Supraventricular tachycardias

• Supraventricular tachycardia (SVT) means a fast heart rhythm that needs tissue at or above the bundle of His to keep going. On the ECG it usually shows as a narrow QRS complex (120 ms or less) at over 100 beats per minute.^[1]
• The commonest cause of a sudden, regular, narrow-complex tachycardia that starts and stops abruptly is a short-circuit loop: AV nodal re-entrant tachycardia (AVNRT) or AV re-entrant tachycardia (AVRT) through an accessory pathway. Together they make up about 90% of paroxysmal SVT.^[2]
• Sinus tachycardia is usually not an arrhythmia to treat but a signal: find the cause (pain, fever, bleeding, hypoxia, thyrotoxicosis) and treat that.^[4][10]
• Management follows an order. If the patient is unstable, give a synchronised shock. If stable, try a modified Valsalva manoeuvre, then adenosine (6 mg, then 12 mg), then verapamil, diltiazem or a beta-blocker. Never give AV-nodal drugs to a patient with pre-excited AF (wide, irregular, very fast).^[1][3][6]
• Catheter ablation cures most re-entrant SVT with success rates of about 92 to 97% and is offered as an initial choice.^[1]

By the end of this page you should be able to:

1. Define SVT and classify it into sinus, atrial, AV-nodal and accessory-pathway types.
2. Explain the mechanism of AVNRT and AVRT, and why a tachycardia that starts and stops suddenly is typical of re-entry.
3. Distinguish physiological from inappropriate sinus tachycardia, and recognise focal and multifocal atrial tachycardia.
4. Work through a regular narrow-complex tachycardia on an ECG and decide the likely mechanism.
5. Manage an episode in guideline order: cardioversion, vagal manoeuvres including the modified Valsalva manoeuvre, adenosine, and second-line drugs, with doses and cautions.
6. Know when adenosine is dangerous and when it helps diagnose atrial tachycardia or flutter.
7. Choose long-term options (ablation, drugs, pill-in-the-pocket) and handle pregnancy, children, driving and low-resource settings.

A normal heartbeat begins in the sinus node in the right atrium, crosses the atria, pauses in the atrioventricular (AV) node, then spreads quickly down the His bundle and bundle branches to the ventricles. The word "supraventricular" simply means that the rhythm depends on tissue from the His bundle upward.^[1] Because the ventricles are still activated through their normal rapid conduction system, the QRS complex is usually narrow.

SVT is a family, not a single disease. The members differ in where the rhythm starts and how it is kept going, and so they differ in how they look on the ECG and how they respond to treatment. Reading this page in order helps: first the types, then the ECG method that sorts them, then treatment.

Atrial fibrillation and atrial flutter are also supraventricular, but they have their own page (see atrial fibrillation and flutter). They matter here because flutter with 2:1 block looks just like AVNRT.

Definition. The 2019 European Society of Cardiology (ESC) guideline defines SVT as a tachycardia whose mechanism involves tissue from the His bundle or above, and uses "narrow QRS tachycardia" for a QRS of 120 ms or less.^[1] A rate above 100 beats per minute is the usual lower limit. Paroxysmal SVT (PSVT) is the clinical name for episodes that begin and end abruptly, with rates typically from just over 100 to about 250 per minute.^[2]

Classification by mechanism. The ESC groups regular narrow-complex tachycardias as physiological sinus tachycardia, inappropriate sinus tachycardia, sinus nodal re-entrant tachycardia, focal atrial tachycardia, atrial flutter with fixed AV conduction, AVNRT, junctional ectopic tachycardia, orthodromic AVRT and idiopathic ventricular tachycardia.^[1] Irregular ones, such as multifocal atrial tachycardia and atrial fibrillation, form a separate group.

In the general population the ESC reports an SVT prevalence of 2.25 per 1000 persons and an incidence of 35 per 100,000 person-years. Women have twice the risk of men.^[1] AVNRT affects women more often than men (about 70:30), whereas AVRT is slightly more often seen in men (female to male about 45:55).^[1] The share of patients with AVRT falls with age, while the share with AVNRT and atrial tachycardia rises.^[1]

A US estimate is that paroxysmal SVT affects about 1 in 300 people and leads to around 250,000 emergency department and hospital visits a year.^[2] Diagnosis is often delayed by years because the episodes are brief, and up to 50% of patients are first misdiagnosed, for example as having anxiety or panic disorder.^[2]

Focal atrial tachycardia is uncommon: in one report its prevalence in people under 50 years without symptoms was as low as 0.34%, with no clear sex difference.^[1]

Most AVNRT and AVRT occur in people with structurally normal hearts, and the rhythm is usually benign unless there is additional structural or coronary disease.^[4] The causes differ by type.

