Supraventricular Tachycardia

• Atrioventricular Nodal Reentrant Tachycardia (AVNRT) Mechanism: AVNRT accounts for approximately 60-70% of all SVT cases and arises from dual nodal physiology within the AV node itself. The AV node contains two functionally distinct conduction pathways with different electrophysiologic properties: the fast (alpha) pathway and the slow (beta) pathway. The fast pathway has a shorter refractory period but slower conduction velocity, while the slow pathway demonstrates slower conduction but shorter refractory period—a critical physiologic paradox that creates the substrate for reentry. During sinus rhythm, impulses travel preferentially down the fast pathway and return via the slow pathway. When a single atrial premature beat occurs, it may encounter the fast pathway still in its refractory period and instead conduct down the slow pathway; if conduction time down the slow pathway allows the fast pathway to recover excitability by the time the impulse reaches the ventricular end of the node, a reentrant circuit is established. The impulse then travels retrogradely up the fast pathway to reenter the atrium and conduct antegrade down the slow pathway again, creating a self-perpetuating macro-reentrant circuit with a cycle length typically of 330-450 ms (rate ~130-180 bpm). This explains why AVNRT typically presents with rates in this range and why vagal maneuvers that slow AV nodal conduction can terminate the rhythm.

• Atrioventricular Reentrant Tachycardia (AVRT) Mechanism: AVRT accounts for approximately 25-30% of SVT cases and depends on an accessory pathway (AP)—an abnormal bundle of muscle that bypasses the normal AV node. AVRT represents a macro-reentrant circuit involving two distinct anatomic limbs: the AV node-His-Purkinje system and the accessory pathway. During sinus rhythm in patients with an AP, dual conduction occurs simultaneously—the normal impulse travels down the AV node while a concurrent impulse travels down the accessory pathway, resulting in Wolff-Parkinson-White (WPW) syndrome if the accessory pathway conducts rapidly. The accessory pathway typically has faster conduction velocity than the AV node but a longer refractory period. AVRT is initiated when an atrial premature beat blocks in the accessory pathway (due to its longer refractory period) and instead conducts down the AV node; if the AV node-mediated impulse then finds the accessory pathway recovered and capable of retrograde conduction, a reentrant circuit is established with antegrade conduction via the AV node and retrograde conduction via the accessory pathway. This mechanism explains the characteristic narrow QRS complexes in orthodromic AVRT (AV node → AP retrograde) and why accessory pathways with longer refractory periods may be less proarrhythmic. Importantly, the rate of AVRT is typically faster than AVNRT (often >180 bpm) because accessory pathways conduct more rapidly than the AV node.

• Atrial Tachycardia Mechanism: Atrial tachycardia (accounting for 10-15% of SVT) arises from abnormal automaticity or triggered activity within atrial tissue. Abnormal automaticity occurs when ectopic pacemaker cells in the atrium develop spontaneous depolarization rates that exceed those of the sinoatrial node, driven by enhanced phase 4 diastolic depolarization due to altered ion channel function, increased intracellular calcium, or enhanced sympathetic tone. Triggered activity—specifically early afterdepolarizations (EADs) or delayed afterdepolarizations (DADs)—represents another mechanism. EADs occur during phase 2-3 of the action potential when intracellular calcium is elevated, causing spontaneous repolarization oscillations that may reach threshold; DADs occur after full repolarization due to spontaneous calcium-induced sarcoplasmic reticulum calcium release and sodium-calcium exchanger activation. Atrial tachycardia presents with rates typically 120-250 bpm and is often incessant or persistent. Critically, atrial tachycardia differs from AVNRT and AVRT in that the P wave is clearly visible and dissociated from the preceding QRS-T complex, reflecting the ectopic atrial origin.

