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Cardiology: An Integrated Approach >

Chapter 9: Arrhythmias and Antiarrhythmic Drugs

Sandeep Banga; Nagib T. Chalfoun

Learning Objectives
Learning Objectives

By the end of this chapter the student will be able to:

Classify both bradyarrhythmias and tachyarrhythmias.

Identify the rhythm disorders.

Elicit the mechanisms of dysrhythmias.

Determine the best treatment modality for a specific arrhythmia.

Classify the antiarrhythmic drugs.

Describe the dosage and the mechanism of action of some antiarrhythmic drugs.

Apply the above knowledge in a clinical setting.

Introduction
The electrical activity of the heart can be a ected by disrupting the conduction system, which can lead to rhythm disorders. The cardiac arrhythmias
are classified into either bradyarrhythmias or tachyarrhythmias. Bradycardia is defined as a heart rate less than 60 beats per minute (bpm), whereas
tachycardia is defined as a heart rate greater than 100 bpm. The former includes sinus bradycardia and various degrees of atrioventricular (AV) blocks.
Tachyarrhythmias include both atrial and ventricular tachycardias.

There are many ways in which tachyarrhythmias can be classified. These can be based on the regularity of the rhythm, the site of origin of the rhythm,
the duration of the QRS complex, and the mechanisms involved in the arrhythmia. Depending on the site of origin, the tachyarrhythmias can be
classified into:

1. Atrial tachyarrhythmias

2. Ventricular tachyarrhythmias

Depending on the duration of the QRS complex, the tachyarrhythmias can be classified into:

1. Narrow QRS complex tachycardia (QRS ≤120 ms)

2. Wide QRS complex tachycardia (QRS >120 ms)

Bradyarrhythmias are treated by reversing the cause of the bradycardia or implanting a pacemaker. Tachyarrhythmias are also treated by reversing the
cause if possible, or by using medications such as antiarrhythmics or ablations.

Normal Heart Rate

The normal heartbeat originates from the sinus node, also called the natural pacemaker of the heart. The normal heartbeat rate ranges from 60 to 100
bpm. The initial impulse is generated from the sinus node, and is conducted down to the AV node, which is e ectively a “bridge” between the signals
from the atrium to the ventricles. The impulse then travels from the AV node to the His-Purkinje system and separates into the le bundle (which
activates the le ventricle) and the right bundle (which activates the right ventricle).

Normal Sinus Rhythm

The normal heart generates an impulse from the sinus node, which is regular, that is, the time interval between 2 beats (the R-R interval) is constant.
Sinus arrhythmia is also a normal impulse from the sinus node but is slightly variable due to the vagal tone. The electrocardiography (ECG) findings in
sinus rhythms or sinus arrhythmias consist of P wave morphology, in general, it is upright in leads 2/3 and aVF and biphasic in lead V1.

Sinus Arrhythmia

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The physiological variation in sinus rhythm in response to phases of the respiratory cycle can be observed in sinus arrhythmia. This variation is seen by
changes in the R-R interval during inspiration and expiration. This is commonly seen in children. Sinus arrhythmia occurs due to the changes in the
vagal tone that cause an alteration in respiration, which does not require any treatment.

CLINICAL CORRELATION 9.1

R-R interval increases during inspiration, and decreases during expiration.

Bradyarrhythmias
There are 2 main causes of bradyarrhythmias: either there is disease of the main pacemaker cells of the heart (ie, sinus node) or disease of the AV node
conduction system that serves as the main communication bridge between the sinoatrial (SA) node and the ventricle.

Diseases of the Sinus Node

1. Sinus bradycardia: Sinus bradycardia occurs when the rate of generation of impulses from the sinus node is reduced to less than 60 bpm. This can
be a normal phenomenon and is not necessarily pathologic. It is common in athletes and also occurs in states of low adrenergic tone such as during
sleep. Increased vagal tone is a common mechanism of sinus bradycardia. Medications with negative chronotropic e ects (such as β-blockers and
calcium channel blockers) are also a common cause. Asymptomatic bradycardia does not require any treatment. See Table 9.1.

2. Sick sinus syndrome: Intrinsic disease of the SA node, causes sick sinus node syndrome. Involvement can progress into the SA node itself and into
the perinodal area.

Table 9.1
Causes of bradycardia

Causes of physiological sinus bradycardia

1. High vagal tone (ie, in athletes)

2. Sleep
3. Medications such as β-blockers and calcium channel blockers
4. Hypothyroidism

Causes of pathological sinus bradycardia

1. Degenerative sinus node disease

2. Infiltrative disorders of the heart (sarcoidosis/amyloidosis)
3. Damage to the sinus node during cardiac surgery, or catheter ablation
4. Ischemic heart disease (IHD)

The following electrocardiographic types can be seen:

1. Symptomatic sinus bradycardia (Fig. 9.1)

2. Sinus pauses and sinus arrest: Sinus pauses are the cessation of the generation of impulses in the SA node (Fig 9.1)

3. Sinus node exit block: This occurs when an impulse generates normally in the sinus node but fails to conduct within the SA node or perinodal tissue
(Tables 9.2 and 9.3).

4. Tachy brady syndrome/Sick sinus syndrome: A condition that occurs when tachyarrhythmia and bradycardia alternate with each other. The
tachyarrhythmias can be atrial fibrillation, atrial flutter, or atrial tachycardia; the rapid rhythm suppresses the natural pacemaker (the SA node) and
as soon as the tachyarrhythmia terminates, the SA node tries to take over. A healthy SA node should be able to quickly resume conduction. A
diseased SA node, such as in sick sinus syndrome, may exhibit a long pause a er the termination of the rapid rhythm. A slow junctional rhythm or
sinus bradycardia may take over a er the pause.

CLINICAL CORRELATION 9.2

Sinus pauses of more than 3 seconds are an indication for a permanent pacemaker if associated with symptoms.

Figure 9.1
ECG showing sinus bradycardia with sinus pauses.

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Table 9.2
Types of sinus node exit blocks (mimics AV block classification)

Type ECG findings

First degree Normal ECG, EP study shows prolonged SACT (sinoatrial conduction time)

Second degree Type I: Progressive shortening of P-P intervals until a P wave disappears (Wenckebach pattern)
Type II: Sudden absence of one or more P waves at a regular interval from the prior P wave

Third degree or complete Absent P waves with long pauses leading to a lower pacemaker escape rhythm

For further information, see Vijayaraman P, Ellenbogen KA. Bradyarrhythmias and pacemakers. In: Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed.
New York: McGraw-Hill; 2011:chap. 43 [1].

Table 9.3
Treatment for di erent types of sinus node dysfunction

Type of sinus node dysfunction Treatment

Symptomatic sinus bradycardia Dual-chamber pacemaker

Symptomatic sinus pauses for more than 3 seconds Dual-chamber pacemaker

Sinus node exit block (third degree) Dual-chamber pacemaker

Tachy brady syndrome/sick sinus syndrome Dual-chamber pacemaker with or without antiarrhythmic drugs to treat the tachycardia component

For further information, see Epstein AE, DiMarco JP, Kenneth A, et al. ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities: a report
of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline
Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for Thoracic Surgery and Society
of Thoracic Surgeons. J Am Coll Cardiol. 2008;51:el. [2].

CLINICAL CORRELATION 9.3

Sinus node disease can present with symptoms of confusion, dizziness, fatigue, presyncope, or syncope. Syncope can present in patients with tachy
brady syndrome as a result of long pauses following the suppression of tachyarrhythmia, and hence, reduced cardiac output that a ects the blood
supply to the brain during bradycardia.

Diseases of the AV Conduction System

The AV conduction system is comprised of the AV node, the bundle of His and its le and right bundle branches. There are 3 degrees of AV blocks
depending on the extent of impaired conduction.

1. First-degree AV block: Usually, this a benign condition of the AV node. It is characterized by a prolongation in the PR interval of more than 200 msec.
The 1:1 conduction of the AV node is well preserved and one P wave corresponding to one QRS complex on the surface ECG is observed.

The causes are usually reversible. These include (1) medications (β-blockers and calcium channel blockers) that depress AV node conduction, (2)
maneuvers that increase vagal tone (eg, during sleep), (3) transient ischemia such as during angioplasty of the right coronary artery, or (4) metabolic
causes such as hyperkalemia. The PR interval will normalize as soon as the responsible factors are reversed.

The irreversible causes of a first-degree AV block include chronic sclero-degenerative disease of the AV node, myocardial injury during infarction, or
trauma during cardiac surgery or ablations.

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A first-degree AV block, in general, does not require any treatment but should be closely monitored when medications are added that can a ect the
AV node, thus increasing the first-degree AV block to a higher level of block.

