Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 16. Ventricular Arrhythmias

The three preceding chapters have focused on supraventricular arrhythmias, which are rhythm disturbances arising in the sinus node, atria, or atrioventricular (AV) junction with normal ventricular depolarization. This chapter considers another major ECG topic—ventricular arrhythmias. Ectopic (nonsinus) beats frequently arise in the ventricles themselves, producing premature ventricular beats (or complexes), ventricular tachycardia (VT), and sometimes ventricular fibrillation (VF) leading to cardiac arrest.


Ventricular premature beats (VPBs)[*] are premature depolarizations arising in the ventricles, analogous to atrial premature beats (APBs) and junctional premature beats (JPBs), which are supraventricular. Recall that, with APBs and JPBs, the QRS complex is usually of normal width because the stimulus spreads normally through the bundle branches to the ventricles. With VPBs, however, the premature depolarizations arise in either the right or left ventricle. Therefore the ventricles are not stimulated simultaneously, and the stimulus spreads through the ventricles in an aberrant direction. Thus the QRS complexes are wide with VPBs, just as they are with the bundle branch block patterns. Examples of VPBs are shown in Figures 16-1 to 16-8 [1] [2] [3] [4] [5] [6] [7] [8].

FIGURE 16-1  A ventricular premature beat (VPB) is recognized because it comes before the next normal beat is expected and it has a wide aberrant shape. (Notice also the long PR interval in the normal sinus beats, indicating first-degree AV block.)

FIGURE 16-2  Notice the wide aberrant shape of a ventricular premature beat (VPB) compared to the QRS complexes of an atrial premature beat (APB), which generally resembles the sinus QRS complexes.

FIGURE 16-3  Notice that the same ventricular premature beat (marked X) recorded simultaneously in three different leads has different shapes. By comparison, notice that the multiform ventricular premature beats shown in Figure 16-9 have different shapes in the samelead.

FIGURE 16-4  Two ventricular premature beats (V) are referred to as a pair or a couplet. They also show the “R on T” phenomenon (see text and Fig. 16-10 ).

FIGURE 16-5  Notice the two very short bursts of nonsustained ventricular tachycardia (VT). Compare this with the sustained VT shown in Fig. 16-12A .

FIGURE 16-6  A, Ventricular bigeminy, in which each normal sinus impulse is followed by a ventricular premature beat (marked X). B, Ventricular trigeminy, in which a ventricular premature beat occurs after every two sinus pulses.

FIGURE 16-7  Some ventricular premature beats (VPBs) cause a fully compensatory pause, with the interval between the two sinus beats that surround the VPB (R3 and R4, in this case) being two times the normal interval between sinus beats (R1 and R2). Notice that the P waves (P) come on time, except that the third P wave is interrupted by the VPB and therefore is not conducted through the AV junction, which is still refractory. The next (fourth) P wave also comes on time. The fact that the sinus node is continuing to pace despite the VPB results in the fully compensatory pause.

FIGURE 16-8  Sometimes a ventricular premature beat (X) falls between two normal beats, in which case it is interpolated.

VPBs have two major characteristics[†]:



They are premature and occur before the next normal beat is expected.



They are aberrant in appearance. The QRS complex is abnormally wide (usually 0.12 sec or more), and the T wave and QRS complex usually point in opposite directions.

VPBs usually precede a sinus P wave. Occasionally, they appear just after a sinus P wave but before the normal QRS complex (see Fig. 16-7 ). Sometimes they are followed by a nonsinus P wave (negative in lead II) that has arisen because of retrograde stimulation of the atria by the VPB.

*  In the ECG literature, the terms ventricular premature beat, ventricular premature depolarization, ventricular extrasystole, and premature ventricular complex or contraction (PVC) are used interchangeably.
†  The basic electrophysiologic mechanisms responsible for VPBs are a subject of active investigation. VPBs may arise by at least three mechanisms: reentrant waves, increased spontaneous depolarizations of ventricular cells (enhanced automaticity), and triggered activity orafterdepolarizations (i.e., premature firing of ventricular cells triggered by the previous depolarization).

Clinicians tend to comment on a number of features of VPBs that may have clinical relevance.


The frequency of VPBs refers to the number that is seen per minute or other unit of time. The VPB frequency may range from one or an occasional isolated premature depolarization to many.

