# 20 - 259 Approach to Ventricular Arrhythmias

### 259 Approach to Ventricular Arrhythmias

TABLE 258-3  Recommendations for Catheter Ablation in Patients with 
Atrial Fibrillation (AF)
LEVEL OF 
EVIDENCE
RECOMMENDATIONS
CLASS

A
In patients with symptomatic AF in whom antiarrhythmic 
drugs have been ineffective, contraindicated, not 
tolerated or not preferred, and continued rhythm 
control is desired, catheter ablation is useful to improve 
symptoms.
PART 6
Disorders of the Cardiovascular System

A
In selected patients (generally younger with few 
comorbidities) with symptomatic paroxysmal AF in whom 
rhythm control is desired, catheter ablation is useful 
as first-line therapy to improve symptoms and reduce 
progression to persistent AF.

A
In patients with symptomatic or clinically significant atrial 
flutter, catheter ablation is useful for improving symptoms.
2a
B
In patients who are undergoing ablation for AF, ablation 
of additional clinically significant supraventricular 
arrhythmias can be useful to reduce the likelihood of 
future arrhythmia.
2a
B
In patients (other than younger with few comorbidities) 
with symptomatic paroxysmal or persistent AF who are 
being managed with a rhythm-control strategy, catheter 
ablation as first-line therapy can be useful to improve 
symptoms.
Source: Reproduced with permission from JA Joglar et al: 2023 ACC/AHA/ACCP/
HRS Guideline for the Diagnosis and Management of Atrial Fibrillation: A report of 
the American College of Cardiology/American Heart Association Joint Committee on 
Clinical Practice Guidelines. J Am Coll Cardiol 83:109, 2024.
of atrioesophageal fistula is important because delayed diagnosis 
leads to likely death. Diagnosis is made by chest CT scan with 
water-soluble oral and IV contrast. Endoscopy should be avoided 
in patients with a suspected fistula because of the risk of air/
esophageal fluid embolus. Definitive repair of the atrioesophageal 
fistula with emergent surgery is required. Pulsed-field ablation 
is associated with a significantly reduced risk of pulmonary vein 
stenosis, phrenic nerve injury, and left atrial esophageal fistula.
Surgical ablation of AF is most frequently performed concomitant 
with cardiac valve or coronary artery surgery and less commonly as 
a stand-alone procedure. There is no significant difference in the rate 
of freedom from AF between patients who undergo pulmonary vein 
isolation and those who undergo the biatrial maze procedure.
However, for patients with persistent AF, surgical or hybrid pro­
cedures (a combination of a surgical and catheter-based approach, 
most often in separate procedures) appear to have comparable effi­
cacy to catheter ablation. Risks include sinus node injury requiring 
pacemaker implantation and higher morbidity with surgical abla­
tion. Surgical removal of the left atrial appendage may reduce stroke 
risk, although thrombus can form in the remnant of the appendage 
or if the appendage is not completely ligated.
RISK FACTORS FOR AND LIFESTYLE 
IMPACT ON ATRIAL FIBRILLATION
There is strong evidence that AF is associated with a sedentary lifestyle, 
obesity, hypertension, smoking, alcohol use, and sleep apnea. Aggres­
sive treatment of these risk factors can substantially reduce AF episodes 
in some patients and is warranted in all patients, as additional benefits 
to the patient are likely beyond AF improvement. The amount of exer­
cise appears to have a complex relationship with the risk of AF develop­
ment. In males, a U-shaped curve exists, where AF risk is high among 
those with sedentary lifestyles and those who participate extensively in 
endurance athletics such as long-distance running or cycling. Moder­
ate exercise appears to confer a lower risk of AF. On the other hand, in 
females, a linear relationship exists between exercise and AF risk, with 
risk of AF decreasing continuously with increasing exercise activity. 
Although caffeine intake is often invoked as a risk for AF development 
or as a trigger for AF episodes in patients with a known AF diagnosis, 
large cohort studies have demonstrated, in contrast, a modest decrease 
in AF risk with modest caffeine intake. Other proposed risk factors are 