2. Second-degree AV block: The next stage of an AV block when an intermittent conduction occurs. There are 2 types of second-degree AV blocks:

a. Mobitz type I is usually a benign condition of the AV node. This is characterized on the ECG by a gradual progression of the PR interval with each
beat until a QRS does not follow a P wave for a single beat (ie, a P wave without a conducted QRS). On the beat that follows, the PR interval
returns to baseline and the whole cycle starts again. The R-R interval typically gets shorter until the QRS drops (Fig. 9.2).

This condition is related to the AV node and the majority of the time does not involve the His bundle. It can occur in subjects with a high vagal
tone such as athletes or during high vagal tone states such as sleep. Rarely, patients may experience symptoms of fatigue and dizziness and may
require a pacemaker.

b. Mobitz type II is characterized on an ECG by a sudden loss of the QRS complex following a P wave without progressive P-R lengthening on prior
beats. Typically, most P waves conduct in a 1:1 fashion with similar PR intervals, and one P wave suddenly does not conduct to a QRS.
Sometimes 2 sequential P waves are followed by a QRS complex in the case of a 2:1 Mobitz type II AV block and 3 sequential P waves followed by
a QRS complex if there is 3:1 Mobitz type II AV block (Fig. 9.3). This condition involves structures below the AV node and the His bundle/Purkinje
system. It is usually an irreversible condition, unless it is caused by a metabolic disorder such as hyperkalemia. This can be seen during aging
due to sclerodegeneration of the AV node. It is also commonly associated with extensive myocardial injury such as during myocardial infarction,
or during cardiac surgery or ablation procedures. If no reversible etiologies are found, a permanent pacemaker is the best treatment even if the
patient is asymptomatic as it can progress to a sudden complete heart block.

3. Third-degree AV block: The most severe level of the AV blocks as because there is a lack of conduction across the AV node. Also called a complete
heart block (CHB), the atria and ventricles beat independently of one another. Hence, this is a type of AV dissociation. An AV dissociation is
characterized on an ECG by the lack of a relationship between the P wave and the QRS complex (Fig. 9.4). P waves are seen marching out with a rate
di erent than the ventricular escape rhythm. Patients usually present with symptoms of lightheadedness, fatigue, shortness of breath, or
presyncope and syncope. During a third-degree AV block, the blood supply to the brain can be insu icient, leading to a loss of consciousness.

Most conditions that cause a third-degree AV block are usually irreversible. These commonly occur during aging due to sclero-degeneration of the
AV node, extensive damage during a MI, and during catheter ablation and cardiac surgery of the valves. Infiltrative diseases of the heart such as
sarcoid diseases should also be considered, especially in young patients without any other apparent cause. CHB usually requires a permanent
pacemaker, unless a readily reversible cause can be found. The reversible causes are usually metabolic in nature such as hyperkalemia. This
condition commonly occurs in renal disease particularly in patients on hemodialysis or patients who are on angiotensin-converting enzyme (ACE)
inhibitors. AV nodal blocking drugs including β-blockers, calcium channel blockers, or digoxin can also cause potentially reversible AV block. Like
Mobitz type II, if no reversible etiologies are found, a permanent pacemaker is the best treatment even if the patient is asymptomatic as it can
progress to sudden death.

Figure 9.2
ECG showing Mobitz type I AV block with Wenckebach phenomenon.

Figure 9.3
ECG showing Mobitz type II with a 2:1 to 3:1 AV block.

Figure 9.4
ECG showing a third-degree AV block with no association between the P waves and QRS complexes.

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CLINICAL CORRELATION Box 9.4

Patients who su er from myocardial infarction (MI) involving the right coronary artery can sometimes have a Mobitz I block, which is usually reversible.

CLINICAL CORRELATION 9.5

Adams-Stokes (or Stokes-Adams) attacks are attacks of syncope or presyncope in the setting of a third-degree AV block.

CLINICAL CORRELATION 9.6

Congenital CHB that occurs in young children and teenagers can be asymptomatic. Pacemaker implantation can usually be delayed until patients are
older or symptomatic. However, because of the small increased risk of sudden death even in asymptomatic CHB, a pacemaker is usually the ultimate
recommendation.

Tachyarrhythmias
Tachyarrhythmias can be divided into 2 general categories depending on the site of origin: supraventricular (SVT)/atrial or ventricular (see Table 9.4A).
There are many forms of atrial arrhythmias that o en cause symptoms but are usually not life-threatening. On the other hand, ventricular tachycardias
not only cause symptoms but are o en life-threatening. Atrial tachyarrhythmias usually present with a narrow complex QRS (≤120 ms), whereas
ventricular arrhythmias present with a wide complex QRS (>120 ms). However, there are some exceptions when an atrial tachyarrhythmia can have a
wide QRS; this is termed supraventricular tachycardia with aberrancy (see Table 9.5).

Atrial tachyarrhythmias are the most common types of tachycardias. There are many types of atrial tachyarrhythmias (Table 9.4B). The di erential
diagnosis includes sinus tachycardia, paroxysmal supraventricular tachycardia (PSVT), atrial fibrillation, atrial flutter, and multifocal atrial tachycardia
(MAT). PSVT is commonly divided into 3 categories: (1) AV nodal reentrant tachycardia (AVNRT), (2) orthodromic reentrant tachycardia (ORT), and (3)
atrial tachycardia (Tables 9.4B and 9.5). These usually present with a narrow complex QRS. However, atrial tachyarrhythmias can also present with a
wide QRS. These include SVT with aberrancy, or SVT using an accessory pathway (antidromic reentrant tachycardia).

Table 9.4A
Types of tachyarrhythmias (based on site of origin)

1. Atrial tachyarrhythmia/supraventricular tachycardia

2. Ventricular tachycardia

Table 9.4B
Types of atrial tachyarrhythmias

1. Inappropriate sinus tachycardia

2. Sinus tachycardia
3. Paroxysmal supraventricular tachycardia: AVNRT/atrial tachycardia/orthodromic reentrant tachycardia (ORT)
4. Atrial flutter
5. Atrial fibrillation

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Table 9.5
Types of tachyarrhythmias (based on QRS morphology)

1. Narrow QRS tachycardias a. Sinus tachycardia (ST)

b. Paroxysmal supraventricular tachycardias (PSVT)
c. Atrial flutter(AFl)
d. Atrial fibrillation (AFib or AF)
e. Junctional ectopic tachycardia (JET)

2. Wide QRS tachycardias a. PSVT with aberration

b. Antidromic reentrant tachycardia (preexcited)
c. Ventricular tachycardia (VT)

Atrial Tachycardia

1. Focal atrial tachycardia

Mechanism—Automaticity is usually the mechanism responsible for this type of tachycardia. This means that a focal cell triggers a continuous
repetitive impulse.

ECG findings—These include a P wave with a di erent morphology than a P wave originating from the sinus node with a heart rate more than 100
beats/min.

Characteristic features—The tachycardia is usually paroxysmal and resolves spontaneously. However, some can become incessant and may need
pharmacologic or electric cardioversion to terminate. They can be asymptomatic and short-lasting in clinical presentation. But if they become
symptomatic, treatment is required. Pharmacological treatment includes β-blockers, calcium channel blockers, or antiarrhythmic drugs.
Tachycardias can also o en be o en cured by radiofrequency ablation.

2. Multifocal atrial tachycardia

Mechanism—Automaticity is the mechanism responsible for this type of tachycardia. As the name denotes, there are multiple foci for the origin of P
waves other than the sinus node.

ECG findings—ECG features include P waves with more than at least 3 P waves with di erent morphologies. Usually, these P waves have varying PR
and R-R intervals.

Characteristic features—These are usually irreversible conditions and o en occur in the setting of significant lung disease. The tachycardia can be
controlled using AV nodal blocking agents such β-blockers and calcium channel blockers. This condition can also be seen in digitalis toxicity, which
is reversible.

CLINICAL CORRELATION 9.7

Radiofrequency ablation (RFA) has no role in the treatment of MAT.

Atrial Flutter

Atrial flutter is a pathological condition that occurs in normal hearts as well as structural heart disease.

Mechanism—Reentry is the mechanism responsible for this type of tachycardia. This means that a continuous circuit of impulses is created. This circuit
can be entrained during electrophysiology study.

ECG findings—Characteristic ECG features include fast sequences of P waves in a sawtooth pattern (Fig. 9.5). The atria contract is typically at around 300
bpm, though the range can be as low as 150 and as high as 350 bpm. Because the AV node has decremental conduction properties, it slows impulse
conduction to the ventricle, so typically there is a 2:1, 3:1, or 4:1 block from the atrium to the ventricle, resulting in a ventricular frequency of 150, 100,
or 75 bpm, respectively, if the atrial rate is 300 bpm. O en the grade of block changes every couple of beats, resulting in for example, 2:1 or 3:1 blocks
and a somewhat irregular ventricular heart rate over a period of ECG monitoring.

