Supraventricular Tachycardia (SVT) – ECG

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ECG Clinical Interpretation

Supraventricular Tachycardia (SVT)

A systematic approach to recognizing regular and irregular supraventricular tachyarrhythmias, identifying atrial activity and AV relationships, and distinguishing AVNRT from other narrow-complex tachycardias.

Foundational to advancedClinicians & trainees~15 min readECG pattern recognition

Representative source tracing: regular narrow-complex tachycardia with typical AVNRT features. Source PDF, page 8.

1. Definition and clinical context

Supraventricular tachycardia (SVT) is an umbrella term for tachyarrhythmias arising above the level of the bundle of His. It includes atrial tachyarrhythmias and tachycardias involving the atrioventricular (AV) node or an accessory pathway. In everyday clinical usage, “SVT” is sometimes used more narrowly to describe a regular, paroxysmal, usually narrow-QRS tachycardia—often AV nodal re-entrant tachycardia (AVNRT).

Paroxysmal SVT describes abrupt onset and termination, a pattern characteristic of re-entry mechanisms such as AVNRT and AV re-entrant tachycardia (AVRT). A narrow QRS is common when ventricular activation proceeds through the normal His–Purkinje system, but bundle-branch block, rate-related aberrancy, or pre-excitation can produce a wide QRS.

Interpretive principle: Do not diagnose the mechanism from QRS width alone. First describe the rhythm (regularity, QRS width, rate, atrial activity and AV relationship); then determine the most likely mechanism.

SVT classification by origin and regularity

Pattern	Examples
Regular atrial	Sinus tachycardia, focal atrial tachycardia, atrial flutter with fixed conduction, inappropriate sinus tachycardia, sinus node re-entry tachycardia.
Irregular atrial	Atrial fibrillation, atrial flutter with variable AV block, multifocal atrial tachycardia.
Regular AV/junctional	AVNRT, AVRT, automatic junctional tachycardia.

The supplied reference emphasizes classification by site of origin and regularity; QRS width is also influenced by pre-existing or rate-related conduction abnormalities and accessory pathways.

2. Electrophysiology: why AVNRT occurs

AVNRT is a functional re-entry tachycardia involving two electrophysiologically distinct pathways in or near the AV node. It is not the same circuit as AVRT, which uses an accessory atrioventricular connection (classically the bundle of Kent) as part of an anatomical re-entry loop.

Fast pathway (β)Rapid conduction · relatively long refractory period

Slow pathway (α)Slow conduction · relatively short refractory period

Initiation of typical slow–fast AVNRT

A premature atrial contraction (PAC) reaches the AV node while the fast pathway is still refractory.
The impulse conducts antegradely down the slow pathway.
By the time it reaches the lower common pathway, the fast pathway has recovered; the impulse travels retrogradely up the fast pathway.
Repeated circulation sustains the re-entry circuit, activating the ventricles antegradely and the atria retrogradely.

This short cycle length produces a rapid, usually regular tachycardia. Other AVNRT variants use different antegrade and retrograde limbs.

AVNRT versus AVRT: AVNRT is a functional circuit within the AV nodal region. AVRT requires an accessory pathway linking atrium and ventricle. A concealed accessory pathway may support AVRT without producing a delta wave during sinus rhythm.

3. Characteristic ECG features

Rate: often rapid; the supplied AVNRT reference describes approximately 140–280 bpm, although slower atypical forms occur.

Regularity: usually very regular in AVNRT and AVRT.

QRS: typically narrow (<120 ms) unless BBB, aberrancy or pre-excitation is present.

Atrial activity: P waves may be hidden, occur just after QRS, or be visible before QRS in long-RP forms.

RP relationship: short RP is typical of slow–fast AVNRT; longer RP suggests atypical AVNRT, AVRT or atrial tachycardia.

ST–T: rate-related ST depression may occur and is not, by itself, proof of acute coronary ischaemia.

