synthesis of adenosine

triphosphate.361,362 It may also have membrane-stabilizing properties, enhance the antioxidant effects of vitamin E, and stabilize

calcium-dependent slow channels. In animal models, it has positive inotropic effects, although weaker than those from digoxin.

More than 18 open-label and double-blind, randomized clinical

trials have been conducted of coenzyme Q in patients with HF

ranging from NYHA classes II to IV.361 Doses varied from 50 to

200 mg/day. In contrast to hawthorn, the patients in many of these

trials were also taking diuretics, ACE inhibitors, and digoxin.

Different trials used different end point measurements. Positive

effects on subjective symptoms, NYHA class improvement, EF,

quality of life, and hospitalization rates have all been observed.

Two trials, however, failed to demonstrate significant changes

in EF, vascular resistance, or exercise tolerance. None of the

trials had sufficiently large samples sizes or adequate duration of

assessment to detect reduction in mortality. Side effects were consistently minimal, but included nausea, epigastric pain, diarrhea,

heartburn, and appetite suppression. Mild increases in lactate

dehydrogenase and hepatic enzymes have been rarely reported

with coenzyme Q doses in excess of 300 mg/day.

It can be concluded that hawthorn and coenzyme Q are both

safe in the treatment of HF and might provide symptomatic

improvement, especially in patients with mild HF (NYHA class

II). Only coenzyme Q has been shown to be of benefit as an

adjunct to conventional therapies. It is unknown whether using

hawthorn and coenzyme Q together, as prescribed for W.L., will

have an additive effect. No conclusion can be drawn about their

effects on mortality rates.

W.L. has poorly controlled systolic HTN and HF that is

beginning to interfere with his activities of daily life. Although

evidence indicates that patients with NYHA class II HF obtain

symptomatic improvement with hawthorn and coenzyme Q,

this does not address W.L.’s HTN. (As reviewed by Tran et al.,361

conflicting data exist on the value of coenzyme Q in lowering

BP.) Furthermore, the results of the SPICE trial did not demonstrate any mortality benefits. Also, no incremental benefits were

seen when combined with standard therapy. Even if W.L. and

his naturopath are both satisfied with his responses to hawthorn

and coenzyme Q, significant concern still exists about what will

happen when and if his disease progresses. Uncontrolled HTN in

patients with HF can further lead to cardiac remodeling, resulting

in worsening HF. Currently he is presenting with symptomatic

HF; therefore he should be started on a diuretic to alleviate his

symptoms. Starting with a 20-mg dose of furosemide and titrating

slowly may be one approach. For all of the reasons cited throughout this chapter, one must also argue strongly for starting an ACE

inhibitor to control his HTN. He should be counseled that the

urinary frequency he experienced previously should diminish

after a few days.

He is being started on both hawthorn and coenzyme Q simultaneously. If he does improve, it will be difficult to assess whether

it is because of only one of the agents or the combination. With

this in mind, it might be more logical to continue hawthorn

alone at a dose of 450 mg BID. If no benefit is derived after

1 month, hawthorn should be stopped and coenzyme Q started

at 100 mg/day.

The use of natural supplements is not routinely recommended

by the guidelines.2 The guidelines clearly state that natural products should not be used to treat symptomatic HF. Agents such as

ephedra (which contain catecholamines), ephedrine metabolites,

or imported Chinese herbs are contraindicated in HF because of

increased risk of mortality and morbidity. Also no regulatory

oversight, quality control, or regulations exist on the use of natural supplements.

488 Section 2 Cardiac and Vascular Disorders

KEY REFERENCES AND WEBSITES

A full list of references for this chapter can be found at

http://thepoint.lww.com/AT10e. Below are the key references

for this chapter, with the corresponding reference number in this

chapter found in parentheses after the reference.