Sinus tachycardia is a normal response to emotion, exercise, pain, pregnancy and sexual intercourse.^[1] In a sick patient it responds to infection, anaemia, blood loss, heart failure and pain.^[4] A search for explainable causes includes anaemia, hyperthyroidism, hypoglycaemia, acute heart failure, dehydration, electrolyte problems, adrenal dysfunction, and drugs such as amphetamines.^[10] Pulmonary embolism should also be considered when the tachycardia is unexplained.^[10]

Multifocal atrial tachycardia is usually seen with pulmonary disease, and also with theophylline therapy and low magnesium.^[1] Chronic obstructive pulmonary disease (COPD), hypoxia, and acute lung illness are the classic backdrop.

Focal atrial tachycardia arises from a small atrial focus. It can follow previous atrial surgery or ablation, or arise in an otherwise normal heart. After atrial fibrillation ablation, atrial tachycardias of focal or macro-re-entrant type are common, and re-ablation is best deferred for at least 3 months where possible.^[1]

AVNRT occurs mostly in people without heart disease; no clear cause is found. AVRT needs a congenital accessory pathway, a strand of muscle bridging the atrium and ventricle outside the AV node (see Wolff-Parkinson-White syndrome).

Pregnancy makes sustained SVT more frequent.^[1]

SVT is explained by three mechanisms: abnormal automaticity, triggered activity and re-entry. Re-entry matters most.

In re-entry, an electrical wave travels round a loop and, instead of dying out, finds the tissue it just left ready to conduct again, so it goes round and round. Two conditions are needed. First, there must be two pathways joined at both ends, with different conduction speed and recovery time. Second, a premature beat must reach the loop when one pathway is still recovering (blocked) but the other is ready. The impulse then travels down the ready pathway, turns, and climbs back up the recovered one. Once the loop is complete, each lap fires the rest of the heart, so the heart rate equals the lap rate.

This explains the typical clinical picture: sudden onset triggered by an ectopic beat, a steady regular rate that does not vary, and sudden termination when something breaks the loop. The AV node is part of the loop in both AVNRT and orthodromic AVRT, which is why a drug or manoeuvre that briefly blocks the AV node (vagal tone, adenosine) ends both.^[1][4]

AVNRT is re-entry in the region of the AV node.^[1] The exact circuit remains uncertain, but the usual teaching model is that the AV node region has two inputs: a fast pathway that conducts quickly but recovers slowly, and a slow pathway that conducts slowly but recovers quickly. In sinus rhythm the impulse travels the fast path. A premature atrial beat finds the fast path still recovering, travels down the slow path, and by the time it arrives the fast path has recovered and carries it back up to the atria. A loop forms.

In the common (typical, "slow-fast") form the impulse goes down the slow path and up the fast path. The atrium and the ventricle are therefore activated almost at the same moment, so the P wave is hidden inside the QRS or appears just after it, and the retrograde P wave is constantly related to the QRS.^[1] Atypical AVNRT makes up about 6% of AVNRT.^[1] Ablation targets the slow pathway in the area of the nodal extensions.^[1]

An accessory pathway (AP) is an extra strand of muscle that conducts between atrium and ventricle outside the AV node. It conducts fast and has no decrement like the AV node. AVRT is a re-entry circuit with two limbs, the AV node and the accessory pathway.^[1]

• Orthodromic AVRT is the common form. The impulse goes down the AV node and the His-Purkinje system, so the QRS is narrow, and returns to the atrium up the accessory pathway.^[1]
• Antidromic AVRT is the reverse: down the accessory pathway, so the ventricles are activated through muscle outside the normal system and the QRS is wide (pre-excited), and back up the AV node or another pathway.^[1]
• Concealed pathway. Some pathways conduct only backwards (from ventricle to atrium). In sinus rhythm there is no delta wave, so the resting ECG looks normal even though the patient has AVRT.^[1] A normal resting ECG does not exclude AVRT.

In Wolff-Parkinson-White (WPW) syndrome the pathway conducts forwards too, producing a delta wave and a short PR interval at rest. The danger of WPW is atrial fibrillation: the pathway can conduct very fast, leading to ventricular fibrillation (see Wolff-Parkinson-White syndrome).

