Ventricular arrhythmias

• Ventricular arrhythmias start in the ventricles, below the AV node. They range from harmless single extra beats (premature ventricular contractions, PVCs) to ventricular tachycardia (VT, three or more beats faster than 100 per minute) and ventricular fibrillation (VF), which is cardiac arrest.^[1]
• A wide-complex tachycardia (QRS over 120 ms, rate over 100 per minute) is treated as VT until proven otherwise, especially in anyone with previous myocardial infarction or heart failure. Never give verapamil or diltiazem for an undiagnosed wide-complex tachycardia.^[9]
• Unstable VT, or VT with no pulse, needs a shock: a synchronised shock if there is a pulse, an unsynchronised defibrillation shock for VF or pulseless VT. Stable monomorphic VT: procainamide is preferred (RCUK, ESC, AHA/ACC/HRS); amiodarone if there is severe heart failure, acute infarction, long QT or end-stage kidney disease, or if procainamide is not available.^[4][7]
• Torsades de pointes is polymorphic VT with a long QT interval. Treat with intravenous magnesium sulphate, correct potassium, stop the offending drugs, and speed the heart up if it keeps recurring.^[11]
• Survivors of VF or poorly tolerated VT without a reversible cause usually need an implantable cardioverter-defibrillator (ICD). Catheter ablation and beta-blockers reduce recurrences.^[12][2]

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

1. Define PVCs, non-sustained and sustained VT, monomorphic and polymorphic VT, VF and torsades de pointes, and recognise each on an ECG.
2. Explain the three mechanisms behind ventricular arrhythmias and why scar from a previous infarct is the commonest substrate.
3. Decide when PVCs are harmless and when they call for investigation or treatment, including PVC-induced cardiomyopathy.
4. Work through a wide-complex tachycardia with the ECG clues (AV dissociation, capture and fusion beats, concordance, QRS width) and the Brugada and Vereckei algorithms.
5. Run a shockable cardiac arrest from the current Resuscitation Council UK and American Heart Association algorithms, with energies and drug doses.
6. Manage stable and unstable VT, torsades de pointes and electrical storm.
7. Describe the work-up after a ventricular arrhythmia, ICD indications for secondary and primary prevention, and the role of ablation.
8. Apply special considerations for acute infarction, heart failure, pregnancy, children, driving and sport, and low-resource settings.

Every heartbeat is meant to start in the sinus node and pass down the AV node and His-Purkinje system, which spreads the impulse to both ventricles in a fraction of a second. A ventricular arrhythmia is any rhythm that originates in the ventricular muscle or Purkinje fibres themselves, outside this fast pathway. The impulse then crosses the muscle cell to cell, which is slow, so the QRS complex is wide (over 120 ms).^[9]

The group matters because it contains both the most common and the most lethal rhythm disturbances. PVCs are very common: about half of people show them on 24 hours of monitoring. At the other extreme, sudden cardiac death accounts for roughly 10 to 20% of all deaths, and in up to half of cases sudden death is the first sign of heart disease.^[2] Most sudden cardiac deaths are caused by VT that degenerates into VF.

Congenital long QT syndrome has its own page (Long QT syndrome). The broader approach to fast rhythms is in Approach to tachyarrhythmias.

The 2019 international ablation consensus statement gives the working definitions used in this page.^[1]

• PVC (premature ventricular complex): an early ventricular depolarisation, with or without a felt contraction. The statement prefers "complex" to "contraction" because an early electrical event does not always produce a pumping beat.
• VT: a ventricular rhythm faster than 100 beats per minute lasting three or more consecutive beats, independent of atrial or AV nodal conduction.
• Non-sustained VT (NSVT): VT that stops by itself within 30 seconds.
• Sustained VT: VT lasting 30 seconds or longer, or needing an intervention (such as a shock) to stop it.
• Monomorphic VT: the QRS looks the same from beat to beat. Polymorphic VT: the QRS shape changes from beat to beat.
• Incessant VT: sustained VT that keeps returning promptly despite repeated treatment over several hours.
• Electrical storm (VT storm): at least three separate sustained VT episodes in one day, each needing an intervention to stop it.^[1][2]

Ventricular fibrillation is chaotic, unorganised ventricular activity with no effective pumping. Torsades de pointes is a polymorphic VT in a heart with a prolonged QT interval, in which the QRS appears to twist around the baseline.^[11]

In cardiac arrest, VF and pulseless VT are called shockable rhythms because a defibrillation shock can restore a perfusing rhythm. Asystole and pulseless electrical activity are non-shockable.^[5]

