Approach to tachyarrhythmias

• A fast pulse is a sign, not a diagnosis. Most often it is sinus tachycardia, the normal heart responding to fever, pain, blood loss, anxiety or illness. The task is then to treat the cause, not the number.
• The first question for any fast rhythm is: is the patient stable? Low blood pressure, a clouded mind, ischaemic chest pain, shock or acute heart failure caused by the rhythm means an immediate synchronised shock, whether the QRS is narrow or wide.^[1][2]
• If the patient is stable, ask two questions of the 12-lead ECG: is the QRS narrow or wide (0.12 seconds is the dividing line), and is the rhythm regular or irregular? Those two answers sort almost every tachyarrhythmia into four boxes.
• A regular wide-complex tachycardia is treated as ventricular tachycardia until proved otherwise. Never give verapamil or diltiazem to an undiagnosed wide-complex tachycardia, and never give atrioventricular (AV) nodal blockers in pre-excited atrial fibrillation.
• Doses and energies are given in detail in the disease topics; this page is the decision map that links them.

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

1. Separate causes of a fast pulse by urgency and by mechanism (sinus, supraventricular, ventricular).
2. Recognise the features that make a tachyarrhythmia unstable and state what to do at once.
3. Take a focused history and examination for palpitations and know which first tests to order.
4. Choose an ambulatory monitor for a patient whose palpitations come and go.
5. Use QRS width and regularity to place a stable tachyarrhythmia in one of four groups, and name the safe first actions and the drugs to avoid in each.
6. Apply the approach to pregnancy, children, older adults, athletes and settings without a monitor or defibrillator.

A "tachyarrhythmia" is a rhythm disturbance with a fast heart rate, in adults usually taken as above 100 per minute.^[6] It sounds like one condition but is a family of very different problems. Some can be ignored, some can be treated with a breath-holding manoeuvre, and some will kill the patient within minutes. The skill is not memorising each rhythm but knowing the order of questions, so that the dangerous ones are caught first.

This page is the map. The detailed rhythms are in supraventricular tachycardias, atrial fibrillation and flutter, ventricular arrhythmias, Wolff-Parkinson-White syndrome and long QT syndrome. Reading an ECG is covered in ECG interpretation.

A fast pulse has three kinds of cause: the sinus node is being driven faster by the body's needs, the rhythm has switched to an abnormal circuit above the ventricles, or it comes from the ventricles themselves. Sorting by mechanism tells you what the ECG will show; sorting by urgency tells you what to do first.

Sinus tachycardia is the commonest arrhythmia, and in most cases it is a normal, useful response to physical or emotional stress, driven by more sympathetic nerve activity and circulating catecholamines (adrenaline and related hormones), and less vagal tone.^[6] Like fever, it is a non-specific sign. The sinus node itself is working properly; it is being asked to work faster.

Secondary (pathological) causes are the ones you must look for in a sick patient. A review of sinus tachycardia lists dehydration, hyperthyroidism, haemorrhage, iron-deficiency anaemia, hypoxia, pulmonary embolism, heart failure, trauma and inflammatory states or infection.^[6] The Resuscitation Council UK adds pain.^[3] Medicines matter: stimulants and beta-agonist inhalers raise the rate directly, and diuretics can raise it indirectly by causing volume depletion.^[6]

Some patients have persistent sinus tachycardia without a trigger, for example inappropriate sinus tachycardia or postural orthostatic tachycardia syndrome; these are diagnoses of exclusion after the causes above have been sought.^[6] They are discussed in the supraventricular tachycardias topic.

