SVT and palpitations: diagnosis, acute management, and when to ablate

Palpitations — the subjective awareness of one’s own heartbeat — are one of the most common presentations in Australian general practice. The spectrum runs from benign ectopic beats in an anxious young adult to life-threatening ventricular tachycardia in a patient with ischaemic cardiomyopathy. The GP’s primary clinical task is distinguishing benign causes from pathological arrhythmias, and capturing an ECG during an episode is the single most valuable diagnostic step.

Supraventricular tachycardia (SVT) encompasses all regular tachycardias arising above the bundle of His. The most common type is AVNRT (atrioventricular nodal re-entry tachycardia), accounting for ~60% of paroxysmal SVT, in which a re-entrant circuit within the AV node produces sudden-onset regular palpitations at 140–220 beats per minute. AVRT (atrioventricular re-entry tachycardia), involving an accessory pathway such as in Wolff-Parkinson-White syndrome, accounts for most of the remainder.

The ESC 2019 SVT guidelines and Therapeutic Guidelines (eTG) converge on catheter ablation as the preferred long-term management for symptomatic recurrent SVT — a curative rather than suppressive approach — with PBS funding making this accessible in Australia.

A. Core clinical — the AU general practice framework

Palpitation differential

Benign and physiological causes:

• Sinus tachycardia — physiological response to exercise, emotional stress, pain, or fever; pharmacological (caffeine, decongestants, beta-agonists, stimulants, ADHD medications, levothyroxine); underlying states (anaemia, dehydration, thyrotoxicosis).
• Ectopic beats — atrial premature complexes (APCs) or ventricular premature complexes (VPCs/PVCs) causing an irregular awareness of the heartbeat, often described as a “missed beat” or “thud.” Ectopics in a structurally normal heart are benign; high burden (>10% of beats on Holter) warrants echocardiographic assessment.
• Anxiety and panic disorder — the commonest driver in young adults; palpitations are often the leading symptom; a gradual-onset racing heart with anxiety triggers, hyperventilation, and other somatic symptoms is characteristic.
• Hyperthyroidism — see related articles; TFT as part of palpitation workup.

Pathological arrhythmias:

• SVT (AVNRT, AVRT, atrial tachycardia, atrial flutter) — typically abrupt onset/offset, regular, rates 140–220 bpm for SVT; flutter with 2:1 block presents at 150 bpm (the “150 bpm clue”).
• Atrial fibrillation (AF) — irregular irregular; common; requires anticoagulation assessment; see the dedicated AF article.
• Ventricular tachycardia (VT) — wide-complex, regular; always a red flag; associated with structural heart disease, ischaemic cardiomyopathy, channelopathies. Assume wide-complex tachycardia is VT until proven otherwise.
• Bradyarrhythmias and heart block — sinus node dysfunction, complete heart block; can cause palpitations through escape rhythms or rate variability.

History

The history aims to characterise onset, duration, pattern, and associated features:

• Onset and offset — abrupt onset and sudden termination is the hallmark of re-entrant SVT; gradual onset/offset is more consistent with sinus tachycardia or anxiety.
• Rate and rhythm perception — regular racing (“machine-gun”) suggests SVT or VT; irregular thumping suggests ectopics or AF.
• Duration — seconds (ectopics), minutes to hours (paroxysmal SVT), days (AF).
• Triggers — exercise, caffeine, alcohol, sleep deprivation, position change, eating, stress, menstrual cycle.
• Termination — spontaneous, vagal manoeuvre, bearing down.
• Associated symptoms — chest pain, syncope, presyncope, dyspnoea, and post-episode polyuria (classic for SVT — atrial natriuretic peptide release).
• Red-flag symptoms — syncope, chest pain, severe dyspnoea, or haemodynamic compromise require urgent assessment.
• Family history — sudden cardiac death under 40, known channelopathy (long QT, Brugada, ARVC, hypertrophic cardiomyopathy).
• Medications and substances — caffeine, alcohol, illicit drugs (cocaine, methamphetamine), prescribed stimulants, beta-agonists, decongestants.