Key References

Bardy GH et al. Amiodarone or an implantable cardioverterdefibrillator for congestive heart failure [published correction

appears in N Engl J Med. 2005;352:2146]. N Engl J Med. 2005;352:

225. (332)

Barnes MM et al. Treatment of heart failure with preserved ejection fraction. Pharmacotherapy. 2011;31:312. (19)

Felker GM et al. Diuretic strategies in patients with acute decompensated heart failure. N Engl J Med. 2011;364:797. (111)

Granger CB et al. Effects of candesartan in patients with chronic

heart failure and reduced left-ventricular systolic function intolerant to angiotensin-converting-enzyme inhibitors: the CHARMAlternative trial. Lancet. 2003;362:772. (176)

Hunt SA et al. 2009 focused update incorporated into the

ACC/AHA 2005 Guidelines for the Diagnosis and Management

of Heart Failure in Adults: a report of the American College

of Cardiology Foundation/American Heart Association Task

Force on Practice Guidelines: developed in collaboration with

the International Society for Heart and Lung Transplantation

[published correction appears in Circulation. 2010;121:e258]. Circulation. 2009;119:e391. (1)

Lindenfeld J et al. HFSA 2010 Comprehensive Heart Failure Practice Guideline. J Card Fail. 2010;16:e1. (2)

[No authors listed]. Effect of metoprolol CR/XL in chronic heart

failure: Metoprolol CR/XL Randomised Intervention Trial in

Congestive Heart Failure (MERIT-HF). Lancet. 1999;353:2001.

(209)

Packer M et al. Comparative effects of low and high doses of the

angiotensin-converting enzyme inhibitor, lisinopril, on morbidity and mortality in chronic heart failure. ATLAS Study Group.

Circulation. 1999;100:2312. (165)

Packer M et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart

Failure Study Group. N Engl J Med. 1996;334:1349. (214)

Pitt B et al. Eplerenone, a selective aldosterone blocker, in

patients with left ventricular dysfunction after myocardial infarction [published correction appears inNEnglJMed. 2003;348:2271].

N Engl J Med. 2003;348:1309. (67)

Pitt B et al. The effect of spironolactone on morbidity and mortality in patients with severe heart failure. Randomized Aldactone

Evaluation Study Investigators. N Engl J Med. 1999;341:709. (66)

Rathore SS et al. Association of serum digoxin concentration

and outcomes in patients with heart failure. JAMA. 2003;289:871.

(241)

Tang AS et al. Cardiac-resynchronization therapy for mild-tomoderate heart failure. N Engl J Med. 2010;363:2385. (339)

Zannad F et al. Eplerenone in patients with systolic heart failure

and mild symptoms. N Engl J Med. 2011;364:11. (61)

Cardiac Arrhythmias 20

C. Michael White, Jessica C. Song, and James S. Kalus

CORE PRINCIPLES

CHAPTER CASES

ATRIAL FIBRILLATION (AF)/FLUTTER

1 Chest palpitations, lightheadedness, and reduced exercise tolerance are the most

common symptoms of AF, but stroke is among the severe complications. The goals

of therapy are to control the ventricular rate and reduce the risk of stroke.

Case 20-1 (Questions 1, 2)

2 Digoxin, β-blockers, and nondihydropyridine calcium-channel blockers are

appropriate rate-controlling medications. Digoxin is usually adjunctive therapy.

Antiarrhythmic drugs are recommended in patients with symptoms but not needed

in asymptomatic patients (no symptoms other than palpitations).

Case 20-1 (Questions 3–7)

3 Before converting AF to sinus rhythm, assurance of a lack of clot is important but not

required if someone is unconscious or cannot mentate. People with a CHADS2 score

of 2 or greater should receive chronic antithrombotic therapy with warfarin or

dabigatran. Those with a score of 0 can receive aspirin, and those with a score of 1

can receive aspirin or antithrombotic therapy.

Case 20-1 (Questions 8, 13)

4 Antiarrhythmic drugs convert patients out of AF 50% of the time, whereas electrical

shock is successful 90% of the time. To maintain sinus rhythm after conversion,

class Ib agents cannot be used, class Ic agents cannot be used in patients with

structural heart disease (left ventricular hypertrophy, myocardial infarction, or heart

failure), and class Ia and III agents can increase the risk of torsades de pointes.

Propafenone, sotalol, dronedarone, dofetilide, and amiodarone are commonly used

antiarrhythmic agents for AF.

Case 20-1 (Questions 9–12)

5 Atrial flutter is less common than AF, but similar rate control and antiarrhythmic

strategies can be tried. Radiofrequency ablation can be used to terminate atrial

flutter.

Case 20-2 (Question 1)

6 A large percentage of patients exhibit AF after cardiac surgery. β-Blockers and

amiodarone have been shown to decrease clinical manifestations of AF and reduce

hospital length of stay. If AF occurs, it should be managed with rate control.