PVCs are very common. About 1 to 4% of people have one on a single ECG, but with 24 to 48 hours of monitoring around 50 to 75% of people show them. They become more common with age and with structural heart disease and hypertension.^[8]

Sudden cardiac death is responsible for around 10 to 20% of all deaths in the general population. Out-of-hospital cardiac arrest is estimated at about 300,000 events a year in Europe, and overall survival is under 15%.^[2] A previous myocardial infarction is the commonest cause of the scar that supports sustained monomorphic VT.^[1] Inherited cardiomyopathies and channelopathies (inherited disorders of the heart's ion channels) are also important causes.^[2][3]

The causes fall into four groups, and the same patient often has more than one.

• Ischaemic heart disease and previous infarction. Scar tissue is the commonest substrate for sustained monomorphic VT. Acute ischaemia more often triggers polymorphic VT and VF.^[1][18]
• Cardiomyopathies and structural disease. These include dilated cardiomyopathy, hypertrophic cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC, in which heart muscle is replaced by fat and scar), cardiac sarcoidosis, myocarditis, amyloidosis, and congenital heart disease. Heart failure of any cause adds risk (see Heart failure).^[3]
• Inherited electrical diseases (channelopathies). Long QT syndrome, Brugada syndrome, catecholaminergic polymorphic VT (CPVT) and short QT syndrome cause arrhythmias in a structurally normal heart.^[2] These are covered in their own topics apart from long QT.
• Idiopathic VT. In a heart with no structural disease, the commonest sites are the right and left ventricular outflow tracts. The usual mechanism is triggered activity.^[1]
• Triggers and modifiers. Low potassium and magnesium, hypoxia, volume overload, drugs (QT-prolonging drugs, digoxin, tricyclic antidepressants, stimulants), tobacco and alcohol.^[8][9] Thyroid function is part of the work-up of PVCs.^[8] Caffeine is often blamed, but a study in the Journal of the American Heart Association of 1,388 older adults found no relationship between chronic coffee, tea or chocolate intake and ventricular ectopy.^[8]
• Sodium-channel-blocking antiarrhythmics (Class I). Flecainide and propafenone cause VT and increase mortality in patients with previous myocardial infarction or impaired ventricular function, so they are avoided in those patients.^[4]

An arrhythmia needs a trigger and a substrate. Three mechanisms are described.^[8]

1. Re-entry. An impulse travels around a circuit of tissue instead of dying out. A scar left by an infarct has islands of dead muscle separated by slowly conducting surviving channels. The impulse can go down one channel, return through another, and re-excite tissue that has just recovered, round and round. Scar-related re-entry is the commonest cause of sustained monomorphic VT in structural heart disease, and a previous infarct is the commonest scar.^[1]
2. Triggered activity. Oscillations after the action potential (early or late afterdepolarisations) reach threshold and fire an extra beat. They are provoked by low potassium, ischaemia, high calcium, and drugs such as digoxin and QT-prolonging agents.^[8] This is the usual mechanism for outflow tract VT.^[1]
3. Abnormal automaticity. Cells, often Purkinje fibres, depolarise spontaneously too early. Acute ischaemia, electrolyte disturbance and catecholamine excess promote this.^[8]

VT can degenerate into VF: a fast rhythm reduces filling and coronary perfusion, and the resulting ischaemia makes the circuit unstable and fragments it into chaos.

A PVC is an early beat from the ventricle. This section covers the ECG, patterns, the burden that matters, causes, work-up and treatment.

A PVC is an early, wide QRS (over 120 ms) with no P wave in front of it and a T wave pointing in the opposite direction to the QRS.^[8]

It is usually followed by a compensatory pause. The ventricular beat travels backwards into the AV node and makes it refractory, so the next sinus impulse arrives while the AV node cannot conduct it. The next conducted beat is therefore delayed, and the R-R interval across the PVC is about twice the normal interval.^[8]

The shape of the PVC points to its origin. A PVC with a left bundle branch block pattern and an inferior axis comes from the right ventricular outflow tract (RVOT). A PVC with a right bundle branch block pattern and an inferior axis, with early transition in the chest leads, comes from the left outflow tract. These two sites account for about two thirds of PVCs.^[8] PVCs with several different shapes (multifocal) carry a higher risk of death and major cardiac events.^[8]