Investigations

• 12-lead ECG — during every consultation; capturing an ECG during the palpitation episode is the single highest-yield diagnostic step. Request the patient present immediately or go to nearest facility with ECG capability during future episodes.
• Holter monitor (24–48 hours) — appropriate for daily or multiple-times-daily palpitations; item 11700.
• Event monitor or patch monitor (7–14 days) — for less frequent palpitations; Zio XT patch (14-day wear) is increasingly used in Australia; Medicare-rebatable in selected indications.
• Implantable loop recorder (ILR) — for recurrent unexplained palpitations or suspected high-risk arrhythmia where shorter monitoring is negative; inserted under the skin by cardiology.
• Smartwatch/wearable ECG (Apple Watch, Kardia) — useful for episode documentation; clinical decision-making should always be confirmed with a 12-lead ECG rather than relying on consumer device rhythm strips alone.
• Echocardiogram — structural heart disease assessment, LVEF, atrial size, valve function; indicated before initiating antiarrhythmic medications and in any patient with red-flag features.
• Bloods — TFT, FBE (anaemia), electrolytes, magnesium, calcium, glucose/HbA1c; BNP if heart failure suspected; drug screen if clinically relevant.

ECG patterns

AVNRT: Narrow QRS (below 120 ms), regular, 140–220 bpm. P waves typically hidden within or immediately after the QRS — look for pseudo-S waves in II/III/aVF or pseudo-R’ in V1.

Atrial flutter: Sawtooth flutter waves most visible in II/III/aVF and V1, atrial rate 250–350 bpm. Ventricular rate 150 bpm at 2:1 block is characteristic — the “150 bpm clue.”

WPW pattern (between episodes): Short PR (below 120 ms), delta wave (slurred initial QRS upstroke), widened QRS — indicates an accessory pathway with antegrade conduction. This is not SVT on a resting ECG but identifies a patient who may have antidromic AVRT or, critically, pre-excited AF.

Wide-complex tachycardia: Assume VT until proven otherwise — especially in patients with structural heart disease. Features of VT: AV dissociation, capture beats, fusion beats, concordance (all positive or all negative across precordial leads), QRS >160 ms.

B. Evidence appraisal — modified Valsalva, adenosine, and ablation

Modified Valsalva — REVERT trial

The REVERT trial (Appelboam et al., Lancet 2015) randomised 428 patients with SVT to standard Valsalva versus modified Valsalva (blow into 10 mL syringe for 15 seconds, immediately lie supine with legs raised to 45 degrees for 15 seconds): modified technique converted SVT to sinus rhythm in 43% versus 17% with standard Valsalva. The modification works by leveraging the rapid venous return on assuming the supine position, enhancing the vagal response. This is now the recommended first-line vagal manoeuvre for acute SVT.

Adenosine for SVT termination

Adenosine transiently blocks the AV node, interrupting the re-entrant circuit in AVNRT and AVRT. The regimen is 6 mg IV rapid bolus through a large-bore antecubital cannula followed immediately by 20 mL normal saline flush and arm elevation; repeated as 12 mg IV if no response within 1–2 minutes; may repeat the 12 mg dose once. Side effects — transient flushing, chest tightness, and brief “doom” sensation — last approximately 20–30 seconds and should be warned about. Caution in asthma (relative contraindication — bronchospasm); dose reduction in heart transplant patients (~1/3 dose). Adenosine also unmasks atrial flutter or atrial tachycardia by transiently slowing AV conduction, revealing flutter waves.

Catheter ablation — curative first-line

Catheter ablation achieves >95% cure rates for AVNRT, AVRT, and typical atrial flutter. The ESC 2019 SVT guideline recommends ablation as first-line management in patients with symptomatic recurrent SVT who prefer definitive treatment over long-term medication. In Australia, catheter ablation for SVT is PBS-funded. Procedural risks: approximately 1% risk of AV block requiring pacemaker (for slow pathway ablation in AVNRT); rare cardiac tamponade; vascular access complications. Most patients resume normal activities within a week.

