Ven t r i c u l a r A r r h y t h m i a s

William F. Dresen, MD*, John D. Ferguson, MBCHB, MD, FHRS

KEYWORDS
 Ventricular tachycardia  Ventricular fibrillation  Catheter ablation
 Implantable cardioverter-defibrillator

KEY POINTS
 Ventricular tachycardia (VT) is the most common form of wide complex tachycardia and associated
with a high mortality rate.
 The electrocardiogram is paramount in diagnosis, but distinguishing VT from supraventricular
tachycardia with aberrant conduction may be difficult; the diagnosis of VT should be assumed until
proven otherwise.
 Catheter ablation of VT is an effective treatment modality typically used after antiarrhythmic drug
failure, but recurrent VT is not uncommon.
 The implantable cardioverter-defibrillator aids in the acute termination of ventricular arrhythmia.
 Its pacing and sensing algorithms are helpful in improving the diagnostic yield and long-term man-
agement of patients with ventricular arrhythmia.

INTRODUCTION near syncope secondary to cerebral hypoperfu-

Ventricular tachycardia (VT) is the most common
cause of wide complex tachycardia.1 It is associ-
ated with ischemic and nonischemic cardiomyopa-
thies, cardiac channelopathies, and toxic metabolic
conditions, or may exist as an idiopathic process in
structurally normal hearts. Of the more than 130
million emergency department (ED) visits in the
United States each year, cardiac dysrhythmias
were the fifth most common reason for presentation
in patients between the ages of 65 and 84 years, ac-
counting for more than 278,000 visits.2 Sustained
VT occurs much less frequently, however, account-
ing for only 0.05% of ED visits in 1 series,3 but oc-
curs at a much higher frequency in critical care
settings, with an incidence of 2% to 7%.4,5
Clinical presentations of ventricular tachyar-
rhythmias may range from the asymptomatic to
implantable cardioverter-defibrillator (ICD) shocks,
cardiogenic shock, and cardiac arrest. Syncope or
sion is relatively common, occurring in 30% of pa-
tients with sustained VT of more than 30 minutes’
duration in individuals not presenting with myocar-
dial ischemia or sudden death. Patients were more
likely to present with syncope when the VT was
greater than 200 bpm and chest pain in those
with a background history of coronary artery dis-
ease (33% vs 12%).6 Similar findings were seen
in another series, in which 77% of patients in sus-
tained VT were hemodynamically stable upon
evaluation.3 Hemodynamic compromise is vari-
able and due to a number of different factors,
including a rate-related decrease in diastolic filling
time, incomplete myocardial relaxation, and a dys-
synchronous ventricular activation pattern result-
ing in decreased pump function, loss of atrial
transport, and possibly mitral regurgitation.7
Ventricular arrhythmia often results in hospital
admission. Those with a hemodynamically
stable VT are most commonly admitted to a
cardiology.theclinics.com

Disclosures: W.F. Dresen and J.D. Ferguson have nothing they wish to disclose.
Department of Cardiovascular Medicine, University of Virginia Medical Center, 1215 Lee Street, Charlottesville,
VA 22908, USA
* Corresponding author.
E-mail address: wfd7t@virginia.edu