Characteristic features—Atrial flutter is divided into 2 major categories: cavotricuspid isthmus (CVI) dependent flutter (ie, typical flutter) and atypical
flutter (ie, non-CVI dependent). (See Table 9.6.)

Figure 9.5
An atrial flutter with a 4:1 AV block.

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Table 9.6
Types of atrial flutters

Forms of atrial flutters Circuit ECG findings

“Typical” atrial flutter: 1. Counterclockwise macro-reentrant circuit (most common) Inverted P waves in the
Cavotricuspid isthmus Wave of tissue activation—Atrial tissue between tricuspid annulus (TA) and coronary sinus opening inferior leads and
dependent (CS) → interatrial septum → posterior right atrium (RA) → roof of RA → RA free wall→ isthmus (atrial upright P waves in lead
tissue) between TA and inferior vena cava (IVC) then recycles V1

2. Clockwise macro-reentrant circuit (common variant) Upright P waves in the

Wave of tissue activation—Atrial tissue between tricuspid annulus (TA) and coronary sinus opening inferior leads and
(CS) → isthmus → RA free wall → roof of RA → posterior RA → interatrial septum → recycles inverted P waves in lead
V1

“Atypical” atrial flutter: Occurs typically in hearts with scarring as a result of open heart surgery around suture lines or a er P wave morphology
Activation is not around radiofrequency ablation in le atrium; can occur in normal hearts variable
cavotricuspid isthmus

For further information, see Prystowsky EN, Padanilam BJ; Waldo AL. Atrial fibrillation, atrial flutter, and atrial tachycardia. In: Fuster V, Walsh RA, Harrington RA, eds.
Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011:chap. 40 [3].

Cavotricuspid Isthmus-Dependent Flutter—Typical Atrial Flutter

This type of flutter usually can occur in structurally normal and abnormal hearts.

Mechanism—The flutter has a macro-reentrant circuit in the right atrium and the direction of propagation is usually counterclockwise around the
cavotricuspid isthmus. The propagation can also be clockwise, and as long as it is around the cavotricuspid isthmus, it is still considered a typical flutter.
The counterclockwise form is seen most o en and is most commonly referred as a “typical flutter.” The more precise and preferred classification is CVI
dependent or atypical (non-CVI dependent). The tissue propagation is described in Table 9.6.

ECG findings—It is commonly depicted by a sawtooth pattern of P waves in the inferior leads. The characteristic ECG changes include inverted P waves
in the inferior leads and upright P waves in lead V1 in a counterclockwise form. Negative P waves in V1 and upright in the inferior leads are seen in a
clockwise form.

Atypical Atrial Flutter

This type of flutter by definition does not involve CVI. It usually occurs in structurally abnormal hearts; for example, a er cardiac surgery around suture
lines or a er radiofrequency ablation. It can also occur around scarring in cardiomyopathies. Atypical atrial flutter occurs in normal hearts as well,
although this is rare.

CLINICAL CORRELATION 9.8

Both CVI dependent and atypical flutter can be treated by RFA (radiofrequency ablation).

Clinical presentations—May be asymptomatic with normal ventricular rates but can become symptomatic when AV conduction increases and the
ventricular rate rises. The most common symptoms include palpitations, exertional dyspnea, and easy fatigability. Rarely, a rapid 1:1 flutter can occur
and present with syncope as the ventricular rates will e ectively be 250 to 300 bpm. An atrial flutter can also present as a cardioembolic stroke.

Treatment—The aim of treatment is to reduce symptoms with either rate control or a return to sinus rhythm. Since the condition can easily be cured
with ablation and the need for long-term anticoagulation for stroke prevention can be avoided, RFA is the preferred treatment strategy in most patients
that are good candidates and do not have any other contraindications.

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There are 3 goals in the treatment of an atrial flutter depending on the clinical scenario at presentation. The initial goal is always rate control, to control
the speed of the arrhythmia. This can be achieved with AV nodal blocking agents including β-blockers and calcium channel blockers. Digoxin can also
be used but is reserved for patients as a third-line drug or for patients that have borderline hypotension as digoxin will not lower blood pressure.
However, digoxin is not as e ective in controlling heart rates as the first 2 drug classes of AV nodal blocking agents and has a narrow therapeutic
window with a significant amount of toxicity. Urgent direct current (DC) cardioversion should be used as an initial treatment goal if the patient is
hemodynamically unstable.

In most patients, once the rate control is achieved or attempted, rhythm control is tried. The goal of rhythm control is to convert the patient back to a
sinus rhythm. This can be achieved with either pharmacologic drugs and antiarrhythmics (class 1C agents, ibutilide, or amiodarone) or DC
cardioversion. RFA is the cure for atrial flutter with success rates approaching 95% for CVI-dependent flutter and is the preferred approach in most
patients who are candidates.

Rhythm control can be achieved if the arrhythmia lasts less than 48 hours without the need for a transesophageal echocardiogram (TEE) to rule out a
le atrial appendage (LAA) clot. If more than 48 hours elapse since symptoms started, then TEE should be performed to rule out an LAA clot.
Anticoagulants should also be started and continued if the arrhythmia lasts more than 48 hours for at least 1 month a er cardioversion. Depending on
the patient’s CHA2DS2-VASc score (Table 9.10), anticoagulants should be continued indefinitely unless an RFA is performed, which is presumed curative.
Patients with a CHA2DS2-VASc score of 1 or more should be considered for anticoagulation. Patients with a score of 2 or more should be on
anticoagulants unless contraindications exist. However, if radiofrequency is performed then anticoagulants can usually be discontinued a er certain
duration based on the success of the ablation and the length of time that the atrial flutter lasted.

Atrial Fibrillation

Atrial fibrillation (AFib) is the most common cardiac arrhythmia. This chaotic rhythm disorder results from disorganized atrial impulses from all over the
atria. Atrial fibrillation is classified depending on the length of episodes: paroxysmal (<7 days), persistent (>7 days), and permanent AFib is sustained
but restoration of a normal sinus rhythm has not been possible or is not seemingly possible and will not be attempted again (Table 9.7).

Mechanism—Multiple reentrant circuits that coexist. There are wavelets, drivers, and rotors that have been proposed [3].

ECG findings—Typically include irregular R-R intervals and an absence of discrete P waves, which are replaced by irregular, chaotic F waves. P waves
occur at a rate between 350 to 600 bpm (Fig. 9.6). Due to the AV node’s decremental conduction properties, the ventricular rates are much slower than
the atrial rates. Heart rates can range anywhere from a slow ventricular response to 250 bpm. Sometimes there are aberrantly conducted beats a er
long-short R-R cycles termed the Ashman phenomenon. When the heart rate is under 60 bpm, it is called atrial fibrillation with a slow ventricular
response. When the rate is greater than 100 bpm, then it is denoted as a fast ventricular response. If the rate is between 60 to 100 bpm, then
electrophysiologists refer to it as atrial fibrillation with a controlled ventricular response.

Clinical presentations—These patients can be asymptomatic, especially with controlled ventricular rates. The most common symptoms associated with
this disease are palpitations, exertional dyspnea, and fatigue. Chest pain, dizziness, near syncope, and syncope can also occur. Unfortunately, many
patients also present with a cardioembolic stroke (cerebrovascular stroke, CVA) as a first symptom, as AFib is a common cause of CVA. If the atrial
fibrillation ventricular rate is le uncontrolled, congestive heart failure can occur.

Causes—The majority of AFibs are idiopathic, but can also be acquired (Table 9.8). Thyrotoxicosis, pericarditis, myocardial ischemia, electrolyte
abnormalities, and alcoholism are other causes that can be reversible. AFib is also very common in postcardiac surgery due to pericarditis and o en
does not recur a er a healing period.

Table 9.7
Classification of AFib depending on the duration at the time of presentation

Type Definition

Paroxysmal Two or more episodes that terminate spontaneously in less than 7 days but more commonly in 24 hours

Persistent AFib is sustained more than 7 days

Or
Requires pharmacological or DC cardioversion if less than 7 days of duration

Long persistent When AFib is sustained for more than a year but restoration of rhythm can still be tried

Permanent When AF is sustained but restoration of normal sinus rhythm is not seemingly achievable and hence will not be tried

For further information, see Fuster V, Rydén LE, Cannom DS, et al. ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice
Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Eur Heart J. 2006;27:1979-2030 [4].

Figure 9.6

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Atrial fibrillation with a varying ventricular rate.