Typical slow–fast AVNRT

In the common slow–fast subtype, retrograde atrial activation is nearly simultaneous with ventricular activation. P waves are frequently buried in the QRS. When visible, terminal QRS notching may create a pseudo-r′ in V₁/V₂ or pseudo-S waves in II, III or aVF. These findings are supportive rather than independently diagnostic.

Actual ECG example: narrow-complex regular tachycardia around 150 beats per minute with no clearly visible P waves and pseudo R-prime waves in V1 and V2 — **Figure 1. Typical slow–fast AVNRT.** Regular narrow-complex tachycardia at approximately 150 bpm; P waves are not clearly visible and pseudo-r′ deflections are present in V1–V2. Source: *Supraventricular Tachycardia (SVT).pdf*, page 8 (Example 1a).

Longer-RP / atypical AVNRT

When retrograde atrial activation is delayed, P waves may be visible after the QRS (fast–slow AVNRT) or may appear before the next QRS (slow–slow AVNRT). A visible P wave does not exclude AVNRT; determine its timing and morphology and compare atrial and ventricular cycle lengths.

Actual 12-lead ECG of fast-slow atypical AVNRT, showing narrow-complex tachycardia and retrograde P waves after each QRS — **Figure 2. Fast–slow AVNRT.** Narrow-complex tachycardia at approximately 120 bpm with retrograde P waves visible after each QRS, particularly in V2–V3. Source: *Supraventricular Tachycardia (SVT).pdf*, page 13 (Example 4a).

QRS alternans and rate-related ST depression

Beat-to-beat variation in QRS amplitude (QRS alternans) may accompany AVNRT or AVRT. Distinguish it from electrical alternans associated with low-voltage states by assessing the overall QRS amplitude and clinical context. ST depression during very rapid SVT can be rate-related; reassess the ECG after conversion and correlate persistent changes with symptoms, risk profile and biomarkers.

Actual ECG showing regular narrow-complex supraventricular tachycardia around 215 beats per minute with beat-to-beat QRS amplitude alternans — **Figure 3. SVT with QRS alternans.** Narrow-complex tachycardia at approximately 215 bpm with beat-to-beat QRS amplitude variation. The source discusses a long-RP differential that includes low atrial tachycardia and atypical AVNRT. Source: *Supraventricular Tachycardia (SVT).pdf*, page 19.

4. AVNRT subtypes: use P-wave timing

Subtype	Approximate proportion in supplied reference	Conduction pattern	Surface ECG clue
Slow–fast (typical)	80–90%	Slow antegrade, fast retrograde	P wave hidden in or at end of QRS; pseudo-r′ in V1 or pseudo-S in inferior leads.
Fast–slow	~10%	Fast antegrade, slow retrograde	Retrograde P wave visible after QRS; longer VA/RP interval.
Slow–slow	1–5%	Slow antegrade and slow retrograde limb	P wave may appear before the next QRS (mid-diastolic).

Quick pattern recognition: P hidden or pseudo-r′/pseudo-S → consider typical slow–fast AVNRT. P after QRS → consider fast–slow AVNRT. P before QRS with a long RP interval → consider slow–slow AVNRT, atrial tachycardia or other long-RP SVT. These are pattern clues, not stand-alone proof.

Actual ECG of fast-slow AVNRT at about 135 beats per minute with retrograde P waves following each QRS — **Figure 4. Fast–slow AVNRT with visible retrograde atrial activity.** The source describes retrograde P waves after each QRS, upright in aVR and V1 and inverted in leads II, III and aVL. Source: *Supraventricular Tachycardia (SVT).pdf*, page 15 (Example 5a).