being evaluated, including psychological stress. Genetic predisposition 
to AF is seen in those with first-degree relatives with AF, and a small 
subset of AF patients can be determined have a familial form of AF.
There is emerging emphasis on an integrated approach to manage­
ment of AF patients, with coordinated management of risk factor 
modification, stroke prevention, rate control, rhythm control, and 
management of associated comorbidities of critical importance. The 
previous classification of AF, which was based only on arrhythmia 
duration (i.e., paroxysmal, persistent, and long-standing persistent), 
although useful, tended to emphasize therapeutic interventions. A 
more recent classification using four stages (i.e., at risk of AF, pre-AF, 
AF, and permanent AF) has been proposed and recognizes AF as a 
disease continuum that requires a variety of strategies at the different 
stages, including prevention, lifestyle and risk factor modification, 
screening, and therapy.
■
■FURTHER READING
Joglar JA et al: 2023 ACC/AHA/ACCP/HRS Guideline for the 
Diagnosis and Management of Atrial Fibrillation: A report of the 
American College of Cardiology/American Heart Association Joint 
Committee on Clinical Practice Guidelines. J Am Coll Cardiol 
83:109, 2024.
Packer DL et al: Effect of catheter ablation vs antiarrhythmic drug 
therapy on mortality, stroke, bleeding, and cardiac arrest among 
patients with atrial fibrillation: The CABANA randomized clinical 
trial. JAMA 321:1261, 2019.
William H. Sauer, Usha B. Tedrow

Approach to Ventricular 
Arrhythmias
There are myriad types of ventricular arrhythmias (VAs), ranging from 
benign to life-threatening, occurring both in patients with normal 
hearts and in those with structural heart disease. An understanding 
of an approach to these arrhythmias is critical to being appropriately 
parsimonious with benign forms, while understanding timely workup 
and management of the malignant forms.
TYPES OF VAs
VAs can arise from focal sites of origin or from reentrant circuits. Focal 
VAs can originate from myocardial or specialized Purkinje cells capa­
ble of automaticity or triggered activity. Reentrant VAs often involve 
areas of scar such as old myocardial infarction or a cardiomyopathic 
process. Less commonly, diseased Purkinje conduction pathways can 
also result in reentrant circuits. VAs are characterized by their electro­
cardiographic appearance and duration. Conduction away from the 
ventricular focus or reentrant circuit exit, propagating through the ven­
tricular myocardium, is slower than activation of the ventricles over the 
normal Purkinje system. For this reason, the QRS complex duration 
during VAs will be wide, typically >0.12 s, though there are unusual 
situations that can arise with narrow QRS duration as well.
Premature ventricular beats (also referred to as a premature ventricular 
contractions or premature ventricular complexes [PVCs]) are single ven­
tricular beats that occur earlier than the next anticipated supraventricu­
lar beat (Fig. 259-1). PVCs that originate from the same focus will have 
the same QRS morphology and are referred to as unifocal (Fig. 259-1A). 
PVCs that originate from different ventricular sites have different QRS 
morphologies and are referred to as multifocal (Fig. 259-1B). Two con­
secutive ventricular beats are ventricular couplets.
Ventricular tachycardia (VT) is three or more consecutive beats at 
a rate faster than 100 beats/min. Three or more consecutive beats at

1000 ms
I
Art. Pr.
A 
B
C
FIGURE 259-1  A. Unifocal premature ventricular contractions (PVCs) at bigeminal frequency. Trace shows electrocardiogram lead 1 and arterial pressure (Art. Pr.). Sinus 
rhythm beats are followed by normal arterial waveform. The arterial pressure following premature beats is attenuated (arrows) and imperceptible to palpation. The pulse 
in this patient is registered at half the heart rate. B. Multifocal PVCs. The two PVCs shown have different morphologies. C. Example of accelerated idioventricular rhythm. 
(See text for details.)
slower rates are designated an idioventricular rhythm. VT that termi­
nates spontaneously within 30 s is designated nonsustained, whereas 
sustained VT persists for >30 s or is terminated by an active interven­
tion, such as administration of an intravenous medication, external 
I
II
aVR
V1
V4
aVL
III
aVF
V1
II
FIGURE 259-2  Repetitive monomorphic nonsustained ventricular tachycardia (VT) of right ventricular outflow tract origin. The VT has a left bundle branch block pattern 
with inferior axis with tall QRS complexes in the inferior leads.

