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Supraventricular Arrhythmias, Part I: Premature Beats and Paroxysmal Supraventricular Tachycardias
General Principles
This chapter and the next two focus on rhythm disturbances with a rapid rate, namely supraventricular ( Fig. 14.1 ) and ventricular tachyarrhythmias.
Key Concepts
For any rapid, abnormal heart rhythm to occur, two major factors have to be present:
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A trigger that initiates the arrhythmia.
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A substrate that allows the arrhythmia mechanism to continue (self-sustain).
Tachyarrhythmias, both supraventricular (see Fig. 14.1 ) and ventricular (see Chapter 16 ), usually start with premature beats that initiate arrhythmias by either focal or reentrant mechanisms ( Fig. 14.2 ).
Focal tachycardias involve repetitive firing of an ectopic (non-sinus) pacemaker. In contrast, reentry involves the nonuniform spread of a depolarization wave through one pathway in the heart, with blockage along a second pathway. If block in the second pathway is unidirectional, the wave may be able to reenter it from the reverse direction and then loop around, traveling back down the first pathway, thereby creating an abnormal “revolving door” circuit.
In many instances, an arrhythmia (e.g., atrioventricular nodal reentrant tachycardia [AVNRT]) initiated by one mechanism (e.g., a premature beat from an ectopic atrial focus) is then sustained by another (e.g., reentry).
The sinus or sinoatrial (SA) node (see Chapter 13 ) is the physiologic (natural or intrinsic) pacemaker of the heart. The SA node normally initiates each heartbeat. However, pacemaker stimuli can arise from other parts of the heart, including the atrial muscle or pulmonary vein areas, specialized conduction system (atrioventricular [AV] junction and His–Purkinje system) or the ventricles themselves.
Ectopic beats are most often premature; that is, they come before the next sinus beat is due. Examples include premature atrial complexes or beats (PACs or PABs/APBs synonymously), premature AV junctional complexes (PJCs), and premature ventricular complexes (PVCs). Ectopic beats can also come after a pause (delay) in the normal rhythm, as in the case of AV junctional or ventricular escape beats (see Chapter 13 ). Ectopic beats originating in the AV junction (node) or atria are referred to as supraventricular, literally coming from above the ventricles.
This chapter and the next describe the major non- sinus supraventricular arrhythmias. Chapter 16 deals with ventricular tachyarrhythmias.
Atrial and Other Supraventricular Premature Beats
Premature atrial complexes (PACs) a
a The terms premature atrial complexes or contractions, atrial premature beats, premature atrial depolarizations, and atrial extrasystoles are used synonymously. Most cardiologists prefer the designations premature atrial complex, beat, or depolarization because not every premature stimulus is associated with an effective mechanical contraction of the atria or ventricles. The same principle applies to the naming of ventricular premature complexes (PVCs; see Chapter 16 ).
result from ectopic stimuli arising from loci in either the left or right atrium, interatrial septum, or pulmonary veins, but not the SA node, itself. After an atrial or junctional premature complex (JPC), the stimulus may spread normally through the His–Purkinje system into the ventricles without affecting the ventricular depolarization (QRS) waveform. However, very early PACs can encroach on the refractory period of the conduction system. This degree of prematurity may cause QRS widening (called “aberration”), manifest by transient right, or less commonly, left bundle branch block. If the PAC is sufficiently premature, it may be completely blocked, producing no QRS. The major features of PACs are listed in Box 14.1 and depicted in Figs. 14.3–14.6 .
Box 14.1
Major Features of Premature Atrial Complexes
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The atrial depolarization (P′ wave) is premature, occurring before the next sinus P wave is due.
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The QRS complex of the premature atrial complex (PAC) is usually preceded by a visible P wave that has a different shape or different PR interval from the P wave seen with sinus beats. The PR interval of the PAC may be either longer or shorter than the PR interval of the normal beats. In some cases the P wave may be subtly hidden in the T wave of the preceding beat.
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After the PAC a pause generally occurs before the normal sinus beat resumes. This delay is due to “resetting” of the sinoatrial (SA) node pacemaker by the premature atrial stimulus. The slight delay contrasts with the longer, “fully compensatory” pause often (but not always) seen after premature ventricular complexes (PVCs) (see Fig. 16.9 ).
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The QRS complex of the PAC is usually identical or very similar to the QRS complex of the preceding beats. With PACs the atrial pacemaker is in an ectopic location, but the ventricles are usually depolarized in a normal way. This sequence contrasts with the generation of PVCs, in which the QRS complex is abnormally wide because of asynchronous ventricular depolarization (see Chapter 16 ).