5. A systematic approach to a tachycardia ECG

Check the tracing. Confirm patient identity, calibration (commonly 25 mm/s and 10 mm/mV), lead placement and artefact. Obtain a 12-lead ECG during symptoms whenever possible.
Calculate the ventricular rate. At a regular rhythm, use 300 divided by the number of large squares between R waves (at 25 mm/s), or count QRS complexes over a timed strip.
Decide regular versus irregular. Mark consecutive R–R intervals. A highly regular rhythm favours AVNRT/AVRT or organized atrial tachycardia; irregularity raises AF, flutter with variable block or MAT.
Assess QRS width and morphology. Narrow (<120 ms) suggests normal His–Purkinje activation. A wide complex requires a broader differential, including VT, SVT with aberrancy and pre-excitation.
Search for atrial activity. Inspect inferior leads and V1; use calipers and compare tachycardia with sinus-rhythm ECG. Look for pseudo-r′, pseudo-S, retrograde P waves or flutter waves.
Establish the AV relationship. Estimate RP and PR intervals, determine whether P waves precede, are buried in, or follow QRS complexes, and assess whether atrial and ventricular rates are linked.
Look for supporting clues. Abrupt onset/termination, short-RP pattern and pseudo-r′/pseudo-S support typical AVNRT. A long-RP pattern requires consideration of atypical AVNRT, atrial tachycardia and other mechanisms.
Integrate clinically. State rhythm, rate, QRS width, regularity, atrial activity and likely mechanism; then document haemodynamic status and relevant clinical context.

Practical reporting template: “Regular [narrow/wide]-complex tachycardia at approximately ___ bpm. Atrial activity is [not clearly visible / retrograde and ___ ms after QRS / preceding QRS]. The pattern is most consistent with ___. Correlate with haemodynamic status and response to vagal manoeuvre/adenosine where appropriate.”

6. Differential diagnosis of regular narrow-complex tachycardia

Rhythm	Clues on ECG	Useful discriminator / caution
Typical AVNRT	Very regular; P often hidden; short RP; pseudo-r′ V1 or pseudo-S inferiorly.	Sudden onset/offset supports re-entry; EP study may be needed for definitive mechanism.
Orthodromic AVRT	Regular narrow QRS; retrograde P often follows QRS.	Accessory pathway participates in circuit; baseline ECG may show pre-excitation, but concealed pathways have no delta wave.
Focal atrial tachycardia	Discrete, often monomorphic P waves with a stable atrial cycle length; P may be hidden in QRS/T.	Adenosine may cause AV block and reveal continuing atrial activity; some triggered ATs may terminate.
Atrial flutter (often 2:1)	Regular ventricular response may be near 150 bpm; flutter activity may be subtle.	Inspect inferior leads and V1; transient AV block may unmask flutter waves.
Sinus tachycardia	Sinus P before each QRS, usually with consistent PR; rate varies with physiological drive.	Usually gradual onset/offset and an identifiable cause rather than abrupt paroxysms.
Junctional tachycardia	Regular narrow QRS; P may be absent, retrograde or dissociated.	Automaticity and clinical setting differ; AV dissociation can occur.

Do not miss a wide or irregular tachycardia

Safety first: An undifferentiated wide-complex tachycardia should be treated as ventricular tachycardia until adequately established otherwise. An irregular wide-complex rhythm may represent pre-excited atrial fibrillation. Avoid AV-nodal blocking agents (including adenosine, beta-blockers, verapamil/diltiazem and digoxin) in pre-excited AF because preferential accessory-pathway conduction can precipitate ventricular fibrillation.

7. Clinical presentation and significance

Patients commonly report sudden-onset, rapid, regular palpitations. Associated symptoms can include light-headedness, presyncope or syncope, chest discomfort, dyspnoea and anxiety. Polyuria is occasionally reported and may relate to atrial natriuretic peptide release. Episodes may terminate spontaneously or persist until treatment is given.

AVNRT is often encountered in people without structural heart disease, but it can also occur in patients with chronic cardiac disease. Symptoms and tolerance depend on rate, duration, ventricular function, comorbidity and the haemodynamic response.