Red flags are features that mean the rhythm is the problem and time is short. The 2025 AHA algorithm asks whether a persistent tachyarrhythmia is causing hypotension, acutely altered mental status, signs of shock, ischaemic chest discomfort or acute heart failure.^[1] The Resuscitation Council UK uses a similar list: shock, syncope with severe or ongoing hypotension, myocardial ischaemia, severe heart failure with pulmonary oedema, and a patient who is immediately post return of spontaneous circulation (ROSC) after a cardiac arrest.^[2]

Each flag has a mechanism. Hypotension, confusion and cold, clammy skin are the brain and the body failing to receive enough output. Chest pain or ST changes mean the coronary arteries are being starved during short diastoles. Breathlessness with crackles means the left atrium and ventricle are not emptying, so fluid backs into the lungs (see heart failure).

Two further warning signs call for early expert help even in a stable patient: syncope (fainting) during palpitations, and a family history of sudden death at a young age. They raise the possibility of a ventricular arrhythmia or an inherited condition such as long QT syndrome or pre-excitation.

If the patient is stable, a short history is still worth the time, because it often points to the rhythm before the ECG is shown. Ask about the following.

• How it starts and stops. Abrupt on and off like a switch suggests a re-entry circuit (AVNRT or AVRT), whereas a gradual rise and fall suggests sinus tachycardia. A sinus rhythm that accelerates over a few seconds fits a focal atrial source (the "warm-up" pattern).^[5] The review of sinus tachycardia also stresses the pattern in time: when the symptoms occur, how often, and how episodes start and end.^[6]
• Regular or irregular. Ask the patient to tap out the beat. A regular tapping suggests a re-entry circuit or VT; an irregular, chaotic tapping suggests atrial fibrillation.
• Whether a vagal manoeuvre stopped it. Termination with a breath-hold strain, a cold drink or similar suggests an AV-node-dependent re-entry circuit. Vagal manoeuvres have been reported to work in between 19 and 54% of supraventricular episodes.^[5]
• Associated symptoms. Dizziness, near-fainting, chest pain, breathlessness and sweating suggest haemodynamic effect.
• Triggers. Exercise, emotion, caffeine, alcohol, nicotine and recreational stimulants; the menstrual cycle, pregnancy, illness and poor sleep. Review all medicines and supplements, including inhalers, thyroid tablets, decongestants and diuretics.^[6]
• Previous heart disease. Past infarction, heart failure, valve disease, congenital heart disease, cardiac surgery, known pre-excitation or earlier arrhythmias. A wide-complex tachycardia in a patient with an old infarct is ventricular tachycardia until proved otherwise.
• Family history. Sudden death or unexplained drowning or car crash at a young age, inherited arrhythmia or cardiomyopathy, early pacemaker or defibrillator.
• Other illness. Fever, infection, bleeding, weight loss, heat intolerance and tremor (thyroid), cough or leg swelling (pulmonary embolism), vomiting and diarrhoea (volume loss).

The examination has two aims: to judge how sick the patient is, and to find a cause for a sinus tachycardia. Start with the vital signs: pulse rate and rhythm, blood pressure, respiratory rate, oxygen saturation and temperature. Then work through the patient.

• Perfusion. Capillary refill, skin temperature, level of consciousness and urine output.
• Pulse. Count it for a full minute. Is it regular? A truly regular, very fast pulse is the clue for a re-entrant or flutter rhythm; a pulse that is irregularly irregular suggests AF.
• Neck veins and heart sounds. Raised jugular venous pressure and a third heart sound point to heart failure; irregular cannon waves (when the atrium contracts against a closed tricuspid valve) hint at AV dissociation, which supports ventricular tachycardia. Murmurs may reveal valve disease; see cardiac physical examination.
• Lungs and legs. Crackles and ankle oedema suggest heart failure; pleuritic pain or a swollen calf suggests pulmonary embolism.
• Causes of sinus tachycardia. Review the findings that one review lists: orthostatic vital signs, low oxygen saturation, pallor, features of heart failure, signs of infection and an enlarged thyroid.^[6]

Investigations answer three questions: what is the rhythm, what is causing it, and is the heart structurally normal.

