SVTs are rapid heart rhythms that arise from the atrium or require conduction through the AV node. Atrial fibrillation and atrial flutter are technically SVTs, although the term generally pertains to paroxysmal SVTs. SVTs can affect all age groups but frequently occur in younger patients. Prevalence is higher in women than in men. SVTs usually occur in the absence of structural heart disease, although echocardiography should be performed to exclude underlying cardiac dysfunction or structural defects. Patients often have repeated episodes of tachycardia and may report palpitations, a sensation of pounding in the neck, fatigue, lightheadedness, chest discomfort, dyspnea, presyncope, and, less commonly, syncope.
The ECG typically demonstrates a narrow-complex tachycardia; however, wide QRS complexes (>120 ms) may be present in cases of bundle branch block, aberrancy, pacing, or anterograde accessory pathway conduction (antidromic tachycardia). SVTs may be classified electrocardiographically according to the relationship of the P wave and the QRS complex. Short-RP tachycardias (RP interval < PR interval) feature a P wave that closely follows the QRS complex, whereas long-RP tachycardias feature a P wave that is more than half the distance between the RR interval (RP interval > PR interval). Short-RP tachycardias include typical AVNRT, AVRT, and junctional tachycardia. Long-RP tachycardias include atypical AVNRT, sinus tachycardia, and atrial tachycardia.
Vagal maneuvers, including the Valsalva maneuver (bearing down), carotid sinus massage, or facial immersion in cold water, are first-line therapy to restore sinus rhythm in patients with SVT. Adenosine can be used to terminate SVT and simultaneously help diagnose its cause. Tachycardias that terminate with adenosine are typically AV node dependent (AVNRT and AVRT), whereas continued atrial activity (P waves) during AV block is consistent with atrial flutter or atrial tachycardia.
AVNRT accounts for two thirds of all cases of SVT, not including cases of atrial fibrillation and flutter. AVNRT is the result of a reentrant circuit within the AV node that uses both the fast and slow pathways. Typical AVNRT involves conduction down the slow pathway and back up to the atrium over the fast pathway (slow-fast). This conduction pattern results in a short RP interval with a retrograde P wave inscribed very close to the QRS complex (Figure 15). Atypical AVNRT occurs when the impulse travels down the fast pathway and returns to the atrium via the slow pathway (fast-slow), resulting in a long RP interval.
AVNRT may be terminated with vagal maneuvers or adenosine. AV nodal blocking therapy with β-blockers or calcium channel blockers is used to prevent recurrent AVNRT. In patients with recurrent AVNRT and patients who do not tolerate or prefer to avoid long-term medical therapy, catheter ablation should be considered. Catheter ablation of AVNRT has a high success rate, although it is associated with a 1% risk for injury to the AV node necessitating pacemaker implantation.
AVRT is an accessory pathway (bypass tract)–mediated tachycardia that is often observed as preexcitation on ECG (Figure 16). Early ventricular activation over the accessory pathway causes shortening of the PR interval, and the initial part of the QRS complex is slurred because of premature ventricular depolarization in the myocardial tissue adjacent to the accessory pathway. In AVRT, the tachycardia can conduct anterograde over the AV node (orthodromic AVRT) or anterograde over the accessory pathway (antidromic AVRT). Orthodromic AVRT is the most common type of AVRT, accounting for more than 90% to 95% of cases. This type of AVRT has a narrow QRS complex, owing to conduction over the AV node and the His-Purkinje system. Antidromic AVRT is characterized by a wide, slurred QRS complex resulting from conduction over the bypass tract and activation of the ventricle without use of the specialized conduction system. Adenosine can be given to terminate orthodromic AVRT; however, adenosine and other AV nodal blockers are contraindicated in cases of antidromic AVRT.
Wolff-Parkinson-White (WPW) syndrome is defined by symptomatic AVRT with evidence of preexcitation on resting ECG (delta wave). It is often seen in patients with Ebstein anomaly. Atrial fibrillation occurs in up to one third of patients with WPW syndrome. Rapid conduction over an accessory pathway in atrial fibrillation can result in VF and sudden cardiac death (SCD), although this occurs in less than 1% of cases of WPW syndrome.
In patients with preexcitation on ECG, stress testing can effectively risk-stratify patients; patients in whom preexcitation is lost during exercise are generally at low risk for ventricular arrhythmia and SCD. Electrophysiology testing is also helpful in determining the risk for SCD and in localizing the pathway to facilitate catheter ablation. Catheter ablation is first-line therapy for patients with WPW syndrome and has a high success rate; however, ablation success is dictated by the location of the bypass tract. Antiarrhythmic therapy is considered second-line therapy. In patients with accessory pathways close to the AV node, antiarrhythmic drug therapy is particularly useful because catheter ablation carries an unacceptable risk for iatrogenic heart block.
In asymptomatic patients with preexcitation on ECG, management is controversial. Invasive testing is generally not required, unless the patient has a high-risk occupation, such as a commercial airline pilot.
Premature atrial contractions (PACs) are early isolated beats that arise from the atria. They are exceedingly common, and their frequency increases with age. During ambulatory ECG monitoring, only 1% of persons have no PACs. High PAC burden is associated with increased risk for atrial fibrillation. Symptomatic PACs are typically treated with β-blockers or calcium channel blockers.
Atrial tachycardia can arise in the presence or absence of structural heart disease. Drugs can cause atrial tachycardia; digoxin toxicity can cause paroxysmal atrial tachycardia with atrioventricular block. Stopping the causative drug, or initiating β-blocker or calcium channel blocker therapy, is first-line treatment for symptomatic atrial tachycardia. Second-line treatment consists of catheter ablation or antiarrhythmic drug therapy. Ablation success rates are generally lower in patients with atrial tachycardia than in patients with other SVTs.
Multifocal atrial tachycardia is typified by three or more P-wave morphologies and a heart rate greater than 100/min (Figure 17). It is usually seen in patients with end-stage COPD.