Editors: Irwin, Richard S.; Rippe, James M.

Title: Irwin and Rippe's Intensive Care Medicine, 6th Edition

Copyright 2008 Lippincott Williams & Wilkins (Copyright 2008 by Richard S. Irwin,
M.D. and James M. Rippe, M.D.)
> Table of Contents > Section 1 - Procedures and Techniques > Chapter 6 - Cardioversion
and Defibrillation
Chapter 6
Cardioversion and Defibrillation
Naomi F. Botkin
The use of electric countershock to terminate arrhythmia was described over 200 years ago.
Thanks to the pioneering work of Zoll et al. [1], Lown et al. [2], and Alexander et al. [3] in
the second half of the twentieth century, the use of electric countershock gained widespread
acceptance and became a staple in the treatment of cardiac arrhythmia. Cardioversion refers
to the use of direct-current electric countershock to terminate arrhythmias other than
ventricular fibrillation. In order to avoid triggering ventricular fibrillation, shocks are
synchronized with the R wave. Defibrillation, on the other hand, refers to the termination of
ventricular fibrillation with unsynchronized shocks. An understanding of both cardioversion
and defibrillation is critical for intensive care unit personnel.
Physiology of Arrhythmia and Countershock
Electric countershocks are capable of terminating arrhythmias that are due to reentry. Reentry
refers to the phenomenon in which a wave of excitation travels repeatedly over a closed
pathway or circuit of conduction tissue. In order for reentry to occur, there must be
unidirectional block in one branch of the circuit. In addition, conduction down the unblocked
pathway must be slow enough that the blocked pathway recovers excitability by the time the
wave reaches the site of block in a retrograde fashion. Continuous electrical activation in
such a circuit can lead to reentrant arrhythmias.
Most of the commonly encountered arrhythmias are due to a reentrant mechanism, including
atrial fibrillation, atrial flutter, atrioventricular (AV) nodal reentrant tachycardia, most
ventricular tachycardias, and ventricular fibrillation. Cardioversion and defibrillation
terminate these arrhythmias by simultaneously depolarizing all excitable tissue, disrupting the
process of reentry.
Arrhythmias due to disorders all of impulse formation (increased automaticity or triggered
activity) do not respond to countershock. These include sinus tachycardia, focal atrial
tachycardia, and some types of ventricular tachycardia. Table 6-1 categorizes arrhythmias by
their responsiveness to electric countershock.
Insight into the effect of countershock on fibrillating myocardial cells has grown in the past
few decades. Although it was initially thought that all ventricular activation fronts had to be
terminated simultaneously to stop ventricular fibrillation [4], it is now believed that if the vast
majority of myocardium is silenced, the remaining mass is insufficient to perpetuate the
arrhythmia [5]. The effect of shock on fibrillating myocardium is complex and is dependent
on multiple factors including energy, shock waveform, and myocardial refractory state. It is
known that electric countershock at low energy levels may fail to terminate ventricular
fibrillation. Although subthreshold shocks may extinguish fibrillatory wavefronts, they will
often reinitiate new wavefronts elsewhere in the ventricle, leading to the perpetuation of
fibrillation [6]. Thus, it is necessary to deliver shocks above a particular threshold of energy
for defibrillation to be successful. Furthermore, ventricular fibrillation can be triggered in
patients not already in this rhythm if shocks are poorly timed. Synchronization of shocks with
the R wave will minimize the risk.
Indications and Contraindications
Cardioversion and defibrillation are performed for a variety of reasons in the intensive care
setting. In the case of hemodynamic instability due to tachyarrhythmia of nearly any variety,
the urgent use of countershock is strongly indicated. One must be careful, however, not to
mistake sinus tachycardia, which is commonly present in patients who are hypotensive for
noncardiac reasons, for a shockable rhythm. The onset of congestive heart failure or angina in
a patient with a tachyarrhythmia is also an indication for immediate countershock. In the
absence of hemodynamic instability or significant symptoms, cardioversion is usually
considered elective and the risks and benefits of the procedure must be carefully weighed.
Extreme caution should be exercised in patients with digitalis toxicity or electrolyte
imbalance because of their increased risk of ventricular tachycardia or fibrillation after being
shocked. Patients with severe conduction system disease may develop significant
bradyarrhythmia after cardioversion. In addition, patients who have been in atrial fibrillation
for a prolonged or indeterminate length of time are at risk for thromboembolism due to
cardioversion; appropriate measures should be taken to minimize this risk (see below).