The 12-lead ECG is the single most important test. Record it as soon as it can be done without delaying treatment of an unstable patient, and keep a continuous rhythm strip running. The algorithms say: monitor ECG, blood pressure and oxygen saturation, give oxygen if saturation is below 94% (Resuscitation Council UK) or if the patient is hypoxaemic (AHA), establish intravenous access, and record a 12-lead ECG.^[1][2] Look at the following in turn:

1. QRS width, narrow or wide, using the 0.12 second line.^[1][2]
2. Regularity of the R-R intervals, ideally over a long strip.
3. P waves. Is there a P wave before every QRS, a saw-tooth pattern, or no P waves at all? In sinus tachycardia the P waves are normal in shape and precede each QRS, so a regular narrow rhythm without visible P waves points elsewhere.^[6]
4. Rate. In adults the AHA algorithm notes a heart rate typically of 150 per minute or more in a tachyarrhythmia, so a modest rate in a sick patient should first prompt a search for a sinus response to illness.^[1] Children have different normal rates (see Step 1 below).
5. Clues to the underlying problem. Pre-excitation (a short PR with a delta wave), ischaemia, a long QT interval, or bundle branch block on a previous trace (see bundle branch blocks).

If the rhythm stops during recording, keep the strip, then repeat the 12-lead ECG, because the baseline ECG can reveal pre-excitation or a long QT interval that explains the episode. Record the ECG during any treatment, such as adenosine, because the response is a diagnostic clue.^[3]

Bloods are chosen to find a cause, and some can be sent while treatment is under way. The review of sinus tachycardia recommends testing for anaemia, hyperthyroidism, hypoglycaemia, acute heart failure, dehydration, electrolyte disturbances and drug use such as amphetamines.^[6] In practice the useful first panel is:

• Potassium and magnesium. Low levels raise the risk of ventricular arrhythmias and torsades de pointes, and are easy to correct; see ventricular arrhythmias.
• Thyroid function (thyroid-stimulating hormone, TSH). Thyrotoxicosis is a common reversible cause of sinus tachycardia and AF.^[6]
• Full blood count, glucose, urea and creatinine, and a blood film or lactate when infection, bleeding or hypovolaemia is suspected.
• Troponin when there is chest pain or an ECG change, to look for myocardial injury as the cause or the result of the rhythm. Interpret a rise in the light of the whole clinical picture.
• Arterial or venous gas, D-dimer or CT pulmonary angiography when pulmonary embolism is a concern, and a toxicology screen if stimulant use is possible.

An echocardiogram shows ventricular function, valve disease, chamber size and wall thickness. It matters because the safest drug choice depends on the ejection fraction: the Resuscitation Council UK algorithm splits the choice of rate-control drug for AF at an ejection fraction of 40%.^[2] Echocardiography is also part of the work-up of ventricular arrhythmias and new-onset AF to look for structural heart disease; see the topics on ventricular arrhythmias and atrial fibrillation. A chest radiograph can show heart size and pulmonary congestion. Stress testing or cardiac magnetic resonance imaging is chosen case by case after the acute event.

A 12-lead ECG is a 10-second snapshot. When palpitations come and go, the rhythm is usually normal in clinic, so the aim is to record the ECG during an episode. Ambulatory ECG is used for symptoms such as palpitations, syncope, dizziness and chest pain that may reflect intermittent arrhythmias.^[7] The best device depends on how often the symptoms occur.

The statement adds that loop recorders gave a higher yield than 24-hour Holter monitoring and were more cost-effective, and that about 2 weeks of recording gave the best balance between yield and cost.^[7] Event recorders that the patient triggers fit infrequent, unpredictable palpitations but need a patient who can activate them in time.^[7]

This section is the heart of the topic. It has three parts: first decide whether the rhythm is sinus tachycardia, then apply the instability rule, then sort the stable patient by QRS width and regularity.

Treat sinus tachycardia as a sign. The Resuscitation Council UK states that sinus tachycardia is not an arrhythmia, that treatment is directed at the underlying cause, and that trying to slow it in response to most of these situations will make matters worse. Do not treat sinus tachycardia with cardioversion or antiarrhythmic drugs.^[3][2] Slowing a sinus tachycardia that is compensating for blood loss, sepsis, anaemia or heart failure removes the compensation the patient needs.