WPW-specific risk: Pre-excited AF in WPW can conduct preferentially down the accessory pathway, generating very rapid ventricular rates (>300 bpm) with risk of ventricular fibrillation. AV-nodal blocking agents — verapamil, diltiazem, beta-blockers, adenosine, and digoxin — are contraindicated in suspected pre-excited AF or antidromic SVT. Use procainamide IV or synchronised DC cardioversion. Refer promptly for ablation.

C. Acute management — the stepwise approach

Stable narrow-complex regular SVT

Step 1: Modified Valsalva (REVERT technique) — 43% conversion; no drug required; teachable for home use.

Step 2: Carotid sinus massage — only if age below 65 years, no carotid bruit, no recent TIA or stroke; one side for 5–10 seconds with continuous ECG monitoring; avoid bilateral simultaneous massage.

Step 3: Cold stimulus — cold water face submersion engages the diving reflex; particularly effective in children and adolescents.

Step 4: Adenosine 6 mg IV — rapid bolus with saline flush if vagal manoeuvres fail; repeat with 12 mg if no response.

Step 5: Verapamil 2.5–5 mg IV or metoprolol 2.5–5 mg IV — if adenosine fails or contraindicated; avoid verapamil/diltiazem if WPW is suspected.

Step 6: Synchronised DC cardioversion — 50–100 J if haemodynamically unstable or drug failure.

Haemodynamically unstable or wide-complex tachycardia

• Synchronised DC cardioversion if pulse is present and haemodynamically unstable.
• Unsynchronised defibrillation + ALS protocol if pulseless.

WPW with pre-excited AF or antidromic SVT

AVOID AV-nodal blockers (verapamil, diltiazem, beta-blockers, adenosine, digoxin) — they block the normal AV node, forcing all conduction down the accessory pathway and risking VF. Use procainamide IV or synchronised DC cardioversion. Urgent electrophysiology referral for ablation.

D. Australian operations

MBS items

Standard consultations (MBS Online): items 23, 36, 44. Heart Health Check (item 699) for cardiovascular risk assessment (≥30 years; ≥18 years for ATSI). GPCCMP (items 965/967) for chronic arrhythmia management. Better Access Mental Health Care Plan (item 2715) for comorbid anxiety contributing to palpitations — up to 10 sessions per year with a psychologist. ATSI Health Assessment (item 715).

Investigations: 12-lead ECG (Medicare-rebatable); Holter monitor (item 11700) for 24–48-hour recording; patch and event monitors (Medicare-rebatable for selected indications); echocardiogram (items 55113 range); ILR (PBS-listed device inserted by cardiology).

PBS pharmacotherapy

Long-term pharmacotherapy for symptomatic SVT (as alternative or bridge to ablation):

• Beta-blockers (metoprolol, atenolol, bisoprolol, nebivolol) — PBS general; first-line prophylaxis.
• Verapamil, diltiazem — PBS general; alternative for patients where beta-blockers are not tolerated; avoid in WPW.
• Flecainide, propafenone — PBS Authority for specific arrhythmia indications; specialist initiation; structurally normal heart only.
• Sotalol — PBS general; specialist-initiated for most SVT contexts.
• Amiodarone — PBS Authority Required; significant multi-organ side effect profile (thyroid, lung, liver, corneal); specialist; generally reserved for refractory cases.

Specialist services

• General cardiology — initial assessment, Holter interpretation, echo, pharmacotherapy initiation.
• Electrophysiology (EP) — catheter ablation; major tertiary and most secondary metropolitan centres.
• Telehealth cardiology — widely accessible for regional and rural patients; ablation can then be performed at a metropolitan centre.