Focal atrial tachycardia is an organised atrial rhythm of at least 100 beats per minute starting from a discrete site.^[1] Automatic types characteristically speed up over the first few beats ("warm-up") and slow before stopping. The P wave differs from the sinus P wave, and the PR interval is equal to or longer than in sinus rhythm.^[1] Because the AV node is a bystander, not a part of the loop, the rhythm may continue with AV block.

Multifocal atrial tachycardia (MAT) is a rapid, irregular rhythm with at least three different P-wave shapes.^[1] It reflects irritable atrial tissue at several sites, as in hypoxia, lung disease and high sympathetic drive.

The sinus node speeds up in response to sympathetic stimulation or reduced vagal tone. A small group has persistent, symptomatic tachycardia that is out of proportion to need: inappropriate sinus tachycardia.^[1][10] It is separate from postural orthostatic tachycardia syndrome (POTS), in which the rate rises on standing.^[10]

Patients most often describe palpitations, shortness of breath, lightheadedness, fatigue, chest pressure or pain, and presyncope or syncope.^[2] Typical AVNRT or AVRT is described as a sudden "switch on" and "switch off" of a fast, regular heartbeat.^[2]

Rapid rates reduce the time for ventricular filling, so cardiac output and blood pressure can fall. Symptoms are worse with underlying heart disease or lung disease, and a "normal" heart rate may already be too slow for a very sick patient.^[4] In a very rapid tachycardia (usually over 250 per minute) the pulse can become impalpable and consciousness impaired.^[4]

Sinus tachycardia is usually symptomless in itself; the symptoms belong to its cause.

• Pulse and blood pressure. A fast, regular pulse. Look for low blood pressure, cold peripheries or a falling level of consciousness.
• Signs of the cause. Fever, pallor, goitre, wheeze or a pulmonary embolism risk profile for sinus tachycardia; signs of lung disease for MAT.

The Resuscitation Council UK lists these as life-threatening features that make a tachycardia unstable: shock, syncope with severe or ongoing hypotension, myocardial ischaemia, and severe heart failure with pulmonary oedema, plus being immediately after return of spontaneous circulation.^[3] A patient with any of these needs synchronised cardioversion without delay.

The main task is to separate the fast, regular narrow-complex rhythms. All can look alike at a glance.

Other conditions that can mimic or sit beside SVT include panic disorder (a common misdiagnosis), thyrotoxicosis, and wide-complex tachycardias. When the QRS is wide, ventricular tachycardia must be assumed until proven otherwise (see ventricular arrhythmias).

12-lead ECG during the tachycardia is the most useful single test. Record it before treatment if possible, and record the rhythm strip during any vagal manoeuvre or adenosine bolus, because the way the rhythm stops or slows is diagnostic.^[4] Record a 12-lead ECG again after successful treatment: it may show pre-excitation, which was hidden during tachycardia.^[4]

1. Is the QRS narrow (120 ms or less) or wide? Wide means ventricular tachycardia, SVT with a bundle branch block, or pre-excited tachycardia. The ESC advises that if the mechanism is not fully understood the arrhythmia should be treated as ventricular tachycardia.^[1]
2. Is it regular? Irregular narrow-complex tachycardia is most likely atrial fibrillation or flutter with variable block, or MAT if there are at least three P shapes.^[1][4]
3. What is the rate? A regular rate of about 150 per minute should make you think of flutter with 2:1 conduction; rates of 160 or more are unlikely to be flutter with 2:1 conduction.^[4]
4. Where is the P wave? Not seen or just after the QRS suggests AVNRT or AVRT; a P wave before each QRS that differs from sinus suggests atrial tachycardia. A P wave after the last QRS at termination points to AVRT or typical AVNRT and is very unlikely in atrial tachycardia.^[1]
5. Look for AVNRT signs. Typical AVNRT shows, more often than AVRT or atrial tachycardia, a small extra deflection at the end of the QRS in V1 (pseudo r') and a small notch in the inferior leads (pseudo S).^[1]
6. Probe. The response to a vagal manoeuvre or adenosine sorts the rest.