The rate itself is a clue. In adults a rate of 150 per minute or more is typical of a tachyarrhythmia,^[1] so a regular narrow rhythm at 150 with no visible P waves needs a different explanation from a rhythm at 110 with normal P waves. A rate below 150 does not exclude an arrhythmia, and in infants and young children 150 may be a normal sinus rate.^[6] The normal upper limit also falls with age. The 99th percentile for rate in a healthy infant is about 180 per minute shortly after birth, falling to 160 at one year, 110 by age 12 and 100 by age 18, and a highly stressed neonate can reach more than 240 per minute with a sinus rhythm.^[6] Use age-appropriate rates in children, rather than the adult cut-off of 100.

If a persistent tachyarrhythmia is causing haemodynamic instability, treat it with immediate synchronised cardioversion, whatever the QRS width.

This applies to narrow and wide complexes. The exception is unstable polymorphic VT or torsades: the monitor has no consistent R wave to synchronise to, so give an unsynchronised defibrillation shock, as for VF (AHA 2025: polymorphic VT receives a defibrillation dose, not a synchronised one).^[8] If there is no pulse, treat it as cardiac arrest. The ESC states that immediate direct-current cardioversion is the first choice in haemodynamically compromised patients with supraventricular tachycardia.^[5] For a broad-complex tachycardia, the Resuscitation Council UK points out that in a patient with adverse features the distinction between VT and supraventricular rhythm with aberrancy is irrelevant: attempt synchronised cardioversion.^[3] Drugs act more slowly and less reliably than a shock, so electrical treatment is usually preferred for an unstable patient.^[3]

How to do it safely.

1. Call for help and bring the defibrillator and airway equipment.
2. Sedate or anaesthetise if the patient is conscious, using a clinician competent in the technique; the AHA says to sedate whenever feasible, and the Resuscitation Council UK says to consider sedation or anaesthesia if conscious.^[1][2][3] Sedation should not hold up the shock in a patient who is collapsing.
3. Check the machine is in synchronised mode. The shock is then timed to the R wave. An unsynchronised shock could land on a T wave and cause ventricular fibrillation.^[3] If a second shock is needed, reactivate the synchronisation switch if necessary.^[3]
4. Choose the energy by rhythm (Table below), and increase stepwise if the first shock fails.
5. If unsuccessful after up to three attempts, give amiodarone 300 mg IV over 10 to 20 minutes, or procainamide 10 to 15 mg per kg (maximum 1 g) over 20 minutes, and repeat the shock, with expert help.^[2]
6. Look for and treat the cause (hypoxia, electrolytes, ischaemia, drugs).

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.^[8]

In atrial fibrillation or flutter of long or unknown duration, cardioversion normally needs prior anticoagulation (or an echo showing no atrial thrombus) because restoring sinus rhythm can dislodge a clot. The duration threshold differs between guidelines: the Resuscitation Council UK 2026 algorithm uses 24 hours and its 2021 manual uses 48 hours, and other guidelines differ again (see the atrial fibrillation topic). If the duration is unknown, treat it as long. If the patient is unstable, the shock cannot wait; start heparin early ("at the earliest opportunity" in the 2021 manual), as described in atrial fibrillation and flutter.^[2][3]

If the patient is stable, there is time to read the ECG properly and to seek expert help, because the choice of drug depends on getting the rhythm right. The Resuscitation Council UK algorithm splits the next step by QRS width (0.12 seconds) and regularity.^[2]

The sections below add what the flowchart cannot show.

