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Supraventricular Tachycardia (SVT)

Clinical Subject Page

Supraventricular Tachycardia (SVT)

ICD-10

I47.10

Specialty

Cardiology

Onset

Acute

Reviewed

July 2026

On This Page

Overview

Supraventricular tachycardia (SVT) is a group of rapid heart rhythm disorders that originate above the ventricles, involving the atria or the atrioventricular (AV) node. It is caused by abnormalities in the heart’s electrical conduction or pacemaker activity, most commonly due to reentry circuits.

Etiology & Risk Factors

  • Supraventicular Tachycardia (SVT) is caused by abnormal electrical impulse formation or conduction above the ventricles. The main mechanisms are:

    • Reentry circuits (most common)
      • Atrioventricular nodal reentrant tachycardia (AVNRT)
      • Atrioventricular reciprocating tachycardia (AVRT)
    • Abnormal or ectopic pacemaker activity
      • Focal atrial tachycardia (FAT)
      • Multifocal atrial tachycardia (MAT)
      • Junctional tachycardia

    Risk Factors For Supraventricular Tachycardia (SVT)

    • Underlying structural heart disease
    • Family history of Supraventricular Tachycardia (SVT) or sudden cardiac death
    • Use of certain medications (e.g., albuterol, theophylline, methylprednisolone)
    • Illicit drug use (e.g., amphetamines, cocaine)
    • Hypertension
    • Cardiomyopathy
    • Myocardial infarction
    • Infection
    • Alcohol poisoning

Pathophysiology

      • Reentry (most common)
        • An electrical impulse repeatedly travels in a continuous loop, causing ongoing rapid stimulation of the heart.
        • Occurs in:
          • AVNRT: Reentry circuit forms between the fast and slow pathways within the AV node.
          • AVRT: Reentry circuit forms between the AV node and an accessory pathway (e.g., Bundle of Kent in WPW syndrome).
      • Abnormal automaticity (ectopic pacemaker activity)
        • An abnormal focus in the atria or AV junction generates rapid electrical impulses independently of the sinoatrial (SA) node.
        • Seen in focal atrial tachycardia and junctional tachycardia.

      Summary Flow

      Abnormal electrical impulse (reentry or ectopic focus) → Rapid atrial activation → Rapid conduction through the AV node to the ventricles → Supraventricular tachycardia (rapid heart rate) → Reduced ventricular filling time → Symptoms such as palpitations, dizziness, dyspnea, chest pain, or syncope.

Clinical Presentation

  1. Symptoms of Supraventricular Tachycardia (SVT)

    • Sudden onset of palpitations (most common)
    • Fatigue
    • Chest pain or chest discomfort
    • Shortness of breath (dyspnea)
    • Dizziness or lightheadedness (presyncope)
    • Syncope (more common in older adults)
    • Diaphoresis (excessive sweating)

    Characteristic Features of Supraventricular Tachycardia (SVT)

    • Symptoms usually begin and end abruptly.
    • Some patients with AVNRT may experience:
      • Neck pounding or “shirt flapping”
      • Urinary urgency or increased urination after an episode

    Signs of Unstable Supraventicular Tachycardia (SVT)

    • Hypotension
    • Acute pulmonary edema
    • Severe chest pain
    • Altered mental status

History Taking

  • “Are you feeling short of breath?”
  • “Is your breathing worse when lying flat?”
  • “Do you have chest pain or pressure?”
  • “Have you noticed dizziness or fainting?”
  • “Do you feel your heart racing (palpitations)?”
  • “Have you had swelling in your legs or abdomen?”
  • “Have you had a recent viral illness or pericarditis?”
  • “Have you recently had heart surgery or a chest injury?”
  • “Do you have kidney disease, cancer, thyroid disease, or an autoimmune condition?”
  • “Have you had fever or recent infection?”
  • “When did your symptoms start? Did they come on suddenly or gradually?”

