heart transplant is particularly sensitive to adenosine; therefore,

lower doses of adenosine should be used.

Calcium-Channel Blockers

CASE 20-4, QUESTION 5: B.J. is still in PSVT. What other

acute therapeutic options should be considered at this

time?

Nondihydropyridine calcium-channel blockers, verapamil

and diltiazem, can be used in patients with PSVT. Verapamil

(2.5 to 5 mg IV given for 2 minutes) achieves peak therapeutic

effects in 3 to 5 minutes after dosing and can be repeated at 10-

to 15-minute intervals to a maximal dose of 20 mg if needed.

The elderly should receive the verapamil infusion for 3 minutes

to minimize the risk of adverse events. Diltiazem is given as a

0.25-mg/kg IV bolus for 2 minutes, and a second bolus of

0.35 mg/kg can be given 15 minutes later if the effect is inadequate.

Both of these calcium-channel blockers have an 85% conversion

rate.107 However, verapamil should not be used in patients with

wide complex tachycardia of unknown origin because it may lead

to hemodynamic compromise and, potentially, VF. β-Blockers

and digoxin can be used if calcium-channel blockers and adenosine fail.

CASE 20-4, QUESTION 6: B.J. is given 5 mg IV verapamil for

1 minute, followed by an additional 5 mg 10 minutes later.

She converts to normal sinus rhythm 3 minutes after the

second dose. Because she has experienced symptoms that

could be attributed to PSVT in the past, she may be a candidate for chronic therapy to slow conduction and increase

refractoriness at the AV node. Which agents have been evaluated for this indication? Is there a role for radiofrequency

catheter ablation therapy for PSVT?

Radiofrequency catheter ablation is frequently used as a longterm treatment for PSVT. Electrophysiologic testing is used to

determine the location of the re-entrant tract, which then can be

ablated, thereby interrupting accessory pathways and re-entrant

circuits. This treatment approach is potentially curative and is

performed by a specially trained electrophysiologist. Patients

who are not candidates for ablation, or who do not wish to

undergo the procedure, can receive medications on a long-term

basis. PSVT is managed with agents that slow conduction and

increase refractoriness in the AV node, thereby preventing a rapid

ventricular response. These include oral verapamil, diltiazem,

β-blockers, or digoxin. Class Ic and III agents are used occasionally to slow conduction and increase refractoriness of the fast

bypass tract to prevent triggering impulses such as premature

atrial and ventricular contractions.

B.J. has had a few episodes of PSVT in the past and may be

a candidate for ablation. Alternatively, because she responded to

IV verapamil, oral SR verapamil could be prescribed at a dosage

of 240 mg/day.

505Cardiac Arrhythmias Chapter 20

Wolff-Parkinson-White Syndrome

CASE 20-5

QUESTION 1: M.B., a 35-year-old man, presents to the ED

with a chief complaint of chest palpitations for 4 hours. He

relates a history of many similar self-terminating episodes

since he was a teenager. He took an unknown medication

5 years ago that decreased the occurrence of the palpitations, but he stopped taking it because of side

effects. M.B.’s vital signs are BP, 96/68 mm Hg; pulse,

226 beats/minute, irregular; respiratory rate, 15 breaths/

minute; and temperature, 98.7◦F. A rhythm strip confirms

AF, with a QRS width varying from 0.08 to 0.14 seconds. To

control the ventricular rate, 10 mg IV verapamil is administered for 2 minutes. Within 2 minutes of completing the

infusion, VF is noted on the monitor. M.B. is defibrillated,

and normal sinus rhythm is restored. A subsequent ECG

demonstrates a P-R interval of 100 ms (normal, 120 to

200 ms) and delta waves, compatible with WPW. What is

WPW syndrome?