CHAPTER 259
Approach to Ventricular Arrhythmias
cardioversion, antitachycardia pacing, or a shock from an implanted 
cardioverter-defibrillator (Fig. 259-2).
Monomorphic VT has the same QRS complex from beat to beat, 
indicating that the activation sequence is the same from beat to beat 
V5
V2
V3
V6

and that each beat likely originates from the same source (Fig. 259-3A). 
The initial site of ventricular activation largely determines the sequence 
of ventricular activation. Therefore, the QRS morphology of PVCs and 
monomorphic VT provides an indication of the site of origin within 
the ventricles (Fig. 259-4). The likely origin often suggests whether an 
arrhythmia is idiopathic or associated with structural disease. Arrhyth­
mias that originate from the right ventricle or septum result in late 
activation of much of the left ventricle, thereby producing a prominent 
S wave in V1 referred to as a left bundle branch block–like configura­
tion. Arrhythmias that originate from the free wall of the left ventricle 
have a prominent positive deflection in V1, thereby producing a right 
bundle branch block–like morphology in V1. The frontal plane axis of 
the QRS is also useful. An axis that is directed inferiorly, as indicated by 
dominant R waves in leads II, III, and AVF, suggests initial activation 
of the cranial portion of the ventricle, whereas a frontal plane axis that 
is directed superiorly (dominant S waves in II, III, and AVF) suggests 
initial activation at the inferior wall.

PART 6
Disorders of the Cardiovascular System
Very rapid monomorphic VT has a sinusoidal appearance, also called 
ventricular flutter, because it is not possible to distinguish the QRS com­
plex from the T wave (Fig. 259-3B). Relatively slow sinusoidal VTs have 
a wide QRS indicative of slowed ventricular conduction (Fig. 259-3C). 
Hyperkalemia, toxicity from excessive effects of drugs that block sodium 
channels (e.g., flecainide, propafenone, or tricyclic antidepressants), and 
severe global myocardial ischemia are possible causes.
Polymorphic VT has a continually changing QRS morphology indi­
cating a changing ventricular activation sequence. Polymorphic VT 
that occurs in the context of congenital or acquired prolongation of the 
QT interval often has a waxing and waning QRS amplitude, creating a 
characteristic shifting axis referred to as torsades des pointes after the 
classic ballet sequence (Fig. 259-3D).
Ventricular fibrillation (VF) has continuous irregular activation with 
no discrete QRS complexes. Monomorphic or polymorphic VT may 
transition to VF in susceptible patients. Cardiac ischemia is the most 
common cause of VF (Fig. 259-3E).
The term idiopathic ventricular arrhythmia generally refers to PVCs 
or VT that occurs in patients with a normal electrocardiogram (ECG), 
without structural heart disease, and not associated with an underlying 
genetic syndrome or risk of sudden death.
CLINICAL MANIFESTATIONS
Common symptoms of VAs include palpitations, dizziness, exercise 
intolerance, episodes of lightheadedness, syncope, or sudden cardiac 
arrest leading to sudden death if not resuscitated. VAs can also be 
asymptomatic and encountered unexpectedly as an irregular pulse or 
heart sounds on examination or may be seen on a routine ECG, exer­
cise test, or cardiac ECG monitoring. Occasionally when every other 
beat is a PVC (bigeminy), pulse measurements for heart rate can be 
erroneously low (pseudobradycardia) because the PVCs may not gener­
ate a separate pulse wave.
Syncope is a concerning symptom, particularly when occurring 
without prodrome, during exercise, or in the setting of abnormal ECG 
or structural heart disease. Such episodes can be due to VT that pro­
duces severe hypotension, warranting concern for risk of cardiac arrest 
and sudden death with arrhythmia recurrence. Although benign pro­
cesses such as reflex-mediated neurocardiogenic (vasovagal) episodes 
and orthostatic hypotension are the most common causes of syncope, 
it is important to consider the possibility of underlying heart disease or 
a genetic syndrome causing VT. When these are suspected, hospitaliza­
tion for further evaluation and monitoring is often appropriate.
Sustained VT may present as a wide QRS complex tachycardia 
that must be distinguished from supraventricular tachycardia with 
aberrancy (Chap. 253). Symptoms can be minor but more commonly 
include hypotension with syncope and even imminent cardiac arrest, 
particularly in patients with structural heart disease. Sustained VT may 
degenerate to VF, most commonly if it is rapid and polymorphic. Many 
patients who are at risk for VT have known heart disease, and many 
have an implantable cardioverter-defibrillator (ICD). In patients with 
an ICD, VT episodes may cause transient lightheadedness, palpitations, 
or syncope followed by a shock from the ICD (see below).