Types of Supraventricular Tachycardia (SVT)

Cardiology · Supraventricular Tachycardia (SVT) — Classification & Features

150–250
Typical HR (bpm)
in most SVTs
<120
QRS duration (ms)
narrow complex (usual)
AVNRT
Most common SVT
~60% of all cases
WPW
Most dangerous SVT
risk of sudden death in AF
SVT Classification — by mechanism
Re-entry (most common)
AVNRT — AV node re-entry
Typical (slow-fast) ~90%
Atypical (fast-slow, slow-slow)
AVRT — AV re-entry (accessory pathway)
Orthodromic (narrow QRS) ~95%
Antidromic (wide QRS) ~5%
Atrial flutter — macro re-entry
Typical (CTI-dependent)
Atypical (non-CTI)
SANRT — SA node re-entry
Rare; abrupt onset/offset
Intra-atrial re-entry
Scar-related; post-surgical
Enhanced / Abnormal Automaticity
Sinus tachycardia
Physiological response (not true SVT)
Inappropriate sinus tachycardia (IST)
Atrial tachycardia (focal AT)
Ectopic focus outside SA node
Automatic, triggered, or micro-re-entry
Multifocal atrial tachycardia (MAT)
≥3 different P-wave morphologies
Associated with COPD, hypoxia
Junctional tachycardia
Automatic focus in AV node/His
Post-cardiac surgery; digitalis toxicity
Triggered Activity
Atrial fibrillation
Multiple wavelets; irregular
Technically an SVT but classified separately
Focal AT (triggered)
DADs — digitalis, catecholamines
EADs — QT prolongation
Note on AF/AFL:
AF and atrial flutter are SVTs anatomically but are managed as distinct entities — not included in the "paroxysmal SVT" treatment protocols
1 — AVNRT (AV Nodal Re-entry Tachycardia)  Most Common SVT — ~60%
Mechanism
Re-entry circuit entirely within or perinodal to the AV node using two functionally distinct pathways: slow pathway (alpha — slow conduction, short refractory period) and fast pathway (beta — fast conduction, long refractory period).

Typical (slow-fast) ~90%: Antegrade conduction via slow pathway, retrograde via fast pathway. P wave buried in or just after QRS.

Atypical (fast-slow): Antegrade via fast, retrograde via slow — long RP interval; P before next QRS.
Epidemiology
More common in women (2:1). Any age but peaks in middle age. No structural heart disease required. Associated with stress, caffeine, alcohol.
ECG Features
Rate 150–250 bpm, regular
QRS Narrow (<120 ms) unless aberrancy
P wave Typical: buried in QRS or pseudo-R’ in V1 / pseudo-S in inf leads — RP < 70 ms
P wave Atypical (fast-slow): long RP > PR
Axis Retrograde P: negative in II, III, aVF
Onset Abrupt; initiated by PAC
Key distinguishing features
Pseudo-R’ in V1 or pseudo-S in inferior leads — retrograde P distorting terminal QRS
RP interval <70 ms (typical) — shortest RP of all SVTs
No delta wave (no accessory pathway)
Terminates with AV block (adenosine) — confirms AV node is part of circuit
2 — AVRT (AV Re-entry Tachycardia) — Accessory Pathway  ~30% of SVTs
Mechanism
Accessory pathway (Bundle of Kent) — abnormal muscle bridge connecting atria to ventricles outside the AV node. Creates a macro-re-entry circuit involving both the AV node and the accessory pathway.

Orthodromic AVRT (~95%): Antegrade via AV node (normal, narrow QRS), retrograde via AP. Most common. Normal QRS unless aberrancy.

Antidromic AVRT (~5%): Antegrade via AP (pre-excited, wide QRS), retrograde via AV node. Wide complex — can mimic VT. Seen in WPW.
WPW Syndrome
WPW = delta wave + AVRT symptoms. Pre-excitation pattern on resting ECG (delta wave, short PR, wide QRS). Risk of sudden cardiac death if AF develops with rapid antegrade AP conduction (→ VF). AP refractory period <250 ms = high risk.
ECG Features — Sinus rhythm (WPW pattern)
PR Short (<120 ms) — AP bypasses AV node delay
Delta wave Slurred QRS upstroke — slow initial ventricular activation via AP
QRS Wide (≥120 ms) — fusion of AP + AV node activation
ST/T Discordant (secondary changes)
ECG during orthodromic AVRT
Rate 150–250 bpm, regular
QRS Narrow (no delta wave — AP used retrogradely)
P wave Retrograde, RP 70–110 ms — longer than AVNRT; P in ST segment
ST Depression common (rate-related)
Key distinguishing features
RP 70–110 ms — longer than AVNRT, shorter than atypical AVNRT/AT
Delta wave on resting ECG (WPW) — absent during orthodromic tachycardia
Antidromic: wide complex, fully pre-excited — mimics VT
DANGER: Never give adenosine/verapamil in pre-excited AF (WPW + AF) — blocks AV node, forces all conduction via AP → VF
3 — Focal Atrial Tachycardia (AT)  ~10–15% of SVTs
Mechanism
Ectopic focus in atrial tissue (outside SA node) — can be automatic, triggered (DADs/EADs), or micro-re-entry. Common sites: crista terminalis, pulmonary vein ostia, coronary sinus, mitral/tricuspid annuli, His bundle region.