Table 9.8
Causes of atrial fibrillation

Age
Hypertension
Coronary artery disease
Cardiomyopathy—both ischemic or nonischemic
Pericarditis/pericardial intervention
Congenital heart disease
Mitral valve disease
Prior heart surgery—CABG or valvular surgery
Hyperthyroidism
Sleep apnea
Alcohol abuse
Smoking
CO poisoning
Excessive ca eine consumption
Atrial flutter
Others:
Chest infections: pneumonia
Pulmonary disease including lung cancer, COPD—emphysema or pulmonary embolism

For further information, see Estes NAM, Sacco RL, Al-Khatib SM, et al. American Heart Association Atrial Fibrillation Research Summit: a conference report from the
American Heart Association. Circulation. 2011;124(3):363-372 [5].

CLINICAL CORRELATION 9.9

Treatment of AFib depends on the type of AFib diagnosed clinically.

CLINICAL CORRELATION 9.10

Always check the thyroid profile in all patients presenting with AFib.

There is a strong association between AFib and other cardiovascular diseases such as heart failure, coronary artery disease, hypertension, and lung
disorders. All these diseases lead to an increase in LA load and hence LA pressure thus predisposing to AFib.

Treatment

Treatment has 3 goals depending on the clinical scenario at presentation. Initially, it is very similar to the treating and atrial flutter. The first goal is
always rate control in order to control the speed of the arrhythmia. This can be achieved with AV nodal blocking agents including β-blockers and
calcium channel blockers. Digoxin can also be used but is reserved for patients as a third-line drug or for patients with borderline hypotension as it does
not lower blood pressure. However, digoxin is not as e ective in controlling heart rates as the first 2 drug classes of the AV nodal blocking agents. Urgent
DC cardioversion should be used as an initial treatment goal if the patient is hemodynamically unstable.

In most patients, once rate control is achieved or attempted, then rhythm control is attempted, unless the patients are elderly and completely
asymptomatic. The goal of rhythm control is to convert the patient back to a sinus rhythm. This can be achieved with either antiarrhythmics (class 1C
agents, ibutilide, or amiodarone) or DC cardioversion. AAD drugs used for this arrhythmia for long-term maintenance of sinus rhythm include: class 1C
agents, sotalol or dofetilide, or amiodarone (Table 9.9). However, RFA is more successful than antiarrhythmics in maintaining sinus rhythm and is
therefore a good option for patients that qualify usually a er failing with AADs. Because the success rate of AFib ablation is not as high as that of atrial
flutter, it is usually reserved for patients that fail AA drugs and are symptomatic. However, some patients with paroxysmal AFib are also candidates for
ablation as a first-line therapy. Those with persistent AFib have lower success rates with RFA, and therefore usually should first fail antiarrhythmic
therapy.

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Table 9.9
Antiarrhythmic drugs for the treatment of atrial fibrillation

Serial no. Drug Dosage

1. Flecainide 50 mg to 150 mg per dose BID

2. Propafenone 150 to 300 mg per dose TID, SR sustained release also available and dosed BID

3. Dofetilide 500 mcg PO BID or 250 mcg BID depending on renal function: requires hospital observation for initiation

4. Amiodarone 150 given IV bolus over 10 to 20 min then drip initiation

Orally 400 mg TID or BID loading until approximately 8 grams given then maintenance dose of 200 mg daily

5. Dronedarone 400 mg BID

6. Sotalol 80 to 160 mg/dose BID

Note: Similar to atrial flutter, rhythm control can be achieved if the arrhythmia lasts for less than 48 hours without the need for a TEE to rule out a LAA
clot. If more than 48 hours elapses since symptoms started, then a TEE should be performed to rule out an LAA clot. Anticoagulation should also be
started and continued if the arrhythmia lasts more than 48 hours for at least 1 month a er cardioversion regardless of the CHA2DS2-VASc score. Long-
term anticoagulation beyond the 1 month should be continued depending on the patient’s CHA2DS2-VASc score (Table 9.10).

Table 9.10
Showing the CHA2DS2VASc scoring system (The CHA2DS2VASc score is used to estimate the risk of stroke in patients with nonvalvular AFib)

Abbreviation Factors Points

C Congestive heart failure 1

H Hypertension 1

A2 Age ≥75 years 2

D Diabetes mellitus 1

S2 Stroke/TIA/thromboembolism 2

V Vascular disease 1

A Age ≥65 <75 years 1

Sc Sex category/female 1

Lip GYH, Nieuwlaat R, Pisters R, et al. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a novel risk factor-based
approach: the Euro Heart survey on atrial fibrillation. Chest. 2010;137: 263-272 [6].

More on Ablation of Atrial Fibrillation

Ablation can be o ered to patients who fail AA therapy and are symptomatic for both paroxysmal and persistent AFib. It is a complex procedure that
generally targets the elimination of pulmonary vein potentials in the le atrium at a minimum, with other targets and triggers depending on the
etiology of the AFib. It can be performed via radiofrequency ablation or via cryoballoon ablation. The success rates of AFib ablation have a wide range
depending on the types AFib and whether the AFib is paroxysmal or persistent.

Stroke Prevention

This is an important goal of atrial fibrillation treatment due to the morbidity and mortality. Anticoagulation is guided by the CHA2DS2-VASc score (Table
9.10). This is a risk-stratifying system that assigns points to risk factors for a stroke. Anyone with one or more risk factors is a candidate for
anticoagulation for stroke prevention. Patients with a score of zero do not require anticoagulation, whereas those with a CHA2DS2-VASc score of 2 or
more should be on anticoagulants unless contraindications exist. Patients with a score of only 1 have the option of aspirin or an anticoagulant, based on

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their preference and their risk of bleeding; given the understanding that anticoagulation is preferable to aspirin in terms of stroke prevention but at the
expense of more bleeding. Anticoagulants include warfarin, and the new oral anticoagulants include:

1. Dabigatran (direct thrombin inhibitor)

2. Rivaroxaban (factor Xa inhibitor)

3. Apixaban (factor Xa inhibitor)

Paroxysmal Supraventricular Tachycardia

In a heart with normal electrical conduction, the AV node is the only way that the transmission of impulses from the atria to the ventricles occurs (Table
9.11). Supraventricular tachycardia includes any arrhythmia initiating in the atria and involving the AV node (antegrade or retrograde) or an accessory
pathway. Conventionally, atrial flutters and atrial fibrillations are treated as separate entities, although they are also supraventricular tachycardias
(SVTs) by definition since they originate in the atrium.

Table 9.11
Types of paroxysmal supraventricular tachycardias

1. Atrial tachycardia (AT)

2. AV nodal reentrant tachycardia (AVNRT)

3. Orthodromic reentrant tachycardia (ORT) using a concealed bypass track with orthodromic conduction down the AV node and up the pathway

4. Junctional tachycardia

5. Antidromic reentrant tachycardia (ART) using a manifest bypass track with conduction down the pathway and up the AV node

PSVTs are characterized by the following features which distinguish this rhythm from sinus tachycardia (Table 9.12).

Table 9.12
Di erentiating PSVT from sinus tachycardia

PSVT Sinus tachycardia

1. P wave morphology di erent from typical sinus P wave or even hidden P wave morphology typically biphasic in lead V1 and upright in leads 2/3/aVF

2. Paroxysmal (meaning sudden onset and sudden termination) Gradual onset and gradual termination

3. Heart rate is variable but can be up to 280 to 300 bpm depending on age Heart rate usually less than bpm depending on age

4. Usually has a constant rate Rate variable

AV Nodal Reentrant Tachycardia

This is the most common and regular supraventricular tachycardia in adults.

Mechanism—The AV node has a compact part and multiple atrial extensions that are anatomical structures denoting physiological pathways with
di erent velocities. These di erent pathways represent slow and fast pathways. The slow pathway has a slow conduction velocity but a short recovery
period, and the fast pathway has a fast conduction velocity but a long recovery period. These di erences in conduction velocities and recovery periods
create a potential for the creation of reentry. Normally, when the impulse reaches the AV node, it travels down both fast and slow pathways but is
conducted faster by the fast pathway to reach the bundle of His. By the time the impulse that is traveling the slow pathway reaches the bundle of His,
the His is in a refractory phase and therefore this impulse is not conducted further to the ventricles (Fig. 9.7).

When a premature atrial beat occurs, either spontaneous or stimulated, it can be conducted through the slow pathway since it has a faster recovery
than the fast pathway. By the time the impulse travels slowly down the slow pathway, the fast pathway may have recovered and the impulse can travel
retrogradely up the fast pathway and then back down the slow pathway, creating a reentry circuit. This type of AVNRT (atrioventricular nodal reentry
tachycardia) is termed a typical AVNRT, where the impulse travels down the slow pathway then back up the fast pathway. Atypical AVNRT is the reverse
circuit, when the impulse travels down the fast pathway and then up the slow pathway.