Case 20-3 (Questions 1–3)

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA (PSVT)

1 PSVT is caused by re-entry within the atrioventricular (AV) node. Palpitations and

hypotension can occur. The Valsalva maneuver, adenosine, or nondihydropyridine

calcium-channel blockers can be used to treat the arrhythmia.

Case 20-4 (Questions 1–6)

2 In Wolff-Parkinson-White syndrome patients with PSVT, the use of AV nodal blocking

agents such as β-blockers, nondihydropyridine calcium-channel blockers, and

digoxin can increase the risk of cardiac arrest. Ablation can destroy the bypass tract

and cure the patient.

Case 20-5 (Questions 1, 2)

continued

489

490 Section 2 Cardiac and Vascular Disorders

CHAPTER CASES

ATRIOVENTRICULAR (AV) BLOCK

1 β-Blockers, digoxin, and nondihydropyridine calcium-channel blockers should be

withheld in patients with type 1 second- or third-degree AV block. Atropine can be

used to treat this disorder.

Case 20-6 (Questions 1, 2)

VENTRICULAR ARRHYTHMIAS

1 In patients with premature ventricular complexes (PVCs) and myocardial infarction,

β-blockers are the treatment of choice.

Case 20-7 (Questions 1, 2)

2 Patients with myocardial infarction and nonsustained ventricular tachycardia (VT)

should receive β-blockers and need to be risk stratified to determine whether they

should receive an implantable cardioverter-defibrillator.

Case 20-8 (Question 1)

3 Patients with sustained VT should be treated with intravenous antiarrhythmic agents

unless they are hemodynamically unstable, in which case they should be electrically

converted. To prevent death from arrhythmia recurrence, implantable cardioverterdefibrillators are superior to antiarrhythmic drugs, but to decrease the occurrence

of painful shocks, both strategies are usually used simultaneously.

Case 20-9 (Questions 1–3)

TORSADES DE POINTES (TDP)

1 TdP occurs secondary to antiarrhythmic and nonantiarrhythmic medications that

prolong the QTc interval. Class Ia and III antiarrhythmic agents, antipsychotic

agents, fluoroquinolones, macrolides, azole antifungals, and methadone can

prolong the QTc interval. Magnesium is the treatment of choice for

hemodynamically stable TdP.

Case 20-10 (Questions 1–4)

2 Natural products such as omega-3 fatty acids, coenzyme Q10, and carnitine have

been studied to treat atrial and ventricular arrhythmias with the most compelling

evidence for omega-3 fatty acids in patients with coronary disease.

Case 20-10 (Question 5)

CARDIAC ARREST

1 Cardiac arrest should be treated with 2-minute cycles of aggressive

cardiopulmonary resuscitation, electrical shock for VT or ventricular fibrillation (VF),

epinephrine or vasopressin, and amiodarone for refractory VT or VF according to

the advanced cardiac life support guidelines from the American Heart Association.

Case 20-11 (Questions 1–4),

Case 20-12 (Question 1),

Case 20-13 (Question 1)

Adequate blood pumping depends on a continuous, wellcoordinated electrical activity within the heart. This chapter

reviews and discusses cardiac electrophysiology, arrhythmogenesis, common arrhythmias, and antiarrhythmic treatment.

ELECTROPHYSIOLOGY

CELLULAR ELECTROPHYSIOLOGY

An electrical potential exists across the cell membrane, and the

electrical potential changes in a cyclic manner that is related to

the flux of ions across the cell membrane, principally K+, Na+,

and Ca2+. If the change in the membrane potential is plotted

against time in a given cycle of a His-Purkinje fiber, a typical

action potential results (Fig. 20-1).

The action potential can be described in five phases. Phase 0 is

related to ventricular depolarization resulting from sodium entry

into the cell through fast sodium channels. On a surface electrocardiogram (ECG), phase 0 is represented by the QRS complex.

Phase 1 is the overshoot phase in which calcium enters the cell and

contraction occurs. During phase 2, the plateau phase, inward

depolarizing currents through slow sodium and calcium channels are counterbalanced by outward repolarizing potassium currents. Phase 3 constitutes repolarization, which on the ECG is

represented by the T wave. During phase 4, sodium moves out of

the cell and potassium moves into the cell via an active pumping

mechanism. During this phase, the action potential remains flat

in some cells (e.g., ventricular muscle) and does not change until

it receives an impulse from above. In other cells (e.g., sinoatrial

[SA] node), the cell slowly depolarizes until it reaches the threshold potential and again spontaneously depolarizes (phase 0). The

shape of the action potential depends on the location of the cell

(see Fig. 20-1). In both the SA and atrioventricular (AV) nodes, the

cells are more dependent on calcium influx than sodium influx,

resulting in a less negative resting membrane potential, a slow

rise of phase 0, and the capability of spontaneous (automatic)

phase 4 depolarization (Fig. 20-1).