AV node is a bystander — not part of the circuit. AV block can occur during AT without terminating the tachycardia (key diagnostic feature).
Causes
Structural heart disease, prior cardiac surgery
Digitalis toxicity (automatic AT with block)
COPD, hypoxia, metabolic disturbance
Idiopathic (structurally normal heart)
ECG Features
Rate 100–250 bpm; may have warm-up (automatic)
QRS Narrow (unless aberrancy or pre-excitation)
P wave Different morphology from sinus P — shape reveals origin. Long RP > PR (P before QRS or mid-cycle). Isoelectric baseline between P waves
AV block Can occur without terminating AT — pathognomonic of AT
Onset Gradual warm-up (automatic) or abrupt (re-entry)
P wave axis localises focus
Positive P in I, aVL → right atrial origin
Negative P in I, aVL → left atrial origin (PV)
Negative P in inferior leads → low atrial / CS focus
AT continues despite AV block = not AVNRT/AVRT
4 — Atrial Flutter  Macro re-entry in right atrium
Mechanism
Typical (CTI-dependent): Counter-clockwise macro-re-entry circuit in right atrium around the tricuspid annulus, using the cavotricuspid isthmus (CTI) as a critical isthmus. Atrial rate ~300 bpm with 2:1 AV block → ventricular rate ~150 bpm.

Atypical flutter: Clockwise (reverse typical), left atrial flutter, or scar-related re-entry (post-ablation, post-surgical). Variable rate and morphology.
Clinical associations
Structural heart disease (RHD, cardiomyopathy, CHD)
COPD, thyrotoxicosis, post-cardiac surgery
Often coexists with AF (same risk factors)
Thromboembolic risk similar to AF — anticoagulation required
ECG Features
Atrial rate ~300 bpm (240–340)
Ventricular rate ~150 bpm (2:1 block — most common); 100 (3:1); 75 (4:1)
Flutter waves Sawtooth pattern — negative in II, III, aVF (typical); no isoelectric baseline
V1 Positive flutter waves — upright
QRS Narrow; regular if fixed AV block ratio; irregular if variable
Key distinguishing features
Sawtooth flutter waves — best seen in II, III, aVF and V1
Ventricular rate of exactly 150 bpm = flutter until proven otherwise
Carotid sinus massage / adenosine unmasks flutter waves (slows AV conduction transiently)
CTI ablation is curative (>95% success) — preferred over long-term antiarrhythmics
5 — Other SVTs: MAT, SANRT, Junctional Tachycardia
Multifocal Atrial Tachycardia (MAT)
Rate >100 bpm. ≥3 distinct P-wave morphologies with varying PR intervals. Irregular rhythm — often confused with AF.

Cause: COPD, hypoxia, electrolyte disturbance, theophylline toxicity, sepsis. Treat the underlying cause. Verapamil or metoprolol may help. Adenosine ineffective (not re-entrant). NOT cardioverted.
Rate >100 bpm, irregular
P waves ≥3 morphologies, isoelectric baseline
QRS Narrow; variable PR intervals
SA Nodal Re-entry Tachycardia (SANRT)
Rare. Re-entry within or around the SA node. Abrupt onset and offset (unlike sinus tachycardia).

Key feature: P-wave morphology identical to sinus P wave — only clue is abrupt start/stop and slightly faster rate (100–150 bpm).

Responds to vagal maneuvers and adenosine. Treated with beta-blockers, CCBs, or ablation.
Rate 100–150 bpm, regular
P wave Identical to sinus P — key diagnostic trap
Onset Abrupt (distinguishes from sinus tach)
Junctional Tachycardia (JT)
Enhanced automaticity of AV node / His bundle. Rate 70–130 bpm.

