Ventricular arrhythmias

01OverviewDefinition, clinical context and the essential points that orientate the chapter.

Ventricular arrhythmias range from incidental PVCs to sudden cardiac arrest. The first branch is pulse and stability; detailed morphology matters only after immediate threats are addressed.

RCUK 2025/2026 supplies the UK arrest and peri-arrest doses. ESC 2022 supplies the broader diagnostic, inherited-disease, ICD and ablation framework where NICE has no comprehensive ventricular-arrhythmia guideline.

Do not turn the antiarrhythmic list into a rigid ladder. Electrical treatment, procainamide, amiodarone, magnesium, lidocaine, pacing and ablation apply to different mechanisms and haemodynamic contexts.

Key points

A ventricular ectopic is a premature broad QRS without a normal preceding P wave; frequent/complex ectopy is a clue, not by itself an indication for suppression.
NSVT is at least three ventricular beats ending spontaneously within 30 seconds; sustained VT lasts at least 30 seconds or requires earlier termination because of instability.
Monomorphic VT has a stable QRS morphology; polymorphic VT varies beat to beat; torsades is polymorphic VT in the setting of QT prolongation.
Treat an uncertain regular broad-complex tachycardia as VT, especially in structural heart disease or prior MI.
Pulseless VT and VF are shockable cardiac-arrest rhythms; synchronised cardioversion is for VT with a pulse.
RCUK first manual biphasic defibrillation shock is at least 150 J (130-150 J for pulsed biphasic); if the recommended device setting is unknown, use the highest adult setting.
After three total shocks in VF/pVT give adrenaline 1 mg and amiodarone 300 mg; repeat adrenaline every 3-5 minutes and give amiodarone 150 mg after five total shocks.
Stable monomorphic VT is not automatically a drug-only case: RCUK recommends electrical cardioversion with structural heart disease or uncertain myocardial damage; drugs are conditional when sedation/anaesthesia risk is high.
Long-QT polymorphic VT: magnesium 8 mmol IV over 10 minutes, stop QT-prolonging drugs, correct electrolytes and consider overdrive with isoprenaline or temporary pacing; avoid amiodarone.
After stabilisation, investigate substrate—acute ischaemia, cardiomyopathy/scar, inflammation, inherited channelopathy, drug/toxin, electrolytes—and consider ICD/ablation according to cause and recurrence risk.

02AetiologyUnderlying causes, associations and risk factors, with why each one matters.

Ischaemia and infarct scar

Acute myocardial ischaemia creates electrical heterogeneity, while healed infarction leaves fibrotic channels capable of re-entry. Prior myocardial infarction therefore strongly raises concern in broad-complex tachycardia.

Structural myocardial disease

Dilated, hypertrophic or arrhythmogenic cardiomyopathy, myocarditis and repaired congenital heart disease create fibrosis, chamber stress or surgical scar that can sustain ventricular re-entry.

Reversible electrical triggers

Hypokalaemia, hypomagnesaemia, bradycardia, acute illness and QT-prolonging medicines disturb repolarisation. Alone or in combination, they can provoke polymorphic ventricular tachycardia, including torsades.

Inherited arrhythmic disease

Channelopathies and inherited cardiomyopathies may cause ventricular arrhythmia despite little obvious structural disease. Exertional syncope, characteristic ECG patterns or familial sudden death increase suspicion.

03PathophysiologyThe causal sequence from the underlying abnormality to symptoms and harm.

1
Vulnerable substrate
Scar, abnormal ion-channel function or acutely ischaemic myocardium creates regions with differing conduction speed and refractory periods within the ventricles.
2
Triggered ventricular beat
A premature ventricular impulse or sudden cycle-length change may initiate re-entry in vulnerable tissue; afterdepolarisations or abnormal automaticity can provide alternative triggers.
3
Organised tachycardia pattern
A fixed scar circuit often produces monomorphic ventricular tachycardia, whereas changing activation fronts can produce polymorphic tachycardia; prolonged repolarisation permits the twisting pattern of torsades.
4
Haemodynamic deterioration
Rapid uncoordinated ventricular activation shortens filling and weakens contraction. Cardiac output falls further when ventricular function is impaired or atrioventricular synchrony is lost.
5
Ventricular fibrillation
Disorganised activation can replace coordinated ventricular depolarisation, producing ventricular fibrillation with no effective stroke volume and immediate circulatory arrest.