• Molecular Mechanisms and Ion Channel Dysfunction: At the molecular level, SVT pathophysiology depends on alterations in ion channel function. Calcium-handling abnormalities, particularly increased L-type calcium channel activity in nodal cells and increased sarcoplasmic reticulum calcium leak, promote DADs and abnormal automaticity. Potassium channel mutations (e.g., KCNE1, KCNQ1) can predispose to both SVT and sudden cardiac death. Genetic variants in genes encoding AV nodal proteins and accessory pathway tissue composition (such as connexin mutations) influence conduction properties and arrhythmia susceptibility. Additionally, adenosine and adenosine-2A receptor signaling on AV nodal cells creates a critical pharmacologic vulnerability: adenosine hyperpolarizes nodal cells via GIRK (G protein-gated inward rectifier potassium) channel activation, rapidly suppressing conduction and terminating reentrant circuits.

• Autonomic Nervous System Integration: The sympathetic nervous system enhances AV nodal conduction velocity and shortens refractory periods, promoting SVT initiation, while the parasympathetic nervous system produces the opposite effect. This explains why SVT often occurs during emotional stress or exertion (sympathetic activation) and why vagal maneuvers (straining, Valsalva, ice water face immersion) can terminate episodes. Beta-adrenergic receptors on AV nodal cells increase intracellular cAMP and enhance L-type calcium channel activity, explaining why beta-blockers and calcium channel blockers are effective SVT treatments.

• Atrioventricular Nodal Reentrant Tachycardia (AVNRT): AVNRT does not require a structural cardiac abnormality and occurs exclusively due to dual nodal pathways; it is not associated with accessory pathways or overt structural heart disease. Risk factors include female sex (approximately 60-70% of AVNRT cases), middle age (peak incidence 40-60 years), and certain genetic predispositions affecting nodal AV nodal properties. Notably, AVNRT can occur even in patients with structurally normal hearts on imaging. Triggers include emotional stress, caffeine, sympathomimetic agents, and atrial premature beats.

• Atrioventricular Reentrant Tachycardia and Wolff-Parkinson-White Syndrome: AVRT depends on the presence of an accessory pathway that bypasses the normal AV nodal delay. The most common accessory pathways are left-sided (60%), followed by right-sided (25%) and septal (15%) pathways. WPW syndrome affects approximately 1-3 per 1000 people and can be sporadic or familial (autosomal dominant inheritance in some cases, with mutations in PRKAG2 and other genes affecting cardiac metabolism). Accessory pathways may be manifest (conducting during sinus rhythm, causing characteristic delta waves on ECG), concealed (conducting only retrogradely, appearing as a normal ECG during sinus rhythm), or intermittently manifest. Patients with manifest WPW are at risk for rapid ventricular rates during atrial fibrillation because accessory pathways often have shorter refractory periods than the AV node, potentially permitting rates >250 bpm and degenerating to ventricular fibrillation.

• Atrial Tachycardia: Atrial tachycardia can be idiopathic (primary automaticity or triggered activity) or secondary to structural cardiac disease, pulmonary disease, thyroid disease, or metabolic derangements. Common secondary causes include chronic obstructive pulmonary disease (COPD), pneumonia, acute myocardial infarction, heart failure, hypertension, and hyperthyroidism. Medications including sympathomimetics, theophylline, and certain antibiotics may trigger atrial tachycardia through DAD mechanisms. Atrial tachycardia originating from the pulmonary veins may predispose to subsequent atrial fibrillation.

• Focal Atrial Tachycardia: Certain anatomic regions are hotspots for ectopic activity: the crista terminalis on the right atrium, the coronary sinus ostium, the pulmonary vein ostia, and the mitral annulus on the left atrium. These sites have enhanced automaticity due to inherent properties of tissue composition and sympathetic innervation.

