Supraventricular Tachycardia (SVT)

01Pathophysiology

Supraventricular tachycardia (SVT) is a group of tachyarrhythmias that originate at or above the bundle of His. The heart rate is typically between 150 and 250 bpm, and the QRS complex is narrow because ventricular depolarization still occurs through the normal His-Purkinje system in most forms.

The dominant mechanism behind SVT is re-entry. A re-entrant circuit requires two functionally distinct pathways with different conduction velocities and refractory periods, along with a region of unidirectional block that allows an electrical impulse to loop continuously. This is why SVT starts and stops abruptly: the circuit either initiates when a premature beat encounters the right conditions, or breaks when one limb of the circuit fails to conduct.

In AV nodal re-entrant tachycardia (AVNRT), the most common form, the re-entry circuit is confined within the AV node itself. Two pathways exist: a fast pathway with a long refractory period and a slow pathway with a short refractory period. In the typical ("slow-fast") form, a premature atrial beat arrives when the fast pathway is still refractory, conducts down the slow pathway, and then re-enters retrogradely up the now-recovered fast pathway. Because atrial and ventricular activation occur nearly simultaneously, P waves are buried within the QRS or appear just after it as a pseudo-R' deflection in lead V1.

In AV re-entrant tachycardia (AVRT), an accessory bypass tract (such as the Bundle of Kent in Wolff-Parkinson-White syndrome) connects the atrium directly to the ventricle, bypassing the AV node. In orthodromic AVRT (the common form), the impulse travels antegrade through the AV node and retrograde through the accessory pathway, producing a narrow QRS. In antidromic AVRT (uncommon), the direction reverses: the impulse goes antegrade through the accessory pathway and retrograde through the AV node, producing a wide QRS that mimics ventricular tachycardia. During sinus rhythm, the accessory pathway allows pre-excitation of the ventricle, which appears as the classic delta wave on ECG.

In focal atrial tachycardia, the mechanism is either enhanced automaticity or triggered activity from a single ectopic focus in the atrial tissue. Unlike re-entrant SVTs, this form does not depend on the AV node for initiation or maintenance, which is why it does not terminate with adenosine (though adenosine may transiently increase AV block and unmask the atrial activity).

The abrupt onset of symptoms directly reflects the sudden establishment of a re-entrant loop. The rapid rate reduces diastolic filling time, which lowers cardiac output and explains the lightheadedness, presyncope, and diaphoresis. Cannon A waves appear in AVNRT because the atria contract against closed AV valves.

02Classification and Clinical Manifestation

03Diagnostic Workup

The first step when a patient presents with palpitations and a rapid heart rate is a 12-lead ECG. The hallmark finding is a regular, narrow-complex tachycardia. The next critical step is to analyze the relationship between P waves and QRS complexes. In AVNRT, P waves are typically hidden within the QRS or appear as a subtle pseudo-R' deflection in V1 and pseudo-S waves in the inferior leads. In orthodromic AVRT, short RP tachycardia is seen with retrograde P waves falling just after each QRS complex.

When the patient is in sinus rhythm between episodes, look for signs of pre-excitation (delta wave, short PR, wide QRS). This baseline finding is what defines WPW syndrome and changes management entirely.

Adenosine serves a dual role. If the arrhythmia terminates after adenosine, it confirms the AV node is part of the re-entrant circuit (AVNRT or AVRT). If the arrhythmia persists but the ventricular rate transiently slows, the underlying atrial rhythm is unmasked, which helps distinguish atrial tachycardia or atrial flutter from AV node-dependent SVTs.

For patients with recurrent symptoms but no documentation of the arrhythmia, ambulatory monitoring with a Holter monitor (24 to 48 hours) or an event recorder (weeks) should be ordered.

The electrophysiology study (EPS) is the gold standard. It precisely identifies the location and mechanism of the arrhythmia and is performed when catheter ablation is planned. It is not needed for every patient with a single self-limited episode, but it is indicated for recurrent SVT, pre-excitation on baseline ECG, or when the mechanism is unclear.