04Clinical features and red flagsSymptoms, examination findings, patterns of presentation and time-critical warnings.

Monomorphic VTRed flag

Regular broad-complex tachycardia with a consistent QRS shape, usually from a fixed re-entry circuit in scar or cardiomyopathy. AV dissociation, capture/fusion beats and concordance support VT, but absence does not exclude it.

Torsades de pointesRed flag

Polymorphic VT with QRS complexes appearing to twist around the baseline in a patient with prolonged QT, often pause-dependent and triggered by drugs, bradycardia, hypokalaemia or hypomagnesaemia.

VF or pulseless VTRed flag

Unresponsive patient with abnormal/absent breathing and no signs of circulation; VF is chaotic without organised QRS and pVT is an organised ventricular tachycardia without a pulse. Both require immediate defibrillation/CPR.

Life-threatening VT with a pulseRed flag

Shock, syncope with severe/ongoing hypotension, myocardial ischaemia, severe heart failure/pulmonary oedema, or immediately post-ROSC.

High-risk ectopy/NSVT

Syncope, exertional episodes, family sudden death, structural disease, reduced EF, long/short QT, Brugada pattern, exercise-triggered bidirectional/polymorphic VT or a high PVC burden with LV dysfunction requires specialist evaluation.

05InvestigationsWhat to request, why it matters and how to interpret it.

Investigation order

Read from the initial assessment onwards. Tests may run in parallel in urgent care; first-line, preferred, confirmatory, definitive and gold-standard labels appear only when the chapter explicitly states them.

01
Immediate ABCDE, pulse check, continuous ECG/BP/SpO2, defibrillator pads and 12-lead if a pulse is presentFirst step
Why
Separate arrest from peri-arrest VT and capture diagnostic morphology without delaying shock.
Interpretation and limitations
If unresponsive with abnormal breathing, assume arrest. In a perfusing patient, classify stability before pursuing fine ECG distinctions.
02
Electrolytes including potassium, magnesium and calcium; renal function, glucose and blood gas
Why
Identify immediately correctable metabolic drivers and guide magnesium/drug safety.
Interpretation and limitations
Long-QT polymorphic VT with low potassium or magnesium supports torsades; give the RCUK magnesium regimen and correct electrolytes urgently with continuous ECG and serial biochemical monitoring.
03
Medication/toxin review and targeted levels
Why
Find QT-prolonging drugs, digoxin, sodium-channel blockers, stimulants and overdose.
Interpretation and limitations
Mechanism changes treatment: amiodarone can worsen torsades; sodium bicarbonate rather than routine antiarrhythmics may be required in sodium-channel-blocker poisoning.
04
Serial 12-lead ECGs and cardiac troponin when ischaemia is suspected
Why
Identify acute coronary occlusion/ischaemia and baseline QT, Brugada, conduction or scar patterns.
Interpretation and limitations
Do not wait for troponin before activating a clear reperfusion pathway; tachycardia/defibrillation can themselves raise troponin.
05
Echocardiography
Why
Assess EF, regional wall motion, valves and cardiomyopathy.
Interpretation and limitations
Structural disease strongly raises VT probability and informs cardioversion, ICD and heart-failure decisions.
06
Coronary angiography or coronary imaging when clinically indicated
Why
Find and treat an ischaemic substrate, especially after arrest, ongoing ischaemia or new LV dysfunction.
Interpretation and limitations
Revascularisation treats ischaemia but does not automatically remove recurrent scar-VT risk; reassess after recovery.
07
CMR, ambulatory monitoring, exercise testing, device interrogation and genetic/family assessment
Why
Define scar/inflammation, quantify PVC/NSVT burden, expose exercise-triggered disease, review ICD therapy and identify inherited syndromes.
Interpretation and limitations
Choose tests by phenotype and timing; inherited-disease evaluation should use a specialist service with family counselling.