WPW is a pre-excitation syndrome in which there is an accessory bypass tract (known as a Kent bundle) connecting the atria

to the ventricles (Fig. 20-7). An impulse can travel down this

pathway and excite the ventricle before the expected regular

impulse through the AV node arrives (hence the term preexcitation). If there is antegrade conduction over the bypass tract

while the patient is in normal sinus rhythm, the ECG will demonstrate a short P-R interval (<100 ms), a delta wave that represents

a fused complex from pre-excitation, and the regular QRS complex after AV conduction. WPW can occur in children and adults

without overt cardiac disease. PSVT (specifically AVRT) and AF

occur in these patients at a higher incidence than in the general population of the same age.108 Similar to M.B., the rapid

heart rate experienced during the tachycardia may cause palpitations, light-headedness, and fatigue. When patients with WPW

develop AF, there is a danger that the rapid atrial impulses will

be conducted directly to the ventricle through the bypass tract,

causing a rapid ventricular rate that may evolve into VF.

CASE 20-5, QUESTION 2: Why did verapamil cause VF in

M.B.? What drug or drugs would be appropriate for M.B.,

and what drugs should be avoided?

Verapamil can block AV conduction by increasing the effective

refractory period, allowing all impulses from the atrial area to

conduct down the bypass (Kent) tract. Because M.B. had AF, the

rapid atrial impulses were conducted directly down the bypass

tract to the ventricle, causing VF. In addition, verapamil may

enhance conduction over the accessory pathway by shortening

its effective refractory period. Also, peripheral vasodilation can

induce a reflex sympathetic discharge that can, in turn, decrease

the effective refractory period of the accessory pathway.109,110

The most common presentation of WPW syndrome involves

normal antegrade conduction down the AV node and retrograde

conduction back up through the accessory pathway. Thus, drugs

that inhibit antegrade impulse conduction through the AV node

(e.g., verapamil, digoxin) will terminate the re-entrant tachycardia and can be suitable in the absence of AF. The less common

variety of WPW is antegrade conduction through the accessory

pathway with retrograde transmission up through the AV node.

Similarly, AV nodal blocking agents will terminate this type of reentrant tachycardia. In some situations, such as that experienced

by M.B., rapid AF with an accessory pathway occurs, which can

lead to VF and cardiac arrest.

FIGURE 20-8 Bundle branch block. Note that the QRS interval is

prolonged. A 12-lead electrocardiogram is required to make the

diagnosis of left bundle branch block. (Reproduced with permission

from Stein E. Rapid Analysis of Arrhythmias: A Self-Study Program.

2nd ed. Philadelphia, PA: Lea & Febiger; 1992.)

The antiarrhythmic drugs used to treat patients with AF who

have an accessory pathway, such as M.B., include those that

depress conduction and increase the effective refractory period of

the fast sodium channel–dependent tissue of the accessory pathway. This includes most class I antiarrhythmic drugs, with the

class Ib agents being least effective. Propafenone and flecainide

are effective and may be preferred.111–114 Amiodarone and sotalol

may also be effective, but clinical experience is limited.115–117

Radiofrequency ablation of the bypass tract is used more frequently for these patients to prevent VF.

Further therapy for M.B. may not be useful at this time. However, if he has recurrent AF or other symptomatology associated

with WPW, radiofrequency catheter ablation or drug therapy as

outlined previously could be indicated.

CONDUCTION BLOCKS

Various arrhythmias can result from blockage of impulse conduction. These can occur above the ventricle, such as first-, second-,

and third-degree (complete) AV block. Others, such as right or

left bundle branch block (RBBB or LBBB) and trifascicular block,

originate below the bifurcation of the His bundle. Although

conduction blocks can be classified as either supraventricular or

ventricular arrhythmias, they are discussed as a separate group

because their mechanism of arrhythmogenesis is similar and their

treatment is different from other arrhythmias.

CASE 20-6

QUESTION 1: H.T., a 63-year-old man, was admitted to the

coronary care unit (CCU) 12 hours ago with an acute inferior wall MI. He has remained stable. On admission, he had

the rhythm strip shown in Figure 20-8 (left bundle branch

block). Twelve hours later, it has changed to the rhythm strip

shown in Figure 20-9 (Wenckebach or type I, second-degree

AV block). Are these rhythms potentially hazardous to H.T.?