• Blood tests for the cause, especially in sinus tachycardia: full blood count, electrolytes (including potassium and magnesium), thyroid function, glucose, and as indicated troponin, drug levels (digoxin, theophylline).^[10]
• Echocardiography if the rhythm has been prolonged, if heart failure is suspected, or if there is any murmur.
• Ambulatory monitoring (Holter, patch, event recorder or a wearable device) for episodes that do not occur in clinic. Diagnosis in PSVT is often delayed because the episodes are brief and not captured.^[2]
• Electrophysiology (EP) study is both diagnostic and therapeutic: it defines the circuit and leads straight to catheter ablation. In people with pre-excitation and no symptoms, high-risk features at EP study include a shortest pre-excited RR interval in AF of 250 ms or less, an accessory pathway refractory period of 250 ms or less, multiple pathways and inducible AVRT.^[1]

Management follows the order set by the guidelines: stabilise, stop the episode, then prevent recurrence. For stable patients the 2015 ACC/AHA/HRS guideline (issued jointly by the main US cardiology and heart rhythm societies) and the European 2019 guideline broadly agree. Vagal manoeuvres come first, then intravenous adenosine, then intravenous calcium channel blockers or beta-blockers if adenosine fails or is unsuitable, with synchronised cardioversion for instability or when drugs fail.^[2]

Immediate direct-current (DC) cardioversion is the first choice in a haemodynamically compromised patient.^[1] Electrical treatment is usually preferred over drugs in the unstable patient because drugs act more slowly and less reliably.^[4]

• Synchronised shock. The defibrillator must be set to synchronised mode so the shock coincides with the R wave; an unsynchronised shock could land on the T wave and cause ventricular fibrillation.^[4]
• Sedation or anaesthesia. A conscious patient requires sedation or anaesthesia delivered by someone competent in the technique.^[4][5]
• Energy. For regular narrow-complex tachycardia and atrial flutter, the Resuscitation Council UK advises starting at 70 to 120 J with a biphasic defibrillator (100 J monophasic), increasing in steps. For broad-complex tachycardia or AF it advises starting at 120 to 150 J biphasic (200 J monophasic).^[4] The AHA 2025 interim guidance gives initial synchronised energies of 100 J for narrow-complex tachycardia and monomorphic VT, at least 200 J for atrial fibrillation and 200 J for atrial flutter, and an unsynchronised defibrillation dose for polymorphic VT; follow the device-specific energy level where it is known, and use the maximum setting if it is not.^[15] Always follow your local protocol and the manufacturer's guidance for your device.
• Up to three attempts, then amiodarone 300 mg IV over 10 to 20 minutes or procainamide, and repeat the shock, with expert help.^[3]

Vagal manoeuvres raise parasympathetic tone, which slows conduction and can block the AV node, ending a re-entry loop that depends on it.^[2] They are Class I in both major guidelines (2015 ACC/AHA/HRS and 2019 ESC).^[2] The ESC reports that conventional vagal manoeuvres succeed in 19 to 54% of cases.^[1]

Modified Valsalva manoeuvre (REVERT trial). The standard Valsalva manoeuvre, a forced strain against a closed glottis, converts few patients in practice. In the REVERT randomised trial at emergency departments in England, 433 adults with SVT (excluding AF and flutter) were randomised to a standard semi-recumbent Valsalva strain or to a modified version. Both used a 15-second strain at 40 mmHg. In the modified version the patient was laid flat and the legs were raised passively immediately after the strain. The primary outcome was return to sinus rhythm at 1 minute: 43% (93 of 214) with the modified manoeuvre versus 17% (37 of 214) with the standard one (adjusted odds ratio 3.7, 95% CI 2.3 to 5.8). No serious adverse events were recorded.^[6]

How to do it: the patient sits semi-recumbent and strains for 15 seconds at 40 mmHg (in practice, by blowing into a 10 mL syringe hard enough to move the plunger); immediately after the strain they lie flat while an assistant raises the legs passively.^[5][6]

Other vagal methods.

• Carotid sinus massage (gentle pressure on one side of the neck, supine with the neck slightly extended, for 5 to 10 seconds; it should always be unilateral).^[1][12] Avoid it if there is a carotid bruit, previous stroke or TIA, or recent myocardial infarction, and be cautious in older people.^[12][2] The evidence is an observational study, not a guideline.
• Diving reflex (breath-holding with cold exposure of the face, as with an ice-water-filled bag or cold wet towel) slows AV nodal conduction.^[2]

Vagal manoeuvres terminate up to a quarter of episodes by older estimates (carotid massage or Valsalva).^[4] Success is lower when patients try them at home: in two trials of etripamil only 4 to 6% of pre-trained patients converted at home by a vagal manoeuvre.^[2]

Adenosine is the first drug of choice if vagal manoeuvres fail.^[1] It activates adenosine A1 receptors in the heart, which causes a brief AV nodal block that breaks the re-entry circuit.^[2] It converts about 85 to 96% of AV-node-dependent PSVT.^[2] Its half-life is a matter of seconds (under 10 seconds), and it is cleared by red cells and vascular endothelium, so it must be given as a fast bolus into a large vein followed by a rapid saline flush.^[9]

