Ventricular Tachyarrhythmias

Meet the patient

A 64-year-old man, two years out from an anterior ST-elevation MI, is on the ward after a bowel resection when the monitor suddenly alarms. He is awake but grey, sweating, systolic BP 84, and the rhythm strip shows a broad-complex tachycardia at 190 bpm.[1][2]

The two questions that decide his next ninety seconds are the two that decide every ventricular tachyarrhythmia: is there a pulse? (no pulse is cardiac arrest — shock now) and is the QRS broad? (broad and fast in a damaged heart is VT until proven otherwise). Everything else — morphology, mechanism, long-term ICD — comes after you have secured the circulation.[1][2]

What VT is — broad, fast, and from below the His

Ventricular tachyarrhythmias are abnormally fast heart rhythms originating from below the bundle of His — that is, from the ventricular myocardium, the His-Purkinje system, or the ventricular conduction tissue.[1][2] They are unified by a single ECG feature: a broad QRS complex (over 120 ms / over 3 small squares), because ventricular depolarisation does not use the normal rapidly-conducting His-Purkinje network. The spectrum ranges from non-sustained self-terminating runs of VT through sustained VT to the terminal rhythms of ventricular flutter and ventricular fibrillation (VF) — the leading cause of sudden cardiac death (SCD).[1]

The clinical skill the examiner probes in this topic has four parts: [1]

1. Recognise that a broad-complex tachycardia at over 100 bpm is VT until proven otherwise, particularly in any patient with prior MI, cardiomyopathy, or structural heart disease.
2. Distinguish VT from its mimics: SVT with aberrancy, antidromic AVRT, pre-excited AF in WPW, paced rhythm, and artefact — using AV dissociation, capture/fusion beats, concordance and the Brugada/Vereckei algorithms.
3. Stratify stability and apply the right algorithm: pulseless VT/VF → ALS shockable; sustained VT with pulse, unstable → synchronised cardioversion; sustained VT with pulse, stable → IV antiarrhythmic; torsades → magnesium.
4. Stratify long-term SCD risk and apply the ICD primary-prevention criteria (EF under 35% more than 40 days post-MI, more than 3 months post-revascularisation, NYHA II–III) versus secondary prevention (survivor of VT/VF).[1][2]

The most important mind-set — repeated until it becomes reflex — is: broad-complex tachycardia in a structurally abnormal heart is VT until proven otherwise; treat accordingly, never give verapamil, never assume SVT-with-aberrancy.[2]

Classification

Ventricular tachyarrhythmias are classified along three axes — duration (sustained vs non-sustained), morphology (monomorphic vs polymorphic), and presence of a pulse (which determines the emergency algorithm).[1]

By duration: [1]

• Non-sustained VT (NSVT) — three or more consecutive ventricular beats at over 100 bpm, lasting under 30 seconds and not causing haemodynamic collapse. Often an incidental finding on ambulatory monitoring. Prognostic significance depends on substrate: in structural heart disease it predicts SCD; in the structurally normal heart it is usually benign.
• Sustained VT — VT lasting over 30 seconds, OR any VT requiring termination (cardioversion/defibrillation/antiarrhythmic) because of haemodynamic compromise. Always pathological; demands acute management and SCD-risk stratification. [1]

By QRS morphology: [1]

• Monomorphic VT — uniform QRS morphology from beat to beat, indicating a single re-entrant circuit (usually through a fixed scar) or a single automatic focus. The classical post-MI VT.
• Polymorphic VT — varying QRS morphology, indicating multiple foci or an unstable wandering re-entrant circuit. Torsades de pointes is the polymorphic VT that occurs in the setting of a prolonged QT interval, with the characteristic twisting of the QRS axis around the baseline.
• Bidirectional VT — alternating QRS polarity (often alternating right and left axis), classically in digoxin toxicity and catecholaminergic polymorphic VT (CPVT). [1]

By haemodynamic consequence (the decisive clinical split): [1]

• VT with a pulse — perfusion is present; apply the synchronised cardioversion vs antiarrhythmic decision.
• Pulseless VT — no perfusion; treat identically to VF in the ALS shockable-rhythm algorithm. [1]

[11] [4] [18] [14] [15] [23] [17] [22] [25] [24] [28]

Epidemiology & Risk Factors

Sudden cardiac death, of which the ventricular tachyarrhythmias are the dominant mechanism, accounts for 300,000 to 400,000 deaths per year in the United States alone and has an incidence of roughly 50 to 100 per 100,000 per year in developed nations.[1] Approximately 80% of SCD is due to ventricular tachyarrhythmia (VF or pulseless VT); the rest is bradyasystole or pulseless electrical activity.[2]

Substrate-specific incidence: [1]