• Precipitating Factors and Triggers: Acute triggers for SVT initiation include atrial premature beats (APBs), acute metabolic derangements (hypokalemia, hypomagnesemia), hyperthyroidism, fever, infection, myocardial ischemia, alcohol binge drinking ("holiday heart" syndrome), and sympathomimetic use (cocaine, amphetamines, decongestants). Chronic risk factors include heart failure (which can reduce AV nodal refractory period and promote SVT), hypertension, cardiomyopathy, and accessory pathway presence.

• Palpitations: The most common presenting symptom, palpitations are described as a sensation of rapid or forceful heartbeats. Patients may report sudden onset and abrupt termination of episodes ("paroxysmal"), distinguishing paroxysmal SVT from sinus tachycardia. The rapid rate creates an amplified cardiac stroke volume and reduced diastolic filling time, enhancing the sensations of individual beats. Palpitations may be accompanied by awareness of heartbeats that patients describe as "fluttering," "pounding," or "racing." This symptom alone does not differentiate SVT from sinus tachycardia or other arrhythmias, necessitating ECG confirmation.

• Dyspnea and Chest Discomfort: Dyspnea occurs due to increased metabolic demand from the elevated heart rate and reduced time for diastolic ventricular filling, decreasing stroke volume and cardiac output. The tachycardia reduces the diastolic interval during which coronary perfusion occurs, potentially causing demand ischemia, especially in patients with underlying coronary artery disease or in those with rates sustained >180 bpm for prolonged periods. Chest discomfort is often described as pressure or tightness and may be indistinguishable from acute coronary syndrome; troponin elevation can occur with demand ischemia in sustained rapid SVT.

• Syncope and Presyncope: These occur when the tachycardia reduces cardiac output sufficiently to cause cerebral hypoperfusion. Syncope is more common with very rapid rates (>200 bpm), prolonged episodes, or underlying cardiac dysfunction reducing baseline contractility. Presyncope may present as lightheadedness, dizziness, or visual dimming. Notably, syncope during SVT should prompt evaluation for underlying structural heart disease or ventricular involvement.

• Fatigue and Weakness: Sustained or frequently recurrent episodes of SVT can lead to chronic fatigue, reduced exercise tolerance, and generalized weakness, particularly if the rhythm is incessant (constant) or persistent (frequent episodes). This is especially true in atrial tachycardia, which may be persistent and lead to tachycardia-mediated cardiomyopathy if untreated.

• Physical Examination Findings:
• Rapid, Regular Pulse: SVT produces a pulse rate typically 130-250 bpm with a regular rhythm; this regularity distinguishes SVT from atrial fibrillation (irregular) and sinus tachycardia (usually more gradual onset/offset and rate variation).
• Prominent Neck Veins with Cannon A Waves: In AVNRT, simultaneous contraction of the atrium against a closed tricuspid valve (occurring during the circuit when the atrium depolarizes during ventricular systole) generates prominent cannon waves (large positive deflections) in the jugular venous pulse. Cannon waves occur irregularly in AVNRT ("variable cannon waves") because the timing of atrial depolarization changes beat-to-beat. This finding is highly specific for AVNRT but may be difficult to appreciate clinically.
• Hypotension and Decreased Perfusion: In severe cases, sustained SVT may cause systolic blood pressure <90 mmHg with cool extremities, altered mental status, and signs of inadequate tissue perfusion, constituting hemodynamic instability.
• Heart Sounds: S1 may be diminished due to variable AV relationships; in AVNRT, atrial sounds may be absent or merged with ventricular sounds due to near-simultaneous ventricular and atrial contraction. In AVRT, an audible S1 is typically preserved.

• Important Clinical Variants:
• Permanent Junctional Reciprocating Tachycardia (PJRT): A form of AVRT utilizing a slowly-conducting concealed pathway, typically presenting as incessant or persistent SVT in infants and young children, at risk for tachycardia-mediated cardiomyopathy.
• Atrial Tachycardia with AV Block: Atrial tachycardia may conduct with variable AV block (e.g., 2:1 conduction), creating a ventricular rate lower than the atrial rate; this pattern is highly suggestive of atrial tachycardia and helps differentiate it from AVNRT or AVRT, which should demonstrate 1:1 conduction.
• Antidromic AVRT: Rare (<5% of AVRT cases), antidromic AVRT utilizes antegrade conduction via the accessory pathway and retrograde conduction via the AV node, producing wide QRS complexes that mimic ventricular tachycardia; recognition is critical to avoid inappropriate treatments.