The upward slope of phase 0, referred to as Vmax, is related to

the conduction velocity. The steeper the slope, the more rapid

the rate of depolarization. Another influence on Vmax is the point

at which depolarization occurs. The less negative the threshold

potential, the slower Vmax will be, and hence conduction velocity

491Cardiac Arrhythmias Chapter 20

Action Potentials

0

1

2

3

4

Time (sec)

0.2 0.4 0.6

P

QRS

T

U

AV Node

SA Node

Common Bundle

Bundle Branches

Purkinje Fibers

entricular Muscle

A

B

C

V

FIGURE 20-1 The cardiac conduction system. A: Cardiac conduction system anatomy. B: Action potentials of specific

cardiac cells. C: Relationship of surface electrocardiogram to the action potential. SA, sinoatrial; AV, atrioventricular.

is slowed. Drugs can affect Vmax and conduction velocity by blocking the fast sodium channels or by making the resting membrane

potential less negative (e.g., class I agents).

The action potential duration (APD) is the length of time from

phase 0 to the end of phase 3. The effective refractory period is

the length of time that the cell is refractory and will not propagate

another impulse. Both of these measurements can be obtained

from intracardiac recordings of the action potential. Class Ia and

III agents prolong the refractoriness of the heart.

NORMAL CARDIAC ELECTROPHYSIOLOGY

Normal cardiac electrical activity begins with automatic impulse

generation (automaticity) at the SA node and then normal

impulse conduction through the heart.

AUTOMATICITY

Automaticity is the ability of cells (often referred to as pacemaker cells) to depolarize spontaneously. These cells are located

in the SA and AV nodes and the His-Purkinje system. The SA

node is normally the dominant pacemaker because it reaches

the threshold faster than other nodes in a normal heart, resulting in 60 to 100 depolarizations per minute. The innate AV node

and Purkinje rate of depolarization is 40 to 60 and 40 depolarizations per minute, respectively. In the healthy heart, the AV node

and Purkinje fibers are prevented from spontaneous depolarization (overridden) by the more frequent impulses from the SA

node. If the normal conduction system is disrupted (e.g., after a

myocardial infarction [MI]), the AV node or Purkinje fibers may

temporarily become the dominant pacemaker.

CONDUCTION

An impulse normally originates in the SA node and travels down

the specialized intranodal pathways to activate the atrial muscle and the AV node. The AV node holds the impulse briefly

before releasing it to the bundle of His. It then travels to the right

and left bundle branches and out to the ventricular myocardium

via the Purkinje fibers. The ECG tracing consists of a series of

complexes that correspond to electrical activity in a specific location or anatomic site. By convention, these electrical deflections

have been labeled the P wave, QRS complex, and T wave. The

P wave represents depolarization of the atria, whereas the QRS

complex reflects ventricular depolarization. The T wave reflects

repolarization of the ventricles. To evaluate the intact conduction

system, conduction intervals at different sites can be obtained.

The normal intervals as measured by ECG or intracardiac electrodes are shown in Table 20-1. Drugs and ischemia can alter the

conduction and hence the ECG intervals. The effects of antiarrhythmic agents on the ECG are described in Table 20-2.

An Approach to Reading

Electrocardiograms

ELECTROCARDIOGRAPHIC PAPER

Calculation of the various intervals and widths is facilitated by

recording the ECG waveforms on graph paper consisting of large

squares defined by heavier lines, which in turn are composed

of smaller squares. Each small square is 1 mm long and represents 0.04 seconds. The larger squares are composed of five small

squares (5 mm in length) and represent 0.20 seconds (Fig. 20-2).