• Ischaemic heart disease is by far the dominant substrate — roughly 80% of SCD occurs in patients with coronary disease, usually as VF or scar-related monomorphic VT in the months to years after MI. Acute ischaemia at the moment of arrhythmia accounts for about 20 to 30% of out-of-hospital VF.
• Cardiomyopathies (dilated, hypertrophic, arrhythmogenic right-ventricular) account for 10 to 15% of SCD.
• Channelopathies (long QT syndrome, Brugada syndrome, CPVT) account for 1 to 2% but are over-represented in young, structurally normal hearts and in athletes.
• Idiopathic VF / early repolarisation syndromes account for the remainder in structurally normal hearts. [1]

Risk factors cluster into four groups:[1][2]

LV ejection fraction is the single most powerful predictor of SCD in structural heart disease — and is the dominant criterion for primary-prevention ICD.[4][8]

[1]

Pathophysiology

Ventricular tachyarrhythmias arise by four fundamental mechanisms, each with its own substrate, trigger, and characteristic ECG.[1][2]

Mechanism 1 — Scar-related re-entry (the commonest sustained VT)

Roughly 80% of sustained VT in structural heart disease is driven by re-entry through a fixed anatomical circuit formed by surviving myocyte channels within a healed infarct scar or fibrotic cardiomyopathic substrate.[2] The scar provides the substrate; an extrasystole (often a ventricular premature beat from a different site) provides the trigger. The wavefront enters the scar at one entrance, travels slowly through a protected channel of surviving myocardium (the diastolic pathway, conducting so slowly that the rest of the ventricle has time to recover excitability), exits at a fixed site, and re-enters — completing a self-sustaining loop. Because the exit site and the path through the scar are fixed, every beat has the same QRS morphology — this is monomorphic VT. The clinical correlate is critical: monomorphic VT in a patient with prior MI = scar-related re-entry until proven otherwise.

Re-entry requires the three classical conditions: (1) an anatomical or functional circuit of two interconnected limbs; (2) different conduction velocities and refractory periods between the two limbs; and (3) a unidirectional block in one limb that allows the wavefront to travel only one way around the loop, returning to its origin after the first limb has recovered excitability. In scar-related VT the protected channel within the scar is the slow-conducting diastolic pathway, while the normal myocardium outside the scar is the fast limb. [1]

Mechanism 2 — Enhanced (abnormal) automaticity

A single ventricular focus depolarises faster than the sinus node and takes over the rhythm. This is the mechanism of outflow-tract VT (especially RVOT) and of digoxin-toxic VT. Automaticity is not dependent on a re-entrant circuit, which is why it does not terminate with overdrive pacing or vagal manoeuvres. The trigger is usually a catecholamine surge (exercise, emotion) in idiopathic RVOT VT; in digoxin toxicity the trigger is Na-K ATPase inhibition → intracellular Na rise → increased Na/Ca exchange → Ca overload → delayed after-depolarisations (DADs). The classical end-result of digoxin toxicity is bidirectional VT with alternating QRS polarity. [1]

Mechanism 3 — Triggered activity from delayed after-depolarisations (DADs)

Triggered activity is the mechanism underlying catecholamine-sensitive RVOT VT and digoxin-toxic bidirectional VT. The cellular mechanism is intracellular Ca overload during the action potential, leading to spontaneous Ca release from the sarcoplasmic reticulum (SR) after repolarisation. The Na/Ca exchanger then extrudes this Ca, generating a net inward (depolarising) current — the delayed after-depolarisation (DAD). If a DAD reaches threshold potential during diastole, it fires off an action potential — and if this recurs, the rhythm self-perpetuates as VT. DADs are amplified by anything that raises intracellular Ca: sympathetic stimulation, digoxin (Na-K ATPase inhibition), high heart rates, ischaemia. The therapeutic corollary is that beta-blockers and verapamil (Ca-channel block) work; adenosine transiently blocks the focus by adenosine-A1 receptor-mediated suppression of cAMP, which is why RVOT VT is adenosine-sensitive (a diagnostic and therapeutic clue). [1]

Mechanism 4 — Triggered activity from early after-depolarisations (EADs) — torsades de pointes

The pathophysiology of torsades de pointes centres on prolongation of the action-potential duration (APD) in mid-myocardial (M) cells and Purkinje cells — the cellular equivalent of QT prolongation on the surface ECG.[14][15] Prolongation of phase 3 repolarisation is most often caused by block of the rapidly activating delayed rectifier potassium current (IKr), encoded by KCNH2 (hERG). QT-prolonging drugs (macrolides, fluoroquinolones, antipsychotics, methadone, ondansetron, sotalol, amiodarone, haloperidol, certain antihistamines) almost universally block IKr. The prolonged plateau phase allows reactivation of L-type calcium channels, generating a depolarising current during phase 2 or 3 — the early after-depolarisation (EAD). The EAD triggers an extrasystole (typically from the Purkinje network), which falls on the vulnerable phase of the preceding T wave (R-on-T) and initiates a polymorphic VT with twisting of the QRS axis — the eponymous torsades de pointes. The twisting axis reflects the transmural dispersion of repolarisation (epicardium repolarises faster than mid-myocardial cells, generating a window of vulnerable heterogeneity).

