Supraventricular tachycardia (SVT) is a general term that is used to describe any arrhythmia with a ventricular rate greater than 100 bpm that originates at or above the level of the His bundle. This term encompasses atrioventricular nodal reentrant tachycardia (AVNRT), atrioventricular reentrant tachycardia (AVRT), ectopic atrial tachycardia (EAT), atrial flutter, focal atrial tachycardia (AT), junctional tachycardia, and inappropriate sinus tachycardia. The epidemiology of SVT is difficult to define given the wide range of rhythms that fall in this category; however, it is estimated that the prevalence of SVT in the general population is 2.29 per 1000 persons with approximately 89,000 new cases diagnosed per year.¹ Gender and age are independent risk factors, with women having twice the risk of men, and those older than 65 years of age being at fivefold risk for developing paroxysmal SVT when compared to those younger than 65 years of age.¹,² The frequency of the different types of SVT changes over the course of a person’s life. AVRT is the most common form of SVT in childhood and adolescence; however, in those middle-aged and older, AVNRT and AT are more common.¹,²

As implied by the name, this rhythm is a reentrant tachycardia that utilizes two functional limbs of the atrioventricular (AV) node, in the setting of a phenomenon known as dual AV node physiology. Dual AV node physiology can be recognized when invasive testing shows that the conduction pattern into the AV node is discontinuous, reflecting separate slowly and rapidly conducting pathways with distinct refractory periods. The typical form of AVNRT is most often initiated when a premature atrial contraction (PAC) blocks in one of these functional pathways (the fast pathway) and instead enters the AV node through the alternate pathway (the slow pathway). By the time the electrical impulse has traveled through the alternate pathway, the first pathway has recovered. This permits retrograde conduction back to the atrium where it can perpetually reenter the circuit. This is the most common form of AVNRT; however, atypical forms exist, where impulse propagation occurs through “fast-slow” or “slow-slow” AV nodal pathways.

This is a second form of reentry, and is the most common form of SVT in children. Accessory pathways (APs) are extranodal AV muscular connections that are classified by their conduction properties (decremental vs. nondecremental) and by the direction over which the electrical wavefront travels (antegrade, retrograde, or both). APs with antegrade conduction will display a classic delta-wave on the surface electrocardiogram (ECG; Figure 55.1). This is the result of early ventricular depolarization at the insertion of the AP. If this finding is present and there are symptoms compatible with SVT, this is termed Wolff-Parkinson-White (WPW) syndrome. Reentry occurs when a PAC blocks in the AP but conducts down the AV node and the His-Purkinje system; by the time the electrical impulse reaches the AP, it has recovered and allows the electrical impulse to travel in a retrograde direction from the ventricle to the atria, thus completing the loop needed for reentrant tachycardia. Reentry can also initiate when a premature ventricular complex (PVC) occurs and blocks in the His-Purkinje system but conducts to the atrium by the AP.

Concealed APs are those that only allow retrograde conduction (from the ventricle to the atria). The mechanism of SVT is identical to that of WPW; however, there will be no evidence of preexcitation during sinus rhythm. Paroxysmal junctional reciprocating tachycardia is a unique type of concealed AP where the pathway has decremental properties with repetitive or incessant behavior, sometimes associated with tachycardia-induced cardiomyopathy. Mahaim fibers are another rare type of APs. These are AV node-like structures that are located in the right parietal AV annulus with insertions into the distal right bundle branch or surrounding myocardium. They have antegrade decremental conduction, but unlike the AV node, have not been shown to exhibit retrograde conduction.

Atrial flutter is another broad term that is used to describe any tachycardia with a macroreentrant circuit in the atria. The most common of these is cavotricuspid isthmus-dependent flutter, also referred to as counterclockwise atrial flutter or typical atrial flutter. This rhythm is characterized by an electrical wavefront that propagates around the tricuspid annulus (up the atrial septum and down the right atrial free wall) with obligate conduction through the isthmus between the inferior vena cava and tricuspid valve.⁵ In cases where the electrical wavefront propagates in the reverse direction, the tachycardia is referred to as reverse typical flutter or clockwise atrial flutter.

