Paroxysmal Supraventricular Tachycardia

Key mechanisms of PSVT

• Atrioventricular nodal reentrant tachycardia (AVNRT) (~50-60% of cases): Results from dual AV nodal pathways with slow and fast conduction properties. The slow pathway (located inferiorly near the tricuspid annulus) demonstrates decremental conduction and faster recovery, while the fast pathway conducts rapidly with slower recovery. During sinus rhythm, anterograde conduction proceeds via the fast pathway. A critically timed atrial premature beat blocks in the fast pathway (longer refractory period) but conducts slowly through the slow pathway, allowing the fast pathway to recover and conduct the impulse retrogradely, creating a circuit within or near the AV node. The resulting rhythm is typically regular with rates of 140-250 bpm.

• Atrioventricular reentrant tachycardia (AVRT) (~30-40% of cases): Involves an accessory pathway (AP) connecting atrial and ventricular tissue, bypassing the AV node. In orthodromic AVRT (most common, >90% of cases), anterograde conduction proceeds down the AV node with retrograde conduction via the accessory pathway, resulting in narrow QRS complexes. In antidromic AVRT (rare), conduction is reversed with wide QRS complexes. Accessory pathways are present in Wolff-Parkinson-White (WPW) syndrome (0.1-0.3% of population), which predisposes to AVRT. Atrial preexcitation demonstrates a short PR interval (<120 ms) with a delta wave (slurred QRS upstroke) on baseline ECG.

• Atrial reentrant tachycardia (ART) and atrial tachycardia (~10% of cases): Less common mechanisms involving reentry within atrial tissue or focal atrial automaticity. Atrial flutter can present as regular narrow complex tachycardia when conduction occurs with fixed AV block.

Major etiologies and associated conditions

• Dual AV nodal pathways (AVNRT): The anatomic substrate for AVNRT is present in ~10% of the population but becomes symptomatic in only a fraction. Risk factors include female sex, advancing age, and increased sympathetic tone. AVNRT can occur without structural heart disease; however, association with hypertension, aortic stenosis, and mitral stenosis exists.

• Accessory pathways (AVRT/WPW): Develop embryologically from muscularization of the AV groove; multiple pathways are present in ~5% of AVRT cases. Associated with hypertrophic cardiomyopathy (HCM), Ebstein's anomaly (pathognomonic association with right-sided pathways), congenital heart disease (ASD, VSD, Tetralogy of Fallot), and rare syndromes (Pompe disease, LAMP2 cardiomyopathy).

• Atrial reentry and focal atrial tachycardia: Associated with underlying atrial disease including atrial fibrillation history, atrial enlargement, chronic lung disease, thyroid dysfunction, and post-cardiac surgery.

• Precipitating factors: Acute illness, fever, dehydration, anemia, thyrotoxicosis, catecholamine surge (stress, exercise, stimulant use), caffeine/alcohol excess, and hypoxia can trigger PSVT in susceptible individuals.

• Genetic factors: AVNRT and AVRT show familial clustering, suggesting inherited substrate predisposition. Specific gene mutations affecting nodal conduction properties have been identified in some families.

Cardinal symptoms

• Palpitations: Sudden-onset awareness of rapid heartbeat, often described as "racing," "pounding," or "fluttering." Onset is characteristically abrupt ("sudden as a light switch"), distinguishing PSVT from sinus tachycardia which has gradual onset.
• Syncope or near-syncope: Occurs particularly with rapid rates (>180 bpm) or prolonged episodes (>30 seconds), resulting from reduced cerebral perfusion. More common in patients with impaired ventricular function or hemodynamically significant accessory pathways.
• Dyspnea: Results from rapid rate, reduced diastolic filling time, and sympathetic activation. May be severe if cardiomegaly or ventricular dysfunction develops from frequent episodes (tachycardia-induced cardiomyopathy).
• Chest discomfort: Described as chest tightness, pressure, or sharp pain; typically substernal and may mimic acute coronary syndrome, particularly in older patients.
• Fatigue and weakness: Occur during sustained episodes due to reduced cardiac output and metabolic stress.