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ECG findings—Patients with AVNRT have a narrow QRS (that can be wide when associated with aberrancy), with a width less than 120 msec. P waves are
not o en distinct as they will merge in the distal portion of the QRS complex if it is typical AVNRT. In typical AVNRT, an inverted P wave in the terminal
portion of the QRS (or buried within the QRS) can be observed, particularly in leads II, III, and aVF as the retrogradely conducted atrial impulse moves
away from the inferior leads (Fig. 9.8).

Clinical presentation—The incidence of AVNRT is more prominent in females and can occur at any age. Common symptoms include palpitations
(classical sudden onset and sudden disappearance), dyspnea, weakness, lightheadedness, angina, or rarely syncope.

Figure 9.7
Mechanisms of supraventricular tachycardias.

Figure 9.8
ECG showing paroxysmal supraventricular tachycardia. (Reproduced, with permission, from Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of
Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill; 2010.)

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CLINICAL CORRELATION 9.12

There are atypical AVNRTs in which the conduction can be down the fast pathway then up the slow pathway (termed fast-slow) or down a slow pathway
and up another even slower pathway (slow-slow). These result in distinct inverted P waves further away from the QRS complex because of the slow
conduction retrograde up the slow pathway.

CLINICAL CORRELATION 9.11

The part of the AV nodal tissue that has transitional cells and fibers conducts slower than the tissue without them. The first group constitutes the slow
pathway and the latter constitutes the fast pathway.

Treatment

The treatment is to reduce the AV nodal conduction by vagal maneuvers or AV node inhibition with the use of drugs (Tables 9.13A, B and 9.14). The use
of IV adenosine is quite helpful if the tachycardia is narrow or wide and regular. If the patient has tachycardia with a QRS duration of ≤120 msec and a
constant R-R interval then it is called a narrow QRS tachycardia with a regular R-R interval. If the tachycardia is regular and the QRS duration is >120
msec, it is defined as a wide QRS tachycardia. If the tachycardia is wide and irregular then adenosine is not recommended since the arrhythmia can be
AFib conducted down an accessory pathway (see next section on Wol -Parkinson-White). AV nodal drugs such as calcium channel blockers and β-
blockers can suppress the arrhythmias, although they are not very e ective.

Radiofrequency ablation is the treatment of choice in patients with recurrent PSVT. The success rate is greater than 95% for RFA. During RFA, if an AVNRT
is confirmed, the slow pathway is ablated.

Table 9.13A
Maneuvers for AVNRT reversal to normal sinus rhythm

Maneuvers

1. Carotid sinus massage

2. Valsalva maneuver

3. Coughing

4. Head immersion in cold water

Table 9.13B
Pharmacological treatments for AVNRT

Pharmacological treatment

1. Adenosine—At 6 to 12 mg IV bolus

2. Calcium channel blockers

a. Verapamil
b. Diltiazem

3. β-blockers
a. Esmolol
b. Metoaprolol
c. Bisoprolol
d. Carvedilol
e. Atenolol

Other: Antiarrhythmic drugs such as amiodarone or class 1 agents, but significant side e ects can occur

For further information Table 9.13A, B, Calkins H. Supraventricular tachycardia: atrioventricular nodal reentry and Wol -Parkinson-White syndrome. In: Fuster V, Walsh
RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011:chap. 41 [8]; Marchlinski F. The tachyarrhythmias. In: Longo DL, Fauci AS, Kasper DL,
Hauser SL, Jameson JL, Loscalzo J, eds. Harrison’s Principles of Internal Medicine. 18th ed. New York: McGraw-Hill; 2012:chap. 233 [9].

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Table 9.14
Di erentiating mechanisms for di erent types of SVTs

Serial Pharmacological/Ablation
Type of arrhythmia Mechanism ECG changes for recognition
no. treatment

1. Unifocal atrial tachycardia Automaticity a. Narrow QRS a. β-blockers

b. Usually regular, but may have some irregularity b. Calcium channel
c. P wave during tachycardia is di erent from sinus P wave blockers
d. Terminates with narrow QRS complex c. Adenosine
sometimes works
d. Ablation

2. AV nodal reentry tachycardia Reentry a. Narrow QRS a. Adenosine

b. Regular b. β-blockers
c. P wave is merged in QRS or just a er QRS c. Calcium channel
d. Pseudo S wave (retrograde P wave) in II, III, aVF, and pseudo R blockers
(retrograde P wave) in lead V1 d. Ablation
e. Terminates with a retrograde P wave or QRS complex

3. ORT (orthodromic reentrant Reentry a. Narrow QRS during tachycardia a. β-blockers

tachycardia) b. Regular b. Calcium channel
c. During sinus rhythm, a short PR interval, delta wave, and wide blockers
QRS may be present c. Adenosine
d. Retrograde P wave is usually farther away from QRS d. Ablation
e. QRS alternans can be seen
f. Terminates with a retrograde P wave or QRS complex

For further information, see Prystowsky EN, Padanilam BJ; Waldo AL. Atrial fibrillation, atrial flutter, and atrial tachycardia. In: Fuster V, Walsh RA, Harrington RA, eds.
Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011:chap. 40 [3]; Calkins H. Supraventricular tachycardia: atrioventricular nodal reentry and Wol -Parkinson-White
syndrome. In: Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill; 2011:chap. 41 [8].

Atrioventricular Reentrant Tachycardia and Wol -Parkinson-White Syndrome

Atrioventricular reentrant tachycardias (AVRTs) are SVTs that are caused by the presence of an accessory pathway. There are 2 types: ORT and
antidromic reentrant tachycardia (ART); see Table 9.15. These accessory pathways are “extra” connections that are present between the atria and the
ventricles in addition to the normal conduction system of the heart. These accessory pathways are actually myocytes spanning between the upper and
lower chambers of the heart across the AV groove. This tissue is distinct from the normal conduction pathway of the heart. These connections disappear
during the normal development of the human heart during fetal life but in some cases, they can persist. Many of these pathways remain benign and can
disappear over time while others can be responsible for SVTs. AVRTs are most common in children, accounting for approximately 30% of all SVTs. The
prevalence of accessory pathways in the general population is 0.15% [10].

Table 9.15
Antidromic versus orthodromic AVRT

Orthodromic AVRT Antidromic AVRT

Most common type Occurs in 10% of patients with WPW syndrome with tachycardia

Impulses transmit anterogradely down the AV node to the ventricles and then Impulses transmit anterogradely down the accessory pathway to the
retrogradely to the atria up through the accessory pathway ventricles and then retrogradely to the atria up through the AV node

Narrow QRS complexes during tachycardia Wide QRS complex during tachycardia

Accessory pathways can conduct antegradely or retrogradely. If they conduct antegradely then they can usually be seen on a baseline ECG and are
represented by a delta wave. These are termed as “manifest” preexcitations since the pathway is obvious on the ECG by the presence of the delta waves.
On the other hand, a pathway may not be obvious on an ECG and only conduct retrogradely during an SVT. In this case, it is termed as “concealed” since

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in e ect the pathway is hidden on the surface of the ECG. Patients with manifest pathways are also labeled as having Wol -Parkinson-White (WPW)
syndrome or ventricular preexcitation.

The ECG manifestation of WPW syndrome includes a short PR interval and a delta wave (Fig. 9.9). The short PR interval occurs because there is early
ventricular activation through the accessory pathway. The QRS has a slurred delta upstroke because there is slower ventricular activation from myocyte
to myocyte initiated by the accessory pathway, as opposed to the usual rapid conduction of the His-Purkinje system. The widening of the QRS complex
is a result of the fusion of the 2 electrical waveforms from the normal conduction system down the AV node and the accessory pathway activation of the
ventricle merging together.

Figure 9.9
ECG showing normal sinus rhythm and delta waves (arrow) with a short PR interval in a patient with WPW syndrome. (Reproduced, with permission,
from Knoop KJ, Stack LB, Storrow AB, Thurman RJ. The Atlas of Emergency Medicine. 3rd ed. New York, NY: McGraw-Hill; 2010.)

The presence of the accessory pathway can set up the reentry and therefore SVT. The direction of the flow of the cardiac impulse during SVT through
this circuit defines the type of AVRT, of which there are 2 types (Table 9.15). If the initial impulse travels down the AV node and retrogradely up the
pathway, then it is termed as “orthodromic reentrant tachycardia” and the resultant ECG shows a narrow QRS (<120 msec) because the impulse travels
down the AV node. If, however, the pathway can conduct antegradely, then “antidromic reentrant tachycardia” (ART) is possible. In this type of reentry,
the impulse travels down the pathway first and then retrogradely up the AV node. In this situation, the ECG shows a wide complex QRS (>120 msec)
since the impulse initially travels down the pathway.