492 Section 2 Cardiac and Vascular Disorders

TABLE 20-1

Normal Electrophysiological Intervals

Normal

Interval Indices (ms) Electrical Activity Measured By

PR 120–200 Atrial depolarization Surface ECG

QRS <140 Ventricular depolarization Surface ECG

QTca <400 Ventricular repolarization Surface ECG

J-Tb — Ventricular repolarization Surface ECG

aQTc interval is the QT interval corrected for heart rate. A common method for

calculating QTc is the QT interval/(R-R interval)1/2 (Bazett formula). b J-T interval is obtained by subtracting the QRS interval from the QT interval.

ECG, electrocardiogram.

RHYTHM INTERPRETATION

ECG tracings are evaluated through a systematic review as

described below:

1. Is the rate fast or slow? A simple method to determine the

rate is to count the number of complexes occurring within 6

seconds and multiply by 10. Most ECG recording paper places

vertical lines at the top of the grid, 3 seconds apart. Therefore,

if eight complexes appear within a 6-second length of strip,

the rate is 80 beats/minute.

2. Are there P waves before each QRS complex, and is their configuration normal? Are the P wave–to–P wave and R wave–to–

R wave intervals regular or irregular? If the rhythm is irregular,

is the pattern of irregularity consistent (regularly irregular)

or totally random (irregularly irregular)? P waves appearing

before the QRS complex usually indicate that the impulse

originated in the SA node and subsequently was conducted

to the ventricle. Abnormal-appearing P waves indicate that an

atrial site other than the SA node is initiating the beat. Irregular rhythms may be caused by an impulse originating from

a site other than the SA node before the normal pacemaker

can fire (premature beat); they also may result from failure to

conduct impulses from the atria.

3. Are the P-R and QRS complexes within normal limits? Is the

QRS complex normal in its configuration? Impulses originating above the ventricles with normal conduction through

the bundle branches and myocardium produce a normalappearing, narrow QRS complex. Impulses originating in the

ventricle give rise to wide, bizarre-appearing QRS complexes.

TABLE 20-2

Pharmacologic Properties of Antiarrhythmic Agents

Surface ECG

PR QRS QT Conduction Refractory

Type Interval Interval Interval Velocity Period

Ia 0/↑ ↑ ↑↑ ↑↓a ↑

Ib 0 0 0 0/↓ ↓

Ic ↑ ↑↑ ↑ ↑ 0

II ↑↑ 0 0 ↓b ↑b

III 0c 0 ↑↑ 0 ↑

IV ↑↑ 0 0 ↓b ↑b

aConduction increases at low dosages and decreases at higher dosages.

b On atrial and atrioventricular nodal tissue.

c May cause PR prolongation independent of class III antiarrhythmic activity.

ECG, electrocardiogram.

Pathophysiology

ABNORMAL IMPULSE FORMATION

Abnormal impulse formation can arise from abnormal automaticity or triggered activity originating from the SA node (e.g.,

sinus bradycardia) or other sites (e.g., junctional or idioventricular

tachycardia). Causes of abnormal automaticity include hypoxia,

ischemia, or excess catecholamine activity.

Triggered activity occurs when there is an attempted depolarization before or after the cell is fully repolarized, but not

by a pacemaker cell. These after-depolarizations may occur in

phase 2 or 3 (early) or phase 4 (delayed) of the action potential. Early after-depolarizations (EAD) arise from a reduced level

of membrane potential and may require a bradycardic state.

Torsades de pointes (TdP), a form of polymorphic ventricular

tachycardia (VT), is thought to be initiated by EAD. Delayed

after-depolarizations (DAD), often seen with digoxin toxicity,

are thought to be secondary to an overload of intracellular free

calcium.

ABNORMAL IMPULSE CONDUCTION

RE-ENTRY

The most common abnormal conduction leading to arrhythmogenesis is re-entry. A re-entrant circuit is formed as normal conduction occurs down a pathway that bifurcates into two pathways

(e.g., AV node or left and right bundle branches). The impulse

travels along one pathway (Fig. 20-3), but encounters unidirectional antegrade block in the other pathway (see Fig. 20-3). The

impulse that passed through the unblocked pathway propagates

in a retrograde manner (i.e., moves backward) through the previously blocked pathway. This abnormal impulse can travel down

the first pathway again when it is not refractory. Supraventricular

and monomorphic VT are both examples of re-entrant arrhythmias (see Case 20-4, Question 3).

BLOCK

Another form of abnormal impulse conduction occurs when the

normal conducting pathway is blocked and the impulse is forced

to travel through nonpathway tissues to cause depolarization.