Clinical Competence
A clinical competence statement by the American College of Cardiology and American Heart
Association outlines the cognitive and technical skills required for the successful and safe
performance of elective external cardioversion (Table 6-2). A minimum of eight
cardioversions should be supervised before a physician is considered competent to perform
the procedure independently. In addition, a minimum of four procedures should be performed
annually to maintain competence [7].
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Table 6-1. Classification of Tachyarrhythmias Based on Predicted Responses to

Cardioversion/Defibrillation
Responsive (reentrant)
Supraventricular arrhythmias
Atrial fibrillation
Atrial flutter
Sinoatrial nodal reentrant tachycardia
AV nodal reentrant tachycardia
AV reciprocating tachycardia
Ventricular arrhythmias
Monomorphic ventricular tachycardia due to scar or bundle branch reentry
Polymorphic ventricular tachycardia
Ventricular flutter
Ventricular fibrillation
Unresponsive (automatic)
Supraventricular arrhythmias
Sinus tachycardia
Focal atrial tachycardias
Junctional tachycardia
Ventricular arrhythmias
Idiopathic monomorphic ventricular tachycardia
Accelerated idioventricular rhythm
Methods
Patient Preparation
In the case of unconsciousness due to tachyarrhythmia, countershock must be performed
urgently. In more elective settings, patient safety and comfort become paramount. As with
any procedure, informed consent should be obtained. Patients should refrain from eating and
drinking for several hours in order to decrease the risk of aspiration. Constant heart rhythm
monitoring should be used throughout the procedure and a 12-lead electrocardiogram should
be obtained before and after the countershock.
Table 6-2. Cognitive and Technical Skills Necessary for Performing External
Cardioversion
Physicians should have knowledge of the following:
Electrophysiologic principles of cardioversion
Indications for the procedure
Anticoagulation management
Proper use of antiarrhythmic therapy
Use of sedation and the management of overdose
Direct current cardioversion equipment, including the selection of appropriate energy and
synchronization.
Treatment of possible complications, including ACLS, defibrillation, and pacing
Proper placement of paddles or pads
Appropriate monitor display and recognition of arrhythmias
Baseline 12-lead electrocardiogram reading, recognition of acute changes, drug toxicity,
and contraindications
Physicians should have the following technical skills:
Proper preparation of skin and electrode placement
Achievement of artifactfree monitored strips and synchronization signal/marker
Technically acceptable 12-lead electrocardiograms before and after DCCV
Temporary pacing and defibrillation capabilities
Ability to perform advanced cardiac life support, including proper airway management
From Tracy CM, Akhtar M, DiMarco JP, et al: American College of Cardiology/American
Heart Association Clinical competence statement on invasive electrophysiology studies,
catheter ablation, and cardioversion. J Am Coll Cardiol 36:17251736, 2000.
Medications with rapid onset and short half-life are favored for achieving analgesia, sedation,
and amnesia. The combination of a benzodiazepine, such as midazolam, and a narcotic, such
as fentanyl, is a frequent choice in the absence of anesthesiology assistance. Propofol is often
used when an anesthesiologist is present to assist with airway management and sedation.
Existing hospital policies for monitoring during conscious sedation should be followed,
including frequent assessment of blood pressure and pulse oximetry. Supplemental oxygen is
delivered via nasal cannula, face mask, orin the case of heavier sedationAmbuBag.
The goal of sedation should be minimal or no response to verbal stimulus. In such a state, a
patient may cry out during the actual cardioversion but will nonetheless usually have no
recollection of the procedure after recovery.
Shock Waveforms
Defibrillators that employ biphasic waveforms have largely replaced those utilizing
monophasic waveforms. The chief advantage of biphasic waveforms is a lower defibrillation
threshold, meaning shocks using biphasic waveforms require less energy to achieve
defibrillation. It is thought that the first phase of the biphasic waveform stimulates the
myocardium to defibrillate while the second phase lowers the defibrillation threshold,
although the mechanism is not well understood [8]. Biphasic truncated exponential waveform
and biphasic rectilinear waveform are both commercially available, with the former being
more common. Randomized trials comparing the two types of waveforms in the
cardioversion of atrial fibrillation have failed to show any significant difference in efficacy
[9,10,11].
The efficacy of biphasic shocks in the termination of VF has been well established [12,13].
