide may pharmacologically restore sinus
rhythm. If the AF persists, repeat cardioversion can be performed, and if successful the patient may be placed on longterm antiarrhythmic therapy.
Electrolyte disturbances, digitalis toxicity, and thyrotoxicosis may result in failure to cardiovert and should be corrected prior to cardioversion.
Table 1258 Factors Associated with Failed Cardioversion of Atrial Fibrillation
Structural heart disease (eg, congestive heart failure, valvular disease)
Underlying illness (eg, thyrotoxicosis)
Dilated left atrium
Extent of atrial fibrosis
Longer duration of atrial fibrillation
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Too low energy
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Technique
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alternate electrode pad configuration, or a biphasic device can be used on repeat attempts. In patients in whom AF recurs acutely or cardioversion
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fails, the combination of AV nodal blocker plus intravenous loading with amiodarone, procainamide, or ibutilide may pharmacologically restore sinus
rhythm. If the AF persists, repeat cardioversion can be performed, and if successful the patient may be placed on longterm antiarrhythmic therapy.
Electrolyte disturbances, digitalis toxicity, and thyrotoxicosis may result in failure to cardiovert and should be corrected prior to cardioversion.
Table 1258 Factors Associated with Failed Cardioversion of Atrial Fibrillation
Structural heart disease (eg, congestive heart failure, valvular disease)
Underlying illness (eg, thyrotoxicosis)
Dilated left atrium
Extent of atrial fibrosis
Longer duration of atrial fibrillation
Too low energy
Technique
Pregnancy
Successful cardioversion has been performed in all three trimesters of pregnancy without adverse consequences to the mother or fetus. Cardioversion
does not affect the rhythm of the fetus though it is recommended that the fetal heart rhythm be monitored during the procedure.
Implantable Pacemakers and CardioverterDefibrillators
Several precautions are necessary when performing cardioversion in a patient with a permanent implanted device (pacemaker or ICD). Electrical
cardioversion can change the settings of the device and may damage the pulse generator, the lead system, or myocardial tissue resulting in device
dysfunction. To prevent this, the electrode pads should be placed at least 12 cm from the implanted device, preferably in the anteriorposterior
position. Elective cardioversion should be initiated at low energies to reduce the risk of damage. The implantable device should be interrogated before
and after cardioversion to ensure normal device function. When these precautions are employed, cardioversion with either monophasic or biphasic
shocks is safe and effective in patients with implantable devices.
Consultation
In 2000, an ACC/AHA task force on clinical competency published recommendations for technical and cognitive skills needed to perform external
electrical cardioversion. The ACC/AHA also recommends that the minimum training necessary for competence to perform external electrical
cardioversion should include competence in the interpretation of 12lead ECGs. Previous ACC/AHA task forces recommended a minimum of eight
supervised electrical cardioversions as a minimum requirement. The competence in electrical cardioversion may be achievable without formal training
in cardiovascular disease. For physicians without adequate experience with electrical cardioversion, a cardiologist should be enlisted to assist with or
perform the procedure. There are no published clinical competency recommendations for the use of pharmacologic cardioversion with antiarrhythmic
drugs. For physicians without adequate experience with antiarrhythmic drugs, a cardiologist may be enlisted to assist with pharmacologic
cardioversion as well.
Quality Improvement to Address Performance Gaps
Secondary Prevention
Maintenance therapy with antiarrhythmic drugs is not typically recommended after electrical cardioverson in patients with a first episode of AF,
particularly those at low risk for recurrence (eg, short duration and normal left atrial size) or those with a reversible cause (eg, cardiac surgery,
pulmonary embolus, or hyperthyroidism). In other patients with recurrent paroxysmal or persistent AF, maintenance antiarrhythmic drug therapy may
be administered to reduce the risk of recurrence if a rhythm control strategy is chosen. Because of the adverse effects associated with antiarrhythmic
drugs and no difference in outcomes between rhythm and rate control strategies, many authorities reserve the use of longterm antiarrhythmic drug
therapy to patients that remain symptomatic with rate control (Table 1259).
Table 1259 EvidenceBased Medicine: Key References for Cardioversion
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Study Methodology Results Limitations Bottom Line Page 18 / 21
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Botto GL, Politi A, Bonini W, et Randomized 301 patients enrolled; higher success Exclusion criteria An AP paddle position is
al. External cardioversion of controlled trial rate of conversion to NSR in AP group included patients with AF superior to an AL location
pulmonary embolus, or hyperthyroidism). In other patients with recurrent paroxysmal or persistent AF, maintenance antiarrhythmic drug therapy may
be administered to reduce the risk of recurrence if a rhythm control strategy is chosen. Because of the adverse effects associated with antiarrhythmic
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drugs and no difference in outcomes between rhythm and rate control strategies, many authorities reserve the use of longterm antiarrhythmic drug
therapy to patients that remain symptomatic with rate control (Table 1259).
Table 1259 EvidenceBased Medicine: Key References for Cardioversion
AF, atrial fibrillation; AFL, atrial flutter; AL, anterolateral; AP, anteroposterior; DCCV, direct current cardioversion; NSR, normal sinus rhythm; TEE, transesophageal echocardiogram; VT, ventricular
tachycardia.
Transitions of Care
After cardioversion, all patients should receive warfarin therapy for at least 4 weeks. A plan for anticoagulation and followup with INR monitoring with
a primary physician, cardiologist, or specialized Coumadin clinic should be established. Patients with AF at high risk from thromboembolic events
based on CHADS2 score may require longterm anticoagulation. Patients with newonset AF should undergo thyroid function testing and receive an
echocardiogram. Patients with no recurrence can follow up with their primary care physicians as outpatients and do not require any additional testing.
Patients with either recurrent, symptomatic AF (despite attempts at rate control) or patients who prefer a rhythm control strategy should be referred to
a cardiologist. Cardiology referral for initiation of an antiarrhythmic drug, if required, may also be indicated unless the physician is experienced with
and knowledgeable of administration of these drugs. Because most antiarrhythmic agents can also be proarrhythmic, and because many have
dangerous side effects to monitor, their initiation and maintenance should be performed by a clinician experienced in their use.
Suggested Readings
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[PubMed: 12595839]
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Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). J Am Coll Cardiol. 2006;48: e149–
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Niebauer MJ, Brewer JE, Chung MK, et al. Comparison of the rectilinear biphasic waveform with the monophasic damped sine waveform for external
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Stambler BS, Wood MA, Ellenbogen KA, et al. Efficacy and safety of repeated intravenous doses of ibutilide for rapid conversion of atrial flutter or
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Niebauer MJ, Brewer JE, Chung MK, et al. Comparison of the rectilinear biphasic waveform with the monophasic damped sine waveform for external
cardioversion of atrial fibrillation and flutter. Am J Cardiol. 2004;93:1495–1499. [PubMed: 15194019]
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1999;340:1849–1854. [PubMed: 10369847]
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