Causes: Post-cardiac surgery (esp. pediatric), digitalis toxicity, myocarditis, inferior MI, electrolyte disturbance.

AV dissociation may occur. Retrograde P waves (if present) buried in or after QRS. Does NOT respond to adenosine (automatic, not re-entrant). Treat the cause; amiodarone if needed.
Rate 70–130 bpm (non-paroxysmal)
P wave Retrograde or AV dissociation
QRS Narrow; gradual onset (warm-up)
SVT Type Rate (bpm) P Wave RP Interval QRS Adenosine Distinguishing Clue
Typical AVNRT 150–250 Buried in QRS; pseudo-R’ V1 / pseudo-S inf <70 ms (shortest) Narrow Terminates Pseudo-R’ in V1 — absent in sinus rhythm
Atypical AVNRT 150–250 Before QRS; negative inf leads Long RP > PR Narrow Terminates Long RP — mimics AT; EPS differentiates
Orthodromic AVRT 150–250 In ST segment; retrograde, negative inf 70–110 ms Narrow Terminates Delta wave on sinus ECG (WPW); RP longer than AVNRT
Antidromic AVRT 150–250 Retrograde after QRS Variable Wide (pre-excited) Terminates (caution) Fully pre-excited wide QRS; mimics VT
Focal AT 100–250 Different morphology from sinus; long RP Long RP > PR Narrow AV block only — AT continues Continues despite AV block; P morphology different from sinus
Atrial Flutter Atrial ~300; Ventricular ~150 Sawtooth — no isoelectric baseline N/A Narrow Unmasks flutter waves Ventricular rate 150 = flutter until proven otherwise
MAT >100, irregular ≥3 morphologies; isoelectric baseline Variable Narrow No effect Irregular + multiple P morphologies; associated with COPD
SANRT 100–150 Identical to sinus P Normal Narrow Terminates Abrupt onset/offset; P wave = sinus P (main trap)
Junctional Tachycardia 70–130 Retrograde or AV dissociation Short or AV dissoc. Narrow No effect Post-surgery; warm-up; AV dissociation possible
Acute management of SVT — stepwise approach
Step 1 — Vagal Maneuvers
First-line (if hemodynamically stable)
Valsalva maneuver — modified (supine, legs raised): most effective; ~40–50% success
Carotid sinus massage — right side first; contraindicated if carotid bruit, recent TIA/stroke
Ice-cold water facial immersion — especially effective in children (diving reflex)
Works for re-entrant SVTs (AVNRT, AVRT) that require AV node in circuit
Step 2 — Adenosine
6 mg IV rapid bolus → 12 mg → 18 mg
Transiently blocks AV node — terminates re-entrant SVTs; unmasks flutter/AT (P waves visible)
Half-life <10 seconds — given as rapid IV push + 20 mL saline flush into large antecubital vein
Doubles dose if on theophylline / caffeine. Halves dose if on dipyridamole or central line
Avoid in pre-excited AF (WPW + AF), asthma (bronchospasm), 2nd/3rd degree block
Side effects: flushing, chest tightness, transient asystole — warn patient beforehand
Step 3 — Further options
If adenosine fails or contraindicated
Verapamil 5–10 mg IV (avoid in WPW, HF, hypotension)
Metoprolol 5 mg IV slow (avoid in acute decompensated HF)
Amiodarone 150 mg IV over 10 min — for pre-excited AF or when others contraindicated
DC cardioversion — synchronized 100–200 J if hemodynamically unstable (hypotension, chest pain, altered consciousness) — immediate first-line in unstable patient
Procainamide — drug of choice for pre-excited AF if hemodynamically stable

Investigations

    • 1. 12-Lead ECG – First-line Investigation

      • Confirms the diagnosis
      • Typical findings:
        • Regular tachycardia
        • Heart rate >100/min (usually >150/min)
        • Narrow QRS complex (<120 ms) (may be wide with aberrant conduction)

      2. Ambulatory ECG Monitoring

      • Holter monitor (24–48 hours)
      • Event recorder
      • Implantable loop recorder (for infrequent episodes)