• Bigeminy: a PVC after every normal beat. Trigeminy: a PVC after every two normal beats.
• Couplet: two PVCs in a row. Triplet: three in a row. More than three consecutive PVCs counts as VT.^[8]
• Coupling interval: the gap between the normal beat and the PVC. It is fixed if the same each time, variable if it changes.^[8]
• Burden: the percentage of all beats over 24 hours that are PVCs. The 2017 AHA/ACC/HRS definition of "frequent" is more than 30 PVCs per hour, and many studies use more than 20% of all beats.^[8]

Most people have no symptoms and PVCs are found on a routine ECG or pulse check. Symptoms include palpitations (often a thump from the stronger beat after the pause), dizziness, chest discomfort and breathlessness. In patients who already have heart disease, frequent PVCs can cause presyncope or haemodynamic compromise.^[8][1] Breathlessness on exertion, orthopnoea and swelling suggest heart failure from long-standing frequent PVCs.^[8]

A very high burden of PVCs can weaken the left ventricle, probably because abnormal ventricular activation makes the muscle contract out of step. The cardiomyopathy is potentially reversible when the PVCs are removed.^[8]

• The 2022 ESC guideline advises considering PVC-induced cardiomyopathy when there is an unexplained reduced ejection fraction and a PVC burden of 10% or more, and considering cardiac magnetic resonance (CMR) in that situation.^[3]
• Risk is higher with a high burden (one frequently cited study found a burden over 24% separated those who developed cardiomyopathy, with sensitivity 79% and specificity 78%), a very wide QRS (over 140 to 150 ms), an epicardial origin, and PVCs that cause no symptoms and so go unnoticed for years.^[8]
• The burden alone is not a perfect guide: some patients with about 10% PVCs develop cardiomyopathy, and some with about 50% keep a normal ejection fraction.^[8]
• PVC-induced cardiomyopathy is a diagnosis of exclusion, because it is often hard to tell whether frequent PVCs caused the weak ventricle or arose from it.^[8]

Work-up is usually a history, examination, 12-lead ECG, and ambulatory ECG for at least 24 hours (longer, or an event recorder, if symptoms are not captured). A transthoracic echocardiogram is advised in most symptomatic patients to look for structural heart disease. Blood tests include potassium and magnesium, and where relevant thyroid function, troponin, BNP, digoxin level and a drug screen.^[8] Stress testing, coronary imaging or CMR are chosen case by case. The ESC advises CMR for PVCs or VT with a pattern that is not typical of an idiopathic origin, even when the echocardiogram is normal.^[3]

Features that raise concern: heart failure symptoms, a reduced ejection fraction, multifocal or very wide PVCs, runs of VT, exercise-induced PVCs in the recovery phase of a stress test, syncope, or a family history of cardiomyopathy or sudden death.^[8][3]

• Reassure and treat causes. Correct low potassium and magnesium, stop stimulants and offending drugs, check thyroid function and treat any abnormality found, and treat sleep apnoea, ischaemia and heart failure. In patients with no structural heart disease and infrequent PVCs, no drug is needed.^[8]
• Beta-blockers are first-line when treatment is needed, especially for exercise-related PVCs, after infarction and in structural heart disease. Non-dihydropyridine calcium channel blockers (verapamil, diltiazem) are an alternative, particularly for outflow tract PVCs in a structurally normal heart.^[8][3] Verapamil and diltiazem must be avoided in left ventricular dysfunction or heart failure with reduced ejection fraction, hypotension, and pre-excited atrial fibrillation.^[4]
• Flecainide or propafenone are options for symptomatic PVCs in a structurally normal heart, but are contraindicated in coronary disease or heart failure. Amiodarone is reserved for structural heart disease with severe symptoms, often as a bridge to ablation. Sotalol has no mortality benefit and increased death in systolic heart failure.^[8][4]
• Catheter ablation is first-line (ESC class I) for symptomatic idiopathic PVCs or VT from the RVOT or the left fascicles, and for a cardiomyopathy suspected to be caused by frequent, mostly monomorphic PVCs. Beta-blockers, calcium channel blockers or flecainide are alternatives where ablation is unavailable, unwanted or risky.^[3] Ablation may also be considered (class IIb) in asymptomatic patients with a burden over 20%.^[2]
• Frequent PVCs that prevent effective biventricular pacing in heart failure are another indication for ablation or an antiarrhythmic drug.^[3][8]

VT is a regular, wide-complex tachycardia that starts below the AV node. This section covers the presentation, ECG clues and differential diagnosis.