A
B
C
D
E
FIGURE 259-3  A. Monomorphic ventricular tachycardia (VT) with dissociated 
P waves (short arrows). B. Ventricular flutter. C. Sinusoidal VT due to electrolyte 
disturbance or drug effects. D. Polymorphic VT resulting from prolongation of QT 
interval (torsade de pointe VT). E. Ventricular fibrillation. (See text for details.)
EVALUATION OF PATIENTS WITH 
DOCUMENTED OR SUSPECTED 
VENTRICULAR ARRHYTHMIAS
There are several important considerations that guide evaluation of 
patients with documented or suspected cardiac arrhythmias. First, 
establish whether a VA is the cause of the symptoms or clinical presen­
tation. Second, determine whether the arrhythmia is associated with a 
cardiac disease, and establish the prognostic significance of that disease 
and, in particular, whether it is associated with a risk of sudden cardiac 
death. Finally, define the likelihood of arrhythmia recurrence and the 
symptoms and risk imposed by the recurrence. The risks of cardiac 
arrest and sudden cardiac death are largely determined by the cause of 
the arrhythmia and the associated underlying heart disease.
The diagnosis of VAs can be established by recording the arrhythmia 
on an ECG, by an ambulatory or implanted cardiac monitor, by an 
implanted rhythm management device such as a pacemaker or ICD, or 
in some cases, initiation of the arrhythmia during an electrophysiologic

II
III
II, III AVF = Inferior axis
superior origin
LV
RV
V1 = LBBB
Septal or RV origin
V1 = RBBB
LV origin
II
III
II, III AVF = Superior axis
inferior origin
FIGURE 259-4  Site of ventricular tachycardia origin based on QRS morphology. (See text for details.) 
LBBB, left bundle branch block; LV, left ventricle; RBBB, right bundle branch block; RV, right ventricle.
study. A 12-lead ECG of the arrhythmia should be obtained when pos­
sible and often provides clues to the potential site of origin and possible 
presence of underlying heart disease (see above) (Fig. 259-4).
For patients with sustained wide-complex tachycardia, initial man­
agement is guided by the patient’s hemodynamic stability. The approach 
to sustained wide-complex tachycardia is discussed in Chap. 261. The 
management of VT that causes cardiac arrest is discussed in Chap. 317. 
Once hemodynamic stability is restored, further management is guided 
by the possibility of a recurrence and the risk imposed by a recurrence.
■
■EVALUATION OF THE PATIENT WITH 
ARRHYTHMIA SYMPTOMS
When symptoms are intermittent, initial evaluation aims to establish 
symptom severity, provocative factors, and presence of underlying 
heart disease. Syncope or near syncope raises concern that an arrhyth­
mia is causing episodes of hypotension and that there may be a risk of 
cardiac arrest. Symptoms that occur with exertion suggest arrhythmias 
that are provoked by sympathetic stimulation but can also be related to 
exertional ischemia in patients with coronary artery disease, although 
nonarrhythmia causes must also be considered. A past history of any 
cardiac disease is important. A review of all medications is relevant. 
Medications that prolong the QT interval predispose to polymorphic 
VT (Chap. 262). Adrenergic stimulants can provoke PVCs.
Family history should determine the presence of premature coro­
nary artery disease, cardiomyopathy, or cardiac arrhythmias, particu­
larly a history of sudden death. Family history may also suggest that 
the possibility of a genetic cause of an arrhythmia warrants careful 
consideration. Details of premature deaths are relevant. Sudden death 
victims are often said to have died of a “massive heart attack” despite 
absence of definite confirmation of thrombotic myocardial infarction 
and when other causes such as arrhythmia may have been possible.
The physical examination focuses on evidence of structural heart 
disease with assessment of pulse, jugular venous pressure lung fields, 
and cardiac auscultation. Stigmata of neuromuscular disease or dys­
morphic features may suggest a genetic arrhythmia syndrome.