Furthermore, clinical studies of elective cardioversion have established the superiority of
biphasic over monophasic waveform shocks [14,15]. For instance, one study demonstrated
the equivalent efficacy of a 120 J to 200 J biphasic sequence with a 200 J to 360 J
monophasic sequence [15]. Biphasic waveforms allow fewer shocks to be given and a lower
total energy delivery [14]. Whether or not this translates into a significant clinical advantage
remains to be demonstrated. However, there is evidence that biphasic shocks result in less
dermal injury [14]. Although an animal model suggested better maintenance of cardiac
function after biphasic shocks [16], human data on myocardial function are unavailable.
Electrodes
Until recently, hand-held paddles coated with conductive gel were the sole type of electrode
used to deliver countershock. Self-adhesive pads have become more common in the past few
years, although paddles are still used, especially in emergent cases. Limited data are available
comparing the two modalities, but one study suggested the superiority of paddles over pads in
cardioverting atrial fibrillation [17]. This phenomenon might be explained by the lower
transthoracic impedance achieved with paddles [18]. Whichever modality is used, impedance
can be minimized by avoiding positioning over breast tissue, by clipping body hair when it is
excessive [19], and by delivering the shock during expiration [20].
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FIGURE 6-1 A: Self-adhesive defibrillator pads in the anterior and lateral positions. B: Self-
adhesive defibrillator pad in the posterior position. When posterior positioning is used, the
second pad is placed anteriorly.
The optimal anatomic placement of pads and paddles is controversial. Anterior-lateral and
anterior-posterior placements are both acceptable (Fig. 6-1). The anterior paddle is placed on
the right infraclavicular chest [21]. In anterior-lateral placement, the lateral paddle should be
located lateral to the left breast and should have a longitudinal orientation, since this results in
a lower transthoracic impedance than horizontal orientation [22]. When anterior-posterior
positioning is used, the posterior pad is commonly located to the left of the spine at the level
of the lower scapula, although some physicians favor placement to the right of, or directly
over, the spine. There are data to suggest that anterior-posterior placement is more successful
in the cardioversion of atrial fibrillation than anterior-lateral positioning when monophasic
waveforms are used [23]. It is thought that anterior-posterior positioning directs more of the
delivered energy to the atria than anterior-lateral placement. Since it has been shown that
only 4% of the current flow from shock reaches the myocardium with the anterior-lateral
position [24], any method that directs more energy to the atria should be beneficial. However,
a study using defibrillators employing a biphasic waveform suggested pad position was not
associated with cardioversion success [25].
Table 6-3. Checklist for Performing Cardioversion
Preparing the patient:

1. Ensure NPO status

2. Obtain informed consent
3. Apply self-adhesive pads (clip hair if needed)
4. Achieve adequate sedation
5. Monitor vital signs and cardiac rhythm throughout

Performing the cardioversion:

1. Select initial energy appropriate for specific device

2. Select the synchronization function
3. Confirm that arrhythmia is still present
4. Charge, clear, and deliver shock
5. If no change in rhythm, escalate energy as appropriate

NPO, nil per os.

Using the Defibrillator
External defibrillators are designed for easy operation. After the patient is adequately
prepared and the electrodes are applied, attention may be turned to the device itself. If the
QRS amplitude on the rhythm tracing is small and difficult to see, a different lead should be
selected. If cardioversionrather than defibrillationis to be performed, the
synchronization function should be selected. The appropriate initial energy is
selected. Finally, the capacitor is charged, the area is cleared, and the shock is delivered. One
should be aware that the synchronization function is automatically deselected after each
shock in some devices, meaning that it must be manually reselected prior to any further shock
delivery.
Table 6-3 provides a checklist for physicians involved in cardioversion. Table 6-4 gives
recommendations for the initial energy selection for defibrillation and cardioversion of
various arrhythmias. Recommendations specific to each device are available in the
manufacturers' manuals and should be consulted by physicians unfamiliar with their
particular device.