How is second-degree AV block different from first- or thirddegree AV block?

P-R

1

P-R

2

P-R

3

QRS Missing

P PPP P P P

FIGURE 20-9 Second-degree atrioventricular block type I

(Wenckebach). The P-R interval progressively prolongs until, after

the third complex, a QRS complex is not conducted. (Reproduced

with permission from Stein E. Rapid Analysis of Arrhythmias: A

Self-Study Program. 2nd ed. Philadelphia, PA: Lea & Febiger; 1992.)

506 Section 2 Cardiac and Vascular Disorders

Regular

PP intervals

Irregular

RR intervals

*

 = nonconducted P waves

* * * *

FIGURE 20-10 Sinus rhythm with second-degree AV block, Type II; note constant PR interval. (Reprinted with

permission from Smeltzer SC, Bare BG. Textbook of Medical-Surgical Nursing. 9th Ed. Philadelphia: Lippincott

Williams & Wilkins; 2000.)

H.T.’s rhythm strip revealed a diagnosis of LBBB. Bundle

branch block occurs when the electrical impulse cannot be conducted along the left or right fascicle of the His-Purkinje system

(see Fig. 20-1). In H.T., the impulse travels down the right bundle

normally, and the right ventricle contracts at the normal time.

The left bundle is blocked, and, therefore, the left side is depolarized from an impulse conducted from the right ventricle. This

impulse must travel through atypical conduction tissues (with

slower conduction), and hence the left side depolarizes later.

This is revealed on the ECG by a widened QRS complex. Bundle branch blocks, particularly in the left fascicle, are associated

with coronary artery disease, systemic hypertension, aortic valve

stenosis, and cardiomyopathy.118 Typically, they do not lead to

clinical cardiac dysfunction on their own. Because H.T. has LBBB,

he can develop complete heart block (third-degree block) if for

any reason his right fascicle is damaged.

First-degree AV block usually is asymptomatic. The ECG will

show P waves with a prolonged P-R interval (normal, <200 ms),

but each P wave is followed by a normal QRS complex. Firstdegree AV block is a common finding in patients taking digoxin,

verapamil, or other drugs that slow AV conduction.

Second-degree heart block consists of two types. Mobitz type

I (Wenckebach) is characterized by progressive lengthening of

the P-R interval with each beat and a corresponding shortening

of the R-R interval until finally an impulse is not conducted; the

cycle then starts over again. Mobitz type II (Fig. 20-10) impulse

conduction is blocked in a fixed, regular pattern (e.g., 3:1 block,

in which for every three P waves, only one is conducted).

Third-degree heart block (complete heart block) occurs when

none of the impulses from the SA node are conducted to the

ventricles. During third-degree block, the ventricle must develop

its own pacemaker (escape rhythm), which may be too slow to

provide adequate cardiac output, causing the patient to become

symptomatic. A mechanical pacemaker is needed for treatment

of third-degree AV block. AV blocks can be caused by drugs

(β-blockers, calcium-channel blockers, digoxin), acute MI, amyloidosis, and congenital abnormalities.119

Atropine

CASE 20-6, QUESTION 2: How should H.T.’s heart block be

treated?

H.T. is experiencing a Wenckebach rhythm, which often is

transient after an inferior wall MI. As long as he is hemodynamically stable, he should be monitored closely. If his heart rate and

BP drop, atropine 0.5 mg IV bolus (maximum 2 mg) can increase

the heart rate. This is only a short-term therapy; if the hemodynamic compromise persists, a pacemaker must be inserted to

initiate the impulse to control the heart rate.