Non-sustained VT is often silent or causes brief palpitations. Sustained VT can cause palpitations, dizziness, shortness of breath, chest pain, low blood pressure, syncope and collapse, and can degenerate into VF.^[1] How badly a patient tolerates VT depends on the rate, the length of the episode, and how weak the ventricle already is. A patient with a normal heart and slow VT may be comfortable for hours, while a patient with a weak ventricle may collapse in minutes.

Examination during VT can support the diagnosis. Cannon A waves in the jugular venous pulse (the atrium contracting against a closed tricuspid valve) and a first heart sound that changes in loudness from beat to beat indicate AV dissociation.^[9]

A wide-complex tachycardia (WCT) has a QRS over 120 ms and a rate over 100 per minute. It has four causes: VT; SVT with aberrant conduction (a bundle branch block, existing or rate-related); SVT with pre-excitation through an accessory pathway; and a ventricular paced rhythm.^[9]

The practical rule is to treat WCT as VT until proven otherwise, for three reasons.

1. VT is far more dangerous than the alternatives.^[10]
2. VT is much more likely in patients over 35 years old, and in anyone with previous myocardial infarction (that history alone had a sensitivity of 97% and specificity of 100% for VT in one study), heart failure or angina.^[9]
3. Drugs aimed at SVT can be harmful in VT. Verapamil and other AV-nodal blockers may be counterproductive and can cause haemodynamic collapse in VT.^[9] The Resuscitation Council UK algorithm advises treating a regular broad-complex tachycardia as VT, and using adenosine only where SVT with aberrant conduction is strongly suspected.^[7]

For wide-complex tachycardia in pre-excited atrial fibrillation (irregular, very fast, with varying QRS width), see Wolff-Parkinson-White syndrome and Atrial fibrillation and atrial flutter. AV-nodal blocking drugs must also be avoided there.^[4][7] See also Supraventricular tachycardias for SVT, and Bundle branch blocks for the baseline conduction patterns that can mimic VT.

No single sign is perfect. Look for as many of these as you can find on the 12-lead ECG.^[9]

QRS shape in V1 and V6 can help. With a right bundle branch block pattern, a triphasic QRS in V1 and an R/S ratio over 1 in V6 favour SVT with aberrancy, while a single tall R in V1 and an R/S ratio under 1 in V6 favour VT. With a left bundle branch block pattern, a narrow initial R wave in V1 with a sharp downstroke favours SVT, while notching of the S downstroke or a long interval from QRS onset to the S nadir (over 60 ms) favours VT.^[9]

Two stepwise algorithms are widely taught. They add up several clues in a fixed order.

• Brugada algorithm. It works through the chest leads in order: no RS complex in any chest lead (VT); otherwise, an interval from the start of the R wave to the lowest point of the S wave of more than 100 ms in any chest lead (VT); then AV dissociation (VT); then QRS shape criteria in V1-V2 and V6 (VT). If none is met, the rhythm is called SVT with aberrancy. The original paper reported 99% sensitivity and 96.5% specificity, but other studies did not reproduce these figures.^[9]
• Vereckei aVR algorithm. It uses a single lead, aVR: an initial R wave, an initial R or Q wave over 40 ms, a notch on the downslope of a negative QRS, and the ratio of the speed of the first to the last 40 ms of the QRS (Vi/Vt). A ratio of 1 or less suggests VT.^[9]

A 2023 meta-analysis of 14 studies with 3,966 patients found that the algorithms are good at not missing VT and only moderately good at excluding it: pooled sensitivity was 90% for Brugada and 90% for Vereckei aVR, with pooled specificity of 64% and 61%.^[10]

The consequence is practical. An algorithm that points to SVT does not make it safe to give AV-nodal drugs, and an algorithm that is uncertain should be treated as VT.

The doses in this flowchart come from the Resuscitation Council UK tachyarrhythmia algorithm.^[7][5]

• Idiopathic outflow tract VT. In a structurally normal heart, repeated bursts of non-sustained monomorphic VT and frequent PVCs of the same shape, usually from the RVOT (left bundle branch block pattern, inferior axis). Adrenergic forms increase with exercise or mental stress. Adenosine is often advised to stop it.^[1][4]
• Fascicular VT. A VT arising in the left fascicles, with a relatively narrow QRS (under 140 ms) that can be mistaken for SVT with aberrancy.^[9] Verapamil is often advised to stop it.^[4]
• Warning that apparently idiopathic VT may have a structural cause: poor tolerance, sustained VT, a tachycardia cycle length under 250 ms, a QRS over 140 ms, several VT shapes, an abnormal resting ECG, an abnormal echocardiogram, or no response to adenosine.^[4]

VF is the commonest shockable rhythm. The patient is unresponsive and not breathing normally, with no pulse. VF is mainly fatal through a delay to defibrillation: every minute without a shock lowers the chance of survival.