VPBs may occur in various combinations. Two in a row (see Fig. 16-4 ) are referred to as a pair or couplet. Three or more in a row are, by definition, VT (see Fig. 16-5 ). Sometimes, as shown in Figure 16-6 A, isolated VPBs occur so frequently that each normal beat is followed by a VPB. This produces a distinctive repetitive grouping of one normal beat and one VPB, which is called ventricular bigeminy. The sequence of two normal beats with a VPB is ventricular trigeminy.


As you might expect, the appearance of the VPBs will differ depending on the site(s) in the ventricles from which the VPBs originate. VPBs originating in the right ventricle generally have a left bundle branch block morphology, since the left ventricle is stimulated after the right ventricle. VPBs originating in the left ventricle generally have a right bundle branch block morphology. VPBs originating in the interventricular septum also often have a left bundle branch block morphology.

Coupling Interval

The term coupling interval is applied to the interval between the VPB and the preceding normal beat. When multiple VPBs are present, fixed coupling often occurs, with the coupling interval approximately the same for each VPB (see Fig. 16-6 A). At other times, VPBs may show a variable coupling interval.

Compensatory Pause

As you may have noticed, APBs and VPBs are usually followed by a pause before the next normal beat. The pause after a VPB is usually but not always longer than the pause after an APB. A fully compensatory pause indicates that the interval between the normal QRS complexes immediately before and immediately after the VPB is twice the basic RR interval (see Fig. 16-7 ). A fully compensatory pause is more characteristic of VPBs than APBs. Sometimes a VPB falls almost exactly between two normal beats; in such cases, the VPB is said to be interpolated (see Fig. 16-8 ).

Uniform and Multiform VPBs

The terms uniform and multiform are used to describe the appearance of VPBs in any lead. Uniform VPBs have the same appearance in any lead and arise from the same anatomic site (focus) (see Fig. 16-6 ). (Of course, they have different shapes in different leads, just as normal beats do.) By contrast, multiform VPBs have different morphologies in the same lead ( Fig. 16-9 ). Multiform VPBs often but not always arise from different foci. Uniform VPBs are unifocal, but multiform VPBs are not necessarily multifocal. Uniform VPBs may occur in normal hearts and hearts with underlying organic heart disease. Frequent multiform VPBs often indicate that organic heart disease is present.

FIGURE 16-9  These multiform ventricular premature beats (VPBs) have different shapes in the same lead. (Compare this tracing with the one in Figure 16-6 A.)

R on T Phenomenon

The R on T or VPB on T phenomenon refers to VPBs that are timed so that they fall at the peak[*] of the T wave of the preceding normal beat (see Figs. 16-10 and 16-16 [10] [16]). Those falling on the T wave are noteworthy in that they may precipitate VT or VF, particularly in the course of an acute myocardial infarction (MI) or myocardial ischemia or with very long QT intervals (discussed later in this chapter). Recall from the discussion of synchronized direct-current (DC) cardioversion that the peak of the T wave is a time during which an external stimulus is especially likely to produce VF (seeChapter 15 ). VT and VF most commonly occur, however, without a preceding “R on T” beat, and most “R on T” beats do not precipitate a sustained ventricular tachyarrhythmia.

FIGURE 16-10  A ventricular premature beat (X) falling near the peak of the T wave of the preceding beat may be a predisposing factor for ventricular tachycardia or ventricular fibrillation, particularly when this “R on T” phenomenon occurs in the setting of acute myocardial ischemia or infarction or with long QT(U) intervals.

FIGURE 16-16  Accelerated idioventricular rhythm (AIVR) and nonsustained polymorphic ventricular tachycardia (VT) occurring together. Notice the “VPB on T” beats that initiate both the AIVR and the VT episodes.

*  Equivalently, the VPBs may fall at the nadir of a negative T wave.

VPBs are among the most common arrhythmias. They may occur in normal hearts and with serious organic heart disease. Individuals with VPBs may be asymptomatic, or they may complain of palpitations (i.e., sensations of a “skipped” or “extra” beat). VPBs may be a stable and benign finding, or they may be a marker of severe organic heart disease associated with an increased risk of cardiac arrest and sudden death from VF. Clearly, clinicians need certain ground rules to help decide when VPBs are of concern. A few general principles are discussed here.