VENTRICULAR ARRHYTHMIAS

Recognition and Definition

Ventricular arrhythmias arise from irritable ectopic foci within

the ventricular myocardium. Impulses from these ectopic foci

generate wide, bizarre-looking QRS complexes leading to PVCs

(Fig. 20-11). PVCs can arise from the same ectopic site (unifocal)

or can be multifocal in origin. They can be simple (e.g., isolated

Normal

QRS Complex

Abnormal QRS

from Ventricular Focus

QRS = 0.12 sec

FIGURE 20-11 Premature ventricular contraction. Every other beat is a premature ventricular (ectopic) contraction.

507Cardiac Arrhythmias Chapter 20

FIGURE 20-12 Nonsustained ventricular tachycardia. (Reprinted with permission from Mhairi G et al. Avery’s

Neonatology Pathophysiology & Management of the Newborn. 6th ed. Philadelphia: Lippincott Williams & Wilkins;

2005.)

or infrequent) or complex (e.g., R on T, in which the R wave

of a PVC falls on top of a normal T wave). Other presentations

include runs of two or more beats, bigeminy (every other beat is a

PVC), or trigeminy (every third beat is a PVC). Three consecutive

PVCs usually are defined as ventricular tachycardia (VT), which

can be nonsustained or sustained. Ventricular flutter, VF, and

TdP are other serious forms of ventricular arrhythmias. The

presentation, etiology, treatment, and ion channels associated

with TdP are discussed separately.

Nonsustained ventricular tachycardia (NSVT) (Fig. 20-12)

commonly is defined as three or more consecutive PVCs lasting

less than 30 seconds and terminating spontaneously. Sustained

VT (SuVT) is defined as consecutive PVCs lasting more than

30 seconds, with a rate usually in the range of 150 to 200 beats/

minute. P waves are lost in the QRS complex and are indiscernible. SuVT (Fig. 20-14) is a serious development because it

can degenerate into VF. Ventricular flutter is characterized by

sustained, rapid, regular ventricular beats (normal, >250 beats/

minute) and usually degenerates into VF. VF (see Fig. 20-13)

is characterized by irregular, disorganized, rapid beats with no

identifiable P waves or QRS complexes. It is thought to be triggered by multiple re-entrant wavelets in the ventricle. There is

no effective cardiac output in patients with VF.118,119

Etiology

Common factors that cause ventricular arrhythmias are

ischemia, the presence of organic heart disease, exercise,

metabolic or electrolyte imbalance (e.g., acidosis, hypokalemia

or hyperkalemia, hypomagnesemia), or drugs (digitalis, sympathomimetic amines, antiarrhythmic drugs). It is essential to

identify and remove any treatable cause (e.g., metabolic or electrolyte imbalance and proarrhythmic drugs) before initiating

antiarrhythmic drug therapy.

Evaluation of Life-Threatening

Ventricular Arrhythmias

An episode of life-threatening ventricular arrhythmia (i.e., SuVT,

TdP, VF) carries a significant risk of morbidity and mortality.

Adequate documentation of the arrhythmia and its suppression

by either drugs or a mechanical device are essential. Patients

suspected of having, or documented to have, symptoms of a

life-threatening arrhythmia (e.g., syncope, out-of-hospital cardiac arrest) should be admitted to the hospital and evaluated.

At present, the ACC/AHA/ESC practice guidelines recommend

FIGURE 20-13 Ventricular fibrillation.

standard testing with a 12-lead ECG in all patients undergoing evaluation for ventricular arrhythmias. The writing group

assigned a class I rating for exercise testing in two groups of

patients with ventricular arrhythmias: (a) adults at intermediate

risk of having coronary heart disease (CHD) by sex, age, and

symptoms to induce ischemic changes or ventricular arrhythmias, and (b) patients with established or suspected exerciseinduced ventricular arrhythmias, with the intent of provoking

the arrhythmia, achieving a diagnosis, and assessing the patient’s

response to tachycardia. Pharmacological stress testing is preferred over exercise testing in patients with an intermediate probability of CHD if they are physically incapable of performing a

symptom-limited exercise test. Two additional approaches are

used to evaluate the arrhythmia and the effectiveness of therapy:

ambulatory monitoring and electrophysiologic studies.118

AMBULATORY MONITORING

The frequency of suspected ventricular arrhythmias determines

the ambulatory monitoring device indicated for patients.119 For

more frequent occurrences (once daily) of arrhythmias, Holter

monitoring during a 24- to 48-hour period represents the firstline ambulatory monitoring device. The patient wears a portable

