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

Part II. CARDIAC RHYTHM DISTURBANCES

Chapter 14. Supraventricular Arrhythmias

Section I Premature atrial and AV junctional beats, paroxysmal supraventricular tachycardias, and AV junctional rhythms

The sinus node, or sinoatrial (SA) node, is the physiologic, intrinsic pacemaker of the heart and normally initiates each heartbeat. Pacemaker stimuli can, however, arise from other parts of the heart, such as the atria muscle, the atrioventricular (AV) junction, or the ventricles. The terms ectopy, ectopic pacemaker, and ectopic beat are used to describe these nonsinus heartbeats.

Ectopic beats are often premature; that is, they come before the next sinus beat is due. Thus atrial premature beats (APBs), AV junctional premature beats (JPBs), and ventricular premature beats (VPBs) may occur. Ectopic beats can also come after a pause in the normal rhythm, as in the case of AV junctional or ventricular escape beats. Ectopic beats originating in the AV junction (node) or atria are referred to as supraventricular (i.e., coming from above the ventricles).

In this chapter and the next, ectopic atrial and AV junctional (supraventricular) rhythms are described. Chapter 16 discusses ventricular ectopy.

ATRIAL AND AV JUNCTIONAL (NODAL) PREMATURE BEATS

APBs[*] result from ectopic stimuli; that is, these beats arise from somewhere in either the left or right atrium but not in the SA node. The atria therefore are depolarized from an ectopic site. After an atrial or junctional depolarization, the stimulus may spread normally through the His-Purkinje system into the ventricles. For this reason, ventricular depolarization (QRS complex) is generally not affected by APBs or JPBs.

APBs have the following major features (Figs. 14-1 to 14-3 [1] [2] [3]):

 

1.   

The atrial depolarization is premature, occurring before the next normal P wave is due.

 

2.   

The QRS complex of the APB is often preceded by a visible P wave that usually has a slightly different shape and/or different PR interval from the P wave seen with normal sinus beats. The PR interval of the APB may be either longer or shorter than the PR interval of the normal beats. In some cases, the P wave may be “buried” in the T wave of the preceding beat.

 

3.   

After the APB, a slight pause generally occurs before the normal sinus beat resumes. This usually slight delay is due to “resetting” of the SA node pacemaker by the premature atrial stimulus. This slight delay contrasts with the longer, “compensatory” pause often (but not always) seen after VPBs ( Fig. 16-7 ).

 

4.   

The QRS complex of the APB is usually identical or very similar to the QRS complex of the preceding beats. Remember that with APBs the atrial pacemaker is in an ecto-pic location, but the ventricles are usually depolarized in a normal way. This finding contrasts with VPBs, in which the QRS complex is usually very wide because of abnormal depolarization of the ventricles (see Chapter 16 ).

 

5.   

Occasionally, APBs result in aberrant ventricular conduction, so that the QRS complex is wider than normal. Figure 14-3 shows an example of such beats causing delayed depolarization of the right ventricle. Thus these APBs are associated with right bundle branch block aberrancy. APBs with left bundle branch block aberrancy may also occur.

 

6.   

Sometimes when an APB is very premature, the stimulus reaches the AV junction just after it has been stimulated by the preceding normal beat. Because the AV junction, like all other conductive tissues, requires time to recover its capacity to conduct impulses, this premature atrial stimulus may reach the junction when it is still refractory. In this situation the APB may not be conducted to the ventricles and no QRS complex appears. The result is a blocked APB. The ECG shows a premature P wave not followed by a QRS complex (see Fig. 14-1B ). After the blocked P wave, a brief pause occurs before the next normal beat resumes. The blocked APB therefore produces a slight irregularity of the heartbeat. (If you do not search carefully for these blocked APBs, you may overlook them.)

FIGURE 14-1  A, Notice the atrial premature beat (APB) after the fourth sinus beat (arrow). B, Notice also the blocked atrial premature beat, again after the fourth sinus beat (arrow). The premature P wave falls on the T wave of the preceding beat and is not followed by a QRS complex because the atrioventricular node is still in a refractory state.