As mentioned, VPBs are not uncommon in normal adults of all ages although they occur more frequently with advancing age. Young adults, for example, may have VPBs because of anxiety or excessive caffeine intake. Certain drugs used in asthmatics (e.g., epinephrine, isoproterenol, and aminophylline) can provoke VPBs in normal hearts. Nevertheless, if a patient has frequent VPBs, you should search carefully for underlying cardiac disease (heart murmurs, abnormal echocardiographic findings, and so on) and also obtain a careful drug history. Occasional or even frequent isolated VPBs in an otherwise healthy person without organic heart disease are not usually a source of concern. VPBs are also common with mitral valve prolapse, and they may be seen with virtually any type of heart disease. For example, a patient with valvular, hypertensive, or ischemic heart disease with or without MI may have them. VPBs are the most common arrhythmia seen with acute MI.

As noted, VPBs can be caused by the effects on the heart of numerous drugs, including epinephrine, isoproterenol, and aminophylline, which are cardiac stimulants. Ventricular ectopy is also an important sign of digitalis toxicity (see Chapter 18 ). VPBs may be seen in patients with electrolyte disturbances such as hypokalemia or hypomagnesemia and in patients with lung disease or hypoxemia from any cause.


As mentioned, VPBs are common in healthy people. Even in patients with underlying heart disease, the suppression of frequent isolated VPBs or even short runs of VT with antiarrhythmic drugs has not been shown to improve survival. In fact, the drugs used to treat ventricular ectopy (e.g., quinidine, procainamide, disopyramide, mexiletine, propafenone, moricizine, amiodarone, and flecainide) all have serious and sometimes life-threatening side effects. Furthermore, antiarrhythmic drugs may actually make the situation worse by increasing the severity of the ectopy (proarrhythmic effect). Indeed, treating a patient with so-called antiarrhythmic drugs may sometimes provoke a potentially fatal, sustained ventricular tachyarrhythmia.

For patients with frequent VPBs associated with very bothersome palpitations, beta-blocker therapy is sometimes used. Beta blockers may also be helpful in patients who have ventricular ectopy associated with coronary artery disease and in patients who have certain types of cardiomyopathy.

These complex and sometimes controversial therapeutic issues are discussed more completely in texts cited in the Bibliography . Again, whenever you see a patient with frequent VPBs, you must search for potentially reversible causes and contributors, particularly hypokalemia, hypomagnesemia, and certain stimulant drugs. Underlying structural heart disease should be assessed by history and physical examination, and by noninvasive techniques such as echocardiography and exercise testing where specifically indicated.



VT is, by definition, simply a run of three or more consecutive VPBs. Examples are shown in Figures 16-5, 16-11, and 16-12 [5] [11] [12]. VT is usefully classified by duration (nonsustained and sustained) and by morphology (monomorphic and polymorphic) ( Box 16-1 ).

FIGURE 16-11  The monitor lead shows short bursts of ventricular tachycardia.

FIGURE 16-12  A, Long run of monomorphic ventricular tachycardia. B, Normal sinus rhythm restored after direct-current (DC) cardioversion.

BOX 16-1 

Classification of Ventricular Tachycardia


Nonsustained (lasting three beats to 30 sec)

Sustained (lasting 30 sec or more, or somewhat shorter runs if associated with symptoms of syncope or near-syncope)





With long QT(U) syndrome: torsades de pointes


Without long QT(U) syndrome: for example, polymorphic ventricular tachycardia with acute ischemia

Sustained VT (typically lasting longer than 30 sec) is usually a life-threatening arrhythmia for two major reasons:



Most patients are not able to maintain an adequate blood pressure at very rapid ventricular rates and eventually become hypotensive.



The condition may degenerate into VF ( Fig. 16-13 ), causing immediate cardiac arrest.

FIGURE 16-13  Ventricular fibrillation (VF) may produce both coarse and fine waves. Immediate defibrillation should be performed.

VT, whether sustained or not, can also be characterized as monomorphic (see Fig. 16-12 A) or polymorphic (see Fig. 16-16 ), depending on whether consecutive VPBs have the same or a variable appearance in a single lead.

Very rapid VT with a sine-wave appearance is sometimes referred to as ventricular flutter. This arrhythmia often leads to cardiac arrest with VF ( Fig. 16-14 ).

FIGURE 16-14  Ventricular tachycardia (VT) and ventricular fibrillation (VF) recorded during the onset of cardiac arrest. The rapid sine-wave type of VT seen here is sometimes referred to as ventricular flutter.