Unlike the AV nodal pathways, accessory pathways do not have decremental properties. The AV node has the intrinsic property of slowing down
impulses from the atrium to avoid very rapid signals from conducting in a 1:1 fashion to the ventricle. However, accessory pathways, in general, do not
have decremental properties and therefore can conduct very rapid impulses from the atria. There are some pathways that do exhibit decremental
conduction, but these are in the minority. Rare but life-threatening arrhythmias can occur in patients with WPW syndrome when an atrial flutter or atrial
fibrillation is present and the accessory pathway conducts in an anterograde fashion to the ventricles at extremely fast rates due to the short refractory
periods of these pathways. These impulses, when conducted to ventricles at over 300 bpm depending on the rate of the atrial flutter or atrial fibrillation,
can lead to ventricular fibrillation and sudden death.

Treatment

Radiofrequency ablation is the treatment of choice in patients with WPW syndrome, which show evidence of preexcitation and are symptomatic.
Patients with symptomatic WPW syndrome have an increased risk of sudden death due to the potential rapid conduction of the accessory pathway
during an atrial flutter or AFib as described above, and therefore ablation is recommended as first-line therapy. An asymptomatic patient with WPW
syndrome can be observed and treated conservatively unless the patient is in a high-risk profession such as an airline pilot. AV nodal agents should be
avoided in WPW syndrome if the tachycardia is irregular as the agents may preferentially allow conduction down the accessory pathway by inhibiting
the AV node (due to the presence of an underlying atrial fibrillation). Procainamide can be used acutely versus DC cardioversion in patients presenting
with WPW syndrome and SVT (Table 9.16A, B).

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Table 9.16A
Treatment in patients with WPW syndrome with tachyarrhythmia

Hemodynamic stability Treatment of choice

STABLE Class IA drugs, eg, procainamide

Class III drugs, eg, ibutilide

UNSTABLE DC cardioversion

Table 9.16B
Pharmacological treatment for WPW syndrome

Indicated Contraindicated

1. Class IA, IC, III 1. Calcium channel blockers, β-blockers, and digoxin are contraindicated if the
All these drugs slow the conduction and increase the refractory period in tachycardia is irregular and wide
the AV node as well as the accessory pathway They slow the conduction through the AV node only

2. Procainamide slows conduction in the accessory pathway more than 2. They can precipitate ventricular fibrillation in a patient who has atrial flutter
the AV node or atrial fibrillation by blocking the AV node only
Or
Ibutilide increases the refractory period in the accessory pathway

Patients with SVT and a narrow complex without a manifest pathway can be treated with AV nodal blocking agents or radiofrequency ablation
depending on their preference. Ablation can be used as a first-line treatment or reserved until medical therapy fails, depending on the patient’s
preference. As opposed to the patients with manifest accessory pathways, patients with a narrow complex SVT who cannot conduct anterograde down
their accessory pathway are not at an increased risk of sudden death compared to the general population since the maximum rate of conduction to the
ventricle anterograde is still limited by the AV node, which has decremental properties.

Ventricular Tachycardia

Characteristic Features

Ventricular tachycardia (VT) is defined when there is a run of 3 or more ventricular premature beats on an ECG. They are therefore wide complex
tachycardias with QRS duration >120 msec (Fig. 9.10). These commonly occur in structurally abnormal hearts and may be life-threatening. However,
they can also occur in completely normal hearts and be well-tolerated. Common associated diseases include myocardial ischemia or injury (ie,
myocardial infarction), cardiomyopathies, congenital heart diseases, valvular heart diseases, long QT syndromes/channelopathies, and postcardiac
surgery due to scarring. There are also metabolic causes including hypokalemia, hypomagnesemia, and hypoxia.

Figure 9.10
ECG showing ventricular tachycardia. (Used with permission from the Innovation Department of the Spectrum Health Fred and Lena Meijer Heart
Center, Grand Rapids, Michigan.)

CLINICAL CORRELATION 9.13

Wide QRS regular tachycardia with a hemodynamic compromise; always suspect VT first.

Ventricular tachycardias are classified based on the uniformity of the morphology of the wide QRS complexes. They can be divided into monomorphic
VT and polymorphic VT. Monomorphic VTs have a uniform morphology of the wide QRS complex; o en these are regular tachycardias but can be

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irregular. Polymorphic VTs have multiple morphologies of the QRS complex with a duration of more than 120 msec. Polymorphic VTs are usually
irregular. If the axis of the QRS changes during polymorphic VT then it can be termed torsades de pointes. Other features are enumerated in Table 9.17.

Table 9.17
Di erentiating monomorphic from polymorphic VTs

Monomorphic VT Polymorphic VT

1. Uniform morphology of QRS complexes 1. Multiple morphologies of QRS complexes

2. May be related to ischemia, metabolic causes, or scarring 2. O en associated with ischemia or channelopathies

3. Rate of rhythm is mostly constant 3. Rate varies all through the rhythm

4. Reentry is a common mechanism; triggered activity can occur in normal hearts and 4. Automaticity or unstable reentry circuits are a common
idiopathic VT mechanism

5. Structural abnormalities and scarring are common causes, although can occur in completely 5. Channelopathies and ischemia are common causes
normal hearts

Ventricular tachycardias can also be classified based on the etiology of the structural heart disease with which they are associated, as either ischemic,
nonischemic, or idiopathic. Ischemic VT, as the name implies, is associated with coronary artery disease and usually occurs as a result of scarring from a
myocardial infarction that causes a reentrant circuit for the VT. These are usually considered to be monomorphic VTs. Ischemia can also cause
polymorphic VT, torsades de pointes, and ventricular fibrillation. Nonischemic VT occurs in patients with structurally abnormal hearts without
associated coronary artery disease, such as in patients with severe le ventricular (LV) dysfunction.

A monomorphic idiopathic VT occurs in the setting of structurally normal hearts without le LV dysfunction or coronary artery disease. These usually
have a good prognosis but in rare instances can be life-threatening (Table 9.18). If an “idiopathic” VT is polymorphic in the setting of an otherwise
normal heart then it is usually due to channelopathies such as Brugada syndrome, long QT syndrome, catecholaminergic polymorphic VT (CPVT), or
short QT syndrome.

Table 9.18
Types of idiopathic VTs

Types of idiopathic VTs ECG findings

1. RVOT VT (right ventricular outflow tract VT) LBBB with inferior axis

2. LVOT VT (le ventricular outflow tract VT) Broad R in V1 with early transition

3. Fascicular VT Narrower QRS usually 120 to 150 msec and with a typical RBBB or LBBB pattern

4. Annular VT RBBB with le -axis deviation

For further information, see Rho RW, Page RL. Ventricular arrhythmias. In: Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill;
2011:chap 42 [11].

CLINICAL CORRELATION 9.14

Channelopathies leading to polymorphic VT include Brugada syndrome, long QT syndrome, and CPVT (catecholaminergic polymorphic VT).

Last, VT can be further described as sustained (>30 sec) and nonsustained (<30 sec) depending on the duration of the arrhythmia (Table 9.19). It is
important to distinguish VT from SVT with aberrancy to streamline the proper treatment (Table 9.20). Recall from the earlier discussion in this chapter
that SVT with aberrancy is an atrial tachyarrhythmia which appears wide on an ECG (QRS >120 msec) because of an “aberrant” or slow conduction of
the ventricular conduction system during a SVT. Di erentiating SVT with aberrancy from VT has important clinical treatment implications and
prognoses. This is not always an easy task but there are certain ECG observations and clinical features that can be helpful (Table 9.20).

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Table 9.19
Di erentiating nonsustained VT from sustained VT

Features Nonsustained VT Sustained VT

Duration Less than 30 seconds More than 30 sec

Associated symptoms—including presyncope, syncope, Usually transient if any at Usually present

palpitations all

Termination Spontaneous termination DC cardioversion/antiarrhythmic drugs/or

spontaneous

For further information, see Rho RW, Page RL. Ventricular arrhythmias. In: Fuster V, Walsh RA, Harrington RA, eds. Hurst's The Heart. 13th ed. New York: McGraw-Hill;
2011:chap 42 [11].