Treatment of Ventricular Fibrillation and Pulseless Ventricular Tachycardia
The algorithm for the treatment of pulseless ventricular tachycardia and ventricular
fibrillation in the most recently published American Heart Association guidelines [21]
contains some important changes from the previous guidelines. Rather than beginning with
three stacked shocks, the guidelines
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recommend only one shock followed by five cycles of cardiopulmonary resuscitation (CPR)
before the rhythm is reassessed. This change was prompted by the observation that delivering
three closely timed shocks involves a substantial interruption in CPR, which has been shown
to be associated with a decreased chance of successful termination of ventricular fibrillation
[26]. In the new algorithm, vasopressors (epinephrine or vasopressin) may be given before or
after the second shock, and antiarrhythmics such as amiodarone and lidocaine may be
considered before or after the third shock (Table 6-5). Both ventricular fibrillation and
pulseless ventricular tachycardia are treated with unsynchronized, high-energy shocks of 360
J in the case of devices that use monophasic waveforms and 120 to 200 J with biphasic ones.
Table 6-4. Suggested Initial Energy for Cardioversion and Defibrillation
Rhythm MonophasicBiphasic
Ventricular fibrillation, pulseless ventricular tachycardia360 J 120200 J
Ventricular tachycardia with pulse 100 J unknown
Atrial fibrillation 100200 J 100120 J
Atrial flutter 50100 J unknown
Table 6-5. Treatment of Ventricular Fibrillation and Pulseless Ventricular Tachycardia
Assess airway, breathing, and circulation
Assess rhythm
Deliver 1 shock
Monophasic: 360 J
Biphasic: use device specific energy; if unknown, 200 J
Resume compressions immediately and perform 5 cycles of CPR
Check rhythmif still VT/VF, shock again
Monophasic: 360 J
Biphasic: same as first shock or higher dose
Resume compressions immediately and perform 5 cycles of CPR
Give a vasopressor during CPR, either before or after the second shock
Epinephrine 1 mg IV/IO, repeat every 35 min, OR
Vasopressin 40 U IV/IO may replace First or second dose of epinephrine
Check rhythmif still VT/VF, shock again
Consider an antiarrhythmic before or after third shock:
Amiodarone 300 mg IV/IO once, then consider additional 150 mg once OR
Lidocaine 1 to 1.5 mg/kg first dose, then 0.5 to 0.75 mg/kg IV/IO, maximum 3 doses.
IO, intraosseous; IV, intravenous; VF, ventricular fibrillation; VT, ventricular tachycardia.
Treatment of Wide Complex Tachycardia with a Pulse
When a pulse is present, a regular, wide complex tachycardia may be either ventricular
tachycardia or a supraventricular tachycardia with aberrant conduction. If signs of instability
such as chest pressure, altered mental status, hypotension, or heart failure are present, urgent
cardioversion is indicated. A starting energy of 100 J is recommended when a monophasic
shock waveform is being used. The optimal initial energy with biphasic devices is unknown.
The energy should be escalated with each successive shock, such as 100 J, 200 J, 300 J, and
360 J [21].
If the patient is stable, however, one might consider enlisting the assistance of an expert in
distinguishing between ventricular and supraventricular arrhythmia. If this is not possible, it
is safest to assume a ventricular etiology. Stable ventricular tachycardia may be treated
initially with antiarrhythmic agents such as amiodarone. Elective cardioversion is usually
performed.
Wide complex tachycardia that appears irregular is usually atrial fibrillation with aberrant
conduction rather than ventricular tachycardia. Treatment should follow the
recommendations for atrial fibrillation below, unless the Wolff-Parkinson-White Syndrome is
suspected.
Treatment of Supraventricular Tachycardia
The most common regular, narrow complex tachycardia is sinus tachycardia.
Supraventricular tachycardia with a reentrant mechanism and atrial flutter are the next most
common. Supraventricular tachycardia should be suspected when the arrhythmia starts
suddenly, when it is more rapid than typical sinus tachycardia, and when P waves are absent
or closely follow the QRS. Initial therapy involves vagal maneuvers and adenosine. If these
fail, nondihydropyridine calcium channel antagonists or beta-blockers may terminate the
arrhythmia. Cardioversion is indicated only rarely for clinical instability, usually in patients
with underlying heart disease in whom the initial therapies fail.
Treatment of Atrial Fibrillation and Flutter
Rate Control
Although the majority of patients with atrial fibrillation and flutter remain hemodynamically
stable, many develop bothersome symptoms such as palpitations, chest pressure, and,
occasionally, pulmonary edema. Beta-blockers and nondihydropyridine calcium channel
antagonists are used to slow the ventricular response rate by depressing AV nodal
conduction. Many patients become asymptomatic or minimally symptomatic with adequate
rate control, allowing the decision about cardioversion to be made electively.