FIGURE 14-2  Atrial bigeminy in which each sinus beat is followed by an atrial premature beat (or premature atrial complex).

FIGURE 14-3  This rhythm strip shows sinus rhythm with three atrial premature beats. The first two (marked •) are conducted with right bundle branch block aberrancy (rSR′ in lead V1). The third atrial premature beat (○) is conducted with normal ventricular activation. Notice how the first two premature P waves come so early in the cardiac cycle that they fall on the T waves of the preceding sinus beats, making these T waves slightly taller.

The APBs may occur frequently (e.g., five or more times per minute) or sporadically. Two APBs occurring consecutively are referred to as an atrial couplet. Sometimes, as shown in Figure 14-2 , each sinus beat is followed by an APB. This pattern is referred to as atrial bigeminy.

*  The terms atrial premature contractions, atrial premature beats, atrial premature depolarizations, and atrial extrasystoles are used synonymously. Most cardiologists prefer the designations premature beat, depolarization, and complex because not every premature stimulus is associated with an actual mechanical contraction of the atria or ventricles.
CLINICAL SIGNIFICANCE

APBs are very common. They may occur with a normal heart or virtually any type of organic heart disease. Thus the presence of APBs does not imply that an individual has cardiac disease. In normal people, these premature beats may be seen with emotional stress, excessive intake of caffeine, or the administration of sympathomimetic agents (epinephrine, isoproterenol, theophylline). APBs may also occur with hyperthyroidism. APBs may produce palpitations; in this situation, patients may complain of feeling a skipped beat or an irregular pulse. APBs may also be seen with various types of structural heart disease. Frequent APBs are sometimes the forerunner of atrial fibrillation or flutter (see Chapter 15 ) or other atrial tachyarrhythmias.

 

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIAS (PSVTs)

Premature supraventricular beats may occur singly or repetitively. A sudden run of three or more beats constitutes a paroxysmal supraventricular tachycardia (PSVT). Episodes of PSVT may be brief and nonsustained (i.e., lasting from three beats up to 30 sec). Sustained episodes (longer than 30 sec) may last minutes, hours, or longer. The topic of PSVTs is actually quite complex. Therefore the following brief discussion is intended to provide only an introduction and overview.[*]

The three major types of PSVT are atrial tachycardia (AT) and related rhythms, atrioventricular nodal reentrant tachycardia (AVNRT), and AV reentrant tachycardia (AVRT) involv-ing a bypass tract of the type seen in the Wolff-Parkinson-White (WPW) syndrome (see Chapter 12 ). These arrhythmias are depicted schematically in Figure 14-4 .

FIGURE 14-4  Major types of paroxysmal supraventricular tachycardia. A, The reference is normal sinus rhythm. B, With atrial tachycardia (AT), a focus (X) outside the sinoatrial (SA) node fires off automatically at a rapid rate. C, With atrioventricular (AV) nodal reentrant tachycardia (AVNRT), the cardiac stimulus originates as a wave of excitation that spins around the AV nodal (junctional) area. As a result, retrograde P waves may be buried in the QRS or appear immediately before or just after the QRS complex (arrows)because of nearly simultaneous activation of the atria and ventricles. D, A similar type of reentrant (circus-movement) mechanism may occur with a bypass tract (BT) of the type found in Wolff-Parkinson-White syndrome (see Fig. 12-5 ). This mechanism is referred to asatrioventricular reentrant tachycardia (AVRT). Note the negative P wave (arrow) in lead II, somewhat after the QRS complex. (With AVRT, the P wave in lead II may be negative or isoelectric.)

*  See the Bibliography for texts that describe this important area of cardiology in more detail.
ATRIAL TACHYCARDIA

Atrial tachycardia (AT) is defined simply as three or more consecutive APBs ( Figs. 14-4B and 14-5 ). Most episodes appear to involve an ectopic (nonsinus) pacemaker located in either the left or right atrium that fires off “automatically” in a rapid way. A sustained episode that lasts 30 seconds or longer, particularly at a rapid rate, may cause light-headedness or even syncope (fainting) and, in susceptible individuals, can induce angina or congestive heart failure (CHF). The atrial rate with AT may be as high as 200 beats per minute or faster (usual range: 100 to 250 beats/min). AT has been observed in patients without apparent structural cardiac abnormality as well as in those with virtually any type of heart disease.[*] Short episodes may require no special therapy, but longer runs causing symptoms are usually treated with antiarrhythmic drugs or radiofrequency (RF) catheter ablation (see later discussion).