Physical examination findings

• Elevated heart rate and blood pressure: Regular, rapid pulse (typically 140-250 bpm depending on mechanism). Blood pressure may be normal or elevated due to compensatory sympathetic activation.
• Cannon a-waves in jugular venous pulsation (JVP): Visible in AVNRT when atrial contraction occurs against a closed tricuspid valve, producing prominent, regular waves synchronous with carotid pulsations. This is a classic finding distinguishing AVNRT from other SVTs.
• Normal S1 and S2: Heart sounds are usually normal; however, variable intensity of S1 may be noted if hemodynamic changes occur.
• No murmurs or structural findings: Absence of organic cardiac disease in uncomplicated PSVT; new murmur may suggest underlying pathology.
• Signs of hemodynamic compromise: Hypotension, altered mental status, cool extremities, and pulmonary congestion (rales, elevated JVP) indicate significant hemodynamic derangement requiring urgent intervention.

Diagnostic approach

12-lead electrocardiogram (ECG) during tachycardia

• Narrow QRS complex tachycardia (QRS <120 ms): Confirms supraventricular origin; the pattern, P wave location relative to the QRS and T wave, and RP/PR intervals vary by mechanism.
• AVNRT-specific features: Regular narrow complex tachycardia with heart rate 140-250 bpm. P waves are typically buried within or immediately after the QRS or T wave (pseudo-"QRST" or "RP = PR" pattern where retrograde P wave is superimposed on terminal QRS/proximal ST segment). Atrial rate equals ventricular rate (1:1 conduction).
• AVRT-specific features: Regular narrow complex tachycardia (orthodromic) with visible retrograde P waves in the ST segment or early T wave (short RP interval where RP < PR). Longer RP intervals may suggest anteromic AVRT or atypical AVNRT.
• Baseline ECG findings: Assessment for delta waves and short PR interval indicating preexcitation consistent with WPW syndrome. Right-axis deviation and epsilon waves suggest Ebstein's anomaly in AVRT patients.

Electrophysiologic study (EPS)

• Gold standard for mechanism identification and risk stratification; indicated for recurrent symptomatic episodes, diagnostic uncertainty, or when ablation is contemplated.
• AVNRT demonstration: Dual AV nodal pathways identified by demonstrating a "jump" in AV nodal conduction curve—abrupt increase in AH interval (AV nodal conduction time) with a single-beat decrement in atrial pacing cycle length, reflecting shift from fast to slow pathway conduction. Atrial and ventricular electrograms demonstrate concentric atrial activation.
• AVRT demonstration: Accessory pathway localization by earliest retrograde atrial activation mapping. Ventriculoatrial (VA) intervals and differential pacing maneuvers characterize pathway properties (decremental vs. non-decremental conduction).
• Atrial tachycardia/atrial reentry: Focal activation pattern with single site of earliest atrial activation; atrial reentry shows reentrant circuit with conduction lines.
• AV nodal properties: Assessment of AV nodal refractory period, Wenckebach cycle length, and block properties helps identify dual pathways.

Holter monitor and event recorder

• Useful for documenting spontaneous episodes when ECG is not immediately available during symptoms.
• Extended monitoring may capture multiple episodes for pattern characterization.
• Event monitors or smartphone-based monitoring may be more practical for infrequent episodes.

Echocardiography

• Indicated to exclude structural heart disease and assess ventricular function.
• Important in AVRT patients to identify Ebstein's anomaly (displacement of tricuspid valve >8 mm from annulus), HCM, or other associated lesions.
• Evaluation for tachycardia-induced cardiomyopathy (depressed ejection fraction with frequent/incessant PSVT).

Laboratory studies

• Thyroid function tests (TSH) to exclude thyrotoxicosis.
• Electrolytes to assess for hypokalemia or hypomagnesemia that may facilitate arrhythmias.
• Troponins if acute coronary syndrome is suspected.