Cardiol Clin 36 (2018) 129–139

https://doi.org/10.1016/j.ccl.2017.08.007
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130 Dresen & Ferguson
non–intensive care unit setting (72%), but rarely
discharged directly from the ED (16%), which
mostly results from extenuating clinical circum-
stances, such as patient refusal or goals of
care that necessitate a less aggressive clinical
approach. Patients with a hemodynamically un-
stable VT are more likely admitted to an intensive
care unit setting versus a general ward (41% vs
35%), with the remaining unstable patients not
surviving past their initial ED evaluation,3 thus
highlighting the severity of the condition.
Definitions of Ventricular Arrhythmia
 Sustained VT: persists for greater than
30 seconds and/or requiring termination
owing to hemodynamic compromise in less
than 30 seconds.
 Monomorphic VT: single QRS morphology
and stable cycle length.
 Polymorphic VT: QRS morphologies and cy-
cle length vary considerably.
 VT storm: Fewer than 2 to 3 episodes of he-
modynamically significant VT or 3 or more
shocks in 24 hours.
 Incessant VT: unable to maintain sinus rhythm.
 Ventricular fibrillation (VF): rapid (usually >300
bpm) disorganized low-amplitude polymor-
phic ventricular activity.
DIAGNOSIS OF VENTRICULAR ARRHYTHMIA
Differentiation of Ventricular Tachycardia
from Supraventricular Tachycardia on the
12-Lead Electrocardiograph
An important distinction in patients presenting with
wide complex tachycardia is the differentiation of
VT from supraventricular tachycardia (SVT). He-
modynamic instability is not useful in the differen-
tiation but prior myocardial infarction, heart failure,
and recent angina pectoris have a positive predic-
tive value for the diagnosis of VT of 98%, 100%,
and 100%, respectively.8
Multiple algorithms for the ECG diagnosis of VT
have been proposed but none are 100% specific.9
Common criteria used include:
 Absence of an RS complex in the precordial
leads10;
 An RS interval of greater than 0.1 second in
any precordial lead10;
 Atrioventricular dissociation with or without
fusion with or without capture beats10,11; and
 VT is more likely in a right bundle branch block
configuration when11:
 QRS duration is greater than 0.14 second;
 There are QR, R, or RSr’ configurations in
lead V1; and
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 The RS ratio is 1 or greater or there is a QS
wave in lead V6.
 VT is more likely in a left bundle branch block
configuration when11:
 The QRS complex duration is greater than
0.16 second;
 The initial R wave is greater than
0.03 second;
 There is slurring or notching of the down
stroke of the S wave or QRS complex onset
to nadir of S wave is greater than 0.07 sec in
lead V1; and
 There is any Q wave in lead V6.
 When the diagnosis remains uncertain, it is
preferable to assume VT rather than SVT.
The 12-lead ECG is also useful in determining
the exit site of VT and whether it is endocardial
or epicardial, an important distinction when
considering catheter ablation (Fig. 1).
A 12-Lead Electrocardiograph After
Termination of Ventricular Tachycardia
Repeat ECG should be obtained immediately after
termination of VT. This can provide useful clues as
to the underlying etiology. For example,
 Q waves indicative of prior infarction;
 ST segment changes consistent with acute ST
elevation myocardial infarction or myocardial
ischemia;
 ECG changes suggestive of hyperkalemia or
drug intoxication;
 Left ventricular hypertrophy and T wave
changes suggestive of hypertrophic
cardiomyopathy;
 Brugada’s syndrome (Fig. 2);
 Prolonged QTc; and
 Epsilon waves indicative of arrhythmogenic
right ventricular dysplasia.
Specific Etiologies of Ventricular Arrhythmia
1. Idiopathic VT without structural heart disease
 Right ventricular outflow tract tachycardia:
most commonly presents with frequent pre-
mature ventricular contractions, but can
develop both repetitive monomorphic sal-
voes of VT and sustained rapid VT, often pro-
voked by exertion. The ECG morphology is a
left bundle branch block, inferior axis. Unlike
arrhythmogenic right ventricular dysplasia,
the right ventricle is not dilated or scarred.
Beta-blockers may ameliorate symptoms,
but patients with symptomatic high prema-
ture ventricular contraction burden (>10,000/
24 hours) and sustained VT are good candi-
dates for catheter ablation. Ablation is usually
 Ventricular Arrhythmias 131

Fig. 1. Monomorphic ventricular tachycardia (VT) in a patient with a nonischemic cardiomyopathy. Electrocardio-
graphic features that confirm VT include the absence of RS in precordial leads (Brugada), atrioventricular disso-
ciation (Wellens, the paced p waves are denoted by arrows), left bundle branch block morphology with a
QRS interval of greater than 0.160 second (Wellens), slurring of S wave in V1 with onset to nadir of greater
than 0.07 second, Q in V6 (Wellens).