FIGURE 14-5  Atrial tachycardia (a type of paroxysmal supraventricular tachycardia) terminating spontaneously with the abrupt resumption of sinus rhythm. The P waves of the tachycardia (rate: about 150 beats/min) are superimposed on the preceding T waves.

A special type of atrial tachycardia is related to multiple sites of atrial stimulation and is called multifocal atrial tachycardia (MAT). This arrhythmia is discussed in Chapter 20 , a general review of bradycardias and tachycardias.

*  See Chapter 18 for a brief discussion of AT with block resulting from digitalis toxicity.
AV NODAL REENTRANT TACHYCARDIA

AV nodal reentrant tachycardia (AVNRT), which was once mistakenly considered a variant of paroxysmal atrial tachycardia, is actually a distinct arrhythmia caused by a rapidly circulating impulse in the AV node area. The term reentry (introduced in Chapter 12 ) describes situations in which a cardiac impulse literally spins around and around and appears to “chase its own tail.” Reentry can occur in virtually any part of the heart. Atrial flutter is due to a large reentrant circuit usually originating in the right atrium. (In the ventricles, reentry may lead to VPBs and sometimes ventricular tachycardia.)

AVNRT produces a very rapid and regular supraventricular rhythm with rates typically between 140 and 250 beats/min ( Fig. 14-6 ). This arrhythmia may occur with otherwise normal hearts or with underlying heart disease. Runs of AVNRT are generally initiated by an APB.

FIGURE 14-6  Notice the marked regularity of rhythm in this paroxysmal supraventricular tachycardia (PSVT), which has a rate of about 170 beats/min. This tachycardia is probably due to a rapidly circulating impulse in the atrioventricular (AV) node (junction) and thus is referred to as an AV nodal reentrant tachycardia. No P waves are visible (see also Fig. 14-4 C.).

With AVNRT, the reentrant rhythm originates in the AV nodal area and spreads simultaneously or nearly simultaneously up the atria and down the ventricles (see Fig. 14-4B ). As a consequence, the P waves are usually hidden in the QRS complex because the atria and ventricles are activated simultaneously. In other cases, the P waves may appear just before or just after the QRS complex and therefore may be difficult to see. Because of this retrograde (bottom-to-top) activation of the atria, the P waves are negative in lead II. Episodes of AVNRT may cease spontaneously or may require treatment. The initial therapy usually involves attempts to increase vagal tone, since the vagus nerve slows conduction in the AV node. This “braking effect” may interrupt the reentrant mechanism ( Fig. 14-7 ). Vagal tone can be increased with the Valsalva maneuver (i.e., the patient is instructed to strain against a closed glottis by bearing down, as for a bowel movement) or with carotid sinus massage.

FIGURE 14-7  Paroxysmal supraventricular tachycardia (PSVT) treated with carotid sinus massage. The first 14 beats in this rhythm strip show the tachyarrhythmia with a rate of about 140 beats/min and no visible P waves. Carotid sinus massage resulted in its abrupt termination, with the appearance of normal sinus rhythm. The PSVT here is probably an atrioventricular nodal reentrant tachycardia (AVNRT) (see Fig. 14-4 C).