Regular narrow complex. The commonest causes are the re-entry circuits AVNRT and AVRT, and atrial flutter with fixed conduction. Start with a vagal manoeuvre. In the REVERT trial the modified Valsalva manoeuvre worked more often than the standard version (43% versus 17%), and the ESC reports that vagal manoeuvres overall have been successful in between 19 and 54%.^[5] If these fail, adenosine by rapid push into a large vein with a saline flush: a slow injection or a small vein produces an apparent failure.^[3] Failure to terminate a regular narrow tachycardia with adenosine suggests an atrial tachycardia such as atrial flutter (unless it was given too slowly).^[3] Adenosine regimens differ between guidelines; the verified topic supraventricular tachycardias gives the comparison, and this page follows it. Have a defibrillator ready when giving adenosine: it can induce fast AF in AVRT, and it should be approached cautiously in known sinus node disease and used cautiously in asthma, where verapamil may be preferred in severe cases.^[5] Other interactions and contraindications are in the supraventricular tachycardias topic. If adenosine is contraindicated or fails, an IV calcium channel blocker or beta-blocker is the next step if there is no hypotension or heart failure (see Pitfalls).^[5]

Irregular narrow complex. This is most likely AF, and the rate-control drug depends on the ejection fraction: with a preserved ejection fraction (above 40%), a beta-blocker, verapamil, diltiazem or digoxin; with a reduced one (40% or lower), a beta-blocker or digoxin, and anticoagulation if the arrhythmia has lasted longer than 24 hours (Resuscitation Council UK 2026; the 2021 manual uses 48 hours).^[2][3] Flutter with variable block and multifocal atrial tachycardia can also look irregular; the second is a rhythm with at least three different P-wave shapes, typically seen in lung disease.^[5] In multifocal atrial tachycardia treat the lung disease, hypoxia and low magnesium first and be cautious with beta-blockers in bronchospastic lung disease; see the supraventricular tachycardias topic.^[5] Rhythm control for AF, the atrial rate in flutter, anticoagulation risk scoring and the timing of cardioversion in new-onset AF are set out in atrial fibrillation and flutter.

Regular wide complex. It may be VT or a supraventricular rhythm conducted with a bundle branch block (see bundle branch blocks), but when the mechanism is unclear the ESC says to treat it as VT.^[5] The Resuscitation Council UK advises treating as VT with synchronised shock(s); if the risk of sedation or anaesthesia is too high, a drug can be tried first, procainamide being the first choice, with amiodarone if procainamide is unavailable or contraindicated (for example in severe heart failure, acute myocardial infarction or end-stage kidney disease), and a synchronised shock if drugs fail.^[2] The AHA allows adenosine in a regular, monomorphic wide-complex tachycardia, but warns that procainamide should be avoided if the QT is prolonged or in heart failure.^[1] The full discussion is in ventricular arrhythmias.

Irregular wide complex. Two dangerous possibilities dominate: AF conducting down an accessory pathway (pre-excited AF), which is irregular and fast with QRS widths that vary from beat to beat, and polymorphic VT. In pre-excited AF the algorithm suggests procainamide or cardioversion.^[2] Polymorphic VT with a long QT interval (torsades de pointes) is treated with magnesium 8 mmol IV over 10 minutes; consider isoprenaline or temporary pacing to raise the heart rate, and avoid amiodarone.^[2] For details see Wolff-Parkinson-White syndrome and long QT syndrome.

Whatever the rhythm, the first minutes follow the same pattern: assess airway, breathing and circulation; attach a monitor for ECG, blood pressure and oxygen saturation; give oxygen if saturation is low; obtain intravenous access; record a 12-lead ECG; and identify and treat reversible causes such as electrolyte disturbance, hypoxia, ischaemia and drugs.^[1][2] Then decide, with the instability rule and the flowchart above, between a shock and a drug. If an arrhythmia complicates another illness such as infection, myocardial infarction or heart failure, make sure the underlying condition is assessed and treated too.^[3]

After successful treatment, keep the patient on a monitor until the risk of further arrhythmia is low, and record a 12-lead ECG, because it may show pre-excitation, a long QT interval or other abnormalities that were hidden during the tachycardia.^[3]

A few errors are responsible for most harm in tachyarrhythmia care.