Sustained VT, which may lead to syncope or sudden death, rarely occurs in patients without underlying structural heart disease.[*] Most patients with this type of high-grade ventricular ectopy (i.e., long runs of ventricular tachycardia) have some basic structural cardiac abnormality, such as prior MI, cardiomyopathy or valvular disease associated with fibrosis (scarring), or ventricular enlargement. The most common cause of sustained, recurrent monomorphic VT in American adults is coronary artery disease with prior MI.

Despite pharmacologic therapy, some patients are at high risk for life-threatening recurrences of sustained VT or VF. For these patients, a special device called an implantable cardioverter defibrillator (ICD) has been developed to deliver an internal electric shock directly to the heart during a life-threatening tachycardia ( Chapter 21 ).

*  See also references cited in the Bibliography for discussion of the types of VT that may occur without structural heart disease.



Figures 16-15 and 16-16 [15] [16] present a distinctive arrhythmia that has been called accelerated idioventricular rhythm (AIVR) or slow ventricular tachycardia. Recall that, with typical VT, the heart rate is faster than 100 beats/min. With AIVR, the heart rate is usually between 50 and 100 beats/min, and the ECG shows wide QRS complexes without associated sinus P waves.

FIGURE 16-15  Accelerated idioventricular rhythm (AIVR) in a patient with an acute inferior wall infarction. The first four beats show the typical pattern, followed by a return of sinus rhythm, then the reappearance of the AIVR. Notice that the fifth, sixth, twelfth, and thirteenth QRS complexes are “fusion beats” because of the nearly simultaneous occurrence of a sinus beat and a ventricular beat.

AIVR is particularly common with acute MI, and it may be a sign of reperfusion after the use of thrombolytic agents or after interventional coronary artery procedures. This arrhythmia is generally short lived, lasting minutes or less, and usually requires no specific therapy.

In many cases (see Fig. 16-15 ), AIVR appears to be a benign “escape” rhythm that competes with the underlying sinus mechanism. When the sinus rate slows, AIVR appears; when the sinus rate speeds up, the arrhythmia disappears. In other cases (see Fig. 16-16 ), AIVR is initiated by premature beats rather than escape beats. This latter type is more likely to be associated with actual VT.



A distinct type of polymorphic VT is called torsades de pointes (a French term meaning “twisting of the points”). Figures 16-17 and 16-18 [17] [18] show examples of this tachycardia. Notice how the direction of the QRS complexes appears to rotate cyclically, pointing downward for several beats and then twisting and pointing upward in the same lead.

FIGURE 16-17  Notice the shifting polarity and amplitude of the QRS complexes during an episode of nonsustained torsades de pointes. QT(U) prolongation (0.52 sec) is also present in the normal sinus beats.

FIGURE 16-18  Classic pattern of the sustained torsades de pointes type of ventricular tachycardia. Notice the pattern of depolarization in which the QRS axis appears to rotate or turn in a systematic way. Figure 16-17 shows a short, nonsustained run of the same arrhythmia, which typically occurs in the setting of QT(U) prolongation.

Torsades de pointes is important because of its diagnostic and therapeutic implications. As shown in Figure 16-17 , torsades de pointes occurs in the setting of delayed ventricular repolarization, evidenced by prolongation of the QT intervals or the presence of prominent U waves. It is often initiated by a VPB that occurs near or on the T or U wave of the preceding beat. Reported causes and contributors include the following (also see Chapter 24 for a more complete list):



Drugs, particularly quinidine (see Chapter 10 and Fig. 19-7 ) and related antiarrhythmic agents (disopyramide and procainamide), as well as ibutilide, dofetilide, sotalol, amiodarone (less commonly), psychotropic agents (phenothiazines and tricyclic antidepressants), and other noncardiac drugs (e.g., probucol, cisapride, pentamidine, and erythromycin and related antibiotics)



Electrolyte imbalances, especially hypokalemia and hypomagnesemia, and, less commonly, hypocalcemia, which prolong repolarization



Severe bradyarrhythmias (e.g., complete heart block)



Miscellaneous factors, such as liquid protein diets



Hereditary long QT syndromes (see Fig. 19-8 )

