Glenn N. Levine, MD, FACC, FAHA

1. What does the term supraventricular tachycardia (SVT) mean?

    By strict definition, a supraventricular tachycardia is any tachycardia whose genesis is not in the ventricles. Thus, the term can encompass atrial fibrillation and flutter, atrial tachycardia and multifocal atrial tachycardia, and reentrant tachycardias. Others will use the terms SVT or paroxysmal SVT to more specifically refer to the reentrant tachycardias of atrioventricular (AV) nodal reentrant tachycardia (AVNRT) and AV reentrant tachycardia (AVRT), as well as atrial tachycardia and several uncommon supraventricular arrhythmias. For the purposes of this chapter, we will use the term SVT to refer to any tachycardia not caused by ventricular tachycardia, and the term paroxysmal SVT to refer to tachycardias resulting from AVNRT, AVRT, and atrial tachycardia (although the reader should recognize that this is somewhat arbitrary and not universally accepted, and we will not discuss in detail other rare causes of paroxysmal SVT).

2. What is the most common cause of paroxysmal SVT?

    AVNRT accounts for 60% to 70% of paroxysmal SVTs, followed by AVRT.

3. What factors are part of the generic workup for supraventricular tachycardia?

4. What are the causes of narrow complex regular tachycardias (regular referring to fixed R-R intervals—the time or distance between QRS complexes)?

    ECGs of the more common SVTs that cause narrow complex regular tachycardias are shown in Figure 35-1.

5. What are the causes of narrow complex irregular tachycardias (tachycardias with irregular R-R intervals)?

    ECGs of SVTs that cause narrow complex irregular tachycardias are shown in Figure 35-2.

6. How should one determine the correct diagnosis of a narrow complex tachycardia?

    This can be done in two simple steps. First, decide if the rhythm is regular or irregular. Second, look for P waves or atrial activity. Figure 35-3 demonstrates how this simple two-step process will lead to the correct diagnosis.

7. What drug is most commonly implicated in cases of drug-induced atrial tachycardia?

    Digoxin. Digoxin toxicity can cause many arrhythmias, including paroxysmal atrial tachycardia with block. In paroxysmal atrial tachycardia (PAT) with block, there is atrial tachycardia but also AV nodal block, leading to a slow ventricular response rate (Fig. 35-4). In cases of PAT with block, digoxin toxicity should be suspected.

8. What is the most common ventricular response rate in patients who develop atrial flutter?

    Atrial flutter most commonly occurs at a rate of 300 beats/min, although the rate can be somewhat slower in patients on antiarrhythmic agents that slow ventricular conduction (such as amiodarone) or in cases of massively dilated atria. Most commonly, there is 2:1 AV block, meaning that only every other atrial impulse is conducted down to the ventricles. Thus, the most common ventricular response rate is 150 beats/min (see Fig. 35-1, C). The finding of a regular narrow complex tachycardia at exactly 150 beats/min should raise suspicion of atrial flutter as the causative arrhythmia.

9. Which is more common, AVNRT or AVRT?

    AVNRT is more common in the general population. In patients with known preexcitation syndrome (Wolff-Parkinson-White [WPW] syndrome), AVRT, which requires an accessory circuit, is more common. Thus, statistically, the cause of a narrow complex regular tachycardia is more likely to be AVNRT than AVRT, unless the patient has known WPW (or evidence of it on a baseline ECG).

10. What is the most common cause of atrial tachycardia?

    Atrial tachycardia (see Fig. 35-1, B) is most commonly caused by a discrete autonomic focus, although a microreentrant circuit causes a small percentage of atrial tachycardias. Precipitating factors and causes of atrial tachycardia include:

Although textbooks describe the rate of atrial tachycardia as anywhere between 100 and 220 beats/min, a rate of approximately 160 to 180 beats/min is most common. AV conduction is usually 1:1 unless the tachycardia is very rapid, in which case 2:1 conduction may occur. Because most cases of atrial tachycardia are due to an autonomic focus and not a reentrant pathway, the arrhythmia most commonly does not terminate with cardioversion. Adenosine usually (but not always) will not terminate the arrhythmia, but adenosine administration may be useful in cases in which the cause of regular SVT is unclear (see Question 12).