The ESC guideline recommends public access defibrillators and community basic life support training.^[2] Hospitals should aim to defibrillate shockable rhythms in under 3 minutes.^[6]

Both the Resuscitation Council UK (2025, based on the European Resuscitation Council guidelines) and the American Heart Association (2025) use the same logic: confirm arrest, start CPR, attach the defibrillator, check the rhythm, shock if shockable, then two minutes of CPR before the next rhythm check.^[5][6]

The energies, drugs and timings in this flowchart are from the 2025 Resuscitation Council UK and AHA sources.^[6][5]

Points to note from the guidelines:

• Single shocks, not stacked. Give one shock then two minutes of CPR. Up to three stacked shocks may be considered only when VF/pVT begins during a monitored arrest with a defibrillator at hand, such as in a catheter laboratory.^[6]
• Pad position. The lateral pad must sit below the armpit in the mid-axillary line. Switch to an anterior-posterior position if VF persists after three shocks.^[6]
• Adrenaline timing differs by rhythm. Give it as soon as possible in a non-shockable rhythm, but only after the third shock in a shockable one.^[6] In the AHA chart, epinephrine appears in the cycle after the second shock and amiodarone or lidocaine after the third.^[5]
• Calcium, sodium bicarbonate and corticosteroids are not given routinely in cardiac arrest.^[6]
• Waveform capnography guides CPR quality; if end-tidal carbon dioxide is low or falling, reassess compressions.^[5]

Look for and treat these from the first minute.^[5][7]

• The Hs: hypoxia; hypovolaemia; hypo- or hyperkalaemia and other metabolic causes (calcium, magnesium, glucose); hypothermia or hyperthermia. The AHA list also names hydrogen ion excess (acidosis).
• The Ts: thrombosis (coronary or pulmonary); tension pneumothorax; tamponade (cardiac); toxins.

Point-of-care ultrasound can help find tamponade and pneumothorax, but it should not be used to judge whether the heart is contracting.^[6]

Torsades de pointes is a polymorphic VT that occurs when ventricular repolarisation is delayed. The ECG in sinus rhythm shows a prolonged QT interval, and the VT shows QRS complexes that twist around the baseline, rising and falling in amplitude. It comes in bursts that usually stop by themselves, causing dizziness, syncope and sometimes seizures, but it can degenerate into VF and sudden death.^[11]

Causes. In acquired long QT, the main causes are drugs that block the IKr potassium channel, low potassium, low magnesium and low calcium, slow heart rates and pauses, and heart disease. Risk factors include female sex, older age, alcoholic liver disease, recent cardioversion of atrial fibrillation, left ventricular hypertrophy, digoxin or diuretic use, and a QT-prolonging drug given at a high dose or rapidly intravenously.^[11] Premature beats followed by compensatory pauses can set off torsades.^[11] Congenital long QT syndrome is covered in Long QT syndrome. Torsades is unusual if the corrected QT is under 500 ms.^[11]

Treatment.

1. Defibrillate if torsades is sustained and the patient is unstable or pulseless, as for VF.^[11]
2. Intravenous magnesium sulphate is the immediate first-line treatment, even if the serum magnesium is normal. A typical adult dose is 1 to 2 g given over about 5 minutes (2 g is usual, which equals 8 mmol), with a maintenance infusion of 0.5 to 1 g per hour in the 2025 European compendium; the Resuscitation Council UK algorithm gives 8 mmol over 10 minutes. There is no randomised trial, and published infusion rates vary, so follow local protocol and check the formulary.^[4][7][11]
3. Correct potassium to the high-normal range. Sources suggest 4.5 to 5.0 mmol per litre.^[11]
4. Stop QT-prolonging drugs and correct hypoxia and other electrolytes.^[11]
5. Raise the heart rate if torsades keeps coming back, with isoprenaline (isoproterenol) or transvenous pacing, because faster rates shorten repolarisation. The choice of treatment differs in congenital long QT syndrome (see Long QT syndrome).^[11]
6. Avoid amiodarone and other drugs that prolong repolarisation (class Ia and class III agents), which can make torsades worse.^[7][11]

The principles are: decide at once whether the patient is stable; document the rhythm on a 12-lead ECG whenever possible; give treatment appropriate to the type of VT; and look for the cause.