A 12-lead ECG should be obtained even if the 
patient is not having symptoms at the time of 
evaluation. Occasionally, premature ventricular con­
tractions will be detected. Patients with benign idio­
pathic arrhythmias usually have a completely normal 
ECG during sinus rhythm. Any ECG abnormality 
warrants further evaluation. Particularly relevant 
findings include Q waves that indicate prior myo­
cardial infarction, which may have been silent, and 
ventricular hypertrophy, which may indicate hyper­
trophic cardiomyopathy or other ventricular disease. 
An ECG finding is the major diagnostic manifesta­
tion of several genetic arrhythmia syndromes in 
patients without structural heart disease, including 
the long QT syndrome, Brugada syndrome, and 
short QT syndrome.

CHAPTER 259
Approach to Ventricular Arrhythmias
V1
If there is suspicion of structural heart disease, 
cardiac imaging is warranted to assess ventricu­
lar function and structure. Transthoracic echocar­
diography is most frequently employed for initial 
evaluation. Depressed ventricular function increases 
concern for a risk of sudden death and warrants fur­
ther evaluation to establish the cause, which may be 
cardiomyopathy, coronary artery disease, or valvular 
heart disease. Ventricular thickening may indicate 
hypertrophic cardiomyopathy or infiltrative diseases 
such as amyloidosis. Cardiac magnetic resonance 
imaging with gadolinium contrast imaging provides 
similar assessment but also can detect areas of ven­
tricular scar, evident as regions of delayed hyper­
enhancement, which are usually present in patients 
who have sustained monomorphic VT (Fig. 259-5). 
The nature and location of abnormalities are helpful 
in assessing the type of heart disease. Evaluation to 
exclude atherosclerotic coronary artery disease should be performed 
in patients at risk, guided by age and other risk factors.
■
■TREATMENT OPTIONS FOR VENTRICULAR 
ARRHYTHMIAS
Treatment of VAs is guided by the severity and frequency of symptoms. 
For those with structurally normal hearts and normal ECGs, reassur­
ance and removal of aggravating factors (e.g., caffeine or alcohol) may 
be all that is needed. For arrhythmias associated with a sudden death 
risk, ICD implantation is usually indicated and will provide a “safety 
net” to terminate life-threatening VT or VF, preventing sudden death 
but without preventing the arrhythmia. When suppression of the 
arrhythmia is required, antiarrhythmic drug therapy or catheter abla­
tion is a major consideration.
■
■ANTIARRHYTHMIC DRUGS
Use of antiarrhythmic drugs is based on consideration of the risks and 
potential benefit for the individual patient. Efficacy and side effects for 
the individual patient are not always predictable and are assessed by 
individual therapeutic trial. Causes of drug intolerance are mostly non­
cardiac and minor but can sometimes be severe enough to limit their 
use. Cardiac adverse events, however, include the potential for “proar­
rhythmia,” whereby a drug can increase the frequency of arrhythmia 
or cause a new arrhythmia. Aggravation of bradyarrhythmias is also a 
common concern. Although antiarrhythmic drugs are classified based 
on their actions on receptors or ion channels, most have multiple 
effects, affecting more than one channel.
■
■a-ADRENERGIC BLOCKERS
Many VAs are sensitive to sympathetic stimulation, and β-adrenergic 
stimulation may also interact with the electrophysiologic effects of 
many membrane-active antiarrhythmic drugs. The safety of β-blocking 
agents makes them the first choice of therapy for most VAs. β-Blockers 
are particularly useful for exercise-induced arrhythmias and idiopathic 
arrhythmias but have limited efficacy for most arrhythmias associated