Electrolyte imbalance (hypokalaemia, hypomagnesaemia, or both), slow heart rate from sinus bradycardia or heart block, organic heart disease, low serum electrolyte levels, previous torsades and baseline QT prolongation all increase the risk of drug-induced torsades.[14][15] The therapy follows directly: stop the offending drug, give IV magnesium sulfate (magnesium suppresses the early after-depolarisations and triggered activity responsible for the arrhythmia[23]), and accelerate the heart rate with isoprenaline infusion or cardiac pacing — shortening the QT and preventing recurrence (isoprenaline is contraindicated in hypertension or ischaemic heart disease).[14][15]

Ventricular fibrillation — multiple wavelet re-entry

VF is the chaotic, disorganised electrical activity of the ventricles with no organised QRS, no coordinated contraction, no cardiac output. The dominant mechanism is the multiple wavelet hypothesis of Moe and colleagues: a large re-entrant wavefront continuously fragments into multiple daughter wavelets that wander, mutually annihilate, and re-form, never settling into a stable circuit. Modern mapping has refined this to the mother-rotor hypothesis — a single high-frequency stable rotor that breaks down into fibrillatory conduction. Either way, the practical message is unchanged: VF is not a perfusing rhythm, it is a cardiac arrest rhythm, and only defibrillation (a massive synchronised shock that simultaneously depolarises the entire myocardium and extinguishes all wavelets, allowing the sinus node to resume) terminates it.[1]

The channelopathies — molecular VT/VF substrates

Long QT syndrome — mutations in the KCNQ1 gene (LQT1, ~35% — IKs loss of function), KCNH2/hERG (LQT2, ~30% — IKr loss of function) or SCN5A (LQT3, ~10% — late inward Na gain of function that prolongs repolarisation). Triggers vary by genotype: LQT1 — swimming, exertion; LQT2 — auditory stimuli, postpartum; LQT3 — rest, sleep. Treatment: beta-blocker (especially nadolol or propranolol) for all; left cardiac sympathetic denervation for breakthrough; ICD for syncope despite beta-blocker, prior cardiac arrest, or high-risk genotypes (QTc over 500 ms).[1]

Brugada syndrome — loss-of-function mutation in SCN5A (the cardiac sodium channel, ~20 to 30% of cases) reduces the inward Na current, which disproportionately shortens the action-potential dome in the right ventricular epicardium (which is more dependent on the transient outward current Ito).[16] The transmural dispersion of repolarisation sets up phase-2 re-entry: an extrasystole from the depolarised region initiates polymorphic VT/VF. Classically a male in his 30s–40s with syncope or nocturnal agonal respiration; ECG shows coved-type ST elevation in V1–V3 (type 1). Treatment is ICD for symptomatic or spontaneous-type-1 patients; quinidine (blocks Ito) and isoprenaline for electrical storm.[16]

Catecholaminergic polymorphic VT (CPVT) — mutation in the cardiac ryanodine receptor RyR2 (autosomal dominant, ~60%) or calsequestrin CASQ2 (autosomal recessive) causes diastolic Ca leak from the SR during sympathetic activation, generating DADs and bidirectional or polymorphic VT.[1] The classical presentation is exercise- or emotion-induced bidirectional VT in a child or young adult with a structurally normal heart and normal resting ECG. Treatment: beta-blocker (nadolol first-line), left cardiac sympathetic denervation, flecainide, ICD for breakthrough.[2]

Why AV dissociation, fusion beats, and capture beats exist in VT

When a ventricular focus fires faster than the sinus node, the ventricles beat independently of the atria — the sinus node still fires, the atria still depolarise, but the AV node is refractory (still recovering from the previous ventricular beat), so most sinus impulses are blocked. Occasionally: [1]

• A fusion beat arises when a sinus impulse manages to reach the AV node just as a ventricular beat is being generated — both depolarise part of the ventricle, producing a QRS that is a hybrid of the two morphologies (intermediate width and shape).
• A capture beat arises when a sinus impulse gets through the AV node and conducts normally through the His-Purkinje system, fully 'capturing' the ventricle for one beat — producing a normal narrow QRS within the broad-complex tachycardia. [1]

Both fusion and capture beats are pathognomonic for VT — they prove that the atria and the ventricles are running independently (which can only happen in a rhythm of ventricular origin).[1][2]