Electrical Cardioversion
Cardioversion for atrial fibrillation or flutter is usually performed electively. The risk of
thromboembolism dictates a thoughtful decision about treatment options. When cardioversion
is performed, an appropriate initial starting dose is 100 to 200 J for monophasic waveform
shock and 100 to 120 J for biphasic shock. Atrial flutter responds to lower energy, so a
starting dose of 50 to 100 J is recommended with a monophasic waveform. The ideal starting
energy for biphasic devices is unknown [21]. If atrial fibrillation or flutter fails to terminate,
shock energy should be escalated.
Anticoagulation
Patients with atrial fibrillation or flutter may develop thrombus in the left atrial appendage or
left atrial cavity, leading to thromboembolism during or after cardioversion. One study
demonstrated a risk of pericardioversion thromboembolism of 5.3% in patients who were not
anticoagulated and 0.8% in those who were [27].
There is general agreement that cardioversion of patients who have been in atrial fibrillation
for less than 24 to 48 hours is very unlikely to cause thromboembolism. Current guidelines
indicate that pericardioversion anticoagulation with heparin or low molecular weight heparin
is optional in these patients [28]. Patients in whom the arrhythmia has been present for longer
than 24 to 48 hours, or for an undetermined length of time, are felt to be at higher risk. When
these patients do not require
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urgent cardioversion for reasons of symptomatology, there are two reasonable approaches.
In the first case, one may perform a transesophageal echocardiogram to assess for the
presence of thrombus in the left atrial appendage [29,30]. If thrombus is not visualized, the
patient is considered to be at low risk for thromboembolism, and cardioversion may be
performed. Anticoagulation with warfarin to an international normalized ratio (INR) goal of
2.5 (range 2.0 to 3.0) is recommended for 4 weeks after cardioversion [7]. The reason for
such a long period of anticoagulation after cardioversion is that the return of organized atrial
mechanical activity can lag behind the restoration of normal sinus rhythm [31,32].
Unfractionated heparin should be administered until the INR is in the therapeutic range. Low
molecular weight heparin has been demonstrated to be effective in preventing
thromboembolism in small trials of atrial fibrillation patients undergoing cardioversion
[33,34] but has not yet been incorporated into the guidelines.
The second approach is to defer cardioversion until the patient has been anticoagulated at a
therapeutic level for at least 3 weeks. Cardioversion is then performed and the patient
anticoagulated for a minimum of 4 weeks afterward [7].
Pharmacologic Cardioversion
Cardioversion can be achieved not only electrically but also pharmacologically.
Pharmacologic cardioversion is used mainly for atrial fibrillation and flutter of relatively
short duration. Although electrical cardioversion is quicker and has a higher probability of
success, pharmacologic cardioversion does not require sedation. The risk of
thromboembolism with pharmacologic cardioversion has not been well established but is
thought to be similar to that of electric countershock because it is the return of sinus rhythm
rather than the shock itself that is believed to precipitate thromboembolism.
Dofetilide, flecainide, ibutilide, propafenone, amiodarone, and quinidine have been
demonstrated to have some degree of efficacy in restoring sinus rhythm [20]. Each of these
medications has potential toxicities including malignant arrhythmias and hypotension. The
risks and benefits should be carefully weighed when selecting a pharmacologic agent.
Although beta-blockers and calcium channel antagonists are often believed to facilitate
cardioversion, their efficacy has not been established in controlled trials.
Management of Resistant Atrial Fibrillation
Electrical cardioversion is unsuccessful in 10% to 30% of cases of atrial fibrillation [20] and
up to 28% of cases of atrial flutter [35]. The duration of atrial fibrillation is inversely related
to the probability of successful cardioversion.
When cardioversion fails, the operator's technique should be reviewed and modified.
Electrode position may be altered, from anterior-posterior to anterior-lateral or vice versa. If
paddles are being used, firmer pressure may be employed. If a device that delivers
monophasic waveform shocks is being employed, it may be exchanged for one that delivers
biphasic waveform shocks. Synchronized shocks from two separate defibrillators using
electrical switches to coordinate the shocks may be performed [36]. An antiarrhythmic
medication may be initiated prior to another attempt at cardioversion. Finally, transvenous
cardioversion may be attempted (see below).