preferable to long-term membrane active
antiarrhythmic drugs. These patients usually
do not require ICD implantation.
 Left ventricular outflow tract tachycardia: a
less common syndrome than right ventricular
outflow tract tachycardia, but managed in a
similar manner. The ECG morphology is a
prominent R wave in V1 with an inferior axis.
 Left posterior fascicular VT: the ECG
morphology is a right bundle branch block
with left axis deviation (most common). This
VT often involves reentry within the His-
Purkinje system and the QRS duration is usu-
ally less than 0.12 second. Calcium channel
blockers may be effective, but ablation is
usually preferred in patients with recurrent
symptoms.
2. Ischemic cardiomyopathy
 Monomorphic VT is most commonly seen.
Patients usually have a history of prior

Fig. 2. Type I Brugada syndrome with typical downsloping ST elevation in V1 and V2. This finding is dynamic and
changes with heart rate and typically is exaggerated during diagnostic testing with intravenous procainamide.

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132 Dresen & Ferguson
infarction and Q waves on the ECG. The left
ventricle is more commonly involved than
the right ventricle, and the ECG morphology
indicates the exit site of the VT, which can
be targeted with ablation.
 Polymorphic VT and VT storm may occur,
usually in the presence of acute ischemia.
Early revascularization may be helpful in this
setting.
3. Nonischemic cardiomyopathy
 Polymorphic VT is more common than mono-
morphic VT. Myocardial scar is more
commonly localized to the epicardium or
midmyocardium than the endocardium.
Consider sarcoidosis and Chagas disease.
4. Arrhythmogenic right ventricular dysplasia
 The VT may be monomorphic, usually a left
bundle branch block, inferior axis
morphology, but also may be polymorphic
or VF. An ECG may show right ventricular
dilation with systolic dysfunction and cardiac
MRI may reveal patchy right ventricular scar.
 Electrophysiologic study often demonstrates
reduced endocardial voltage indicative of
scar.
5. Hypertrophic cardiomyopathy
 Nonsustained VT, polymorphic VT, and VF
are more common, but sustained mono-
morphic VT may also occur. On ECG, left
ventricular hypertrophy with significant
repolarization changes are common.
 Physical examination may reveal a murmur of
outflow tract obstruction or a bisferiens
pulse.
 Echocardiography, cardiac MRI, or genetic
screening are needed to establish a precise
diagnosis.
 Family history is pertinent; genetic testing of
first-degree relatives is often indicated.
6. Genetic arrhythmia syndromes: consider in pa-
tients with a family history of arrhythmia or pre-
mature sudden death. Genetic screening is
now available for many of these syndromes
and is most helpful in patients with a definite
phenotype and corresponding genotype to
use in screening other family members.
 Long QT syndrome (LQTS): torsade de
pointes in the setting of a prolonged QTc
that should be considered in patients with a
positive family history and syncope. Drug his-
tory is important.
 Brugada syndrome: classically presents with
VF (see Fig. 2).
 Catecholaminergic polymorphic VT: poly-
morphic or bidirectional VT.
 Short QT syndrome: rare syndrome that usu-
ally presents with VF.
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 Early repolarization syndrome: polymorphic
VT or VF.
Clinical Evaluation
An immediate assessment focusing on the hemo-
dynamic status of the patient will determine initial
management. After urgent stabilization, a thor-
ough clinical assessment and review of the medi-
cal record will help determine the underlying
etiology and direct definitive therapies.
 Vital signs
 If hemodynamically unstable (symptoms of
hypoperfusion or traditionally a blood pres-
sure <90/60 mm Hg), perform urgent direct
current cardioversion or defibrillation with
appropriate sedation; and
 A 12-Lead ECG, both during VT and after its
termination.
 History
 Onset, duration, and severity of cardiac
symptoms;
 Prior cardiac history of arrhythmia or under-
lying structural heart disease; and
 Family history of arrhythmia or premature
sudden death, specifically in the setting of
hypertrophic cardiomyopathy, LQTS, ar-
rhythmogenic right ventricular dysplasia,
or Brugada syndrome.
 Medications
 Proarrhythmic medications such as digoxin
or other QT-prolonging agents; and
 Antiarrhythmic drugs, specifically Vaughan
Williams class I and III medications.
 Physical examination
 Determination of clinical well-being and the
status of peripheral perfusion;
 Signs of underlying structural cardiac dis-
ease such as canon A waves, cardiac mur-
murs, heart failure, or prior thoracotomy
scar; and
 Presence of a dialysis fistula or other evi-
dence of systemic disease.
 ICD interrogation
 Urgent device interrogation should be per-
formed (see below).
 Laboratory tests
 Baseline chemistries including magnesium
as well as troponin, B-type natriuretic pep-
tide, and thyroid function studies.
 Imaging
 Chest radiograph: evidence of heart failure,
cardiomegaly, or prior cardiac device
implantation;
 Echocardiogram: assessment of ventricular
size and function, specific wall motion abnor-
malities, valvular disease, and hypertrophy;