PART 6
Disorders of the Cardiovascular System
FIGURE 259-5  Imaging studies of the left ventricle (LV) used to assist ablation for ventricular tachycardia (VT). Left panel is a magnetic resonance image of a longitudinal 
section demonstrating thinning of the anterior wall and late gadolinium enhancement in a subendocardial scar (white arrows). The middle panel shows a two-dimensional 
image of the LV in long axis corresponding to the sector through the mid-LV (arrow in figure on right panel) obtained by an intracardiac echocardiography probe positioned 
in the right ventricle. An electroanatomic three-dimensional map of the LV in the left anterior oblique projection is displayed in the right panel. The purple areas depict areas 
of normal voltage (>1.5 mV). Blue, green, and yellow represent progressively lower voltages, with the red areas indicating scar (<0.5 mV). Channels of viable myocardium 
with slow conduction within the scar are identified with the light blue dots. Areas of ablation delivered to regions involved in reentrant VT are indicated by maroon dots.
with heart disease. Bradyarrhythmias and negative inotropic effects are 
the major cardiac adverse effects.
■
■CALCIUM CHANNEL BLOCKERS
The nondihydropyridine calcium channel blockers diltiazem and vera­
pamil can be effective for some idiopathic VTs. The risk of proarrhyth­
mia is low, but they have negative inotropic and vasodilatory effects 
that can aggravate hypotension.
■
■SODIUM CHANNEL–BLOCKING AGENTS
Drugs whose major effect is mediated through sodium channel 
blockade include mexiletine, quinidine, disopyramide, flecainide, and 
propafenone, which are available for chronic oral therapy. Blockade 
of the fast inward sodium current has been referred to as a class I 
antiarrhythmic drug effect. Antiarrhythmic actions are the result of 
depressing cardiac conduction and membrane excitability. Conduction 
slowing can be manifest as a prolongation of QRS duration. Lidocaine, 
quinidine, and procainamide are available as intravenous formula­
tions. Quinidine, disopyramide, and procainamide also have potas­
sium channel–blocking effects that may prolong the QT interval (class 
III antiarrhythmic drug action), contributing to their antiarrhythmic 
effect. Quinidine also blocks a particular potassium current, Ito, the 
blockade of which can be important in Brugada syndrome. These 
agents have potential proarrhythmic effects and, with the possible 
exception of quinidine, also have negative inotropic effects that may 
have contributed to the increased mortality observed when some were 
administered chronically to patients with prior myocardial infarction. 
Long-term therapy is generally avoided in patients with structural 
heart disease but may be used to reduce symptomatic arrhythmias in 
patients with ICDs.
■
■POTASSIUM CHANNEL BLOCKING AGENTS
Sotalol and dofetilide block the delayed rectifier potassium channel 
IKr, thereby prolonging action potential duration (QT interval) and the 
cardiac refractory period, known as the class III antiarrhythmic drug 
effect. Sotalol also has nonselective β-adrenergic–blocking activity. It 
has been shown to have a modest effect on reducing ICD shocks due 
to ventricular and atrial arrhythmias. Proarrhythmia due to the poly­
morphic VT torsade de pointe that is associated with QT prolongation 
occurs in 3–5% of patients. Both sotalol and dofetilide are excreted 
via the kidneys, necessitating dose adjustment or avoidance in renal 
insufficiency. These drugs must be avoided in patients with other 
risk factors for torsades de pointes, including QT prolongation, other 
administered medications that prolong the QT interval, hypokalemia, 
and significant bradycardia.
■
■AMIODARONE
Amiodarone blocks multiple cardiac ionic currents and has sym­
patholytic activity. It is the most effective antiarrhythmic drug for 
suppressing VAs. It is administered intravenously for life-threatening 