A variety of intravenous drugs are used to interrupt the reentrant mechanism in AVNRT. Clinically, adenosine and verapamil or diltiazem are the drugs most often enlisted in the acute setting. Beta blockers and digoxin also are useful in selected cases.[*]

Younger patients and individuals without significant underlying cardiovascular disease may tolerate heart rates up to 250 beats/min with complaints of only palpitations or light-headedness. In patients with limited cardiac reserve, however, a heart rate above 160 beats/min (or even less) can have disastrous consequences. In these patients, myocardial ischemia or even infarction may occur. They may also develop CHF or hypotension. Electrical cardioversion may be required in emergency circumstances (especially, when any PSVT is associated with angina, pulmonary edema, or severe hypotension and when initial therapy with vagal maneuvers and rapid-acting drugs fails). Electrical cardioversion is the use of a direct-current (DC) shock to treat certain tachyarrhythmias. The electrical shock transiently depolarizes the heart, interrupting a variety of abnormal rhythms and allowing the sinus node to “regain control” of the cardiac electrical cycle. The shock is administered with special paddles placed on the chest wall (see also Chapter 15 and Fig. 15-8 ). An unsynchronized DC shock is used to treat some arrhythmias (e.g., ventricular flutter or ventricular fibrillation). A synchronized DC shock must be used, however, to treat PSVT and other supraventricular arrhythmias (e.g., atrial fibrillation and atrial flutter). The shock is synchronized with the QRS complex so that it does not occur during the vulnerable period of ventricular repolarization (simultaneous with the apex of the T wave). Note that the DC shocks given to the heart during the vulnerable period may produce ventricular fibrillation. Therefore, in treating PSVT, a synchronized DC shock must be given.[*]

FIGURE 14-8  Atrioventricular junctional (nodal) beats produce P waves that point upward in lead aVR and downward in lead II; this is just the opposite of what is seen with sinus rhythm. The P wave may just precede the QRS complex (A), follow it (B), or occur simultaneously with it (C). In the last instance, no P wave is visible.

For patients with recurrent episodes of AVNRT, radiofrequency (RF) catheter ablation may be curative. This special form of therapy involves delivering short pulses of RF current through an intracardiac catheter placed near the AV node during an electrophysiology procedure. The current produces a very small burn that effectively blocks part of the circuit that is supporting the reentrant-type wave.[†]

*  Other drugs that may be used to prevent the reentrant mechanism in AVNRT are discussed in various texts cited in the Bibliography .
*  For details on the use of electrical cardioversion to treat PSVT, see the appropriate texts cited in the Bibliography .
†  AVNRT is due to the presence of so-called dual pathways located within the AV node area. These two pathways have different conduction and recovery (refractory) properties, allowing an impulse to travel down one path and loop back (reenter) along the other. In particular, there is a “fast” pathway that conducts relatively quickly but recovers slowly and a “slow” pathway that conducts more slowly but recovers more quickly. (See Bibliography for more details.)
ATRIOVENTRICULAR REENTRANT (BYPASS TRACT) TACHYCARDIA

A third common cause of PSVT has already been introduced in the discussion of preexcitation syndromes (see Chapter 12 ). As previously mentioned, the WPW syndrome is related to the presence of a so-called bypass tract (accessory pathway), an abnormal tract of cardiac muscle that connects the atria and ventricles, circumventing the AV node. Patients with this type of atrioventricular bypass tract may develop a tachycardia caused by a reentrant mechanism in which the impulse travels down the normal conduction system (AV node and His bundle) into the ventricles, recycles rapidly up into the atria via the bypass tract, and then goes down the AV node again. Repetition of this large reentrant circuit leads to atrioventricular reentrant (bypass tract) tachycardia (AVRT), a type of PSVT.

Of interest is the fact that in some patients the bypass tract is “concealed”; that is, it never becomes evident during sinus rhythm but can conduct in a retrograde direction, allowing a supraventricular tachycardia to occur.[*] The ECG with a concealed-bypass-tract type of PSVT is very similar to the ECG findings described for AVNRT. One subtle difference is that the ECGs of some patients with tachycardia associated with a concealed bypass tract may show P waves occurring visibly after the QRS complexes in the ST segment (see Fig. 14-4D ).

The therapy of PSVT resulting from a concealed bypass tract is quite similar to that of AVNRT. Drugs such as adenosine are used for acute episodes, and electrophysiologic testing is performed to evaluate the patient for possible RF catheter ablation of the bypass tract.