06Differential diagnosisRealistic alternatives and the features that help distinguish them.

SVT with aberrancy

A supraventricular rhythm conducted through bundle-branch block can be broad. A securely documented identical baseline pattern supports aberrancy, but diagnostic uncertainty should remain ventricular-tachycardia safe.

Pre-excited atrial fibrillation

An irregular broad rhythm with beat-to-beat changes in QRS shape and very short intervals suggests atrial fibrillation using an accessory pathway, not monomorphic VT.

Torsades de pointes

This is polymorphic ventricular tachycardia occurring with QT prolongation, often after a pause. Establishing the preceding QT distinguishes its mechanism from polymorphic VT with normal repolarisation.

ECG artefact

Movement or poor electrode contact can simulate broad chaotic activity. A conscious patient with a stable pulse and undisturbed QRS complexes in another lead supports artefact, but clinical assessment must not delay treatment of genuine instability.

Ventricular paced rhythm

Pacing produces broad QRS complexes that may resemble ventricular ectopy or tachycardia. Visible pacing stimuli, a consistent programmed rate and device interrogation clarify the source.

07ManagementImmediate care, first-line treatment, alternatives and escalation.

01Cardiac arrestVF or pulseless VTFirst stepUnresponsive, abnormal breathing and shockable rhythm with no pulse/signs of circulation.

1Start high-quality CPR, call the arrest team and defibrillate as soon as possible. Use one shock followed immediately by two minutes of CPR.
2EscalationManual biphasic first shock: at least 150 J (130-150 J for pulsed biphasic); escalate subsequent shocks when possible. If device recommendations are unknown, use the highest adult energy setting.
3After the third total shock, during CPR give adrenaline 1 mg IV/IO and amiodarone 300 mg IV/IO. Repeat adrenaline 1 mg every 3-5 minutes.
4AlternativeAfter the fifth total shock give amiodarone 150 mg IV/IO. If amiodarone is unavailable or the resuscitation service has selected the RCUK-supported lidocaine alternative, give lidocaine 100 mg after three shocks and an additional 50 mg after five shocks; do not routinely combine the two.
5Treat reversible causes: hypoxia, hypovolaemia, hypo/hyperkalaemia and other metabolic disorders, hypothermia, thrombosis, tamponade, tension pneumothorax and toxins.
6EscalationFor refractory VF after three consecutive shocks, ensure correct pad placement, escalate energy and consider vector change to antero-posterior pads; RCUK does not recommend routine double-sequential defibrillation.

02Unstable with pulseVT causing life-threatening featuresPulse present with shock, syncope/severe hypotension, ischaemia, pulmonary oedema/severe heart failure or immediately post-ROSC.

1Call expert/resuscitation help, attach pads, obtain IV access and treat reversible causes; sedate/anaesthetise conscious patients if feasible without dangerous delay.
2Use synchronised cardioversion for monomorphic VT with a pulse: RCUK initial 120-150 J, then stepwise increases, up to three attempts.
3If cardioversion fails and instability persists, give procainamide 10-15 mg/kg IV (maximum 1 g) over 20 minutes OR amiodarone 300 mg IV over 10-20 minutes according to availability/contraindications, then reattempt synchronised cardioversion.
4Polymorphic VT cannot be reliably synchronised; if unstable or pulseless, deliver an unsynchronised defibrillation shock and follow ALS.

03Stable monomorphic VTElectrical versus pharmacological treatment is conditionalSustained regular broad monomorphic VT with a pulse and no life-threatening feature.