Adult doses. Default adult regimen in RCUK 2026, ESC 2019 and ERC 2025: 6 mg, then 12 mg, then (optional) 18 mg, each by rapid push with a saline flush, 1 to 2 minutes apart. The AHA 2025 algorithm uses 6 mg then 12 mg.^[3][1][5] Where a licensed label differs (US 6/12/12; UK and South Africa Adenocor 3/6/12), follow local protocol.^[7][8][14]

The ESC adds that the mean dose required is about 6 mg and repeat administration is safe within a minute of the last dose.^[1] An 18 mg dose is above the single-dose maximum on the US label.^[7] Patients who develop high-level block on one dose should not be given further doses.^[7]

Technique.

• Use a large cannula in a large vein (for example the antecubital fossa), give the drug as a very rapid bolus (over 1 to 2 seconds) and follow at once with a saline flush.^[4][7] Giving it too slowly or into a small peripheral vein can cause an apparent lack of response.^[4]
• The US label notes that the doses come from studies of peripheral venous bolus dosing and that central venous administration has not been systematically studied; if a central line is the only access, follow your local formulary for the dose. Current RCUK, ERC and ESC guidance gives no separate central dose.^[7]
• Warn the patient that they will feel unwell for a few seconds, with chest discomfort or a sense of impending doom.^[2][4]
• Record a 12-lead ECG during the injection.^[4]

Adverse effects. Transient AV block and asystole, flushing, chest pain, hypotension, dyspnoea, bronchospasm, atrial fibrillation and a feeling of impending doom, usually short-lived because of the short half-life.^[2] Resuscitation equipment should be available. Rarely, ventricular fibrillation has been reported, mostly with concomitant digoxin.^[7]

Cautions and contraindications.

• Second- or third-degree AV block and sinus node disease (sick sinus syndrome, symptomatic bradycardia) are contraindications on the US label unless the patient has a functioning pacemaker.^[7] The ESC advises caution in known sinus node disease.^[1]
• Asthma and COPD. Regulators and guidelines differ. The US label advises caution because of mild to moderate worsening of asthma, and the South African label lists asthma and COPD as contraindications.^[7][8] The ESC says adenosine can be used cautiously in asthma, though verapamil may be better for severe asthma.^[1] The real-world risk may be mostly irritant dyspnoea rather than true obstruction.^[9]
• Dipyridamole blocks adenosine uptake and breakdown and potentiates it about four-fold. Stop dipyridamole 24 hours beforehand, or markedly reduce the adenosine dose.^[8]
• Carbamazepine can increase the degree of heart block produced.^[7][8]
• Methylxanthines (theophylline, caffeine) antagonise adenosine; larger doses may be needed or it may not work.^[7] Caffeine taken within 4 to 6 hours may mean a higher dose is needed.^[9]
• Heart transplant. Labels advise caution and lower doses in the first year after heart transplant; the ESC 2019 guideline notes recent evidence supporting use with no particular cautions. Start low and monitor.^{[1][8][9][14]}
• Long QT syndrome, severe hypotension and decompensated heart failure are listed contraindications on the South African label.^[8]
• AF, flutter and pre-excitation. Adenosine does not convert atrial flutter, AF or ventricular tachycardia.^[7] In AVRT it should be used with caution because it may induce fast AF.^[1] In pre-excited AF, AV-nodal blockers including adenosine should be avoided, as they may precipitate ventricular fibrillation.^[1]
• Wide-complex tachycardia of unknown mechanism. Do not use AV-nodal blockers (adenosine, non-dihydropyridine calcium channel blockers, beta-blockers) in undifferentiated wide-complex tachycardia or suspected pre-excited AF.^[2]

Adenosine as a diagnostic aid. Because it blocks the AV node but does not stop an atrial rhythm, adenosine can unmask what the atria are doing. If the ventricular rate slows briefly and then picks up again, look for atrial activity: atrial flutter or atrial tachycardia.^[4] Failure to terminate a regular narrow-complex tachycardia suggests an atrial tachycardia such as flutter (unless the dose was given too slowly or into a small vein).^[4] Adenosine does not interrupt macro-re-entrant atrial tachycardias.^[1] It may terminate focal atrial tachycardia due to triggered activity.^[1]