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When PACs occur very early after ventricular depolarization before the conduction system if fully recovered, they can result in aberrant ventricular conduction so that the QRS complex is wider than normal, usually in the form of right or, less often left bundle branch block. Figs. 14.5 and 14.6 show examples of such PACs causing delayed (aberrant) depolarization of the right and left ventricles, respectively.
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Sometimes, when a PAC is very premature, the stimulus reaches the atrioventricular (AV) junction just after it has been stimulated by the preceding beat. The AV junction, like other cardiac tissue, has an inherent refractory period. Therefore it requires time to recover its capacity to conduct impulses. Thus a PAC may reach the junction when it is still refractory. In this situation the PAC may not be conducted to the ventricles and no QRS complex appears. The result is a so-called blocked PAC. The ECG shows a premature P wave not followed by a QRS complex (see Fig. 14.3 B). After the blocked P wave, a brief pause occurs before the next normal beat resumes. The blocked PAC, therefore, produces a slight irregularity of the heartbeat. If you do not search carefully for blocked PACs, you may overlook them.
PACs may occur frequently or sporadically. Two PACs occurring consecutively are referred to as an atrial couplet. Sometimes, as shown in Fig. 14.4 , each sinus beat is followed by a PAC. This “grouped” pattern is referred to as atrial bigeminy.
Clinical Significance
PACs, conducted and blocked, are very common. They may occur in people with normal hearts or with virtually any type of organic heart disease. Thus the presence of PACs does not imply that an individual has cardiac disease. Supraventricular premature beats may be associated with emotional stress, excessive intake of caffeinated drinks, or the administration of sympathomimetic agents (epinephrine, albuterol, and other sympathomimetic agents). PACs may also occur with hyperthyroidism. PACs may produce palpitations; in this situation, patients may complain of feeling a “skipped beat” or an irregular pulse (a type of palpitation). PACs may also be seen with virtually any type of structural heart disease. Frequent PACs are sometimes the forerunner of atrial fibrillation or flutter (see Chapter 15 ) or other supraventricular tachyarrhythmias, as discussed in the next sections.
Paroxysmal Supraventricular Tachycardias (PSVTS)
Premature supraventricular beats ( Box 14.2 ) may occur singly or repetitively. A sudden run of three or more such consecutive non-sinus beats constitutes an episode of paroxysmal (or sometimes persistent) supraventricular tachycardia (PSVT). Episodes of PSVT may be nonsustained (i.e., lasting from a few beats up to 30 sec). Sustained episodes (greater than 30 sec) may last for minutes, hours, or longer. These episodes may stop spontaneously, stop after drug therapy, and more rarely require emergency direct current (DC) cardioversion (see Chapter 15 ) or radiofrequency ablation therapy.
Box 14.2
Classification of Major Types of Paroxysmal Supraventricular Tachycardia
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Atrial tachycardia (AT) and related rhythms, including multifocal atrial tachycardia
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Atrioventricular nodal reentrant tachycardia (AVNRT)
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Atrioventricular reentrant tachycardia (AVRT) involving a bypass tract of the type seen in the Wolff–Parkinson–White (WPW) syndrome (see Chapter 18 )
The detailed topic of PSVT is quite complicated. Furthermore, the term PSVT itself is somewhat misleading because sometimes tachyarrhythmias in this class, as just noted, may be long lasting (persistent) or even incessant not just paroxysmal or intermittent. Therefore the following brief discussion is intended to provide trainees and clinicians with a general introduction and overview. Additional material is provided in the online supplement and in the bibliography.
The three major types of PSVT are shown in Fig. 14.7 .
Atrial Tachycardias
Classic (“monofocal” or “focal”) atrial tachycardia (AT) is defined as three or more consecutive PACs coming from a single atrial focus, with each having an identical, non-sinus P wave morphology ( Fig. 14.8 ). The arrhythmic focus can be located in either the right or left atrium (sometimes in the proximal pulmonary vein areas), and it fires off “automatically” in a rapid way. An important variant, discussed later, is multifocal AT ( MAT ), in which the P waves vary because they represent ectopic foci originating from different sites (usually three or more) of abnormally increased automaticity.
Initiation and Termination of Atrial Tachycardias
ATs are initiated by PACs, which may be conducted or blocked (i.e., not followed by a QRS). Termination occurs when the ectopic atrial focus stops firing (either spontaneously or after administration of an antiarrhythmic drug). The last P wave of the tachycardia usually conducts to the ventricles producing a QRS complex at the end of the run. Therefore AT almost always terminates with a QRS complex ( Figs. 14.9 and 14.10 ). This is an important feature for the differential diagnosis of other types of PSVTs (see discussion later in Chapter).
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