 Cardiac catheterization: may be indicated
in patients with chest pain, prior coronary
artery disease or elevated troponin (note
VT and cardioversion may elevate serum
troponin); and
 Cardiac MRI: to assess for cardiac structure
and function, late gadolinium enhancement
indicative of myocardial scar, or other sys-
temic infiltrative processes such as amyloid
or hemochromatosis.
 Electrophysiologic study
 Aid in arrhythmia determination and risk
stratification.
MANAGEMENT
Immediate Considerations
The initial management of VT is predicated upon
the hemodynamic status and clinical condition of
the patient.
 Sustained monomorphic VT associated with
hypotension and/or the presence of presyn-
cope or syncope should be treated with
immediate synchronized direct current car-
dioversion in conjunction with appropriate
sedation.
 In patients without hemodynamic compro-
mise, treatment may include medications
and antitachycardia pacing.
Intravenous procainamide and intravenous
amiodarone carry class IIa recommendations for
the acute treatment of sustained monomorphic
VT.12 A direct comparison between the latter 2
agents was recently completed and intravenous
procainamide was not only associated with a
higher rate of arrhythmia termination (67% vs
38% for intravenous amiodarone), but also fewer
adverse cardiovascular outcomes including hypo-
tension (18% vs 31% for intravenous amiodar-
one).13 When associated with myocardial
ischemia or infarction, intravenous lidocaine may
also be considered (class IIb, level of evidence
C).12 Beta-blockers also carry a class IIa recom-
mendation in patients with repetitive monomor-
phic VT in the setting of coronary artery
disease.12 For patients with an idiopathic VT syn-
drome such as an right ventricular outflow tract
VT, calcium channel blockers and adenosine are
also very effective for arrhythmia termination, but
verapamil in particular may be associated with he-
modynamic deterioration when used in the wrong
clinical context.14
Polymorphic VT, including torsades de pointes,
should be treated with immediate defibrillation if
persistent and if hemodynamic compromise is
present. Withdrawal of offending medications in
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Ventricular Arrhythmias 133
addition to electrolyte replacement should be uni-
versally performed. Intravenous magnesium sul-
fate is recommended in those with a long QT
interval and torsades de pointes. If hemodynami-
cally stable, intravenous beta-blockers or lido-
caine may be considered, especially when of
ischemic origin. Intravenous amiodarone may
also be used in the absence of congenital or ac-
quired LQTS. Finally, isoproterenol may be given
to patients presenting with a pause-dependent
torsades de pointes in the absence of congenital
LQTS.12
Definitive Management
If no reversible cause is found, the clinician must
then decide on definitive management with antiar-
rhythmic drugs, VT ablation, ICD implantation, or a
combination thereof. Most patients with sustained
VT have an indication for a secondary prevention
ICD. However, patients with structurally normal
hearts and an outflow tract VT usually require abla-
tion and not an ICD. Beta-blockers are a mainstay
of therapy in most patients with structural heart
disease and those with catecholaminergic poly-
morphic VT and LQTS. Antiarrhythmic therapy
with sotalol and amiodarone may reduce recurrent
symptomatic arrhythmias and ICD shocks, but
have not been shown to decrease mortality.15
Amiodarone in particular is associated with long-
term adverse effects. Quinidine, mexiletine, and
dofetilide, although not approved by the US
Food and Drug Administration for the treatment
of ventricular arrhythmias, may also be considered
in certain clinical scenarios.
Ablation has traditionally been recommended
when VT recurs despite medical therapy.12,16 The
highest success rates are seen in patients without
structural heart disease,17 with a 77% freedom
from recurrent arrhythmia at 6 years. At 6 years,
patients with an ischemic cardiomyopathy have a
higher arrhythmia-free survival compared with a
nonischemic cardiomyopathy (54% vs 38%).18
Multiple randomized clinical trials in patients with
recurrent VT and an ischemic cardiomyopathy
support its use.19–21
Despite its success and the increase use of VT
ablation, 30% to 50% of patients may recur during
long-term follow-up,18,22,23 necessitating a repeat
procedure or an alternative means of therapy.
Anatomic barriers limiting proper access, abbrevi-
ated mapping owing to hemodynamic instability,
disease progression, and intramural foci beyond
the reach of standard ablation lesion depth are
some of the most common reasons for procedural
failure.24 In carefully selected patients who have