If adenosine fails or is contraindicated, and the patient is stable, an intravenous calcium channel blocker or beta-blocker is the next step. Both classes are Class IIa in the 2015 ACC/AHA/HRS and 2019 ESC guidelines.^[2]

Hypotension, bradycardia and worsening heart failure are the main side-effects. Verapamil should be avoided or given very carefully in small patients because it can cause severe hypotension.^[1] It is not recommended in wide-complex tachycardia of unknown cause.^[1]

For AVNRT specifically, oral diltiazem with a beta-blocker may terminate most episodes, while oral flecainide works too but in fewer. In AVNRT, vagal manoeuvres and adenosine terminate the rhythm less often than they do in AVRT.^[1]

Synchronised cardioversion is used when drug therapy fails or is contraindicated.^[3][1] For SVT that is refractory, seek expert help.

Sinus tachycardia is a rhythm, not a disease. In the peri-arrest setting, the Resuscitation Council UK stresses that treatment is directed at the underlying cause, and trying to slow a sinus tachycardia that has appeared in response to illness will make matters worse. Do not treat it with cardioversion or antiarrhythmic drugs.^[3][4]

Review categories are physiological, pathological, sinus node re-entrant (rare), inappropriate sinus tachycardia and POTS.^[10]

Inappropriate sinus tachycardia (IST) is a resting or minimal-activity sinus rate over 100 beats per minute that is out of proportion to physical, emotional, pathological or pharmacological stress. On 24-hour monitoring the mean rate is typically over 90 and waking rates exceed 100.^[1][10] It occurs even while supine, and is diagnosed only after secondary causes (anaemia, hyperthyroidism, drugs, infection, heart failure, pulmonary embolism) are excluded. POTS differs: a sustained rate rise of 30 beats per minute or more on standing (40 or more in teenagers), or to at least 120, without orthostatic hypotension.^[10]

Treatment of IST: beta-blockers are indicated, and ivabradine, a drug that slows the sinus node rate, can be added or considered.^[1] One review reports ivabradine is generally well tolerated at 2.5 to 7.5 mg twice daily, and in a small randomised crossover trial ivabradine was moderately more effective than metoprolol, which often caused symptomatic hypotension.^[10] Ablation of the sinus node is not established and may cause more harm than good.^[10]

"Paroxysmal atrial tachycardia" is the older term for what is now usually called atrial tachycardia (focal if it comes from one site). A rapid ectopic atrial pacemaker, not the sinus node, drives the rhythm. The rate is over 100 per minute, with a P wave of unusual axis before each QRS.^[1]

• Acute treatment. Beta-blockers or calcium channel blockers are the usual starting points; adenosine may terminate a triggered-activity form; class IA, IC and III drugs may also work.^[1] Adenosine is useful chiefly for unmasking the atrial activity by slowing the ventricular rate.^[4]
• Long-term treatment. Catheter ablation is the treatment of choice for recurrent focal atrial tachycardia, with reported success of 75 to 100% (average table figures: 85% acute success, 20% recurrence, 1.4% complications, 0.1% mortality).^[1]

MAT is a rapid, irregular rhythm with at least three different P-wave shapes. It is associated with pulmonary disease, theophylline and low magnesium.^[1]

• Treat the cause first: treat the lung disease and hypoxia, review theophylline therapy, and correct potassium and magnesium.
• Intravenous magnesium may help even if the serum magnesium is normal.^[1]
• Verapamil is of some help if the patient has no ventricular dysfunction, sinus node disease or AV block. The ESC describes metoprolol as superior to verapamil.^[1] Beta-blockers can cause bronchospasm,^[2] so in a patient with significant bronchospasm they should be avoided or used with great care.
• Antiarrhythmic drugs are generally not helpful.^[1]
• MAT often looks like AF. Look for the distinct P waves. Both are irregular, but MAT has organised P waves of several shapes.

AVNRT is the commonest type of paroxysmal SVT, often seen in people without other heart disease.^[4] The rate is typically in the range of 150 to 250 per minute. The ECG shows regular narrow QRS with P wave hidden or just after the QRS (pseudo r' in V1).^[1] It is usually benign unless there is separate structural or coronary disease, but it may cause symptoms that patients find frightening.^[4] Acute treatment follows the steps above. Ablation of the slow pathway is curative in about 97%.^[1]

AVRT is a re-entry loop that includes an accessory pathway.^[1] Orthodromic AVRT behaves like AVNRT in its acute response. The full discussion of pre-excitation, delta waves, risk stratification and the danger of pre-excited AF is in Wolff-Parkinson-White syndrome.