ECG monitoring device in a purselike carrier, and electrodes

connected to the monitor are taped to the patient’s chest. The

ECG is played back in the laboratory, correlating the presence

of arrhythmias with a written patient activity and symptom log.

In contrast, event recorders are selected for patients presenting with arrhythmias that occur less frequently.119 The event

recorder (or loop recorder) is worn constantly for up to 14 days

(http://www.advmed.ca/ler.asp) and stores and saves data on

instruction by the patient. Whenever a patient experiences symptoms, a switch on the recorder is depressed, resulting in storage

of a record of the patient’s heart rhythm at the time of the event.

A telephone can transfer event recorder data for analysis.

ELECTROPHYSIOLOGIC STUDIES

Electrophysiologic (EP) studies represent another approach to

evaluating ventricular arrhythmias, especially in patients with

sporadic ventricular arrhythmias that may be missed by shortterm monitoring.118 EP testing serves as a diagnostic tool for

evaluating drug effects, assessing the inducibility of VT, determining the risks of recurrent VT or sudden cardiac death (SCD),

guiding ablation, and assessing the need for an ICD (implantable

cardioverter-defibrillator).

Class I recommendations (per ACC/AHA/ESC) on the use of

EP studies apply to the following patient subsets: (a) patients with

FIGURE 20-14 Sustained ventricular tachycardia.

508 Section 2 Cardiac and Vascular Disorders

R waves after axis shift,

negatively deflected

Isoelectric point at which

the electrical axis shifts

R waves positively deflected Rate ª 180 beats/min

Note the difference in QRS configuration from beat to beat

FIGURE 20-15 Torsades de pointes.

remote MI with symptoms indicative of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope; (b) CHD

patients to guide and determine the efficacy of VT ablation; (c)

CHD patients being evaluated for wide-QRS-complex tachycardias of unclear mechanism; and (d) patients with structural heart

disease or impaired left ventricular function who present with

syncope of unknown origin.118

Premature Ventricular Contractions

CASE 20-7

QUESTION 1: A.S., a 56-year-old woman, is admitted to

the CCU with a diagnosis of acute anterior wall MI. Her

vital signs are BP, 115/75 mm Hg; pulse, 85 beats/minute;

and respiratory rate, 15 breaths/minute. Auscultation of the

heart reveals an S3 gallop. Her electrolytes include potassium (K) 3.8 mEq/L (normal, 3.5 to 5.0 mEq/L), and magnesium (Mg) 1.4 mEq/L (normal, 1.6 to 2.4 mEq/L). Otherwise,

her examination is within normal limits. Two days later, an

echocardiogram estimates her ejection fraction to be 35%

(normal, >50%). During her stay in the CCU as well as the

step-down unit, multiple PVCs (15/minute) were noted on

the bedside monitor. No antiarrhythmic agent was ordered.

Should A.S.’s multiple PVCs be treated with a class I antiarrhythmic drug?

Occasional PVCs are a benign, natural occurrence, even in a

healthy heart, and are not an indication for drug therapy. Similarly, asymptomatic simple forms of PVCs, even in patients with

other cardiac disease, usually are not an indication for treatment.