Diagnostic criteria

Acute termination of PSVT

Vagal maneuvers (first-line for hemodynamically stable patients)

• Valsalva maneuver: Sustained increased intrathoracic pressure for 10-15 seconds followed by rapid release; increases intrathoracic pressure, increases AV nodal refractoriness through parasympathetic (vagal) activation, and decreases AV nodal conduction velocity. Most effective in AVNRT. Success rate 40-60%.
• Carotid sinus massage: Gentle unilateral massage of carotid bulb for 5-10 seconds; elicits baroreceptor reflex with vagal discharge. Contraindicated in carotid stenosis or recent stroke.
• Cold water immersion ("diving reflex"): Application of ice-cold water to face activates trigeminal nerve and parasympathetic system. Particularly effective in younger patients.
• Supine positioning with leg elevation: Enhances venous return without performing straining maneuvers.

Adenosine IV (if vagal maneuvers fail and hemodynamically stable)

• Mechanism: Non-selective adenosine receptor agonist that activates G-protein-coupled receptors (A1 and A2A), hyperpolarizing nodal cells and blocking AV nodal conduction by increasing K+ conductance and reducing cAMP. Also slows SA nodal firing.
• Dosing: Initial bolus 6 mg IV rapid push followed by saline flush; second dose of 12 mg if necessary. Effective in >90% of AVNRT and orthodromic AVRT.
• Mechanism identification: Brief AV nodal block may reveal underlying atrial activity, aiding diagnosis; atrial tachycardia may continue briefly unmasking flutter waves.
• Adverse effects: Transient dyspnea, chest discomfort, flushing, and hypotension common but brief (half-life <10 seconds). Bronchospasm in asthmatic patients contraindicates use.
• Special considerations: Less effective in patients on theophylline (competitive antagonist); more effective with dipyridamole or carbamazepine (inhibitors of adenosine reuptake).

Alternative IV agents (if adenosine contraindicated or ineffective)

• Verapamil (non-dihydropyridine calcium channel blocker): IV dose 2.5-5 mg bolus; blocks L-type calcium channels in AV nodal cells, slowing conduction and increasing refractoriness. Effective in AVNRT and orthodromic AVRT. Avoid in patients with hypotension, heart failure, or WPW with rapid AF (accessory pathway may preferentially conduct).
• Diltiazem (alternative calcium channel blocker): IV bolus 0.25 mg/kg; similar mechanism to verapamil with potentially better hemodynamic profile.
• Beta-blockers (metoprolol, esmolol): Less effective for acute termination but useful adjuncts; increase AV nodal refractoriness through beta-2 adrenergic blockade.

Hemodynamically unstable PSVT

• Synchronized DC cardioversion (100-200 J initial monophasic or 50-100 J biphasic): Immediate therapy for hypotension, altered mental status, or signs of shock. Sedation with midazolam or propofol if patient conscious.

Chronic prophylactic management

For frequent symptomatic episodes or patient preference

• Beta-blockers: First-line prophylaxis; metoprolol (100-200 mg daily), atenolol (50-100 mg daily), or bisoprolol. Effective for AVNRT and AVRT; reduce frequency and rate of episodes through increased AV nodal refractoriness and decreased atrial/accessory pathway conduction. Provide additional benefit in patients with hypertension or post-MI.

• Non-dihydropyridine calcium channel blockers: Verapamil (120-360 mg daily) or diltiazem (120-360 mg daily); slow AV nodal conduction and increase refractoriness. Contraindicated in left ventricular dysfunction or hemodynamic instability.

• Class IA or IC antiarrhythmics (less common with modern practice):
• Flecainide (100-300 mg daily): Class IC agent; blocks fast sodium channels slowing conduction in accessory pathways and atrial tissue. Particularly effective for AVRT. Black box warning: Proarrhythmic in structural heart disease; avoid post-MI.
• Procainamide (1-4 g daily divided): Class IA agent; combination of sodium channel blockade and parasympathomimetic effects. Less favored due to side effects and need for QT monitoring.

• Class II antiarrhythmics (digoxin, rarely used):
• Digoxin: Increases AV nodal refractoriness through parasympathomimetic effects and direct AV nodal tissue effects. Limited by narrow therapeutic window, drug interactions, and availability of superior alternatives. May precipitate AF in WPW syndrome.

Non-pharmacological management

• Catheter ablation: Gold-standard definitive therapy for recurrent or frequent PSVT; success rates >95% with low complication rates (<1%).