Common examples are left and right bundle branch blocks in

the ventricles. A block in one path necessitates retrograde conduction through the opposite bundle to stimulate both ventricles.

Typically, the nonpathway tissue conducts the electrical impulse

more slowly than conduction tissues do.

Classification of Arrhythmias

All arrhythmias originating above the bundle of His are

referred to as supraventricular arrhythmias. These may include

sinus bradycardia, sinus tachycardia, paroxysmal supraventricular

tachycardia, atrial flutter, atrial fibrillation (AF), Wolff-ParkinsonWhite (WPW) syndrome, and premature atrial contractions

(PACs). All of these arrhythmias are characterized by normal

QRS complexes (i.e., normal ventricular depolarization) unless

there is a bundle branch block. Not all of these rhythm changes are

necessarily a sign of pathology. For example, athletes with a wellconditioned heart and large stroke volume commonly have slow

heart rates (sinus bradycardia). Vigorous exercise commonly is

accompanied by transient sinus tachycardia.

Arrhythmias originating below the bundle of His are referred

to as ventricular arrhythmias. These include premature ventricular contractions (PVCs), ventricular tachycardia (VT), and

ventricular fibrillation (VF). Conduction blocks often are categorized separately based on their level or location, which can

493Cardiac Arrhythmias Chapter 20

3 sec

0.04 sec

0.2 sec

FIGURE 20-2 Electrocardiogram recording paper.

be a supraventricular site (e.g., first-, second-, or third-degree

AV block, see Case 20-6, Question 2) or in the ventricle (e.g.,

right or left bundle branch block). An alternative method of

classifying arrhythmias is based on the rate: bradyarrhythmia

(<60 beats/minute) or tachyarrhythmia (>100 beats/minute).

Pulmonary Vein

Left Atria

FIGURE 20-3 Re-entrant circuit in the pulmonary vein. In the

pulmonary vein there is a mixing of electrically active cells (shaded

circles) and electrically inactive cells (white circles). While the main

wave of depolarization goes homogenously down the atria a small

depolarization stimuli enters the pulmonary vein and meanders

through the electrically active tissue. In this case, there is a re-entrant

circuit formed where the impulse can continue to rotate through the

pulmonary vein and a route for it to stimulate the atria as well.

There is a website with useful rhythm evaluation tutorials at

http://www.blaufuss.org.

Antiarrhythmic Drugs

On the basis of their electrophysiologic and pharmacologic

effects, there are four Vaughn-Williams antiarrhythmic drug

classes. Class I drugs, sodium-channel blockers, are subdivided

further depending on the duration of channel blockade (class Ia

is intermediate, Ib is quick, and Ic is long). Class II drugs are

β-adrenergic blockers, class III drugs are potassium-channel

blockers, and class IV drugs are calcium-channel blockers. The

classification, pharmacokinetics, and adverse effects of these

agents are summarized in Table 20-3.

Class Ia and class III antiarrhythmic agents increase repolarization time, the QTc interval, and the risk of TdP. Class II and

IV antiarrhythmic agents can decrease the heart rate (may cause

bradycardia), decrease the force of ventricular contractility (may

decrease stroke volume), and prolong the PR interval (may cause

second- or third-degree AV block). Class Ib antiarrhythmic agents

work only in ventricular tissue, so they cannot be used in AF or

atrial flutter. Class Ic antiarrhythmic agents are useful, but should

never be used after an MI or with heart failure (HF) or severe left

ventricular hypertrophy (classified as structural heart diseases)

because increased mortality can result. These drugs are discussed

in greater detail later.

SUPRAVENTRICULAR ARRHYTHMIAS

The specific arrhythmias include (a) those primarily atrial in

origin, such as AF, atrial flutter, paroxysmal sinus tachycardia,

ectopic atrial tachycardia, and multifocal atrial tachycardia; and

(b) AV nodal re-entrant tachycardia (AVNRT) and AV re-entrant

tachycardia (AVRT) involving accessory pathways within the

atria or ventricle. AVNRT and AVRT often self-terminate and

are paroxysmal (episodic) in nature; thus, they are commonly

referred to as paroxysmal supraventricular tachycardias (PSVT).

494 Section 2 Cardiac and Vascular Disorders

TABLE 20-3

Vaughn-Williams Classification of Antiarrhythmic Agents

Drug and Classification Pharmacokinetics Indications Side Effects

Class Ia (can cause torsades de pointes similar