already failed an endocardial ablation and have a
134 Dresen & Ferguson
suspected epicardial focus, such as those with
arrhythmogenic right ventricular cardiomyopathy
and certain nonischemic cardiomyopathies,
epicardial VT ablation may increase success rates
up to 63% to 78%.25–28 Although epicardial VT foci
are seen in ischemic disease, success rates of
epicardial ablation thus far have been lower in
this patient population.29
Secondary to the effects of the autonomic ner-
vous system on arrhythmia propagation and main-
tenance, neuromodulation through cardiac
sympathetic denervation is an alternative therapy
for refractory VT as well as in patients with cate-
cholaminergic polymorphic VT and LQTS. The
procedure involves partial removal of either the
left or bilateral stellate ganglion in addition to the
T2 to T4 sympathetic ganglia. In patients with VT
storm or VT refractory to medications and ablation,
a significant reduction in ICD shocks as well as a
50% freedom from ICD shocks at 1 year was
seen with sympathetic denervation.30 Additional
alternative interventional techniques for refractory
VT, including simultaneous unipolar ablation, bipo-
lar ablation, alcohol ablation, thoracic epidural
anesthesia, and other surgical approaches exist
when conventional therapies have failed, although
the experience remains limited to highly special-
ized centers.24
In the absence of an acutely reversible cause or
an idiopathic VT, an ICD is clinically indicated
owing to its proven mortality benefit in the majority
of patients with sustained VT and structural heart
disease. However, given the potential deleterious
effects of ICD placement, specifically inappro-
priate shocks and the risk of infection, proper pa-
tient selection is necessary.
 Beta-blockers are a mainstay of chronic ther-
apy and, although other antiarrhythmic agents
may be used, they have not shown any mor-
tality benefit.
 VT ablation can be successful in appropriately
selected patients, but recurrence remains
common.
 ICDs have a proven mortality benefit and are
indicated in most patients with VT and struc-
tural heart disease.
VENTRICULAR ARRHYTHMIA IN PATIENTS
WITH IMPLANTABLE CARDIOVERTER-
DEFIBRILLATORS
Between 1993 and 2008, 1.1 million ICDs were
implanted in the United States.31 The prevalence
of patients with ICDs is steadily increasing and is
related to an aging population and expanding indi-
cations for an ICD. The growing number of patients
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with ICDs has transformed the management of
ventricular arrhythmia and a sound approach to
the management of patients with ICDs presenting
to the ED is important. Not only are data from the
ICD interrogation helpful in improving the diag-
nostic accuracy of ventricular arrhythmia, but the
pacing, sensing, and detection algorithms are
crucial in both their immediate and definitive
management.
Recognizing the Implantable Cardioverter-
Defibrillator
Most ICDs are implanted in the left prepectoral re-
gion and are easily palpable. The generator and
leads are also identifiable on chest radiographs.
Subcutaneous ICDs are increasingly used in pa-
tients without a pacing indication. They are posi-
tioned in the left axilla and have a totally
subcutaneous shocking lead traversing the left
chest wall and tracking up to the high sternum
(Fig. 3). Most ICD patients carry a card with the
ICD manufacturer and model, implant date, and
implanting electrophysiologist.
Symptoms of Ventricular Arrhythmia in
Patients with Implantable Cardioverter-
Defibrillators
 ICD shock: described as a ‘thump’ or ‘kick’ in
the chest. There may be preceding palpita-
tions, dizziness, or chest pain depending on
the rate and duration of tachycardia.
 Palpitations: may arise from tachycardia at a
rate below the detection zone, from nonsus-
tained arrhythmias or successful antitachy-
cardia pacing.
 Dizziness or syncope.
 Chest pain.
 ICD alarms: can be programmed to signal
arrhythmia or abnormal battery and lead pa-
rameters. Alarms are usually a beeping tone
with an accompanying vibration.
Implantable Cardioverter-Defibrillator
Interrogation and Interpretation
Patients with an ICD who present to the ED with
symptoms to suggest ventricular arrhythmia
should have their device interrogated. In addition
to information regarding VT/VF, the device may
show details regarding atrial arrhythmia and
heart failure. Arrhythmia logs provide the date,
duration, rate, and therapies of each episode,
and it is useful to correlate this information
with patient symptoms. In addition, a review
of the electrogram details are helpful to
determine the arrhythmia subtype and subse-
quent management. Before closing down the
 Ventricular Arrhythmias 135