1Treat as VT and seek expert help. RCUK recommends electrical cardioversion when structural heart disease exists or myocardial damage is uncertain.
2If sedation/anaesthesia creates increased risk, consider procainamide 10-15 mg/kg IV over 20 minutes (maximum 1 g) with continuous ECG/BP.
3If procainamide is unavailable or contraindicated, use amiodarone 300 mg IV over 10-60 minutes, followed by 900 mg IV over 24 hours.
4If drug treatment fails, use synchronised cardioversion with expert advice. Investigate ischaemia and structural substrate even after apparently successful termination.

04TorsadesPolymorphic VT with QT prolongationPolymorphic VT in a prolonged-QT context, with a pulse or recurrent self-termination.

1If pulseless/unstable, defibrillate and follow ALS; do not wait for magnesium.
2Give magnesium 8 mmol (approximately 2 g magnesium sulfate) IV over 10 minutes.
3Stop QT-prolonging drugs, correct potassium/magnesium/calcium and treat bradycardia/pause dependence.
4With expert help consider isoprenaline infusion or temporary overdrive pacing to increase heart rate in acquired long-QT torsades; avoid amiodarone because it can prolong QT further.
5Congenital long-QT torsades needs specialist genotype/phenotype-directed management; isoprenaline may be inappropriate in congenital disease.

05Secondary preventionFind substrate and prevent recurrenceAfter sustained VT/VF, arrest survival, recurrent ICD therapy or high-risk NSVT/PVCs.

1Correct reversible causes and complete coronary, structural and inherited-disease assessment.
2Discuss ICD for survivors of VT/VF arrest or sustained VT when no completely reversible cause accounts for the event and expected benefit is meaningful; exact indication depends on substrate, EF, timing and goals of care.
3Use catheter ablation for recurrent monomorphic VT/ICD shocks or selected idiopathic VT according to specialist assessment; it is not simply the 'third drug'.
4For electrical storm, use an ICU/electrophysiology pathway: device interrogation/reprogramming, deep analgesia/sedation when needed, correction of triggers, appropriate antiarrhythmic plus sympathetic control, and urgent ablation consideration.

Key medicines and prescribing safety6 treatments · regimens, roles and cautions

Vasopressor during VF/pulseless VT arrest; not treatment for stable VT with a pulse.

Adrenaline in shockable cardiac arrest

1 mg IV/IO after the third total shock, then 1 mg every 3-5 minutes while ALS continues.

Give during CPR without delaying shocks/compressions; confirm route and flush per arrest practice. Post-ROSC bolus dosing is different and requires titration.

Antiarrhythmic for refractory or recurrent shockable cardiac arrest.

Amiodarone in VF/pulseless VT

300 mg IV/IO after the third total shock; a further 150 mg after the fifth total shock.

Use the arrest dose only in cardiac arrest. Do not substitute the slower perfusing-VT infusion regimen. Avoid for torsades/long-QT polymorphic VT.

RCUK-supported alternative when amiodarone is unavailable or the resuscitation service has selected lidocaine.

Lidocaine in VF/pulseless VT

100 mg IV/IO after three shocks, plus 50 mg after five shocks.

Alternative rather than routine add-on to amiodarone; reduce/monitor carefully in severe hepatic impairment, low cardiac output and toxicity.

Conditional drug option when sedation/anaesthesia risk makes immediate cardioversion less attractive; also RCUK rescue after failed shocks.

Procainamide in perfusing monomorphic VT

10-15 mg/kg IV over 20 minutes, maximum 1 g.

UK product availability varies. Use continuous ECG/BP monitoring; avoid or stop with marked hypotension, QRS widening, long QT or decompensated heart failure, and verify the available preparation before administration.

Conditional alternative/rescue for monomorphic VT.

Amiodarone in perfusing VT

Stable VT when procainamide is unavailable/contraindicated: 300 mg IV over 10-60 minutes, then 900 mg IV over 24 hours. Persistent unstable rhythm after failed shocks: 300 mg IV over 10-20 minutes before repeat cardioversion.

Continuous ECG/BP; hypotension, bradycardia, AV block and QT prolongation. Avoid in torsades; long-term use needs thyroid/liver/lung/eye monitoring and interaction review.