• 12-Lead Electrocardiography - Rhythm Strip Analysis:
• QRS Duration: SVT by definition presents with narrow QRS complexes (<120 ms) on the 12-lead ECG, distinguishing it from ventricular tachycardia. However, approximately 15-20% of SVT may manifest bundle branch block aberrancy, widening the QRS to 120-200 ms while maintaining the supraventricular origin. Clinical correlation with baseline ECG is essential to identify pre-existing bundle branch blocks.
• Rate: Typical SVT rates are 130-250 bpm. AVNRT rates typically range 140-180 bpm, AVRT 150-250 bpm, and atrial tachycardia 120-250 bpm (and can be slower). Extremely regular rates at 130-150 bpm with 1:1 AV conduction in a patient with known WPW should raise suspicion for AVRT.
• P Wave Location and Morphology: This is a critical diagnostic feature:
• In AVNRT during the tachycardia, the P wave is typically retrograde (negative in leads II, III, aVF) due to atrial activation traveling backward from the AV node. Critically, the retrograde P wave is often buried within or immediately after the QRS complex or may appear at the terminal portion of the QRS or within the T wave,

Step 1 — Assess hemodynamic stability (2020 AHA ACLS adult tachycardia algorithm)

• Synchronized cardioversion: indicated immediately for hypotension, altered mentation, ischemic chest pain, or acute heart failure. Synchronization to the R wave avoids delivering energy on the T wave and inducing ventricular fibrillation. Narrow regular tachycardias convert at low biphasic energies; sedate the awake patient if time permits.

Step 2 — Vagal maneuvers first in the stable patient (2015 ACC/AHA/HRS SVT guideline, Class I)

• Valsalva or carotid sinus massage: increased vagal tone hyperpolarizes AV nodal cells and prolongs nodal refractoriness, breaking the reentrant limb in AVNRT and orthodromic AVRT. The modified Valsalva (strain supine, then immediate leg elevation) converts more patients than the standard maneuver. Avoid carotid massage with a bruit or prior stroke.

Step 3 — Adenosine (Class I)

• Adenosine 6 mg IV rapid push through a proximal vein with a saline flush, followed by 12 mg if no response. It activates GIRK potassium channels in nodal tissue, producing transient AV block that terminates nodal-dependent reentry and unmasks flutter or atrial tachycardia when it does not.

Step 4 — IV AV nodal blockers if adenosine fails

• Non-dihydropyridine calcium channel blockers (diltiazem, verapamil) or IV beta blockers (metoprolol, esmolol). Avoid verapamil in decompensated HFrEF and in wide-complex tachycardia of uncertain origin.

Definitive therapy

• Catheter ablation: slow-pathway modification for AVNRT, accessory-pathway ablation for AVRT — a Class I option for symptomatic recurrent SVT and preferred over lifelong drugs in most patients per the 2015 ACC/AHA/HRS guideline. Chronic suppression with beta blockers, diltiazem/verapamil, or flecainide/propafenone (structurally normal hearts only) is an alternative.

Contraindicated

• AV nodal blockade in pre-excited atrial fibrillation (irregular, wide, very rapid): adenosine, calcium channel blockers, beta blockers, and digoxin funnel conduction down the accessory pathway and can precipitate ventricular fibrillation. Use procainamide or ibutilide, or cardiovert.
• Adenosine with caution in severe bronchospastic disease and in transplanted (denervated) hearts.