Acute points for AVRT:

• Orthodromic: vagal manoeuvres, then adenosine with caution because it may induce fast AF; AV-nodal drugs are used for orthodromic AVRT.^[1]
• Antidromic, or any pre-excited tachycardia: drugs acting on the accessory pathway (ibutilide, procainamide, propafenone or flecainide), because drugs acting on the AV node are ineffective or dangerous. Amiodarone may be considered in drug-refractory antidromic AVRT, but not in pre-excited AF.^[1]
• Ablation is the treatment of choice for symptomatic recurrent AVRT or pre-excited AF.^[1]

A regular narrow tachycardia at about 150 per minute may be flutter, which can be indistinguishable at first from AVNRT or AVRT.^[4] Adenosine or a vagal manoeuvre that transiently slows the ventricular rate and shows flutter waves makes the diagnosis. Management is covered in atrial fibrillation and flutter, including anticoagulation and the choice between cardioversion and ablation.

The aims are to reduce episodes and symptoms, decide whether to cure the rhythm, and avoid harm.

Catheter ablation is Class I for patients with symptomatic recurrent SVT in the 2015 ACC/AHA/HRS guideline, and the ESC advises offering it as an initial choice for all re-entrant and most focal arrhythmias.^[1][2] Energy is applied through catheters to destroy the critical tissue: the slow pathway in AVNRT, or the accessory pathway in AVRT.

All figures are from the ESC 2019 table.^[1] In AVNRT the risk of AV block that needs a pacemaker was below 1% in earlier reports and is probably close to zero when the inferior nodal extension is targeted in expert centres. For septal accessory pathways, cardiac tamponade occurs in 0.13 to 1.1% and complete AV block in 0.17 to 2.7%.^[1] In adults with congenital heart disease the success rate of AVNRT ablation is lower (82%) and the heart block risk higher (14%).^[1] Large registries report success above 95% for ongoing PSVT, yet only about 15% of eligible patients proceed to ablation, because of the invasive nature, waiting time, reluctance or availability.^[2]

Drugs reduce rather than cure episodes. The ESC reports a success rate of 13 to 82% for drugs in AVNRT and that up to 20% of patients discontinue them, so with the high success of ablation drug therapy has limited long-term value.^[1]

• Beta-blockers, diltiazem, verapamil: may be considered in orthodromic AVRT, only if the resting ECG shows no pre-excitation.^[1] They are also used in AVNRT.
• Flecainide and propafenone: are options only in hearts free of ischaemic or structural disease; their intravenous forms are contraindicated when such disease is present.^[1] They are used in antidromic AVRT only when structural or ischaemic disease is excluded and ablation is not feasible.
• Sotalol: the ESC advises not to use sotalol in patients with SVT.^[1]

For infrequent, well-tolerated, documented episodes, the patient takes an oral drug at the time of symptoms. The 2015 ACC/AHA/HRS guideline gives it a Class IIb (weak) recommendation for AVNRT; the ESC guideline omits it.^[2] The evidence is small and old: for example, in 33 patients with induced PSVT, a crushed single dose of diltiazem 120 mg plus propranolol 80 mg converted 94% within 2 hours, compared with 61% for crushed flecainide (about 3 mg/kg) and 52% for placebo.^[2] Absorption is slowed during an episode, and onset takes about 1 to 2 hours.^[2] It is suitable only for patients with an established diagnosis of regular narrow-complex PSVT and no pre-excitation, who have been taught what to do.^[2]

In 2025 the US Food and Drug Administration approved etripamil nasal spray (70 mg, up to two doses) for self-treatment of AV-node-dependent PSVT. In the RAPID trial 64.3% of patients converted to sinus rhythm within 30 minutes, versus 31.2% with placebo. It is not recommended with undifferentiated wide-complex tachycardia or pre-excitation, and it is not yet in the 2015 or 2019 guidelines.^[2]

Identify and avoid triggers where there are any (caffeine, alcohol, stimulants, sleep deprivation). Teach the modified Valsalva manoeuvre. Review after the first episode and offer a referral to an electrophysiologist for ablation. Advise patients to return urgently, or call emergency services, if palpitations are accompanied by chest pain, severe breathlessness, fainting or confusion.