Clinical Presentation

The clinical presentation of ventricular tachyarrhythmia is determined by whether a pulse is present and by the haemodynamic consequence. [1]

Sustained VT with a pulse — the typical presentation

The patient is usually awake but symptomatic: rapid palpitations, dyspnoea, lightheadedness, presyncope or frank syncope, ischaemic-type chest pain (VT at high rate increases myocardial oxygen demand while decreasing coronary perfusion), and signs of low cardiac output (pallor, sweating, cool peripheries, oliguria). Examination shows a rapid regular pulse at 100 to 250 bpm with a broad QRS on the monitor, variable first heart sound intensity (AV dissociation alters the mitral/tricuspid closure timing beat-to-beat), cannon A waves in the JVP (the right atrium occasionally contracts against a closed tricuspid valve), and signs of poor perfusion (hypotension, confusion).[2]

Pulseless VT/VF — the cardiac arrest presentation

The patient presents as sudden collapse with loss of consciousness, no pulse, no breathing, no response. There may be a brief preceding palpitation, but most patients have no warning. No time for history — the diagnosis is on the rhythm monitor. Time is myocardium and brain: every minute of delay to defibrillation reduces survival by ~10%.[1]

Atypical presentations — examiner favourites

• Elderly patient — may present with syncope alone, falls, new confusion, or exacerbation of heart failure rather than the textbook palpitations. The broad-complex tachycardia on the monitor is often misread as 'SVT with aberrancy'. Maintain a high index of suspicion: syncope in a patient with prior MI or cardiomyopathy is VT until proven otherwise.
• Post-MI patient — new broad-complex tachycardia within hours to weeks of MI is scar-related or ischaemic VT; do not attribute to a benign cause.
• Pregnant patient — palpitations may be attributed to the physiological tachycardia of pregnancy; sustained VT in pregnancy is rare but demands urgent treatment (most antiarrhythmics and synchronised cardioversion are safe).
• Athlete — exercise- or emotion-induced syncope or sudden collapse in a young athlete raises the question of HCM, ARVC, long QT, Brugada, CPVT. All demand a 12-lead ECG, echocardiogram, exercise test, and family-history evaluation. Competitive sport is contraindicated until the cause is identified.
• Torsades de pointes — classically presents with syncope in a patient on a QT-prolonging drug (macrolide, fluoroquinolone, antipsychotic, methadone, antiemetic), or with electrolyte disturbance (diuretic-induced hypokalaemia), or in congenital long QT syndrome (often first manifest at puberty or in the postpartum period). Episodes are usually self-terminating but can degenerate to VF.
• Brugada syndrome — male in his 30s–40s, syncope or nocturnal agonal respiration, family history of sudden death; ECG shows coved ST elevation in V1–V3. Fever is a well-recognised precipitant of VF in Brugada and warrants urgent cooling and monitoring.
• CPVT — child or young adult with exercise-induced syncope or seizure-like activity (cerebral hypoperfusion), structurally normal heart, normal resting ECG. Diagnosis is by exercise test, which reproduces the bidirectional/polymorphic VT.
• Digoxin-toxic patient — nausea, vomiting, visual disturbance (yellow-green halos, xanthopsia), confusion, and on ECG a bidirectional VT or atrial tachycardia with AV block. The bidirectional VT is the high-yield exam clue: bidirectional VT + a patient on digoxin = digoxin toxicity → check level, give Digibind. [1]

Differential Diagnosis

A broad-complex tachycardia (QRS over 120 ms at over 100 bpm) has a small but critical differential — distinguishing VT from its mimics is the most-tested skill in this topic.[1][2]

The single most important rule: broad-complex tachycardia at over 100 bpm in a patient with structural heart disease is VT until proven otherwise. Misdiagnosis as 'SVT with aberrancy' and giving verapamil causes haemodynamic collapse.[2]

The Brugada algorithm (4-step) and Vereckei aVR algorithm (single-lead) are the two bedside ECG algorithms to distinguish VT from SVT-with-aberrancy.[11]

Clinical & Bedside Assessment

The bedside assessment has one decisive branch — stability.[1][2]

First — ABCDE and the monitor. Secure the airway, give high-flow oxygen if hypoxic, attach continuous cardiac monitoring and defibrillator pads to the chest (anterior–apical), establish two large-bore IV cannulae, and take bloods (U&E including Mg and Ca, FBC, troponin, digoxin level if relevant, TFTs, toxicology). [1]

Second — the stability decision. A sustained VT with pulse is unstable if any of: [1]

• Systolic blood pressure under 90 mmHg or shock
• Syncope or reduced GCS
• Ischaemic chest pain
• Acute heart failure / pulmonary oedema
• Signs of end-organ hypoperfusion (oliguria, mottling, altered mental status) [1]

Unstable → synchronised DC cardioversion immediately (do not delay for antiarrhythmics). [1]