• Verapamil or diltiazem in a wide-complex tachycardia. The ESC states that verapamil is not recommended in wide-QRS tachycardia of unknown cause.^[5] If the rhythm is VT, these drugs depress contraction and lower the blood pressure and can cause collapse.
• Calcium channel blockers or beta-blockers in heart failure or hypotension. IV verapamil and diltiazem are contraindicated in hypotension or heart failure with reduced ejection fraction, and IV beta-blockers in decompensated heart failure.^[5] Check the ejection fraction when you can, and see heart failure.
• Treating the number in sinus tachycardia. Slowing a compensatory rate with a beta-blocker in a bleeding or septic patient can precipitate collapse.^[3]
• Missing a long QT. Several drugs used for tachycardia (amiodarone, sotalol, procainamide) prolong the QT interval and may worsen torsades.^[2] Look at the QT on any ECG before and after the tachycardia.
• Missing atrial flutter. A regular narrow tachycardia that does not terminate with a correctly given adenosine bolus suggests an atrial rhythm such as flutter, not a re-entry circuit.^[3]
• Cardioverting AF without considering clots. In AF lasting longer than 24 to 48 hours (guidelines differ), cardioversion should wait for 3 weeks of anticoagulation or an echocardiogram showing no atrial thrombus, unless the patient is unstable.^[3]

Seek expert help (a cardiologist or an anaesthetist/intensivist for sedation) as soon as a patient meets any red flag. The algorithms say seek expert help for the stable pathway and again when life-threatening features persist.^[2] Refer in particular:

• Any patient who needed cardioversion, or who has a wide-complex tachycardia, syncope, or an unclear rhythm.
• Pre-excited AF, or an ECG with pre-excitation and symptoms, because catheter ablation is the treatment of choice for symptomatic and recurrent AVRT and for pre-excited AF.^[5]
• Recurrent supraventricular tachycardia: the ESC advises offering catheter ablation as an initial choice to patients with re-entrant and most focal arrhythmias.^[5]
• Known or suspected structural heart disease, heart failure, long QT, or a family history of sudden death; see long QT syndrome.
• A tachycardia that persists, or palpitations without a documented rhythm after a first-line monitor has been negative.

Safe discharge after a short, self-terminating, well-tolerated supraventricular episode needs a documented rhythm if possible, a normal baseline ECG, and clear advice on when to return (chest pain, breathlessness, fainting, confusion).

Pregnancy. Sustained SVT becomes more frequent in pregnancy, at 22 to 24 per 100,000 pregnancies.^[5] The principles are unchanged. If the mother is unstable, electrical cardioversion is the first choice: it seems safe in all phases of pregnancy because it does not compromise fetal blood flow, and the fetal heart rate should be checked after it.^[5] For stable supraventricular tachycardia, vagal manoeuvres come first, and the ESC advises adenosine as first-line drug treatment in the second and third trimesters.^[5] The disease topics give drug choices in pregnancy.

Children. The normal heart rate depends on age (the 99th percentile for infants is about 180 per minute soon after birth, 160 at one year, 110 by age 12, and 100 by age 18), so a rate that is normal in an infant would be a tachycardia in an adult.^[6] Doses are by weight (see supraventricular tachycardias). The ESC advises that verapamil be avoided, or used very carefully, in small patients because it can cause severe hypotension, and notes that younger children may respond less well to adenosine.^[5] Involve paediatric cardiology early.

Older adults. Atrial fibrillation and flutter become more common, and the ageing heart tolerates fast rates and drug effects poorly; rapid rates of 100 to 150 may already cause instability in people with impaired cardiac function or serious lung disease.^[3] Review medicines, because rate-slowing drugs combined with age-related conduction disease can produce bradycardia afterwards (see bradyarrhythmias and AV block), and the work-up should include anaemia, thyroid and kidney function.