Fig. 3. Anteroposterior and lateral chest radiographs of a conventional transvenous implantable cardioverter-
defibrillator (ICD) (A) and subcutaneous ICD (B).

programmer, it is crucial to confirm that thera-
pies have not been inadvertently disabled but
remain on.
Appropriate Implantable Cardioverter-
Defibrillator Therapies
VT or VF is detected when a tachycardia meets the
detection criteria in a programmed tachycardia
zone. Typical criteria for VT include a ventricular
rate of greater than 162 bpm that is sustained for
a minimum duration (usually 12–20 beats). There
may be programmed discriminators to distinguish
VT from SVT, such as a sudden onset, a ventricular
rate greater than the atrial rate, a stable cycle
length (typically <40 ms variation of an RR interval
to exclude atrial fibrillation), and a QRS
morphology different from baseline. When all
criteria are met, VT is confirmed and therapy,
including antitachycardia pacing or shocks, are
then delivered (Figs. 4 and 5).
ICD therapy is considered appropriate if it is deliv-
ered for true VT/VF and not SVT or electrical artifact.
 In patients with 1 or 2 shocks delivered over a
short period (seconds to minutes) and without
persistent symptoms, the ICD can safely be
interrogated the following day in the cardiol-
ogy office.
 If 2 or more shocks occur over minutes to
hours, patients are advised to go to the ED
for immediate evaluation. These patients
should be screened for ischemia, electrolyte
abnormalities, and heart failure. In patients
with 2 or more shocks, an escalation in ther-
apy is usually required either with antiar-
rhythmic drugs or catheter ablation.
 In patients with rare episodes of monomor-
phic VT successfully treated with antitachy-
cardia pacing, it is often reasonable to
continue with that same antitachycardia pac-
ing alone.

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136 Dresen & Ferguson

Fig. 4. Successful antitachycardia pacing (ATP) for sustained ventricular tachycardia (VT). These electrograms are
from a single chamber implantable cardioverter-defibrillator (ICD). Note the initial onset of nonsustained VT (A),
becoming sustained and more regular VT (B), which is detected as VT (note the denotation of ‘T’ in the marker
channel), 8 beats of ATP are delivered (C), and the VT is terminated to slow atrial fibrillation (D). The near field
electrogram is between the distal bipole of the ICD lead. The far-field electrogram is between the shocking coil in
the right ventricle and the ICD can in the left precordial position. The far-field electrogram is similar to lead III of
a 12-lead electrocardiograph. Note that the VT after the ‘B’ is somewhat irregular with cycle lengths ranging from
305 to 328 ms. The stability criteria for detection of VT on many ICDs is 30 to 40 ms and thus this irregular VT
meets criteria for a stable cycle length. ATP may be felt as palpitations or dizziness, but can also be completely
asymptomatic. Although this VT was asymptomatic, it was one of many episodes of VT within 48 hours despite
amiodarone therapy, and the patient was referred for catheter ablation.