Unstable means any of: shock, syncope with severe hypotension, myocardial ischaemia, severe heart failure with pulmonary oedema (Resuscitation Council UK), or hypotension, altered mental state, signs of shock, ischaemic chest discomfort or acute heart failure (AHA).^[7][5]

• Synchronised cardioversion. The shock is timed to the R wave so it does not land on the T wave and cause VF. Sedate or anaesthetise a conscious patient if feasible, but do not delay the shock. For VT with a pulse the Resuscitation Council UK advises a first shock of 120 to 150 J, then increasing energy if it fails.^[6][7] 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.^[19][5]
• If shocks fail: 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.^[7]
• If the patient becomes pulseless, switch to the cardiac arrest algorithm above with unsynchronised shocks.

When the patient is stable, a few minutes are available to record a 12-lead ECG and give a drug. Document the cycle length, QRS shape and QT interval, and keep a defibrillator close.^[4]

The European compendium (2025) states that for acute termination of stable monomorphic VT of unknown cause, procainamide or amiodarone may be used, with a preference for procainamide, which led to a shorter time to conversion and fewer major cardiac adverse events in the PROCAMIO trial. If the patient has severe heart failure, acute myocardial infarction or end-stage kidney disease, amiodarone is the drug of choice. Intravenous lidocaine is only moderately effective and is kept for recurrent stable VT that does not respond to beta-blockers or amiodarone, or when amiodarone cannot be used. Ajmaline, sotalol and flecainide are not advised if there may be structural heart disease.^[4]

Special cases:

• Idiopathic outflow tract VT is often stopped by adenosine; fascicular VT by verapamil. Verapamil should be used with caution because it depresses contraction and lowers blood pressure, especially if structural heart disease has not been excluded.^[4]
• Incessant slow VT while taking an antiarrhythmic drug may need catheter ablation, usually continuing the drug.^[4]
• Polymorphic VT with ischaemia is treated by relieving the ischaemia with coronary intervention; intravenous beta-blockers and amiodarone are the preferred drugs, and lidocaine may be added.^[4]
• Heart failure. In acute heart failure, class III drugs other than amiodarone (sotalol, dronedarone) and non-dihydropyridine calcium channel blockers are contraindicated. PVCs and non-sustained arrhythmias are common in chronic heart failure and, with a severely reduced ejection fraction, carry a higher risk of sudden cardiac death.^[18]

Electrical storm is three or more separate sustained ventricular arrhythmias within 24 hours, each needing termination by pacing, shock or defibrillation. It affects 10 to 25% of people with an ICD, and mortality in the first 48 hours can be as high as 14%.^[17][2] It adds severe distress as well as risk.

The 2022 ESC guideline gives the storm its own chapter.^[2]

• Address precipitants: ischaemia, electrolytes, drugs, heart failure decompensation.
• In structural heart disease with monomorphic VT, amiodarone and non-selective beta-blockers are first-line (class I), together with mild to moderate sedation to reduce sympathetic drive. Propranolol combined with intravenous amiodarone has been superior to metoprolol with amiodarone in a trial in ICD patients.^[2][4]
• Interrogate and reprogramme the ICD (shocks that are inappropriate, or that continue unnecessarily, can fuel the storm).^[18]
• Catheter ablation in an experienced centre is preferred to deep sedation, autonomic modulation or mechanical circulatory support in recurrent storm. Cardiac sympathetic neuromodulation (such as stellate ganglion block) is used for refractory cases.^[2][17]
• Polymorphic storm: look for ischaemia and QT prolongation. Post-infarct storms triggered by short-coupled PVCs from Purkinje fibres respond to quinidine and resist beta-blockers, lidocaine and amiodarone.^[4]
• Refer early to a specialist centre if the storm continues.^[2]

Finding the substrate decides the long-term plan. The 2022 ESC guideline structures work-up around typical first presentations: incidental NSVT, first sustained monomorphic VT, aborted sudden cardiac arrest, and relatives of someone who died suddenly.^[2]