Table 9.20
Di erentiating features between SVT with aberrancy and monomorphic VT

Features favoring SVT with

  Features favoring VT
aberration

History of heart disease Unusual Common

VA (ventricular/atrial) dissociation Absent Can be present

Morphology of QRS in precordial leads No concordance Concordance in V1-V6 (ie, all QRS vectors up or down) can be
present

Initial R wave in aVR Small R wave in aVR favors SVT Large R wave in aVR common

Fusion/capture beats Absent Can be present

Interval from onset of R to nadir of S wave in any Interval <100 msec Interval ≥100 msec
precordial lead

Clinical Features
The clinical features depend on the type and duration of the ventricular tachycardia. The most common symptoms associated with VT are palpitations,
presyncope, syncope, shortness of breath, chest pain, diaphoresis, or sudden cardiac death. If the VT is nonsustained, it is usually asymptomatic. Some
slower sustained VTs are also asymptomatic. Most sustained VTs, however, are symptomatic and require prompt treatment. As stated above, those that
occur in the setting of structurally normal hearts tend to be tolerated much better than those that occur in abnormal hearts.

Treatment of VT

VT treatment first depends on the hemodynamics of the patient. If the patient is hemodynamically unstable, then DC cardioversion needs to be
performed emergently. If the patient is stable, then a trial at antiarrhythmics can be administered, followed by DC cardioversion if unsuccessful. Most
commonly, IV amiodarone is the first choice, followed by IV lidocaine. If the VT is stable and monomorphic, and one is unsure of whether it is a SVT with
aberrancy or a VT, then adenosine IV bolus can be attempted as a diagnostic maneuver. If it is SVT with aberrancy then the wide complex tachycardia
can terminate. There are also some idiopathic VTs that are adenosine sensitive, which will also terminate.

Long-term treatment of VT involves the use of antiarrhythmic drugs. The choice of antiarrhythmic drugs is complex and usually involves expert
consultation. There are many antiarrhythmics available and several di erent classifications but the Vaughan Williams classification is still the most
commonly used scheme (Tables 9.21 and 9.22).

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Table 9.21
Vaughan Williams classification of antiarrhythmic drugs

Class Site/mechanism of action E ect on action potential

I Sodium channel blockade Reduce phase 0 slope and peak of action potential

Ia Moderate slowing of Moderate reduction in phase 0 slope; increase in action potential duration (APD); increase in e ective refractory
conduction period (ERP)

Ib Minimal slowing of Small reduction in phase 0 slope; reduce APD; decrease in ERP
conduction

Ic Marked slowing of Pronounced reduction in phase 0 slope; no e ect on APD or ERP

conduction

II β-receptor blockade Block sympathetic activity; reduce rate and conduction

III Potassium channel blockade Delay repolarization (phase 3) and thereby increase action potential duration and e ective refractory period

IV Calcium channel blockade Block L-type calcium channels; most e ective at SA and AV nodes; reduce rate and conduction

V Other agents  

For further information, see McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.; Vaughan Williams EM. Classification of
Antiarrhythmic Agents. Berlin: Springer-Verlag; 1989:45 [12].

Table 9.22
Classification of antiarrhythmic drugs

Class Drugs under category

Ia Quinidine, Procainamide, Disopyramide

Ib Lidocaine, Phenytoin, Mexiletine, Tocainide

Ic Flecainide, Propafenone, Moricizine

II Propranolol, Esmolol, Metoprolol, Timolol, Atenolol, Bisoprolol

III Amiodarone, Sotalol, Ibutilide, Dofetalide, Dronedarone

IV Verapamil, Diltiazem

V Adenosine, Digoxin, Magnesium sulfate

For further information, see McGraw-Hill Concise Dictionary of Modern Medicine. © 2002 by The McGraw-Hill Companies, Inc.; Vaughan Williams EM. Classification of
Antiarrhythmic Agents. Berlin: Springer-Verlag; 1989:45 [12].

Most o en, patients with monomorphic VT associated with ischemic or nonischemic cardiomyopathies are treated with antiarrhythmics as a first line. If
these drugs fail, then they can be o ered an ablation, which has variable success rates depending on the etiology. These can be curative but o en
patients with structural heart disease develop either a recurrence of the original VT or occurrences of new ones.

However, patients with idiopathic VT in the setting of a normal heart have an excellent curative potential with ablation. These patients can be o ered
transient antiarrhythmics or a trial of β-blockers or calcium channel blockers. However, the side e ects of long-term therapy of antiarrhythmics need to
be taken into consideration. Since the success rates of ablation are excellent, many patients are o ered ablation.

If the patient has polymorphic VT, then there the role for ablation is small as a particular focus for ablation cannot usually be targeted. These types of VT
are best treated by antiarrhythmics as it is important to reverse the underlying condition such as ischemia or electrolyte abnormality.

Ultimately, patients that present with a VT in the setting of a structurally abnormal heart are o ered an implantable cardioverter defibrillator (ICD).
These are permanent devices that monitor the heart rhythm for any recurrence of the VT and can cardiovert the patient out of the tachycardia. Patients

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with idiopathic monomorphic VT are not usually o ered an ICD since these are normal hearts, usually well tolerated, and have a high cure rate with
ablation.

Ventricular Fibrillation

Ventricular fibrillation (VFib or VF) is a particular type of ventricular tachyarrhythmia that is characterized by a complete disorganized rhythm of the
ventricles (Fig. 9.11). This is usually a terminal rhythm. It requires immediate termination with DC cardioversion; otherwise, it can be life-threatening.

Figure 9.11
ECG showing ventricular fibrillation. (Used with permission from the Innovation Department of the Spectrum Health Fred and Lena Meijer Heart Center,
Grand Rapids, Michigan.)

Mechanism—The mechanism responsible for ventricular fibrillation is the degeneration of electrical impulses into multiple small reentry
circuits/wavelets that travel through the myocardium.

ECGs are characterized by chaotic, bizarre, irregular waveforms without identifiable P waves or QRS complexes with a wandering baseline (Fig. 9.11).

Characteristic features—This is the most common cause of sudden cardiac death post-myocardial infarction. This terminal rhythm is also seen in other
cardiomyopathies or in the setting of channelopathies and severe electrolyte abnormalities.

Death is almost certain if not treated promptly with electrical defibrillation. There are occurrences when VFib spontaneously terminates. The
precipitating factors for this cardiac arrhythmia include hypoxia, electrolyte abnormalities, acidosis, ischemia/myocardial infarction, and
channelopathies.

Clinical features—Include loss of consciousness, convulsions, and death. This is because the ine ective contractions of the heart lead to no cardiac
output and a cessation of the blood supply to the brain with eventual death.

Treatment—Prompt defibrillation is the main treatment. Antiarrhythmic drugs are generally started to prevent recurrences (Tables 9.21 and 9.22) if the
etiology cannot be reversed. ICDs are implanted for secondary prevention if no obvious reversible cause is found such as ischemia or severe electrolyte
abnormalities. In general, ablation has no role here since it is a disorganized rhythm without a particular focus. In some instances, close coupled PVC
can be the trigger to VFib and can be targeted for ablation. However, most of these patients are recommended for ICD as a secondary prevention.

Genetic Association of Ventricular Arrhythmias

Many genetic disorders have been discovered that can cause ventricular tachycardia and VFib. These genetic mutations either encode for
channelopathies (diseases involving ion channels) without significant structural heart disease, or cardiomyopathies that predispose to ventricular
tachyarrhythmias. The 3 main disorders/channelopathies without structural heart disease are Brugada syndrome, long QT syndrome, and
catecholaminergic polymorphic ventricular tachycardia (CPVT). The genetic diseases that code for myopathies with a strong predisposition for
ventricular arrhythmias are hypertrophic cardiomyopathy, arrhythmogenic right ventricular dysplasia (ARVD) and familial dilated cardiomyopathy.
Table 9.23 shows the mode of inheritance and ECG findings.

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Table 9.23
Genetic causes of ventricular arrhythmia in heart disease

Name of cardiac Type of ECG findings during

Genetic mutation ECG findings at rest
disease inheritance ventricular arrhythmia

Brugada syndrome Involves Na channels AD RBBB with ST elevation Ventricular fibrillation

in V1 to V3

LQTS: Mainly LQT1, LQT1 and LQT2 involve K channels Variable Resting QT interval ≥440 Torsades de pointes
LQT2, LQT3 LQT3 involves Na channels msec (polymorphic VT)
LQT1 and LQT2 (exercise
induced)
LQT3 (at rest)

CPVT RYR2 receptor gene—responsible for release of Ca from SR AD Resting ECG is normal Polymorphic VT or VFib
(commonly)
AR (rarely)

Hypertrophic CMP Sarcomere proteins like β myosin heavy chain (45%), AD LVH with deep T Monomorphic VT
cardiac myosin-binding protein C (35%) inversion in V2 to V6

Arrhythmogenic Desmosomal proteins AD in 50% T inversion in V1 to V3 LBBB VT

RV dysplasia Epsilon waves are seen in
50%

Familial dilated Most commonly TTN proteins AD in 90% Commonly have ST RBBB VT
CMP changes
May have baseline LBBB,
AF and AV block

AF, Atrial fibrillation; AD, autosomal dominant; AR, autosomal recessive; ARVD, arrhythmogenic right ventricular dysplasia; CMP, cardiomyopathy; CPVT,
catecholaminergic polymorphic ventricular tachycardia; LBBB, le bundle branch block; RBBB, right bundle branch block; RYR2, cardiac ryanodine receptor gene; TTN,
titin; VF, ventricular fibrillation; VT, ventricular tachycardia.