Inappropriate Implantable Cardioverter- discriminators are enabled, adding atrioven-

Defibrillator Therapies
Inappropriate shocks or antitachycardia pacing
are delivered when SVT, atrial fibrillation, or electri-
cal interference is spuriously classified as VT/VF
and programmed therapy is delivered. Inappro-
priate therapy is most commonly from sinus tachy-
cardia and atrial fibrillation with high rates, often
greater than 180 bpm. Shock therapy during sinus
tachycardia paradoxically results in an increased
heart rate and ongoing sinus tachycardia can
result in multiple inappropriate shocks.
 Rapid inhibition of further inappropriate
shocks can be achieved by placing a magnet
over the device, which disables therapies until
definitive programming changes can be
made. Such patients should be connected to
telemetry and an external defibrillator.
 Ultimately, shocks from SVT with rapid rates
can be prevented by increasing the
arrhythmia detection rates, ensuring the SVT
tricular nodal blocking drugs or performing
atrioventricular nodal ablation.
Electrical Storm
Electrical storm is defined as 3 or more shocks
delivered in a 24-hour period. Between 20% and
40% of patients with an ICD experience an electri-
cal storm.32 The source of multiple shocks can be
recurrence of arrhythmia or, less commonly, elec-
trical artifact such as lead fracture or electromag-
netic interference (Fig. 6). ICDs are usually
programmed to deliver a maximum of 6 shocks
for a single episode of VT before therapies are
considered exhausted and ineffective. If shocks
are effective in terminating tachycardia and there
is a subsequent recurrence of arrhythmia outside
the redetection window, a new episode of VT is
declared and another 6 shocks may be delivered.
Thus, for recurrences of VT, patients can receive
multiple shocks in a short time, even to the extent
of ICD battery depletion, which may result in a

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 Ventricular Arrhythmias 137

Fig. 5. Failed antitachycardia pacing (ATP) followed by a successful implantable cardioverter-defibrillator (ICD)
shock. Note the regular tachycardia before attempted ATP (A). The marker of ‘F’ denotes the tachycardia is in
the ventricular fibrillation (VF) zone with a cycle length of approximately 280 ms. Twelve beats of ATP are deliv-
ered (A), but this fails to terminate the ventricular tachycardia (VT) (B). ATP is commonly programmed in the VF
zone and is often delivered during charging to attempt painless termination of fast VT. Given the ongoing tachy-
cardia in the VF zone the ICD then proceeds to deliver a 36-J shock (C). This successfully restores sinus rhythm.

posttraumatic stress syndrome. Every effort
should be made to prevent recurrent shocks
using antiarrhythmic drugs, magnet application,
device reprogramming, and occasionally general
anesthesia when ongoing device therapies are
required.
Miscellaneous Issues in Implantable
Cardioverter-Defibrillator Management
 Patients may experience symptoms of palpi-
tations or syncope with no corresponding
arrhythmia on ICD interrogation. This may be
related to tachycardia below the detection
zones and reprogramming of the rate, adding
a monitor zone or ECG monitoring may be
required.
 Some patients, particularly those who have
had prior ICD shocks, may experience the
sensation of an ICD shock without ICD
arrhythmia detection or delivered therapy.
These symptoms have been termed phantom
shocks.
 Both antitachycardia pacing and shock ther-
apy can be delivered manually via the pro-
grammer in patients who have tachycardia
below the programmed zones when more
aggressive therapy is required.
 ICD shocks are painful and can cause signifi-
cant distress and even posttraumatic stress

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138 Dresen & Ferguson

Fig. 6. Implantable cardioverter-defibrillator (ICD) shock for electrical interference. This patient presented to the
emergency department after receiving a shock when climbing the steel ladder out of his swimming pool. Inter-
rogation of this single chamber ICD showed electrical interference (A) with no increase in the ventricular rate.
This interference was detected as ventricular fibrillation resulting in a 35-J shock (B) with no change in the heart
rate. The device responded appropriately and electrical testing showed an electrical short in the pool pump,
which was repaired.

disorder. Efforts to prevent recurrent shocks
and, occasionally, sedation to avoid aware-
ness of recurrent shocks should be instituted
as soon as possible.33
 Patients evaluated for arrhythmia and ICD
therapies require follow-up with their electro-
physiologist for long-term management.
Most ICD patients are seen at least every
6 months and generally with remote moni-
toring during the intervening period.
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