Assess stability before rhythm-specific treatment

Assess blood pressure, mental status, perfusion, ongoing ischaemic chest discomfort, acute heart failure and shock.
Obtain a 12-lead ECG, continuous rhythm monitoring, IV access and appropriate clinical investigations.
Record the rhythm before and after intervention whenever feasible; a post-conversion ECG may reveal baseline pre-excitation or residual ST–T abnormalities.

Actual ECG example of very rapid narrow-complex typical AVNRT around 220 beats per minute with pseudo R-prime in V1 and widespread ST depression — **Figure 5. Rapid typical AVNRT with ST depression.** The source describes a narrow-complex tachycardia around 220 bpm, subtle terminal QRS notching in V1 and widespread ST depression. Source: *Supraventricular Tachycardia (SVT).pdf*, page 10 (Example 2a). Persistent ST changes after conversion require clinical evaluation rather than automatic attribution to rate alone.

8. Management principles

Management depends on haemodynamic stability, QRS width, regularity and the suspected mechanism. This section is an educational overview, not a patient-specific treatment order; follow current resuscitation guidance and local protocols.

Unstable tachycardia

Prompt synchronized electrical cardioversion is the priority for tachycardia causing haemodynamic compromise. Do not delay cardioversion for repeated diagnostic manoeuvres or medication trials.

Stable, regular, narrow-complex

Use a monitored approach. Vagal manoeuvres are first-line; a modified Valsalva technique may improve conversion. If unsuccessful, consider rapid IV adenosine according to resuscitation protocol.

Vagal manoeuvres and adenosine

Vagal manoeuvres: modified Valsalva is commonly preferred. Carotid sinus massage, if considered, requires appropriate expertise and monitoring and should be avoided with carotid bruit or prior stroke/TIA.
Adenosine: give as a rapid IV bolus with immediate flush in a monitored setting, with resuscitation equipment available. Adult dosing varies by protocol; the ESC guideline describes incremental 6–18 mg dosing. Warn patients about transient flushing, chest pressure, dyspnoea or a sense of impending doom.
Diagnostic response: termination supports an AV-node-dependent re-entry mechanism (AVNRT/orthodromic AVRT), but is not absolutely specific. Transient AV block without termination may expose atrial tachycardia or flutter activity.

Actual rhythm strips showing typical AVNRT before, during and after administration of 12 milligrams of adenosine — **Figure 6. AVNRT during adenosine administration.** The supplied example shows the tachycardia, transient AV nodal suppression with broad beats during the response, and subsequent sinus rhythm with disappearance of pseudo-r′ waves. Source: *Supraventricular Tachycardia (SVT).pdf*, page 12 (Example 3). Broad beats during adenosine administration require rhythm-context interpretation and should not be assumed to represent a new ventricular arrhythmia without assessment.

Important exclusions: Do not apply the “regular narrow-complex SVT” algorithm to irregular or polymorphic wide-complex rhythms. In pre-excited AF, avoid AV-nodal blockers; obtain expert help and use an appropriate pre-excited AF pathway. For a wide-complex tachycardia of uncertain origin, prioritize safe VT-oriented assessment.

Further / definitive management

For recurrent symptomatic AVNRT, electrophysiology consultation and catheter ablation should be discussed. Beta-blockers or non-dihydropyridine calcium-channel blockers may be considered for selected patients when ablation is not desired or suitable, taking ventricular function, blood pressure, pre-excitation and comorbidities into account. Drug selection should be individualized.

9. ECG interpretation cases

Case 1 · Typical short-RP pattern

A patient presents with abrupt palpitations. ECG shows a regular narrow-complex tachycardia at approximately 150 bpm. P waves are not clearly visible; small terminal deflections are seen in V1–V2.

Reveal interpretation and reasoning

Most likely: typical slow–fast AVNRT. The very regular narrow-complex rhythm, absent/hidden P waves and pseudo-r′ appearance support a short-RP AV nodal re-entry pattern. Orthodromic AVRT remains a differential; surface ECG alone may not establish the mechanism.

