Basic and Bedside Electrocardiography, 1st Edition (2009)

Chapter 15. Supraventricular Tachycardia

Introduction

·         Tachycardia refers to a heart rate >100 beats per minute (bpm). The tachycardia may be supraventricular or ventricular depending on the origin of the arrhythmia.

o    Supraventricular tachycardia (SVT): If the tachycardia originates above the bifurcation of the bundle of His, usually in the atria or atrioventricular (AV) junction, the tachycardia is supraventricular (Fig. 15.1A). Supraventricular impulses follow the normal AV conduction system, activate the ventricles synchronously and will have narrow QRS complexes measuring <120 milliseconds. The QRS may be wide if there is preexistent bundle branch block, ventricular aberration, or the impulse is conducted through a bypass tract.

Figure 15.1: Supraventricular and Ventricular Tachycardia (VT). (A) In supraventricular tachycardia, the impulses originate above the bifurcation of the bundle of His, follow the normal AV conduction system, and activate both ventricles synchronously resulting in narrow QRS complexes. (B) In VT, the impulses originate below the bifurcation of the bundle of His. Activation of the ventricles is not synchronous because the impulse has to spread outside the normal conduction system resulting in wide QRS complexes. The stars represent the origin of the impulse. The horizontal line represents the bifurcation of the bundle of His.

o    Ventricular tachycardia (VT): If the tachycardia originates below the bifurcation of the bundle of His, the tachycardia is ventricular (Fig. 15.1B). The impulse will spread to the ventricles outside the normal AV conduction system. Activation of the ventricles will not be synchronous resulting in wide QRS complexes measuring ≥120 milliseconds.

·         There are other types of tachycardias with narrow QRS complexes other than SVT. These include sinus tachycardia, atrial flutter, and atrial fibrillation. These tachycardias should be distinguished from each other because the treatment of these various arrhythmias is different.

o    Sinus tachycardia: Sinus tachycardia implies that the rhythm originates from the sinus node with a rate that exceeds 100 bpm. Sinus tachycardia is a normal finding, which is usually an appropriate response to a physiologic or pathologic condition. This was previously discussed in Chapter 14, Sinus Tachycardia.

o    Atrial flutter: The diagnosis of atrial flutter is based on the presence of a very regular atrial rate of 300 ± 50 bpm. This will be discussed separately in Chapter 18.

o    Atrial fibrillation: The diagnosis of atrial fibrillation is based on an atrial rate of 400 ± 50 bpm with characteristic baseline fibrillatory pattern and irregularly irregular R-R intervals. This will also be discussed separately.

·         Table 15.1 classifies the different types of narrow complex tachycardias.

·         SVT: SVT is a narrow complex tachycardia originating outside the sinus node but above the bifurcation of the bundle of His, with a rate that exceeds 100 bpm. Several types of SVT are present and are classified according to three general mechanisms: reentry, enhanced automaticity, and triggered activity.

o    Reentry: SVT due to reentry is an abnormality in the propagation of the electrical impulse resulting from the presence of two separate pathways with different electrophysiologic properties (Fig. 15.2A).

o    Enhanced automaticity: This is an abnormality in initiation rather than conduction of the electrical impulse. Some cells in the atria or AV junction may exhibit phase 4 diastolic depolarization and may spontaneously discharge faster than that of the sinus node if the discharge rate is enhanced (Fig. 15.2B).

o    Triggered activity: This is also an abnormality in initiation of the electrical impulse resulting from occurrence of afterdepolarizations. Afterdepolarizations are secondary depolarizations that are triggered by the initial impulse (Fig. 15.2C). The afterdepolarization does not always reach threshold potential, but when it does, it may be followed by repetitive firing of the membrane voltage. Triggered activity is usually seen in association with digitalis toxicity, calcium excess, or increased catecholamines.

·         SVT from reentry usually occurs in normal individuals without evidence of structural cardiac disease. SVT from enhanced automaticity may occur in normal individuals, although they are more frequently associated with structural cardiac diseases, abnormalities in electrolytes and blood gasses, or use of pharmacologic agents. SVT from triggered activity usually occurs with digitalis excess or after cardiac surgery. The differences between SVT from reentry, from enhanced automaticity, and from triggered activity are summarized in Table 15.2.