Atypical flutters are macroreentrant circuits that do not involve the cavotricuspid isthmus. These reentrant circuits are particularly prevalent in patients with congenital heart disease or patients with prior cardiac surgery, and will often use incisional or scar-related substrates as isthmuses for reentry.

Atrial ectopic tachycardia (AET) is a form of enhanced automaticity where single or multiple foci in either the right or left atrium fire rapidly. In the largest study to date, 63% of these foci were in the right atrium, predominantly along the crista terminalis.⁶ Left-sided foci commonly localize to the pulmonary veins. AETs can be paroxysmal or incessant, the latter potentially resulting in tachycardia-induced cardiomyopathy.⁷ Multifocal atrial tachycardia (MAT) is a form of AT where greater than or equal to three distinct P-wave morphologies can be identified; this is an irregular rhythm.

Focal ATs historically referred to ATs from enhanced automaticity; however, in more recent decades, the term has been expanded to include ATs of focal origin from automatic, triggered, and microreentrant etiologies. The pathogenesis of focal ATs cannot be distinguished by the surface ECG. Focal ATs account for 5% to 15% of arrhythmias in adult patients undergoing invasive electrophysiology studies.⁸

This form of SVT occurs when there is abnormal impulse formation originating from the AV junction including the His node. This form of SVT more commonly occurs in the pediatric population and can occur as congenital or in the postcardiac
surgery period. Congenital junctional tachycardia classically presents shortly after birth, and is associated with high morbidity and mortality resulting from an increased incidence of systolic dysfunction.⁹

A relatively rare form of tachycardia defined as sinus in origin (normal P-wave axis, normal PR interval), inappropriate sinus tachycardia has an average 24-hour heart rate greater than 90 bpm in adults without identifiable cause. The mechanism of inappropriate sinus tachycardia is related to disorders of the autonomic nervous system and is typically diagnosed after secondary causes of sinus tachycardia have been excluded.

Clinical evaluation of any arrhythmia starts with a detailed history and physical examination. The chief complaint will often be palpitations or a “racing” heartbeat, but SVT can also present as episodes of dizziness, feeling lightheaded, or syncope. Questions should focus on timing, duration, frequency, and quality of symptoms because these clues can direct the medical provider toward the specific form of SVT. How symptoms start and stop are critical; SVT will typically have a sudden onset and abrupt termination, contrary to sinus tachycardia that is characterized by a gradual increase at the onset followed by a gradual slowing of the heart rate as it returns to normal. Frequency of symptoms is important and can be a clue to the magnitude of the problem, and can direct the provider on the best diagnostic modality to confirm the diagnosis. Beyond palpitations, there are a number of associated symptoms; these can include chest discomfort, shortness of breath, lightheadedness, or even syncope.

Special attention should be paid to syncope, defined as a transient loss of consciousness due to impaired cerebral blood flow, because this could be a “red flag” of a more serious problem. Syncope during tachycardia may represent a hemodynamic compromise. SVT does not commonly present with syncope; thus, syncope could suggest a different arrhythmia such as ventricular tachycardia (VT) or ventricular fibrillation. Patients with preexcitation on their ECG may present with ventricular fibrillation secondary to rapid conduction of atrial fibrillation over their AP. In this setting, this would be a life-threatening event, and urgent evaluation and treatment is warranted. A second exception involves elderly patients with AVNRT; this population is more vulnerable to syncope with the onset of SVT.¹⁰

The physical examination is rarely useful for patients with SVT. The sensation of rapid regular pounding in the neck during tachycardia has been shown to be a positive predictor of AVNRT.¹¹ Nonspecific findings such as a systolic or diastolic murmur could indicate a congenital cardiac anomaly, some of which are associated with specific forms of SVT.