In summary, a PSVT should be suspected when a rhythm strip shows a rapid and typically very regular nonsinus rate at about 140 to 220 beats/min (range: 100 to 250 beats/min). The mechanism may be due to reentry in the AV node (AVNRT), atrioventricular reentrant (bypass tract) tachycardia (AVRT), or ectopic AT. The differential diagnosis of PSVT and other supraventricular tachycardias is discussed further in Chapter 20 .

*  To be evident during sinus rhythm, the bypass tract must conduct impulses rapidly from the atria to the ventricles, bypassing the AV node. This produces a short PR interval, a wide QRS complex, and a delta wave—the classic triad of WPW preexcitation (see Fig. 12-2 ). In some patients with a bypass tract, the pathway does not conduct antegrade effectively, but it can still conduct retrograde under certain conditions, thereby allowing an impulse to reenter the atria from the ventricles. Bypass tracts that conduct only in a retrograde direction, causing PSVT, are said to be “concealed.”

 

AV JUNCTIONAL RHYTHMS

With APBs, the ectopic pacemaker is located somewhere in the atria outside the SA node. Under certain circumstances, the AV junction may also function as an ectopic pacemaker, producing an AV junctional rhythm. In some discussions, the term AV nodal or nodal is used to refer to an AV junctional rhythm. The terms AV junctional, junctional, AV nodal, and nodal are, however, essentially synonymous.

Chapter 4 introduced the basic mechanism of AV junctional rhythms and the patterns seen with AV junctional beats. When the AV junction is the cardiac pacemaker, the atria are stimulated in aretrograde fashion, from bottom to top. An arrow representing the spread of atrial depolarization with junctional rhythm points upward, just opposite the direction of atrial depolarization when normal sinus rhythm is present (see Fig. 4-4 ). This retrograde stimulation of the atria produces a positive P wave in lead aVR and a negative P wave in lead II (see Fig. 4-5 ). With AV junctional rhythm, the ventricles are depolarized normally (unless a bundle branch block is present), resulting in a narrow QRS complex.

In some cases of AV junctional rhythm, the atria are stimulated just before the ventricles. In other cases the stimulus reaches the ventricles first. Finally, in many cases, the atria and the ventricles are stimulated simultaneously. If the atria are stimulated first, the P wave precedes the QRS complex. (A retrograde P wave preceding the QRS complex also occurs with some ectopic atrial beats from the lower part of either atrium. The distinction between such “low” ectopic atrial and AV junctional beats is usually not of clinical importance, however.) If the ventricles are first to be stimulated, the QRS complex precedes the P wave. If atrial and ventricular depolarizations are simultaneous, the P wave is hidden in the QRS and therefore is not seen.

In summary, AV junctional beats can be recognized on the ECG by one of the following patterns ( Fig. 14-8 ):

 

   

Retrograde P waves (positive in lead aVR, negative in lead II) immediately preceding the QRS complexes

 

   

Retrograde P waves immediately following the QRS complexes

 

   

Absent P waves (buried in the QRS), so that the baseline between QRS complexes is flat

AV JUNCTIONAL ESCAPE RHYTHMS

AV junctional escape beats were mentioned in the discussion of sinus arrest (see Chapter 13 ). An AV junctional escape beat ( Fig. 14-9 ) is simply a beat that comes after a pause when the normal sinus pacemaker fails to function. The AV junctional escape beat is therefore a “safety beat.” After this escape beat, the normal sinus pacemaker may resume function. If it does not, a slow AV junctional escape rhythm may continue. An AV junctional escape rhythm is a consecutive run of AV junctional beats. The heart rate is usually slow (30 to 50 beats/min).

FIGURE 14-9  The junctional escape (JE) beat comes after a pause and is followed by a junctional premature complex (JPC). Notice the retrograde (inverted) P wave preceding the JPB in this lead II rhythm strip.

Figure 14-10 shows an example of an AV junctional escape rhythm. Not surprisingly, the basic rate of the AV junction is slower than that of the SA node. If the AV junction had a faster inherent rate, it would compete with the SA node for control of the heartbeat.

FIGURE 14-10  This rhythm strip shows a slow junctional escape rhythm at about 40 beats/min. No P waves are visible, and the baseline between QRS complexes is flat.