      3. Echocardiography (TTE)

      • Evaluates structural heart disease
      • Assesses cardiac function and heart failure
      • Initial imaging test of choice

      4. Laboratory Tests

      • CBC (anemia, infection)
      • BMP (electrolyte abnormalities)
      • TSH (hyperthyroidism or hypothyroidism)

      5. Electrophysiology (EP) Study

      • Gold standard for identifying the mechanism of Supraventricular Tachycardia (SVT)
      • Used when the diagnosis is uncertain or before catheter ablation

      6. Additional Tests (When Indicated)

      • Exercise tolerance testing (e.g., suspected WPW syndrome or catecholamine-dependent arrhythmias)
      • Cardiac stress testing in patients with atherosclerotic cardiovascular disease (ASCVD) risk factors

Diagnosis

Diagnostic Approach

  • Confirm the rhythm with a 12-lead ECG in all patients with suspected Supraventricular Tachycardia (SVT).
  • Investigate the underlying cause with transthoracic echocardiography (TTE) and laboratory tests.
  • If episodes are intermittent, use ambulatory ECG monitoring (Holter monitor or event recorder).
  • Consider an electrophysiology (EP) study if the diagnosis is uncertain or catheter ablation is planned.

ECG Findings (Diagnostic)

  • Regular tachycardia
  • Heart rate >100/min (typically >150/min)
  • Narrow QRS complex (<120 ms) (may be wide with aberrant conduction)
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Management of Supraventricular Tachycardia (SVT)

1. Initial Management

  • Assess hemodynamic stability (ABCDE).
  • Continuous ECG monitoring.
  • Keep a defibrillator available.

2. Unstable Patient

  • Immediate synchronized electrical cardioversion.

3. Stable Patient

Step 1: Vagal maneuvers (first-line)

  • Modified Valsalva maneuver
  • Carotid sinus massage (only if no carotid bruit)
  • Diving reflex (selected cases)

Step 2: If Supraventricular Tachycardia (SVT) persists

  • IV adenosine (first-line if no contraindications)

Step 3: If adenosine is ineffective or contraindicated

  • Verapamil or diltiazem
  • OR β-blocker (e.g., metoprolol or esmolol)

Step 4: If Supraventricular Tachycardia (SVT) still persists

  • Antiarrhythmic drug (e.g., amiodarone or ibutilide)
  • OR synchronized electrical cardioversion

4. Long-Term Management

  • Catheter ablation (often curative and first-line for recurrent symptomatic Supraventricular Tachycardia SVT)
  • Medications if ablation is not suitable:
    • Beta-blockers
    • Verapamil or diltiazem

Complications of Supraventricular Tachycardia (SVT)

      • Hemodynamic instability (especially if the tachycardia is prolonged or very rapid)
      • Syncope
      • Heart failure or worsening of existing heart failure
      • Tachycardia-induced cardiomyopathy (with persistent or recurrent Supraventricular Tachycardia SVT)
      • Sudden cardiac death (rare, mainly in patients with high-risk accessory pathways such as WPW syndrome)

Prognosis of Supraventricular Tachycardia (SVT)

  • Most patients have a good prognosis with appropriate treatment.
  • Many Supraventricular Tachycardia (SVT) are self-limiting or respond well to vagal maneuvers, medications, or electrical cardioversion.
  • Catheter ablation can provide curative treatment for many patients (e.g., AVNRT and AVRT).
  • Prognosis depends on the type of SVT, the presence of underlying heart disease, and whether high-risk accessory pathways (e.g., WPW syndrome) are present.

Key Points / Clinical Pearls of Supraventricular Tachycardia (SVT)

  • Supraventricular Tachycardia (SVT) is a rapid heart rhythm originating above the ventricles.
  • Most common type: AVNRT.
  • Diagnosis: 12-lead ECG (Holter monitor if episodes are intermittent).
  • First-line treatment in stable patients: Vagal maneuvers → IV adenosine.
  • Unstable patients: Immediate synchronized electrical cardioversion.
  • Definitive treatment: Catheter ablation for recurrent symptomatic SVT.
  • Avoid AV nodal blockers in wide-complex tachycardia or when WPW syndrome is suspected unless the diagnosis is established.
  • If the origin of a wide-complex tachycardia is uncertain, treat it as ventricular tachycardia.