11. What is concealed conduction?

    In many patients with preexcitation syndrome (e.g., WPW), conduction from the atrium to the ventricle will result in the appearance of a delta wave on the 12-lead ECG. However, in some patients with WPW, the accessory bypass tract does not conduct in such an antegrade direction but only in a retrograde direction (up from the ventricle to the atrium). No delta wave appears on the baseline ECG because there is no antegrade conduction, but the accessory pathway is capable of retrograde conduction and participating in the genesis of AVRT (impulses travel down the His-Purkinje system, into the ventricle, and then up the accessory pathway into the atrium).

12. In cases of SVT in which the cause is not clear, what is generally considered first-line drug therapy?

    Adenosine is most commonly administered in cases of SVT of unclear origin. Adenosine will transiently block AV nodal conduction. In patients with atrial flutter or atrial tachycardia, it will slow the ventricular response rate and may allow identification of flutter waves or the abnormal P waves of atrial tachycardia. In cases of AVNRT and AVRT, it may break the arrhythmia by interrupting the reentrant circuit. The dosing is 6 mg, administered quickly through a large-bore intravenous (IV) line, followed, if unsuccessful in terminating the arrhythmia, by a first dose of 12 mg, followed in turn by a second dose of 12 mg. Lower doses of adenosine (such as 3 mg) are recommended by some authorities if adenosine is administered through a central line, and adenosine should be used with caution, if at all, and in lower doses, in heart transplant patients.

    Although adenosine is a frontline agent for arrhythmia diagnosis and termination, it is not useful for more sustained ventricular rate control in patients with atrial fibrillation or atrial flutter because of its very short half-life. Patients who do not respond to adenosine can be treated acutely with IV beta-adrenergic blocking agents (β-blockers) or IV diltiazem or verapamil, both of which have onset of action within minutes and are good AV node blocking agents. IV digoxin is not considered a good choice for acute therapy because its onset of action is approximately 1 hour.

13. For what arrhythmia should AV nodal blocking agents not be administered?

    In rare cases of atrial fibrillation in the setting of an accessory bypass tract (WPW syndrome), some conduction of impulses will occur down the AV node and His-Purkinje system into the ventricle, and some conduction will occur down the bypass tract. In such cases, administration of AV nodal blocking agents (adenosine, digoxin, β-blockers, calcium channel blockers) may lead to increased conduction down the accessory bypass tract, producing an increased ventricular response rate and possibly precipitating ventricular fibrillation.

14. Do patients with atrial flutter require anticoagulation before cardioversion?

    Previously it was believed that the risk of embolization during cardioversion for atrial flutter was negligible. However, observational studies have reported rates of embolization with cardioversion of atrial flutter ranging between 1.7% to 7%. Although a collective review showed that the rate of embolization with cardioversion for atrial flutter was lower than for that with atrial fibrillation (2.2% vs. 5% to 7%), expert consensus is that this rate is sufficient to warrant anticoagulation (and/or transesophageal echocardiogram) similar to that used in patients with atrial fibrillation who are to undergo cardioversion.

15. Can SVT cause a wide QRS complex tachycardia?

    Yes, SVT occurring in the setting of baseline bundle branch block will produce a wide complex (QRS width of 120 ms or more) tachycardia. At faster heart rates, patients can also develop what is called rate-related bundle branch block. Rarely, a wide complex SVT can also be caused by AVRT with antidromic conduction.

16. What is AVRT with antidromic conduction?

    In approximately 90% of cases of AVRT, the reentrant circuit is composed of conduction down the AV node and His-Purkinje system, into the ventricle, and then up the bypass tract (this is called orthodromic conduction). However, in about 10% of cases of AVRT, the reentrant circuit is composed of conduction from the atrium down the bypass tract, into the ventricle, and then up the His-Purkinje system and AV node and into the atrium. This is termed antidromic conduction. Because ventricular depolarization occurs without the use of the His-Purkinje system and left and right bundle branches, the QRS complexes appear wide.

17. What factors make the diagnosis of a wide QRS complex more likely to be ventricular tachycardia (VT) than SVT?

Importantly, the presence of stable hemodynamics and no cardiac symptoms does not distinguish between SVT and VT.

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