04Management and Treatment

Acute stabilization begins with assessing hemodynamic status. If the patient is unstable (systolic BP < 90 mmHg, chest pain with ischemic changes, pulmonary edema, or altered consciousness), proceed immediately to synchronized cardioversion without delay.

In the stable patient, vagal maneuvers are the first step. These work by increasing parasympathetic tone at the AV node, transiently slowing conduction and potentially breaking the re-entrant loop. The modified Valsalva maneuver (bearing down in a semi-recumbent position for 15 seconds, then immediately lying supine with passive leg raise) has a higher success rate than the standard technique.

If vagal maneuvers fail, adenosine is the next best step. Adenosine has an extremely short half-life (less than 10 seconds), which is why it must be given as a rapid IV push through a proximal vein (antecubital or above) immediately followed by a 20 mL normal saline flush. The dose is 6 mg initially; if no response, 12 mg is given, and a second 12 mg dose may be attempted. Patients often experience transient chest tightness, flushing, and a brief sense of impending doom, which should be communicated beforehand. Adenosine is contraindicated in severe reactive airway disease (asthma) due to the risk of bronchospasm; in these patients, use IV verapamil or diltiazem instead.

The critical exception in management involves WPW with pre-excited atrial fibrillation. In this scenario, the atrial fibrillation conducts rapidly down the accessory pathway. If you administer AV nodal blocking agents (adenosine, verapamil, diltiazem, digoxin, or beta-blockers), you remove the "braking" effect of the AV node while leaving the accessory pathway unaffected. This preferentially shunts all conduction through the bypass tract and can degenerate into ventricular fibrillation and cardiac arrest. The correct treatment is procainamide (which slows conduction through the accessory pathway) or synchronized cardioversion.

For long-term management, catheter ablation is the definitive treatment. It is recommended as first-line therapy for patients with recurrent SVT or WPW, given its high cure rate and low complication profile. If the patient declines ablation or if it is unavailable, daily oral beta-blockers or calcium channel blockers provide rate control and reduce episode frequency.

05Differential Diagnosis and Distractors

06Traps and High-Yield Pearls

The single most dangerous trap on this topic is WPW with atrial fibrillation. The vignette will describe a young patient with an irregularly irregular wide-complex tachycardia and a history of "episodes of palpitations." The temptation is to treat the atrial fibrillation with standard rate-control agents (beta-blockers, calcium channel blockers, or digoxin). Every one of these choices is wrong and potentially lethal. The answer is either procainamide or synchronized cardioversion. If you see an irregular wide-complex tachycardia in a young patient, think WPW first.

A second common trap is the vignette presenting a regular narrow-complex tachycardia at exactly 150 bpm and asking for the next step. Students reflexively choose adenosine because the rhythm looks like SVT. However, a rate locked at 150 should raise suspicion for atrial flutter with 2:1 block, where the atrial rate is 300 and every other impulse is conducted. Adenosine will not terminate atrial flutter, but it will transiently slow AV conduction and unmask the flutter waves. This distinction matters because flutter often requires different long-term management (rate control, anticoagulation assessment, or ablation targeting the cavotricuspid isthmus).

A third pearl: when a vignette describes a tachycardia that "terminates spontaneously" or "terminates with bearing down," the answer is almost always AVNRT or AVRT. These arrhythmias depend on the AV node, and anything that transiently blocks AV conduction breaks the circuit. Focal atrial tachycardia does not terminate with vagal maneuvers.

Finally, remember the "wide-complex tachycardia in a young patient" rule. When the question stem describes a hemodynamically stable wide-complex tachycardia and asks for the next step, the safest answer when the diagnosis is uncertain is procainamide (or cardioversion if unstable). Never assume SVT with aberrancy without strong evidence; treating VT as SVT can be fatal, but treating SVT as VT is safe.

The core competency being tested across all SVT questions is the ability to read an ECG pattern, match it to the correct mechanism, and choose a management pathway that avoids harm, particularly in the setting of accessory pathway physiology.