Complications of the arrhythmia

• Pre-excited atrial fibrillation degenerating to ventricular fibrillation (emergency): In WPW, AF conducts down an accessory pathway that lacks the decremental properties of the AV node, so ventricular rates can be extreme. The signal is an irregularly irregular, wide, bizarre, varying-morphology tachycardia. The 2015 ACC/AHA/HRS SVT guideline directs immediate synchronized cardioversion if unstable and procainamide or ibutilide (not AV nodal blockers) if stable. This is the mechanism of sudden cardiac death in WPW.
• Tachycardia-induced cardiomyopathy: Incessant or very frequent SVT causes calcium-handling derangement and energetic depletion, producing a dilated, hypocontractile ventricle. Signal: new LV systolic dysfunction on echocardiography with no other cause; largely reversible once the arrhythmia is controlled or ablated.
• Hemodynamic decompensation (emergency): Loss of atrial kick plus abbreviated diastolic filling at rapid rates causes hypotension, syncope, angina, or pulmonary edema — especially in aortic stenosis, HCM, or ischemic disease.

Complications of treatment

• Adenosine: Transient sinus arrest/high-grade AV block and a brief "flatline" pause on the monitor are expected; the real hazards are bronchospasm in reactive airway disease and induction of atrial fibrillation, which is dangerous if an accessory pathway is present. Have a defibrillator at the bedside.
• Non-dihydropyridine calcium channel blockers and beta blockers: Negative inotropy and AV block can cause bradycardia, hypotension, or decompensated heart failure; in pre-excitation they shunt conduction down the accessory pathway (emergency). IV verapamil should not be given for an undifferentiated wide-complex tachycardia.
• Flecainide/propafenone: Class IC agents slow atrial conduction and can convert atrial flutter to slow flutter with 1:1 AV conduction and QRS widening; they are proarrhythmic in structural heart disease or prior MI.
• Catheter ablation: Slow-pathway ablation near the compact AV node risks inadvertent complete heart block requiring a permanent pacemaker; other risks are cardiac tamponade (emergency — hypotension with distended neck veins), vascular access injury, and thromboembolism.
• Cardioversion: Sedation-related apnea and skin burns; rare post-shock bradyarrhythmia.

• "Like a light switch": Abrupt onset and abrupt offset of palpitations in a young, otherwise healthy patient is the stem's signal for PSVT; gradual acceleration and deceleration points instead to sinus tachycardia from pain, fever, anemia, hypovolemia, or thyrotoxicosis.
• Pseudo-R′ in V1 and pseudo-S in the inferior leads: A retrograde P wave buried in the terminal QRS is the classic ECG buzzword for typical (slow-fast) AVNRT. Compare with a baseline tracing if one is available — the "extra deflection" disappears in sinus rhythm.
• Single best next step in a stable patient: Vagal maneuvers first, and if they fail, adenosine 6 mg IV rapid push through a proximal vein with an immediate saline flush, followed by 12 mg if needed (2015 ACC/AHA/HRS SVT guideline). The modified Valsalva with supine repositioning and passive leg raise converts more patients than the standard strain.
• Unstable = shock, not drugs: Hypotension, altered mental status, ischemic chest pain, or acute heart failure mandates immediate synchronized cardioversion per ACLS. Synchronization matters — an unsynchronized shock on the T wave can induce VF.
• The association examiners love: Ebstein anomaly with right-sided accessory pathways and WPW; also recall lithium exposure in utero as the classic Ebstein trigger.
• The distractor to avoid: Never give adenosine, verapamil, diltiazem, beta blockers, or digoxin for pre-excited atrial fibrillation (irregular, wide, polymorphic-appearing). Blocking the AV node funnels conduction down the accessory pathway and can precipitate VF; use procainamide, ibutilide, or electrical cardioversion.
• Asthma/COPD caveat: Adenosine can cause bronchospasm; a nondihydropyridine calcium channel blocker (diltiazem) is the preferred alternative in a stable patient with normal LV function.
• Definitive therapy: Catheter ablation is the guideline-endorsed curative option for recurrent symptomatic AVNRT or AVRT and is the answer when the stem emphasizes a young patient who wants to be off medication or has a symptomatic accessory pathway.