Sustained SVT is more frequent in pregnancy, at 22 to 24 per 100,000 pregnancies.^[1]

• Vagal manoeuvres and adenosine are generally the first-line approach for a stable patient.^[2] The ESC advises adenosine as the first-line drug in the second and third trimesters.^[1] The US label says adenosine should be used in pregnancy only if clearly needed.^[7]
• Electrical cardioversion is the first choice if the patient is unstable, and appears safe at every stage of pregnancy, since it does not reduce blood flow to the foetus. Check the fetal heart rate routinely afterwards.^[1]
• Catheter ablation is best done before pregnancy if SVT is already known, or postponed to the second trimester if possible.^[1]
• Drug exposure should be minimised, especially in the first trimester.^[2]

In children, the principles are similar but doses are by weight. The US label advises, for children under 50 kg, an initial adenosine dose of 0.05 to 0.1 mg/kg, pushed fast (centrally or peripherally) and flushed with saline, then increased in steps of 0.05 to 0.1 mg/kg if the rhythm persists after 1 to 2 minutes, up to a single-dose maximum of 0.3 mg/kg; children over 50 kg receive the adult dose, with a ceiling of 12 mg.^[7] Response may be reduced in younger children.^[1] Verapamil should be avoided or used very carefully in small patients because it can cause severe hypotension, and diltiazem and verapamil are contraindicated under 1 year of age.^[1][13] The UK label gives a first adenosine bolus of 0.1 mg/kg (maximum 6 mg) with increments of 0.1 mg/kg,^[14] and a 2026 paediatric intensive care guideline uses 0.1 mg/kg (maximum 6 mg), then double (maximum 12 mg); its synchronised cardioversion is 1 J/kg first and 2 J/kg second, with non-vasoplegic sedation.^[13] Specialist paediatric cardiology advice should be sought.

The ESC advises that catheter ablation should generally be recommended to all athletes with a history of paroxysmal SVT, and discourages treatment with beta-blockers or sodium channel blockers.^[1]

SVT in congenital heart disease can arise from scar-related re-entry after surgery or from accessory pathways, and management needs individual electrophysiological assessment. Ablation is harder and the choice of drug depends on the ventricular function and surgical history.^[2]

Most AVNRT and AVRT are benign when the heart is otherwise normal.^[4] The harm comes from the following.

• Haemodynamic compromise: syncope, hypotension and pulmonary oedema, particularly with structural heart disease or very fast rates.^[3][4]
• Sudden death in WPW: the estimated risk of cardiac arrest or ventricular fibrillation is 2.4 per 1000 person-years (95% CI 1.3 to 3.9), via rapidly conducted pre-excited AF.^[1]
• Pre-excitation-related arrhythmias. About one in five patients with asymptomatic pre-excitation develop an arrhythmia related to the pathway during follow-up, most often AVRT (80%), followed by AF (20 to 30%).^[1]
• Drug harm: AV-nodal blockers in pre-excited AF, and flecainide-type drugs in structural heart disease.^[1]
• Persistent rapid heart rates are harmful in patients with underlying heart disease.^[10]
• Quality of life. Frequent or prolonged episodes disrupt work, exercise and travel, and repeated emergency visits are costly.^[2]

After successful ablation, outcomes are excellent and most patients need no long-term drug therapy.^[1]

The UK Driver and Vehicle Licensing Agency (DVLA) sets rules for arrhythmias that have caused or are likely to cause incapacity.^[11]

• Car and motorcycle (Group 1): must not drive for at least 4 weeks after an incapacitating arrhythmia, and the DVLA must be notified. Driving can resume 4 weeks after the event if the cause has been identified and treated and there has been no recurrence likely to cause incapacity.^[11]
• Bus and lorry (Group 2): must notify the DVLA and must not drive. Relicensing requires the cause to be identified and treated, no further incapacitating arrhythmia likely for at least 3 months, and a left ventricular ejection fraction of at least 40%.^[11]
• Pre-excitation without arrhythmia: drivers in either group may drive and need not notify the DVLA. If it is associated with an arrhythmia, the arrhythmia rules apply.^[11]
• After a successful ablation (other than for ventricular tachycardia), Group 1 drivers must not drive for at least 2 days and Group 2 drivers for at least 2 weeks, with no notification required.^[11]

The ESC similarly advises that where there is a history of syncope, driving must cease until the condition is satisfactorily controlled or treated.^[1] Other countries have their own rules, so check local law.

• Any unstable tachycardia (while resuscitating).
• Wide-complex tachycardia, pre-excitation on the ECG, or syncope.
• Recurrent or poorly tolerated SVT, for consideration of ablation.
• SVT in pregnancy, children, or with structural heart disease.
• Atrial tachycardia or flutter that does not terminate with adenosine.
• Persistent unexplained sinus tachycardia not explained by a cause.