• Resting 12-lead ECG between episodes, looking for Q waves, bundle branch block, long or short QT, Brugada pattern, epsilon waves.
• Blood tests: potassium, magnesium, calcium, thyroid function, troponin, and a drug screen when relevant.^[8]
• Echocardiography for ventricular size and function, valves, and wall motion. The ejection fraction is the main prognostic variable for ventricular arrhythmias.^[1]
• Coronary evaluation (angiography or non-invasive imaging) whenever ischaemia is possible; polymorphic VT and VF in particular may be ischaemic.^[4]
• Cardiac magnetic resonance (CMR) with late gadolinium enhancement shows scar and inflammation. It is recommended in all survivors of sudden cardiac arrest without a clear cause (class I) and in suspected ARVC and hypertrophic cardiomyopathy.^[2][3]
• Genetic counselling and testing are recommended in survivors with a suspected inherited condition: ARVC, hypertrophic cardiomyopathy, clinically diagnosed long QT syndrome, Brugada syndrome, CPVT, short QT syndrome, and dilated cardiomyopathy with conduction disease or a family history. Blood should be saved after an aborted sudden cardiac arrest, and relatives tested when a pathogenic variant is found.^[2]
• Electrophysiology study with programmed stimulation helps risk stratification in selected patients, for example those with a previous infarct and unexplained syncope (class I in the ESC), or, in coronary disease with an ejection fraction of 40% or less and NSVT, to show whether VT is inducible and an ICD should be considered.^[2][3]

No antiarrhythmic drug other than beta-blockers has been shown to reduce all-cause mortality. Drugs mainly lower the number of arrhythmic episodes and ICD shocks.^[2]

• Beta-blockers are the backbone, and the ESC prefers the non-selective nadolol or propranolol in long QT syndrome and CPVT.^[2]
• Amiodarone plus a beta-blocker prevents ICD shocks better than sotalol, at the cost of more drug-related adverse effects. Sotalol is an alternative that needs monitoring of QT, potassium and kidney function.^[4]
• Class I sodium-channel blockers (flecainide, propafenone) are contraindicated with significant structural disease or previous infarction, because of excess mortality in the CAST trial.^[2][4]
• Mexiletine is used as add-on therapy for recurrent VT, and for long QT type 3.^[4][2]

An implantable cardioverter-defibrillator senses VT or VF and treats it with pacing or shocks. Secondary prevention means an ICD for people who have already survived a life-threatening arrhythmia that is not due to a reversible cause and did not occur within 48 hours of a myocardial infarction, provided they have a good functional status and a life expectancy of more than a year.^[12]

In a patient-level analysis of three trials comparing an ICD with amiodarone after VF or sustained VT, all-cause mortality was 28% lower and arrhythmic mortality 50% lower with the ICD. Patients with an ejection fraction of 35% or less gained the most.^[12]

ESC 2022 adds detail:^[3][2]

• In coronary disease with recurrent symptomatic sustained monomorphic VT, or ICD shocks on chronic amiodarone, catheter ablation is recommended in preference to escalating antiarrhythmic drugs.
• In coronary disease with well-tolerated sustained monomorphic VT and a preserved or mildly reduced ejection fraction (40% or more), catheter ablation can be considered as an alternative to an ICD if the ablation endpoints are met. Trials on this question are lacking.^[3][2]
• In survivors with coronary artery spasm, an ICD should be considered.

The standard criterion is symptomatic heart failure (NYHA class II to III) with an ejection fraction of 35% or less despite optimal medical therapy, with a life expectancy of more than a year and good functional status.^[12] The 2022 ESC guideline added further points.^[2][3]

• In dilated cardiomyopathy, the ESC downgraded the ejection fraction criterion from class I to class IIa after the DANISH trial, and now also considers an ICD when the ejection fraction is 35 to 50% and at least two other risk factors are present (unexplained syncope, scar on CMR, inducible monomorphic VT, or pathogenic variants in LMNA, PLN, FLNC or RBM20).^[2]
• In coronary disease, an ICD should be considered (class IIa) with NYHA class I and an ejection fraction of 30% or less despite at least three months of optimal medical therapy, and also with an ejection fraction of 40% or less, non-sustained VT and inducible VT at electrophysiology study.^[3]
• In ARVC, an ICD should be considered (class IIa) when the diagnosis is definite and symptoms are present, ventricular function is moderately reduced on either side, and there is either non-sustained VT or sustained monomorphic VT that can be induced at electrophysiology study.^[3]
• In inherited conditions, risk calculators (hypertrophic cardiomyopathy, laminopathy, long QT) guide primary prevention.^[2]

Radiofrequency ablation destroys the focus or the critical channel in the circuit. Indications in the 2022 ESC guideline are summarised above for PVCs, idiopathic VT (class I for outflow tract and fascicular sites), and VT with coronary disease. In dilated cardiomyopathy it is considered (class IIa) for drug-refractory recurrent symptomatic monomorphic VT, though results are less good than after infarction. In Brugada syndrome with recurrent shocks it can target VF-triggering PVCs and the epicardial right ventricular outflow substrate (class IIa).^[2] Ablation in low-volume centres has carried higher mortality.^[1]