However, the presence of frequent PVCs is a well-described risk

factor for SCD.120 In patients with a low ejection fraction induced

by the PVCs or NSVT, the risk for SCD can increase 13-fold. However, studies have shown that MI survivors were at increased risk

of SCD when frequent and repetitive forms of ventricular ectopic

activity occurred in patients with lower ejection fractions.118

TYPE IC ANTIARRHYTHMIC AGENTS

Because PVCs are a risk factor for SCD, the National Institutes

of Health launched the Cardiac Arrhythmia Suppression Trial

(CAST)121,122 to assess the benefit of PVC suppression in survivors of MI. The CAST was a prospective, randomized, placebocontrolled trial that evaluated three antiarrhythmic agents: flecainide, encainide, and moricizine (all class Ic agents). The choice

of these drugs was based on results of a pilot study of 1,498

patients that showed adequate suppression of arrhythmia (PVCs)

in the target population. Ten months after initiation of the study,

CAST was discontinued because of excess total mortality and cardiac arrests in patients receiving flecainide and encainide. Fortythree of 755 patients in the flecainide and encainide groups died

of arrhythmia or cardiac arrest versus 16 of the 743 patients taking

placebo. Further, total mortality in the flecainide and encainide

groups was 8.3% (63 of 755 patients) compared with 3.5% (26 of

743 patients) in the placebo group.121 In the moricizine group,

which was reported separately in CAST II, 16 of 660 patients in the

drug group died compared with 3 of 668 patients in the placebo

group in the initial 2 weeks. Subsequent long-term follow-up did

not show a difference between moricizine and placebo.122 It generally is believed that the excessive death rate in the drug-treated

groups was attributable to the proarrhythmic effect of the drugs.

Because the patients enrolled in CAST were asymptomatic and

at low risk for the development of arrhythmias, they were at

greater risk for drug toxicity (relative to benefit). Although many

issues have been raised concerning CAST, one conclusion is that

patients with a recent MI and the presence of asymptomatic PVCs

should not be treated with encainide, flecainide, or moricizine.

Whether other class I antiarrhythmic agents will produce similar

results is unknown. Thus, the decision not to treat A.S.’s PVCs

with class I antiarrhythmic medications was a sound one. The

proarrhythmic effects of the drug may outweigh the potential

danger of PVCs at this time.

CASE 20-7, QUESTION 2: What alternatives to class I antiarrhythmic drugs should be considered for A.S.?

β-BLOCKING AGENTS

It is estimated that SCD accounts for 50% of all deaths among MI

patients.123 In a pooled analysis from 31 clinical trials evaluating

β-blockers in MI, a 20% to 25% reduction in the risks of death

and reinfarction during an average of 2 years of treatment was

documented.124 The beneficial effects of β-blockers on mortality

were primarily attributed to a decrease in SCD, usually caused

by arrhythmias such as VF.125 Similarly, a meta-analysis of 28

randomized trials demonstrated that intravenous followed by

oral β-blocker therapy resulted in a 15% to 20% decrease in the

relative risks of reinfarction and cardiac arrest during the first

7 days of hospitalization for acute MI patients.126

The COMMIT/CCS2 (Clopidogrel and Metoprolol in Myocardial Infarction Trial/Second Chinese Cardiac Study) collaborative group assessed the effect of intravenous metoprolol (up

509Cardiac Arrhythmias Chapter 20

to three 5-mg doses in the first 15 minutes) followed by oral

metoprolol (200 mg/day in divided doses, then 200 mg once

daily) or placebo on cardiovascular outcomes in 45,852 acute

MI patients.127 The two prespecified end points included the

composite of death, reinfarction, or cardiac death, along with allcause mortality. The mean duration of drug therapy was 15 days.

β-Blocker therapy did not result in significant reductions in the

rate of achieving the coprimary study outcomes, but 5 fewer

episodes of VF for every 1,000 patients occurred during therapy with metoprolol (odds ratio, 0.83; 95% confidence interval

[CI], 0.75–0.93; p=0.001). However, metoprolol-treated patients

experienced 11 more episodes of cardiogenic shock for every

1,000 patients during the treatment period (odds ratio, 1.30; 95%

CI, 1.19–1.41; p <0.00001).

The importance of the β-blocking effect after MI is further

illustrated by the results of two trials of sotalol in patients with