Although some patients fail to achieve sinus rhythm, many who are successfully cardioverted
revert to atrial fibrillation within minutes, hours, or days. The administration of
antiarrhythmic pharmacologic therapy decreases this possibility significantly [37]. However,
given the adverse reactions associated with these medications, the necessity of maintaining
sinus rhythm should be carefully considered. When atrial fibrillation is associated with
substantial symptoms that are not alleviated by rate-controlling medications, antiarrhythmic
therapy may be indicated. However, patients in whom the arrhythmia is well tolerated may be
served as well by a strategy of rate control and anticoagulation [38].
Transvenous Cardioversion
Cardioversion using high-energy shocks delivered internally via a right atrial (RA) catheter
and a backplate was described in 1988 [39]. This technique was demonstrated to be more
efficacious than external cardioversion, especially in patients who are obese or who have
chronic obstructive pulmonary disease [40]. Lower energy internal shock using an RA
cathodal electrode and an anode in the coronary sinus or left pulmonary artery has also been
described [41].
Complications
Burns
Countershock can cause first-degree burns and pain at the paddle or pad site. One study
documented moderate to severe pain in nearly one quarter of patients undergoing
cardioversion. Pain was directly related to total energy delivered and number of shocks [42].
Another study showed a lower rate of dermal injury with biphasic rather than monophasic
shocks, probably due to the lower energy necessary with biphasic shocks [14]. The lowest
effective energy should be used to minimize skin injury.
Thromboembolism
Cardioversion of atrial fibrillation and atrial flutter carries a risk of thromboembolism. One
percent to 7% of patients in atrial fibrillation who undergo cardioversion without receiving
anticoagulation may experience this complication [27,43]. The role of anticoagulation to
diminish this risk is discussed above.
Arrhythmia
Bradyarrhythmias such as sinus arrest and sinus bradycardia are common immediately after
countershock and are almost always short-lived. However, patients who have atrial
fibrillation with a slow ventricular response in the absence of medications that slow AV
conduction should be suspected of having conduction disease and are at higher risk for
sustained bradyarrhythmia after cardioversion. The prophylactic placement of a transvenous
or transcutaneous pacemaker may be considered in this situation [20].
Ventricular tachycardia and ventricular fibrillation can occasionally be precipitated by
countershock, particularly in patients with digitalis toxicity or hypokalemia [44,45]. Elective
cardioversion should therefore be avoided in patients with these conditions. If cardioversion
or defibrillation must be performed urgently, one should anticipate the ventricular
arrhythmias to be more refractory to shock than usual.
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Myocardial Damage
Occasionally, one may see transient ST elevations on postcountershock electrocardiograms
[46]. This is unlikely to signify myocardial injury. Although a study of cardioversion using
higher-than-usual energy levels demonstrated an increase in creatine kinase-MB levels above
that expected from skeletal muscle damage in 10% of patients, there was no elevation in
troponin-T or -I seen [47]. This observation suggests that clinically significant myocardial
damage from cardioversion or defibrillation is unlikely. Nonetheless, it has been suggested
that any two consecutive shocks be delivered no less than one minute apart to minimize the
chance of myocardial damage [48]. Of course, this recommendation applies only to
nonemergent situations.
Miscellaneous Topics
Patients with Implanted Pacemakers and Defibrillators
Patients with implanted pacemakers and defibrillators may undergo external cardioversion
and defibrillation safely in most cases. However, one must be aware of the possibility that
external energy delivery may alter the programming of the internal device. Furthermore,
energy may be conducted down an internal lead, causing local myocardial injury and a
resultant change in the pacing or defibrillation threshold [20]. The paddles or pads used for
external electric countershock should never be placed over the internal device. In addition,
interrogation of the device immediately after any external shock delivery is recommended.
Chest Thump
The use of a manual thump on the chest to successfully terminate ventricular
tachycardia was described in several patients in 1970 [49]. The reason for its success is not
well understood. Unfortunately, this technique may inadvertently trigger ventricular
fibrillation if the blow happens to fall during the vulnerable period of the ventricle [50]. For
this reason, chest thump is considered a therapy of last resort, administered only to a
pulseless patient when a defibrillator is unavailable and unlikely to become available soon. It
should not be administered when a pulse is present unless a defibrillator is immediately
available.
Cardioversion and Defibrillation in Pregnancy
Cardioversion and defibrillation have been performed in all trimesters of pregnancy without
obvious adverse fetal effects or premature labor [51,52]. It has been suggested that the fetal
heart rhythm be monitored during cardioversion [53].
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