Stable → IV antiarrhythmic while preparing for cardioversion if deterioration. [1]

Third — get a 12-lead ECG during the tachycardia if at all possible (often not possible in unstable patients). Look for the three pathognomonic signs of VT: [1]

• AV dissociation — independent P waves 'marching through' the tachycardia
• Capture beats — occasional normal narrow QRS within the broad-complex tachycardia
• Fusion beats — QRS of intermediate morphology (hybrid of normal and VT) [1]

Apply the Brugada or Vereckei aVR algorithms to differentiate VT from SVT-with-aberrancy.[11]

Fourth — bedside clinical clues: [1]

• Cannon A waves in the JVP — the right atrium occasionally contracts against a closed tricuspid valve (because the AV node is refractory), producing intermittent large 'cannon' waves in the neck — a bedside clue to AV dissociation and therefore VT.
• Variable intensity of S1 — beat-to-beat variation in mitral/tricuspid closure timing alters the first heart sound — another bedside AV-dissociation clue.
• Carotid sinus massage — may transiently unmask atrial activity (vagal tone blocks AV conduction); never use as the primary diagnostic test in a broad-complex tachycardia — VT can degenerate with vagal manoeuvres. [1]

Investigations

First-line (acute presentation): [1]

• 12-lead ECG — the single most important test. Assess rate, regularity, QRS width, morphology, axis, P-wave timing, AV dissociation, capture/fusion beats, concordance, and the Brugada/Vereckei criteria. For torsades, look for prolonged QT and twisting of the QRS axis; for Brugada, look for coved ST elevation in V1–V3.
• Bloods — U&E (potassium, magnesium, calcium), FBC, troponin (acute ischaemia as cause or consequence), digoxin level if relevant, TFTs (thyrotoxicosis precipitates), toxicology (cocaine), glucose, ABG (hypoxia, acidosis), lactate (perfusion).
• Chest X-ray — heart size, pulmonary oedema, pneumothorax, lines/tubes. [1]

The two ECG algorithms for VT vs SVT-with-aberrancy: [1]

Brugada algorithm (4-step):[2]

1. Absence of RS complex in ALL precordial leads (V1–V6) → VT (stop).
2. R-to-S nadir over 100 ms in any precordial lead → VT (stop).
3. AV dissociation (capture/fusion beats, independent P waves) → VT (stop).
4. Morphology criteria in V1–V2 and V6 — for VT the QRS does not match a typical bundle-branch-block pattern (e.g. absence of rsR' in V1 for RBBB, or notching on the downstroke of S in V1) → VT. [1]

If all four steps are negative, the diagnosis is SVT with aberrancy. Sensitivity for VT is approximately 99%. [1]

Vereckei aVR algorithm (single-lead, simpler):[11]

Diagnose VT if any one of the following is present in lead aVR: [1]

1. Initial R wave (positive deflection)
2. Initial r or q wave over 40 ms
3. Notch on the descending limb of a negative-onset QRS
4. Ventricular activation-velocity ratio (vi/vt) under or equal to 1 — the ratio of vertical deflection in the first 40 ms to the vertical deflection in the last 40 ms of the QRS [1]

Sensitivity ~90%, specificity ~80%; far simpler and quicker than Brugada at the bedside. [1]

Second-line (substrate characterisation — once stabilised): [1]

• Transthoracic echocardiography — LV ejection fraction (the dominant ICD criterion), regional wall-motion abnormalities (scar, ischaemia), structural substrate (HCM with maximal wall thickness over 30 mm, ARVC with RV dilation/dyskinesia, dilated cardiomyopathy, valvular disease, infiltrative cardiomyopathy).
• Coronary angiography if ischaemia suspected (most patients with new VT/VF in the setting of risk factors warrant urgent angiography — ischaemia is the commonest precipitant).
• Cardiac MRI — late gadolinium enhancement to characterise the scar (subendocardial pattern = ischaemic; mid-wall = non-ischaemic, myocarditis, sarcoidosis, DCM; epicardial = ARVC, sarcoid); functional RV assessment for ARVC; tissue characterisation for sarcoidosis, amyloidosis, HCM.
• Electrophysiology study (EPS) — programmed ventricular stimulation to induce VT, map the circuit, identify the critical isthmus/exit site, and plan ablation. EPS is less used diagnostically than historically (modern imaging and ECG criteria suffice) but central to ablation planning.
• Ambulatory ECG / event monitor / implantable loop recorder — to detect NSVT, quantify arrhythmia burden, and guide ICD programming.
• Exercise test — to provoke CPVT (bidirectional/polymorphic VT on exercise), and to unmask ischaemia.
• Genetic testing and family screening — for long QT syndrome (KCNQ1, KCNH2, SCN5A, KCNE1, KCNE2), Brugada syndrome (SCN5A), CPVT (RyR2, CASQ2), ARVC (PKP2, DSG2, DSC2, JUP), and familial screening of first-degree relatives of SCD victims under 40. [1]