For further information, see Rho RW, Page RL. Ventricular arrhythmias. In: Fuster V, Walsh RA, Harrington RA, eds. Hurst’s The Heart. 13th ed. New York: McGraw-Hill;
2011:chap 42 [11].

Key Points
1. Rhythm disorders of the heart include bradyarrhythmias and tachyarrhythmias.

2. Sick sinus syndrome and AV blocks are the important pathological causes of bradyarrhythmias.

3. Mobitz type 2 AV block, complete heart block. and sick sinus syndrome require permanent pacemaker implantation.

4. Supraventricular arrhythmias include atrial flutter, atrial fibrillation, atrial tachycardia, AVNRT, and AVRT.

5. Supraventricular tachycardia with aberrant conduction needs to be distinguished from ventricular tachycardia.

6. Paroxysmal supraventricular tachycardia is treated with di erent maneuvers and pharmacologically with adenosine.

7. DC cardioversion is the treatment of choice in all tachyarrhythmias with hemodynamic compromise.

8. Defibrillation is the treatment of choice for ventricular fibrillation.

9. The prevention of stroke by providing anticoagulants in patients with a diagnosis of atrial fibrillation is calculated on the basis of the CHA2DS2-VASc
score.

10. Radiofrequency ablation is the treatment of choice for AVNRT, AVRT, paroxysmal atrial fibrillation, atrial flutter, and idiopathic VT. ICDs are implanted
in patients that cannot be treated pharmacologically for ventricular tachyarrhythmias.

Case Studies
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CASE 9.1 A 70-year-old man who is hypertensive and nondiabetic presents with a history of recurrent loss of consciousness while sitting on the couch.
There is no past history of seizures or any other neurological disorder. Examination findings show: BP = 1 56/60 mmHg, pulse = 36/min, temperature =
37°C, and RR = 15/min. Cardiovascular examination shows a slow variable S1 with normal chest and abdominal examination findings. His ECG is given
below. The most likely diagnosis for this patient is

a. Complete heart block

b. Atrial fibrillation with a slow ventricular rate

c. Sick sinus syndrome

d. Mobitz type 2 block

e. Ventricular tachycardia

The correct answer is c.

This is a patient who developed syncopal attacks while sitting, likely due to symptomatic sinus bradycardia. This disease is most commonly seen in the
older population who have sclero-degenerative disease of the sinus node. This diseased sinus node is unable to generate cardiac impulses, but the AV
node is able to conduct all the impulses to the ventricle. Due to the long sinus pauses, the blood supply to the brain is impaired leading to neurological
manifestations of the disease. These are managed by permanent pacemaker implantation. Before implantation, reversible causes must be ruled out.
These causes include hyperkalemia, metabolic acidosis, and drugs such as β-blockers and calcium channel blockers. (Used with permission from the
Innovation Department of the Spectrum Health Fred and Lena Meijer Heart Center, Grand Rapids, Michigan.)

CASE 9.2 A 66-year-old female with a history of hypertension, coronary artery disease, and stroke presents in the emergency department with a sudden
onset of palpitations for the last 3 hours at home. These palpitations are irregular and are associated with breathlessness at rest. These symptoms
started while she was sleeping in bed at 5 am and was awakened by the symptoms. She is regularly on aspirin, statins, β-blockers, and ACE inhibitors.
Examination findings show: BP = 156/92, PR = 127/min irregular, normal temperature, and RR = 18/min with variable S1S2 and bilateral basal crackles on
chest examination. Her ECG is given below. What is the best treatment to prevent further cerebrovascular accidents?

a. Continue aspirin without any additional anticoagulants

b. Add an anticoagulant

c. No aspirin or Coumadin is needed

d. Add clopidogrel to the aspirin

The correct answer is b.

This is a patient who presented to the emergency room with paroxysmal atrial fibrillation and a fast ventricular rate manifested by irregular palpitations
and early signs of pulmonary edema secondary to raised le atrial (LA) pressure. This arrhythmia is commonly responsible for embolization to the
central nervous system and patients present with transient ischemic attacks and stroke as seen in this case. The risk stratification for another stroke is
assessed with the CHA2DS2-VASc score system. This score recommends starting anticoagulation in patients with a score ≥2. One should also strongly
consider anticoagulation with a CHA2DS2-VASc score of 1; however, with a score of 1, aspirin is also an option, understanding that aspirin provides
inferior stroke prevention compared to anticoagulation but with the benefit of less bleeding. Patients with CHA2DS2-VASc score of zero are at very low
risk of stroke and therefore do not need anticoagulation; it is controversial whether aspirin has any benefit in this subgroup of patients. The CHA2DS2-
VASc score is 6 for this patient and hence she needs to be treated with anticoagulation to prevent further cardiovascular events. (Used with permission
from the Innovation Department of the Spectrum Health Fred and Lena Meijer Heart Center, Grand Rapids, Michigan.)

References

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1. Vijayaraman  P, Ellenbogen  KA. Bradyarrhythmias and pacemakers. In: Fuster  V, Walsh  RA, Harrington  RA, eds. Hurst’s The Heart. 13th ed. New York,
NY: McGraw-Hill; 2011: chap. 43.

2. Epstein  AE, DiMarco  JP, Kenneth  A,  et al. ACC/AHA/HRS 2008 Guidelines for device-based therapy of cardiac rhythm abnormalities: a report of the
American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002
Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices) developed in collaboration with the American Association for
Thoracic Surgery and Society of Thoracic Surgeons. J Am Coll Cardiol. 2008;51:el.

3. Prystowsky  EN, Padanilam  BJ, Waldo  AL. Atrial fibrillation, atrial flutter, and atrial tachycardia. In: Fuster  V, Walsh  RA, Harrington  RA, eds. Hurst’s
The Heart. 13th ed. New York, NY: McGraw-Hill; 2011:chap. 40.

4. Fuster  V, Rydén  LE, Cannom  DS,  et al. ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation: a report of the American
College of Cardiology/American Heart Association Task Force on Practice Guidelines and the European Society of Cardiology Committee for Practice
Guidelines (Writing Committee to Revise the 2001 Guidelines for the Management of Patients with Atrial Fibrillation). Eur Heart J. 2006;27:1979–2030.
[PubMed: 16885201]  

5. Estes  NAM, Sacco  RL, Al-Khatib  SM,  et al. American Heart Association Atrial Fibrillation Research Summit: a conference report from the American
Heart Association. Circulation. 2011;124(3):363–372.  [PubMed: 21709057]

6. Lip  GYH, Nieuwlaat  R, Pisters  R,  et al. Refining clinical risk stratification for predicting stroke and thromboembolism in atrial fibrillation using a
novel risk factor-based approach: the Euro Heart survey on atrial fibrillation. Chest. 2010;137:263–272.  [PubMed: 19762550]

7. Camm  AJ, Kirchhof  P, Lip  GYH,  et al. Guidelines for the management of atrial fibrillation. Euro Heart J. 2010;31:2369–2429.

8. Calkins  H. Supraventricular tachycardia: atrioventricular nodal reentry and Wol -Parkinson-White syndrome. In: Fuster  V, Walsh  RA, Harrington  RA,
eds. Hurst’s The Heart. 13th ed. New York, NY: McGraw-Hill; 2011:chap. 41.

9. Marchlinski  F. The tachyarrhythmias. In: Longo  DL, Fauci  AS, Kasper  DL, Hauser  SL, Jameson  JL, Loscalzo  J, eds. Harrison’s Principles of Internal
Medicine. 18th ed. New York, NY: McGraw-Hill; 2012:chap. 233.

10. Gutiérrez Rojas  A, Iturralde Torres  P, Colín Lizalde  L,  et al. The familial incidence of accessory atrioventricular pathways (the preexcitation
syndrome). Arch Inst Cardiol Mex. 1999;69(3):228–234.  [PubMed: 10529856]

11. Rho  RW, Page  RL. Ventricular arrhythmias. In: Fuster  V, Walsh  RA, Harrington  RA, eds. Hurst’s The Heart. 13th ed. New York, NY: McGraw-Hill;
2011:chap 42.

12. Vaughan Williams  EM. Classification of Antiarrhythmic Agents. Berlin, Germany: Springer-Verlag; 1989:45.

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