arrhythmias. During chronic oral therapy, electrophysiologic effects 
develop over several days. It is more effective than sotalol in reducing 
ICD shocks and is often used for VAs in patients with heart disease. 
Bradyarrhythmias are the major cardiac adverse effect. Ventricular 
proarrhythmia can occur, but torsades de pointes VT is rare. Noncar­
diac toxicities are a major problem and contribute to drug discontinua­
tion in at least a third of patients during long-term therapy. Hyper- and 
hypothyroidism are related to the iodine content of the drug. Pneumo­
nitis or pulmonary fibrosis occurs in ~1% of patients. Photosensitivity 
is common, and neuropathy and ocular toxicity can occur. Systematic 
monitoring is recommended during chronic therapy including assess­
ment for thyroid, liver, and pulmonary toxicity. Intravenous adminis­
tration of amiodarone via a peripheral vein for >24 h can cause severe 
peripheral thrombophlebitis. Dronedarone has structural similarities 
to amiodarone but without the iodine moiety. Efficacy for VAs is poor, 
and dronedarone increases mortality in patients with heart failure, so 
dronedarone is not typically used for treatment of VAs.
■
■IMPLANTABLE CARDIOVERTER-DEFIBRILLATORS
ICDs detect sustained VT, largely based on heart rate, and then ter­
minate the arrhythmia. In transvenous devices, VF is terminated by a 
shock applied between a lead in the right ventricle and the ICD pulse 
generator. The lead can provide pacing for bradycardia if needed. This 
transvenous form of ICD has the disadvantages of vascular occlusion, 
risk of lead fracture, endocarditis in the event of infection, and dif­
ficulty with removal. Monomorphic VT can also be terminated by a 
burst of rapid pacing faster than the VT, known as antitachycardia 
pacing (ATP) (Fig. 259-6A). If ATP fails or is not a programmed 
treatment, as is often the case for rapid VT or VF, a shock is deliv­
ered (Fig. 259-6B). ICDs can also be subcutaneous or extravascular, 
without a transvenous lead. The rhythm is also sensed by this lead, in 
a manner similar to a surface ECG. The lead is placed overlying the 
left chest with a coil parallel and next to or underneath the sternum. 
No matter the type of ICD, shocks are uncomfortable and distressing 
if the patient is conscious, sometimes leading to a posttraumatic stress 
disorder (PTSD). The most common ICD complication is the delivery 
of unnecessary therapy (either ATP or shocks) in response to an inap­
propriately detected rapid supraventricular tachycardia or electrical 
noise as a result of an ICD lead fracture or electromagnetic interference 
from an external source. ICDs record and store electrograms from 
arrhythmia episodes that can be retrieved by interrogation of the ICD, 
which can be performed remotely and communicated via the internet. 
This assessment is critical after an ICD shock to determine the arrhyth­
mia diagnosis and exclude unnecessary therapy. Device infection is an 
important problem long term and occurs in ~1% of patients. This risk 
may be less for subcutaneous or extravascular implants.
ICDs decrease mortality in patients at risk for sudden death due to 
structural heart diseases. In all cases, ICDs are recommended only if 
there is also an expectation for survival of at least a year with acceptable