Management — Resuscitation

The acute management of ventricular tachyarrhythmia is dictated by whether a pulse is present.[1][2]

Pulseless VT and VF — the ALS shockable-rhythm algorithm

Both are shockable rhythms and managed identically. Immediate action saves lives; every minute of delay to defibrillation reduces survival by ~10%. [1]

1. Confirm cardiac arrest — unresponsive, no pulse, no breathing.
2. Start high-quality CPR — the five critical components: minimise interruptions in chest compressions, provide compressions of adequate rate and depth, allow full chest recoil between compressions, avoid leaning, and avoid excessive ventilation.[22]
3. Attach defibrillator pads (anterior–apical) and analyse rhythm.
4. If shockable rhythm (VF/pulseless VT): deliver one UNSYNCHRONISED shock at the device's standard energy setting.
5. Immediately resume CPR without rhythm check (CPR maintains coronary and cerebral perfusion during the post-shock period).
6. Reassess rhythm; if still shockable, deliver further shocks of equal or escalating energy.
7. Give IV epinephrine (adrenaline) per the ALS drug schedule — PARAMEDIC-2 found it increased 30-day survival (3.2% vs 2.4%) but with more frequent severe neurologic impairment among survivors (31.0% in the epinephrine group).[27]
8. If VF/pulseless VT persists after three or more shocks, give amiodarone 300 mg IV — in the randomised placebo-controlled trial this raised survival to hospital admission from 34% to 44%.[17]
9. Continue the cycle of CPR–shock–drug until either ROSC, the rhythm becomes non-shockable (convert to PEA/asystole algorithm), or resuscitation is discontinued.
10. Reversible causes — the 4 Hs and 4 Ts:
    • Hypoxia — oxygenate, secure airway
    • Hypovolaemia — IV fluids, treat bleeding
    • Hypo-/hyperkalaemia and other electrolyte disturbance — check and correct (magnesium is first-line for torsades de pointes[14])
    • Hypothermia — rewarm
    • Thrombosis (coronary or pulmonary) — consider reperfusion
    • Tension pneumothorax — decompress, then chest drain
    • Tamponade (cardiac) — pericardiocentesis
    • Toxins — identify and give specific antidotes

Post-ROSC care: [1]

• Targeted temperature management (TTM) — the HACA trial cooled comatose survivors of VF arrest to 32 to 34 °C for 24 hours and increased favourable neurologic outcome at six months (55% vs 39%) while reducing mortality.[20] The later TTM trial found that targeting 33 °C and 36 °C gave similar outcomes, so a constant target anywhere in that range is acceptable.[21]
• Optimise oxygenation and ventilation — avoid both hyperoxia and excessive ventilation.
• 12-lead ECG — to look for STEMI and guide coronary assessment.
• Haemodynamic optimisation — support perfusion with fluids, vasopressors or inotropes as required.
• Investigate the cause — ischaemia, electrolyte, channelopathy, drug toxicity.

Sustained VT with a pulse

If unstable (hypotension, syncope, ischaemic chest pain, acute heart failure, reduced GCS): [1]

• Synchronised DC cardioversion — the unstable patient is cardioverted immediately, not treated with drugs first; pre-sedate only if time permits and never delay in the deteriorating patient. In the PROCAMIO randomised comparison the drugs were reserved for the well-tolerated wide-QRS tachycardia: IV procainamide 10 mg/kg over 20 min or IV amiodarone 5 mg/kg over 20 min — procainamide caused fewer major cardiac adverse events (9% vs 41%) and terminated more episodes (67% vs 38%).[18]

If stable: IV antiarrhythmic (below), with cardioversion on standby.[1][2]

Management — Definitive & Stepwise

Stable sustained monomorphic VT

For tolerated (well-perfused) wide-QRS tachycardia, IV procainamide 10 mg/kg over 20 minutes or IV amiodarone 5 mg/kg over 20 minutes.[18] In the PROCAMIO randomised trial of 74 such patients, procainamide had the better safety profile — major predefined cardiac adverse events in 9% versus 41% with amiodarone — and terminated the tachycardia within 40 minutes in 67% versus 38%; the benefit of procainamide also held in the 49 patients with structural heart disease (11% vs 43% adverse events).[18]

Alternative: IV lidocaine. In the ALIVE trial of shock-resistant VF, survival to hospital admission was 22.8% with amiodarone versus 12.0% with lidocaine (OR 2.17) — so amiodarone is the better-supported of the two when shocks fail.[12]

If drug therapy fails or the patient deteriorates: move to synchronised DC cardioversion with the drug regimen on standby.[18]