Driving — Austroads 2022

Symptomatic SVT causing presyncope or syncope affects driving safety. Austroads 2022 guidance recommends not driving during symptom periods; individual assessment post-ablation with resumption once asymptomatic and off medication or with procedure confirmed successful. Document advice given in the clinical record.

E. Special populations

Women. AVNRT is two to three times more common in women. Palpitations are frequently reported in association with the menstrual cycle, pregnancy, and perimenopause — hormonal fluctuations affect autonomic tone and arrhythmia threshold. Adenosine is considered safe in pregnancy; most antiarrhythmics are avoided. Catheter ablation in pregnancy is generally deferred unless the arrhythmia is haemodynamically compromising; electrophysiologist-led assessment is required.

Children and adolescents. SVT is the most common sustained arrhythmia in children. AVRT (often Wolff-Parkinson-White) is more prevalent in the paediatric population than in adults. Cold water face immersion (diving reflex) is highly effective in children. Many paediatric WPW cases undergo ablation in late adolescence; earlier ablation if haemodynamically significant. Paediatric cardiology referral is appropriate.

Athletes. Palpitations in athletes require careful evaluation — physiological sinus bradycardia and ectopics are common, but ARVC, hypertrophic cardiomyopathy, and channelopathies can present in this setting. Family history of sudden cardiac death is an important trigger for cardiology review. Exercise-induced SVT warrants echocardiography and electrophysiology assessment.

Older adults. AF becomes increasingly prevalent with age and may be misidentified as SVT by patients. Carotid sinus massage carries higher embolic risk in older adults with carotid disease — avoid if any bruit is present or recent cerebrovascular event. Adenosine is safe in older adults at standard dosing. Ablation is effective across age groups with appropriate procedural risk assessment.

Stimulant medications. ADHD medications (methylphenidate, amphetamines), decongestants (pseudoephedrine), and illicit stimulants (cocaine, methamphetamine) are common triggers. Dose timing adjustment and stimulant reduction or cessation may resolve palpitations without further intervention.

When to escalate

• Wide-complex regular tachycardia — assume VT; emergency department immediately.
• Haemodynamic instability (hypotension, pallor, syncope, chest pain) during palpitations — 000.
• Suspected WPW with AF or antidromic SVT — emergency; avoid AV-nodal blockers.
• Family history of sudden cardiac death under 40 — cardiology for channelopathy/structural workup.
• First SVT episode with structural heart disease or reduced LVEF — urgent cardiology.
• Symptomatic recurrent SVT — cardiology referral for ablation assessment.
• SVT in pregnancy with haemodynamic compromise — obstetric–cardiology assessment.
• Palpitations with syncope — cardiology same-day; implantable loop recorder consideration.

What this article is and is not

This is general health information drawn from current Australian guidelines — Therapeutic Guidelines, Heart Foundation Australia, and AMH — and the ESC 2019 SVT guideline and REVERT trial. It is not personal medical advice and does not create a doctor–patient relationship. Decisions about whether palpitations represent a significant arrhythmia, which monitoring modality is appropriate, whether catheter ablation is suitable, and how to manage medications are made by your own GP and treating cardiologist based on your complete clinical picture.

For Australian consumer resources: HealthDirect — Palpitations, Heart Foundation Australia, Better Health Channel — Palpitations.

For acute chest pain or palpitations with dizziness or near-fainting: call 000.

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Sources cited

1. Therapeutic Guidelines (eTG) — Cardiovascular / Arrhythmia
2. ESC 2019 Guidelines for the management of supraventricular tachycardia
3. Appelboam A et al. — REVERT trial (Lancet 2015)
4. Heart Foundation Australia
5. Australian Medicines Handbook (AMH)
6. RACGP
7. PBS — antiarrhythmics, beta-blockers, CCB
8. MBS Online — items 23, 699, 715, 965/967, 2715, 11700, 55113
9. Austroads — Assessing Fitness to Drive 2022
10. HealthDirect — Palpitations
11. Better Health Channel — Palpitations