TABLE 15.1 Narrow Complex Tachycardia

 Sinus Tachycardia

SVT

Atrial Flutter

Atrial Fibrillation

 Sinus Rate >100

Reentrant

·         AVNRT

·         AVRT

·         Intraatrial

·         Sinoatrial

Automatic

·         Atrial

○ Focal or unifocal

○ Multifocal

·         Junctional

○ Paroxysmal

○ Nonparoxysmal

Atrial Rate
300 ± 50

Atrial Rate
400 ± 50

 

Atrial Rate 200 ± 50

   

 Table shows the different tachycardias that can result in narrow QRS complexes. Generally, the atrial rate of atrial fibrillation is 400 ± 50  bpm, for atrial flutter 300 ± 50 bpm, for SVT approximately 200 ± 50 and for sinus tachycardia >100 bpm. AVNRT, atrioventricular nodal  reentrant tachycardia; AVRT, atrioventricular reciprocating tachycardia; SVT, supraventricular tachycardia.

         

Figure 15.2: Mechanisms of Supraventricular tachycardia (SVT). (A) Reentry is the most common mechanism of all SVT. In reentry, two separate pathways with different electrophysiologic properties are present. (B) Diagram of action potential of a cell with automatic properties. These cells exhibit slow phase 4 diastolic depolarization, which may dominate as the pacemaker if the discharge rate is enhanced. (C) Diagram of action potential of a cell with triggered activity. Oscillations occur early during phase 2 or phase 3, or late during phase 4 of the action potential. The dotted horizontal lines in (B) and (C) represent threshold potential. Numbers 0 to 4 represent the different phases of the action potential. Adapted and modified from Wellens and Conover.

 

TABLE 15.2 Differences between SVT because of Reentry, Enhanced Automaticity, and Triggered Activity

 

Reentry

Enhanced Automaticity

Triggered Activity

 Mechanism

This is an abnormality in impulse conduction. A reentrant circuit is present.

This is an abnormality in impulse initiation. Cells with automatic properties become the dominant pacemaker.

Early or late after - depolarizations are present.

 Initiation

Initiated by premature impulses or by rapid pacing.

Initiated by increased firing rate of automatic cells in the atria or AV junction.

Initiation is not well defined.

 Termination \

Terminated by vagal maneuvers, AV nodal blockers, ectopic impulses, overdrive pacing, or electrical cardioversion.

Not usually terminated by vagal maneuvers, AV nodal blockers, ectopic impulses, overdrive pacing or electrical cardioversion.

May be terminated by premature impulses, overdrive pacing, or electrical cardioversion.

 Underlying Condition

Frequently seen in structurally normal hearts.

Frequently seen in patients with metabolic or pulmonary disorders or patients on adrenergic drugs, caffeine, theophylline, or other agents.

Frequently seen in patients with digitalis toxicity or postcardiac surgery.

 Examples of SVT

·         AV nodal reentry

·         AV reentry

·         Sinoatrial reentry

·         Intraatrial reentry

·        AT

○ Focal AT

○ Multifocal AT

·         Junctional tachycardia

○ Focal or paroxysmal

○ Nonparoxysmal

Atrial tachycardia with 2:1 AV block

Nonparoxysmal junctional tachycardia

 SVT, supraventricular tachycardia; AT, atrial tachycardia; AV, atrioventricular.

Suggested Readings

Conover MB. Arrhythmogenesis. In: Understanding Electrocardiography. 5th ed. St. Louis: Mosby; 1988:31-41.

Wellens HJJ, Conover M. Drug induced arrhythmic emergencies. In: The ECG in Emergency Decision Making. 2nd ed. St. Louis: Saunders Elsevier; 2006:178.

Wit AL, Rosen MR. Cellular electrophysiology of cardiac arrhythmias. Part I. Arrhythmias caused by abnormal impulse generation. Mod Concepts Cardiovasc Dis. 1981; 50:1-6.

Wit AL, Rosen MR. Cellular electrophysiology of cardiac arrhythmias. Part II. Arrhythmias caused by abnormal impulse conduction. Mod Concepts Cardiovasc Dis. 1981; 50:7-12.