Torsades de pointes — the management is distinct

Torsades is treated differently from other VT because its mechanism (EAD-driven triggered activity in prolonged repolarisation) is fundamentally different.[14][15]

1. Stop ALL QT-prolonging drugs (consult a QT-drug list — CredibleMeds; common culprits include sotalol, amiodarone, quinidine, procainamide, macrolides, fluoroquinolones, methadone, haloperidol, droperidol, certain antipsychotics, ondansetron, tacrolimus).
2. IV magnesium sulfate — the treatment of choice and first-line therapy for torsades. Magnesium suppresses the early after-depolarisations and triggered activity responsible for the arrhythmia, and has the advantage of safety and simplicity over conventional therapy.[14][15][23]
3. Correct electrolyte disturbance — hypokalaemia and hypomagnesaemia (alone or together) are recognised precipitants.[14][15]
4. Accelerate the heart rate — shortening the QT prevents recurrence: isoprenaline (isoproterenol) infusion or cardiac pacing. Isoproterenol is contraindicated in hypertension or ischaemic heart disease; pacing requires skilled personnel and fluoroscopy — magnesium avoids both limitations.[14][15]
5. Identify and remove the trigger — drug, electrolyte disturbance, bradycardia.
6. Long-term — for acquired LQTS: stop the culprit drug and avoid all QT-prolonging drugs; if a QT-prolonging therapy cannot be avoided, modify the dose if the QT reaches 560 to 600 ms, and stop and hospitalise if syncope or increasing ventricular ectopy occurs.[15]

Idiopathic VT (structurally normal heart)

• RVOT VT — adenosine-sensitive VT is due to cAMP-mediated triggered activity, typically originates from the right ventricular outflow tract, and occurs in patients with apparently normal hearts; in the Cornell series VT terminated with adenosine in every patient, was sensitive to vagal manoeuvres in 9 of 11 and to verapamil in 10 of 12.[25] Definitive: catheter ablation.
• Fascicular (Belhassen) VT — verapamil-sensitive left fascicular monomorphic VT, a re-entrant circuit whose ablation targets are now well defined in inducible and non-inducible patients.[24] Definitive: catheter ablation.

Long-term prevention of SCD — the ICD

The implantable cardioverter-defibrillator (ICD) is the cornerstone of long-term SCD prevention. It detects VT/VF and delivers anti-tachycardia pacing (ATP) or a shock to terminate the arrhythmia.[1][2]

ICD indications: [1]

Secondary prevention (survivors of VT/VF): [1]

• Survivors of cardiac arrest due to VT/VF, where the cause is not reversible (i.e. not acute ischaemia, drug toxicity, electrolyte disturbance, or early post-MI) — ICD indicated.
• Spontaneous sustained VT in structural heart disease — ICD indicated.
• Syncope with inducible sustained VT/VF on EPS — ICD indicated. [1]

Primary prevention (no prior event, but high risk): [1]

• LV ejection fraction under 35%, NYHA II–III, more than 40 days after MI, more than 3 months after revascularisation, optimal medical therapy for at least 3 months (MADIT-II, SCD-HeFT criteria).[4][8]
• LV ejection fraction under 40%, prior MI, NSVT on monitoring, and inducible VT on EPS that is not suppressible by class I antiarrhythmics (MADIT-I criteria).[3]
• LV ejection fraction under 40%, prior MI, NSVT, inducible VT on EPS (MUSTT criteria).[5]
• Non-ischaemic DCM, EF under 36%, NSVT or PVCs (DEFINITE criteria — significant reduction in arrhythmic death).[6]
• Hypertrophic cardiomyopathy with one major SCD risk factor (maximal wall thickness over 30 mm, family history of sudden death, prior unexplained syncope, NSVT, abnormal BP response to exercise).
• Arrhythmogenic right-ventricular cardiomyopathy with sustained VT/VF, or with high-risk features (syncope, extensive disease).
• Long QT syndrome with syncope despite beta-blocker, or prior cardiac arrest, or high-risk genotype (QTc over 500 ms).
• Brugada syndrome with spontaneous type 1 ECG and syncope or sustained VT.
• CPVT with syncope or sustained VT on beta-blocker.

ICD is NOT implanted: [1]

• Within 40 days of MI — DINAMIT showed no mortality benefit and excess non-arrhythmic death (the LV may yet recover).[7]
• Within 3 months of CABG/PCI — the LV may recover.
• Within 3 months of starting optimal medical therapy in newly diagnosed non-ischaemic DCM — re-assess EF before deciding.
• NYHA IV symptoms (refractory heart failure) — unless CRT-D planned or transplant-bridging.
• Life expectancy under 1 year (comorbidity, frailty).
• Incessant VT or electrical storm — ablate or stabilise first, then ICD.