Case 2 · Visible retrograde P waves

A regular narrow-complex tachycardia occurs at approximately 120–135 bpm. A discrete P wave follows each QRS and is most apparent in V2–V3.

Reveal interpretation and reasoning

Consider: fast–slow (atypical) AVNRT. The longer VA/RP interval allows retrograde P waves to be seen after QRS complexes. Orthodromic AVRT and atrial tachycardia remain important alternatives; assess RP timing, P-wave morphology, baseline ECG and response to AV nodal manoeuvres.

Case 3 · Adenosine response

A regular narrow-complex tachycardia terminates after adenosine, with return to sinus rhythm and disappearance of the pseudo-r′ deflections.

Reveal interpretation and reasoning

This response is consistent with an AV-node-dependent re-entry tachycardia such as AVNRT. Adenosine response alone does not prove AVNRT; integrate the tachycardia ECG, clinical history and any electrophysiology findings.

10. Common pitfalls and limitations

Calling every narrow tachycardia “AVNRT”. SVT is a broad category; atrial tachycardia, flutter and AVRT may look similar.
Assuming absent P waves. P waves may be buried in QRS/T or very small; inspect V1 and inferior leads carefully.
Using rate alone. A ventricular rate near 150 bpm should prompt a search for 2:1 atrial flutter, not an automatic AVNRT label.
Overcalling pseudo-r′ or pseudo-S. Compare with sinus-rhythm ECG and avoid mistaking baseline QRS morphology for a tachycardia-specific deflection.
Equating ST depression with ACS—or dismissing it. Rate-related changes may resolve after conversion, but persistent changes and clinical risk require evaluation.
Misclassifying wide-complex tachycardia. Pre-existing BBB, aberrancy and pre-excitation can widen SVT, but VT must remain a priority differential.
Interpreting adenosine response as definitive. AV block can unmask atrial activity; termination is supportive but not uniquely diagnostic of AVNRT.
Ignoring instability. The haemodynamic assessment takes priority over fine mechanism classification.

11. Clinical pearls and take-home points

Start with regularity and QRS width, then identify atrial activity and the RP/PR relationship.
Typical slow–fast AVNRT is usually a regular narrow-complex, short-RP tachycardia with hidden P waves; pseudo-r′ in V1 or pseudo-S in inferior leads can be helpful.
Visible retrograde P waves after QRS suggest a longer VA interval and should prompt consideration of atypical AVNRT and AVRT.
Transient AV block after adenosine can reveal flutter or atrial tachycardia; tachycardia termination suggests an AV-node-dependent circuit but is not definitive.
Rate-related ST depression may resolve after conversion. Reassess the post-conversion ECG and clinical picture.
Unstable tachycardia requires prompt synchronized cardioversion. Irregular wide-complex tachycardia with pre-excitation is a high-risk situation.

12. References

Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. European Heart Journal. 2020;41(5):655–720. doi: 10.1093/eurheartj/ehz467.

Fox DJ, Tischenko A, Krahn AD, et al. Supraventricular tachycardia: diagnosis and management. Mayo Clinic Proceedings. 2008;83(12):1400–1411. doi: 10.4065/83.12.1400.

Jazayeri MR, Massumi A, Mihalick MJ, Hall RJ. Sinus node reentry: case report and review of electrocardiographic and electrophysiologic features. Texas Heart Institute Journal. 1985;12(3):249–252.

Burns E, Buttner R. Supraventricular Tachycardia (SVT). Life in the Fast Lane, ECG Library. 1 August 2020. User-supplied PDF reference; ECG figure pages cited individually in captions.

Medical education disclaimer: This page is intended for educational use by healthcare professionals. It does not replace clinical assessment, professional judgment, current resuscitation guidance, institutional protocols or patient-specific decisions. Management must be adapted to the patient’s haemodynamic status and the precise rhythm diagnosis.