First drug for polymorphic VT with QT prolongation while correcting cause; shock first if unstable/pulseless.

Magnesium sulfate for torsades

8 mmol magnesium (approximately 2 g magnesium sulfate) IV over 10 minutes.

Monitor BP, respiratory status and reflexes with repeated/high doses; renal failure increases toxicity. Magnesium does not replace defibrillation in arrest.

08ComplicationsImportant consequences, why they occur and why they matter clinically.

Syncope and traumatic injury

Abrupt loss of cardiac output reduces cerebral perfusion, causing presyncope or syncope. Unheralded collapse adds substantial risk of head injury, driving incidents or occupational harm.

Cardiogenic shock

Sustained rapid activation can markedly reduce forward flow, producing hypotension, myocardial ischaemia, pulmonary oedema and multiorgan hypoperfusion even while a pulse remains palpable.

Ventricular fibrillation and sudden death

Ventricular tachycardia may destabilise into fibrillation, abolishing effective circulation. Without prompt defibrillation and resuscitation, irreversible neurological injury or death can follow rapidly.

Arrhythmia-induced cardiomyopathy

Frequent ventricular ectopy or recurrent sustained tachycardia can depress left-ventricular function through dyssynchrony and persistent rate stress, potentially improving when the arrhythmia burden falls.

Electrical storm

Clusters of recurrent ventricular tachycardia or fibrillation cause repeated haemodynamic insults and device therapies, indicating an unstable substrate that requires urgent specialist management.

09Monitoring and follow-upTreatment response, safety checks and longer-term review.

During any sustained VA: continuous ECG, BP, SpO2, defibrillator pads and frequent perfusion/mental-state reassessment.
During CPR: two-minute cycles, minimise peri-shock pauses, waveform capnography when an advanced airway is present, and rhythm/drug timing documentation.
After ROSC/termination: serial ECG including QT, potassium/magnesium/calcium, renal function, glucose, troponin when appropriate and temperature/oxygen/ventilation management.
Procainamide: QRS, QT and BP throughout infusion; amiodarone: BP, rate, conduction and QT; magnesium: BP/respiration and renal context.
Long term: EF/structural reassessment, ambulatory PVC/NSVT burden when relevant, ICD interrogation and shock review, and specialist family screening for suspected inherited disease.

10Special situationsVariants, exceptions and circumstances that change the usual approach.

Shock type follows pulse and morphology

Pulseless VT/VF and unstable polymorphic VT need unsynchronised defibrillation; monomorphic VT with a pulse is synchronised to avoid an R-on-T shock.

Stable does not mean benign

A patient can perfuse during sustained VT and still deteriorate abruptly. Pads, expert help and a pre-agreed cardioversion plan should accompany any drug trial.

Torsades is a mechanism-specific exception

Amiodarone is useful for many ventricular arrhythmias but can worsen long-QT torsades. Magnesium, electrolyte correction and faster pacing/chronotropy are the relevant branch.

PVC treatment starts with phenotype

Symptoms, burden, morphology and LV function matter. Suppressing incidental ectopy without defining structural/inherited risk can expose a patient to proarrhythmia without benefit.

Reversible cause is a demanding standard

A transient electrolyte or ischaemic trigger does not always explain away scar or cardiomyopathy. ICD decisions require complete reassessment rather than a superficial label.

11Common pitfallsFrequent interpretation and management errors.

01
Giving synchronised cardioversion to a pulseless rhythm or trying to synchronise polymorphic VT.
02
Delaying defibrillation to obtain IV access, a 12-lead or antiarrhythmic drugs.
03
Giving adrenaline before the third shock in a shockable arrest under the RCUK algorithm.
04
Combining amiodarone and lidocaine routinely instead of treating lidocaine as the RCUK alternative.
05
Giving amiodarone for torsades with prolonged QT.
06
Calling a regular broad tachycardia SVT because the patient is young or haemodynamically stable.