Recognition of torsades de pointes is critical because this type of potentially lethal ventricular tachycardia is often caused by drugs conventionally recommended for the treatment of arrhythmias. Therefore the therapy of torsades de pointes must include removing or correcting causative factors such as drug effects, electrolyte imbalance, or underlying bradycardia. In emergency settings, a temporary pacemaker may be inserted to accomplish “overdrive” suppression of the arrhythmia by increasing the underlying heart rate and shortening of the QT interval, thereby decreasing ventricular repolarization time and inhomogeneity. Intravenous magnesium sulfate has proved useful for suppressing this arrhythmia. Drug therapy with isoproterenol has been used in selected cases. Sustained episodes of torsades de pointes associated with cardiac arrest require attempted cardioversion. The arrhythmia usually recurs, however, unless causative factors are corrected.[*]

Polymorphic VT may also occur without QT prolongation (see Fig. 16-16 ), for example, in the setting of acute myocardial ischemia.

*  Consult texts cited in the Bibliography for further discussions of torsades de pointes.



With VF (see Figs. 16-13 and 16-14 [13] [14]), the ventricles do not beat in any coordinated fashion but instead fibrillate or quiver asynchronously and ineffectively. No cardiac output occurs, and the patient becomes unconscious immediately. VF is one of the three major ECG patterns seen with cardiac arrest. The other two are brady-asystolic patterns and pulseless electrical activity (see Chapter 19 ).

The ECG in VF shows characteristic fibrillatory waves with an irregular pattern that may be either coarse or fine (see Fig. 16-13 ).

VF requires immediate defibrillation with an unsynchronized DC shock. Patients who have just been resuscitated from an episode of VF are generally given an immediate dose of an intravenous antiarrhythmic drug in an attempt to suppress further ventricular ectopy.

This lethal tachyarrhythmia can occur in patients with heart disease of any type. It may be preceded by a warning arrhythmia (e.g., VPBs or VT), or it may occur spontaneously. VF is the most common cause of sudden cardiac death (see Chapter 19 ) in patients with acute MI, although it may also occur in normal hearts, sometimes because of drugs (e.g., epinephrine, cocaine).

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Goldberger: Clinical Electrocardiography: A Simplified Approach, 7th ed.

Copyright © 2006 Mosby, An Imprint of Elsevier


Ventricular premature beats (VPBs) may occur normally or with organic heart disease. VPBs have the following characteristics:



They are premature, occurring before the next normal beat is expected.



They have an aberrant shape. The QRS complex is abnormally wide, usually 0.12 second or more in duration, and the T wave and QRS complex usually point in opposite directions.

VPBs may occur with varying frequency. Two in a row are called a couplet. Three or more in a row constitute ventricular tachycardia (VT). When a VPB occurs regularly after each normal beat, the grouping is called ventricular bigeminy. When the rhythm is two normal beats followed by a VPB, this grouping is termed ventricular trigeminy.

A VPB is often followed by a compensatory pause before the next beat. Uniform VPBs have the same shape in a single lead. Multiform VPBs have different shapes in the same lead.

A VPB occurring simultaneously with the apex of the T wave of the preceding beat is called an R on T phenomenon. It may be the precursor of VT or ventricular fibrillation (VF), particularly in the setting of acute myocardial infarction or long QT syndromes.

VT is a run of three or more VPBs. Short runs of VT are called nonsustained. In sustained VT, episodes last longer than 30 seconds and may lead to syncope or even cardiac arrest. VT may be classified as monomorphic or polymorphic. Torsades de pointes is a particular type of polymorphic VT associated with prolonged repolarization syndromes such as long QT(U) syndrome.

Accelerated idioventricular rhythm (AIVR) is a ventricular arrhythmia that resembles a slow VT with a rate between 50 and 100 beats/min. It is commonly seen with MI and is usually self-limited.

Torsades de pointes is a form of VT in which the QRS complexes in the same lead appear to twist periodically and turn in the opposite direction. It is generally seen in the setting of delayed ventricular repolarization (increased QT interval or prominent U waves) caused by drugs (quinidine, procainamide, disopyramide, dofetilide, ibutilide), electrolyte abnormalities (hypokalemia, hypomagnesemia), or other factors summarized in Chapter 24 .

VF occurs when the ventricles stop beating and, instead, fibrillate or twitch in an ineffective fashion. It is one of the three major ECG patterns seen with cardiac arrest; the other two are brady-asystoleand pulseless electrical activity (see Chapter 19 ).





What is the arrhythmia shown below?




Which arrhythmia does this rhythm strip show? 




Name three potentially treatable causes of ventricular premature beats.



What is the arrhythmia here?