Complications of the arrhythmia

• Degeneration of pre-excited atrial fibrillation into ventricular fibrillation (emergency): an accessory pathway with a short antegrade refractory period conducts atrial impulses without nodal filtering; the signal is an irregularly irregular, wide, bizarre, extremely rapid complex tachycardia. This is the mechanism of sudden cardiac death in WPW and mandates immediate cardioversion or procainamide, never AV nodal blockade.
• Tachycardia-mediated cardiomyopathy: incessant atrial tachycardia or PJRT causes chronic calcium-handling derangement and ventricular remodeling; signalled by a new drop in LVEF with chamber dilation that reverses after rhythm control or ablation.
• Demand ischemia: shortened diastole reduces coronary perfusion time while raising myocardial oxygen demand; presents as chest pressure with ST depression and a modest troponin rise even with normal coronaries. Do not reflexively label this a type 1 MI.
• Syncope with injury and hemodynamic collapse (emergency): from cerebral hypoperfusion at very rapid rates or with impaired baseline contractility.

Complications of treatment

• Adenosine effects: transient sinus arrest/high-grade AV block, flushing, chest tightness, and a sense of impending doom; bronchospasm in reactive airway disease. Adenosine can also induce atrial fibrillation, which is hazardous in manifest pre-excitation — have a defibrillator at the bedside.
• Verapamil/diltiazem: negative inotropy and vasodilation causing hypotension and bradycardia, particularly with concurrent beta blockade or HFrEF.
• Catheter ablation: complete heart block requiring a permanent pacemaker (highest with slow-pathway or septal-pathway ablation), cardiac tamponade, and vascular access injury; signalled by post-procedure bradycardia, hypotension, or a pulsus paradoxus.
• Class IC antiarrhythmics (flecainide, propafenone): proarrhythmia and increased mortality when structural heart disease or prior infarction is present — hence their restriction to structurally normal hearts.
• Cardioversion: thromboembolism if an unrecognized atrial arrhythmia has been present beyond 48 hours, and skin burns from poor pad contact.

• Unstable = shock, stable = vagal then adenosine: the single most tested "next best step" is synchronized cardioversion for hypotension or altered mentation, and modified Valsalva followed by adenosine 6 mg IV push for the stable patient (2020 AHA ACLS, 2015 ACC/AHA/HRS).
• **Delta wave + short PR interval on the resting ECG = *Wolff-Parkinson-White*. The examiner's favorite association is WPW plus irregular, wide, very fast atrial fibrillation — give procainamide** or cardiovert. Adenosine, verapamil, beta blockers, and digoxin are the classic distractors and can precipitate ventricular fibrillation.
• ***Pseudo-R′ in V1* and *pseudo-S in the inferior leads*** during tachycardia that vanish in sinus rhythm are retrograde P waves buried in the QRS — typical AVNRT, the most common SVT.
• Adenosine is diagnostic even when it fails: transient AV block unmasks sawtooth flutter waves (atrial flutter) or continued atrial activity with AV block (atrial tachycardia). Termination of the tachycardia implies the AV node was part of the circuit (AVNRT or AVRT).
• Wide-complex regular tachycardia of unknown origin is ventricular tachycardia until proven otherwise — antidromic AVRT mimics it. Verapamil in that setting can cause collapse. The shockable pulseless rhythms remain ventricular fibrillation / pulseless VT.
• Catheter ablation is curative and is a first-line option, not a last resort, for symptomatic recurrent AVNRT or AVRT per the 2015 ACC/AHA/HRS guideline; slow-pathway ablation risks AV block requiring a pacemaker.
• **≥3 distinct P-wave morphologies with an irregular rhythm = *multifocal atrial tachycardia***, classically in decompensated COPD; treat the hypoxia and metabolic derangement — it does not respond to cardioversion.
• Incessant SVT with a falling ejection fraction = tachycardia-mediated cardiomyopathy, which is reversible with rate or rhythm control.