A
Anti-tachycardia pacing
B
ICD shock
FIGURE 259-6  Implantable cardioverter-defibrillator (ICD) and therapies for ventricular arrhythmias. A. A monomorphic ventricular tachycardia (VT) is terminated by a 
burst of pacing impulses at a rate faster than VT (antitachycardia pacing). B. A rapid VT is converted with a high-voltage shock (arrow). The chest x-ray in the panel C shows 
the components of an ICD capable of biventricular pacing (yellow arrows). ICD generator in the subcutaneous tissue of the left upper chest, pacing leads in the right atrium 
and the left ventricular (LV) branch of the coronary sinus (LV lead), and a pacing/defibrillating lead in the right ventricle (RV lead) are shown.
functional capacity. The exception is in cases of patients with endstage heart disease who are awaiting cardiac transplantation outside 
the hospital or who have left bundle branch block QRS prolongation 
such that they are likely to have improvement in ventricular function 
with cardiac resynchronization therapy from a biventricular ICD or 
conduction system pacing (Fig. 259-6C). In these cases, an ICD may 
be warranted despite a guarded prognosis. A wearable ICD system with 
electrodes incorporated into a vest and an external battery pack is also 
available for short-term use in patients pending a decision regarding a 
permanent implanted system, or when a permanent system cannot be 
implanted for other reasons such as an ongoing infection.
Despite prompt termination of VT or VF by an ICD, the occur­
rence of these arrhythmias predicts subsequent increased mortality 
and risk of heart failure. Occurrence of VT or VF should therefore 
prompt assessment for potential causes including worsening heart 
failure, electrolyte abnormalities, and ischemia. Repeated shocks, even 
if appropriate, often induce posttraumatic stress disorder. Antiarrhyth­
mic drug therapy, most commonly amiodarone, or catheter ablation is 
often required for suppression of recurrent arrhythmias. Antiarrhyth­
mic drug therapy can alter the VT rate and the energy required for 
defibrillation, thereby necessitating programming changes in the ICD’s 
algorithms for detection and therapy.
■
■CATHETER ABLATION FOR VT
Catheter ablation is usually performed by applying radiofrequency 
(RF) current to cause thermal injury by resistive heating of cardiac 
tissue responsible for the arrhythmia. An electrode catheter with an 
electroanatomic mapping system is used to map local electrical activity 
to identify the ventricular myocardium that is causing the arrhythmia, 
referred to as the arrhythmia substrate. The size and location of the 
arrhythmia substrate determine the ease and likely effectiveness of the 
procedure, as well as the potential complications. When the arrhythmia 
originates from the endocardium, as is most commonly the case, it 
can be reached from an endovascular approach via a femoral vein or 
artery. Less commonly, arrhythmias originate from the subepicardium, 
and percutaneous pericardial puncture, similar to pericardiocentesis, 

CHAPTER 259
Approach to Ventricular Arrhythmias
Atrial
lead
ICD
LV
lead
RV
lead
C
is required to insert a catheter into the pericardial space for mapping 
and ablation. In patients with scar-related VT due to prior infarction 
or cardiomyopathy, ablation typically targets abnormal regions in the 
scar or region of fibrosis. Because these scars often contain multiple 
reentry circuits over relatively large regions, extensive areas of ablation 
can be required, and these areas are often identified as regions of low 
voltage displayed on electroanatomic reconstructions of the ventricle 
(Fig. 259-5).
Catheter ablation is often performed in patients with recurrent 
VAs associated with poor cardiac function, and the procedure-related 
mortality in this situation is 0.5–3%. Outcomes are better for patients 
with prior infarction and VT than for patients with nonischemic car­
diomyopathies in which the scar locations are more variable and often 
intramural or subepicardial. Ablation can be lifesaving for patients 
with very frequent or incessant VT. Methods of delivering ablative 
energy to intramural areas or areas requiring very extensive ablation 
are under development. These include needle catheters capable of 
delivering ablative energy into intramural sources, and bipolar ablation 
where radiofrequency energy is delivered across two ablation catheters. 
Stereotactic body radiation therapy (SBRT), classically used for treating 
thoracic tumors, has been used to direct radiation therapy to a specific 
portion of the scar substrate to noninvasively ablate VT with encourag­
ing early studies.
Idiopathic VTs and PVCs that occur in the absence of structural heart 
disease usually originate from a small focus, for which catheter ablation 
typically has a higher success rate for preventing recurrent arrhythmia. 
Long-term arrhythmia-free survival in these patients is excellent.
ARRHYTHMIA SURGERY
When antiarrhythmic drug therapy and catheter ablation fail or are not 
an option, surgical cryoablation, often combined with aneurysmec­
tomy, can be effective therapy for recurrent VT due to prior myocardial 
infarction and has also been used successfully in a few patients with 
nonischemic heart disease. Few centers now maintain the expertise for 
this therapy, though some use this therapy as an adjunct to ventricular 
assist device implantation.