Athletes. Athletes with palpitations need the same assessment as others, with extra attention to exercise-related syncope, which raises concern about ventricular arrhythmia or structural disease. For a documented paroxysmal SVT in an athlete, the ESC says ablation should generally be recommended.^[5]

• No 12-lead ECG. Even a single-lead rhythm strip from a monitor or defibrillator shows regularity, and a narrow or wide QRS can be judged on it. A pulse that is regular and very fast in an otherwise stable patient justifies a vagal manoeuvre (the modified Valsalva manoeuvre needs only a bed) before any drug.^[5]
• No adenosine. The Resuscitation Council UK algorithm gives verapamil or a beta-blocker when vagal manoeuvres and adenosine are ineffective; verapamil and diltiazem are contraindicated in hypotension or heart failure with reduced ejection fraction.^[2][5]
• No sedation expertise. Do not delay a shock in a dying patient. For a stable wide-complex tachycardia when sedation is risky, drug treatment first is acceptable.^[2]
• No echocardiography. Treat the possibility of heart failure as real in an older patient with breathlessness and raised jugular venous pressure, and avoid verapamil and diltiazem if you cannot exclude it.^[5]
• Palpitations that come and go. Teach the patient to record an ECG at the time of symptoms with an event recorder or a smartphone device if available, or to feel the pulse and note its rate and regularity.^[7]

Case 1: a regular narrow-complex tachycardia in a young woman. A 26-year-old woman has sudden palpitations while sitting at her desk. She is anxious but alert; her blood pressure is 118/74, her pulse is very fast and regular, and her ECG shows a narrow regular tachycardia at 190 per minute with no visible P waves. She has no chest pain, breathlessness or syncope. Reasoning. She is stable, so there is time. The rhythm is regular and narrow, so this is an SVT (most likely AVNRT or AVRT). First, a vagal manoeuvre: the modified Valsalva manoeuvre (semi-recumbent strain, then lying flat with the legs raised). If it fails, adenosine 6 mg by rapid IV push into a large vein with a saline flush, then 12 mg, with the rhythm recorded, given only if there is no known pre-excitation on a resting ECG and with a defibrillator at hand.^[2][5] A resting ECG after conversion should be checked for pre-excitation. Recurrent episodes mean referral for ablation.

Case 2: wide, regular and unstable in an older man. A 68-year-old man with a past anterior myocardial infarction feels light-headed. His blood pressure is 82/50, he is confused and sweaty, and the monitor shows a regular wide-complex tachycardia at 170 per minute. Reasoning. Hypotension and confusion mean he is unstable, so the instability rule applies. Wide and regular in a man with an old infarct is VT until proved otherwise, and the distinction between VT and SVT with aberrancy is irrelevant when adverse features are present.^[3] He needs a synchronised shock, with sedation or anaesthesia if he is conscious and if it can be arranged without delay, starting at 120 to 150 J biphasic and increasing stepwise if it fails.^[3][4] After up to three attempts, amiodarone 300 mg IV over 10 to 20 minutes or procainamide, then another shock.^[2] Verapamil would be dangerous. He then needs potassium and magnesium checked and a cardiology referral for the cause.

Case 3: wide, irregular and very fast in a young man. A 24-year-old man has had palpitations for an hour, with a pulse that is wildly irregular. His blood pressure is 110/70. The ECG shows a wide-complex tachycardia, irregular, with QRS shapes varying from beat to beat, at rates up to 250 per minute. His resting ECG from a school medical shows a short PR interval and a delta wave. Reasoning. The rhythm is stable at present. The combination of wide, irregular and fast, with pre-excitation on an old ECG, points to pre-excited AF. The key is what not to give: no adenosine, verapamil, diltiazem, beta-blockers, digoxin or amiodarone, because AV-nodal blockers can speed conduction down the accessory pathway and risk ventricular fibrillation.^[3][5] The algorithm suggests procainamide or cardioversion.^[2] If he deteriorates, he needs an immediate synchronised shock. Afterwards he needs an electrophysiology referral for ablation.^[5]