VF and polymorphic VT in the first hours of an infarct arise from acute ischaemia and are treated with rapid defibrillation and reperfusion by coronary intervention. A VF episode within 48 hours of an infarct does not usually count as an ICD indication for secondary prevention, because the substrate is acute and may not recur.^[12] Correct potassium and magnesium; one study found the lowest rate of ventricular arrhythmia in infarct patients with potassium between 3.5 and 4.5 mmol per litre.^[8] Prophylactic lidocaine to prevent VF was abandoned after later studies reported higher mortality.^[4]

Ventricular arrhythmias are both a complication and a cause of heart failure (see the VT management section). Optimal heart failure therapy (see Heart failure) lowers arrhythmic risk; ICDs and cardiac resynchronisation add to it in selected patients.^[12]

If the mother is unstable, electrical cardioversion is the treatment of choice for any arrhythmia, and evidence from case reports supports its safety.^[14] Antiarrhythmic drugs are best avoided in the first trimester because of teratogenic risk; beta-blockers are preferred in pregnancy, while amiodarone and dronedarone are avoided because of the risk of fetal harm.^[4] Catheter ablation during pregnancy has been done safely with a specialised team.^[14] Any pregnant woman with a ventricular arrhythmia needs a multidisciplinary team, because an underlying cardiomyopathy or channelopathy may be present.

PVCs are common in children: Holter studies find them in up to 41% of children, usually in a normal heart. In asymptomatic children with a structurally normal heart, one study found no correlation between PVC burden and left ventricular function, unlike adults. PVCs are more common with congenital heart disease, such as tetralogy of Fallot. Catheter ablation is used for symptomatic, frequent or haemodynamically significant PVCs that do not respond to medicines.^[16] Sustained ventricular arrhythmias in congenital heart disease should prompt a search for residual lesions or new structural abnormalities.^[3]

Rules differ between countries and each patient's circumstances; check the local regulator. In the UK, the DVLA applies the following to ordinary (Group 1) car and motorcycle drivers.^[13]

• A ventricular arrhythmia leading to an ICD recommendation: a 6-month break from driving. For an ICD implanted for sustained ventricular arrhythmia, driving may resume 6 months after implantation, and 6 months after any appropriate shock or pacing therapy. The DVLA must be notified.
• A prophylactic (primary prevention) ICD: no driving for one month after implantation, DVLA notified; the secondary-prevention rules apply if the device later delivers therapy.
• After successful VT ablation in a patient with impaired ventricular function or congenital heart disease: no driving for at least 4 weeks, with no need to notify the DVLA.
• Vocational (Group 2, lorry and bus) licences: permanently refused or revoked with an ICD; after VT ablation relicensing needs arrhythmia control for at least 3 months and an ejection fraction of at least 40%.^[13]

For sport, ICDs were once viewed as barring vigorous or competitive sport; contemporary registry data are reassuring that selected athletes can take part without the catastrophic outcomes once feared, but the data are not definitive. The ICD protects against arrhythmia but not against the underlying disease, so decisions on return to sport are individual and shared with the athlete.^[15]

Prognosis depends on the heart, not just the rhythm. Isolated PVCs in a normal heart are benign, though a single PVC on a resting ECG was associated with more than a twofold increase in death from coronary disease and sudden cardiac death in one large cohort, which is why they prompt a look for undiagnosed disease.^[8] VT with a low ejection fraction carries a high risk of recurrence and death; an ICD lowers this risk. Out-of-hospital cardiac arrest survival remains under 15% overall.^[2] The ejection fraction and the extent of scar on CMR predict ventricular arrhythmias.^[1] Electrical storm carries a substantial early mortality.^[17]

• Electrocardiogram (ECG) interpretation: the basics of reading a rhythm and measuring QRS and QT.
• Long QT syndrome: congenital and acquired long QT, the setting for torsades de pointes.
• Approach to tachyarrhythmias: the overall approach to a fast rhythm.
• Supraventricular tachycardias and Wolff-Parkinson-White syndrome: the other causes of tachycardia, and pre-excitation that can mimic VT.
• Bundle branch blocks: baseline conduction patterns that can look like VT.
• Heart failure: the commonest setting for ICD decisions.
• Atrial fibrillation and atrial flutter: the commonest sustained arrhythmia, and the usual cause of an irregular fast rhythm that can be mistaken for VT.
• Bradyarrhythmias and atrioventricular block: slow rhythms, including those that predispose to torsades de pointes.