AV junctional escape rhythms can be seen in a number of clinical settings, including the sick sinus syndrome (see Chapter 20 ), digitalis toxicity (see Chapter 18 ), excessive effects of beta blockers or calcium channel blockers (diltiazem and verapamil), acute myocardial infarction, hypoxemia, and hyperkalemia. The cause determines the treatment (e.g., stopping a toxic drug or oxygenating the patient). If the heart rate becomes excessively slow with an AV junctional rhythm, drugs such as atropine (a vagal blocker) or isoproterenol (a sympathomimetic stimulant) are sometimes used acutely. A pacemaker may be required.

AV JUNCTIONAL TACHYCARDIAS

As is true of AV junctional escape rhythms, AV junctional tachycardias can arise in a number of settings. Probably the most common type is AVNRT (see Fig. 14-4C ), an arrhythmia that results from a rapidly recirculating impulse in the nodal part of the AV junction. AV junctional tachycardias can also occur because of abnormally enhanced automaticity. This finding may, for example, occur with digitalis toxicity (see Chapter 18 ).[*]

*  Additional information can be obtained from references cited in the Bibliography .

 

REVIEW

Stimuli that pace the heart can arise not only in the sinoatrial (SA) node but also in other cardiac tissues, such as the atria, atrioventricular (AV) junction, or ventricles. The terms ectopy, ectopic pacemaker, ectopic contraction, and ectopic beat are used to describe these stimuli. Ectopic beats can be divided into two major categories:

 

1.   

Premature beats are extra beats that come before the next normal beat is expected. Examples include atrial premature beats (APBs), junctional premature beats, and ventricular premature beats. These beats originate in the atria, AV junction, and ventricles, respectively.

 

2.   

Escape beats are usually AV junctional or ventricular beats that are not premature but come after a pause in the normal rhythm.

APBs show the following ECG patterns:

 

1.   

Usually, the P wave has a different shape, and the PR interval is longer or shorter than in the preceding sinus complexes. Sometimes the P wave is hidden in the T wave of the preceding normal beat.

 

2.   

Not uncommonly, the atrial stimulus cannot penetrate the AV junction. In such cases of blocked APBs, the premature P wave is not followed by a QRS complex.

Paroxysmal ventricular tachycardia (PSVT) is a sudden run of three or more supraventricular beats. PSVT has three common types (see Fig. 14-4 ):

 

1.   

Atrial tachycardia (AT)

 

2.   

AV nodal reentrant tachycardia (AVNRT)

 

3.   

AV reentrant tachycardia (AVRT), which is associated with a bypass tract

AV junctional rhythms have the following features:

 

1.   

The P wave, when seen, is negative in lead II and positive in lead aVR, which is just the reverse of the pattern seen with normal sinus rhythm. These are called retrograde P waves.

 

2.   

The retrograde P wave may immediately precede or follow the QRS complex.

 

3.   

In many cases, the retrograde P wave is buried within the QRS complex. When this occurs, the baseline between QRS complexes remains completely flat.

AV junctional rhythms are categorized as junctional escape rhythms and junctional tachycardias. An AV junctional escape rhythm is a run of AV junctional beats with a slow rate, generally between 30 and 50 beats/min. AV junctional tachycardia, by contrast, is a more rapid run of three or more consecutive beats originating in the AV junction. A common type is AVNRT. Other types are due to increased automaticity of AV junctional pacemaker cells.

 

QUESTIONS

 

1.   

Based on the rhythm strip shown below, why might this patient complain of occasional palpitations?

 

 

2.   

What is the beat marked X?

 

 

3.   

Examine the rhythm strip shown below and answer the questions on the next page:

 

 

a.   

What is the heart rate?

 

b.   

What type of tachyarrhythmia is present?

 

(1) 

Sinus tachycardia

 

(2) 

Paroxysmal supraventricular tachycardia (PSVT)

 

(3) 

Atrial flutter

 

(4) 

Atrial fibrillation

 

(5) 

Multifocal atrial tachycardia

 

4.   

True or false: Paroxysmal supraventricular tachycardia (PSVT) represents sinus tachycardia at a very rapid rate at rest (above 150/min).