Antiarrhythmic drugs for long-term suppression

• Beta-blockers (metoprolol, bisoprolol, carvedilol, nadolol) — first-line in HCM, LQTS, CPVT, post-MI; reduce sympathetic triggering of arrhythmia.
• Amiodarone — for VT storm, adjunctive to ICD, in refractory idiopathic VT. Toxicity is the limiting factor: pulmonary fibrosis (baseline CXR + PFTs), thyroid (hypo- and hyper-thyroidism — TFTs 6-monthly), hepatic (LFTs 6-monthly), corneal microdeposits, photosensitivity (grey-blue skin discolouration), peripheral neuropathy, bradycardia, QT prolongation (but low torsades risk).
• Sotalol — class II + class III (IKr-blocking) action; effective but torsadogenic — QT must be monitored; contraindicated in severe HF, hypokalaemia, and women (longer baseline QT).
• Mexiletine — oral class Ib (lidocaine analogue), useful adjunct in long-QT type 3 (LQT3) and HCM.
• Quinidine — blocks Ito, useful in Brugada syndrome (normalises ECG and suppresses VF) and short QT syndrome. [1]

Catheter ablation

Catheter ablation is the definitive therapy for idiopathic VT (RVOT, fascicular — cure rate over 85 to 90%) and an adjunct in scar-related VT (reduces VT recurrence and ICD shocks by ~75% but is not curative — multiple circuits and unmappable channels remain).[2] Indications: idiopathic VT with recurrent symptoms, scar-related VT with frequent ICD therapies, electrical storm, bundle-branch re-entry VT.

Electrical storm

Electrical storm is defined as the occurrence of three or more distinct episodes of ventricular tachycardia or ventricular fibrillation within 24 hours, requiring defibrillator intervention (anti-tachycardia pacing or shock).[19] It is a medical emergency — mortality is high both in the acute phase and in the long term. Management ladder:

1. Sedation and analgesia — reduces the sympathetic surge that drives the storm.
2. Intubation and mechanical ventilation if unstable.
3. Intensive medical therapy — in most cases the storm can be interrupted by medical therapy (antiarrhythmic drugs plus beta-blockade).[19]
4. Mechanical circulatory support if cardiogenic shock.
5. Urgent catheter ablation — transcatheter radiofrequency ablation is an effective treatment for refractory cases.[19]
6. Identify and treat reversible precipitants — ischaemia, electrolyte disturbance, infection, drug withdrawal or overdose.

Specific Subtypes & Scenarios

• Monomorphic scar-related VT (post-MI) — fixed re-entry circuit through infarct scar; uniform broad QRS; treat per sustained-VT algorithm; long-term ICD (MADIT-II, MUSTT showed survival benefit in this population[4][5]); ablation adjunctive.
• Torsades de pointes — polymorphic VT + long QT; stop the drug, IV magnesium sulfate, accelerate the heart rate with isoprenaline or pacing.[14][15]
• Bidirectional VT — alternating QRS polarity; classical for digoxin toxicity (magnesium effectively abolished ventricular tachyarrhythmias of digitalis intoxication[23]) and CPVT.
• RVOT VT — adenosine-sensitive, cAMP-mediated triggered activity, apparently normal heart; terminates with adenosine, sensitive to verapamil.[25]
• Fascicular (Belhassen) VT — verapamil-sensitive re-entrant left fascicular tachycardia with well-defined ablation targets.[24]
• Bundle-branch re-entry VT — typically in dilated cardiomyopathy; circuit through the His-Purkinje system; ablation is the definitive therapy.
• CPVT — an inheritable disorder causing exercise- and stress-induced sudden death in young individuals; beta-blockers are the mainstay, but up to a third of patients still have complex arrhythmias despite beta-blockade — flecainide and left cardiac sympathetic denervation are newer options.[28]
• Brugada syndrome — an inherited disorder with right bundle-branch block, persistent ST-segment elevation in precordial leads V1–V3 and sudden death, linked to SCN5A mutations; the coved ST pattern carries the higher risk of VT/VF and sudden death.[26]
• Ventricular flutter — regular sine-wave appearance at 250 to 300 bpm; treated as VF — immediate defibrillation.
• Pulseless VT — treated identically to VF in the ALS shockable-rhythm algorithm.

Complications & Pitfalls

Complications: [1]

• Sudden cardiac death — the dominant feared outcome; up to 25% of structural-heart-disease VT degenerates to VF within 1 year if untreated.
• Syncope and traumatic injury from syncope.
• Tachycardiomyopathy from incessant VT — especially focal/incessant idiopathic VT (RVOT, fascicular) — reversible with ablation.
• Cardiogenic shock and acute heart failure from sustained VT.
• Anoxic brain injury after cardiac arrest — function of downtime and quality of resuscitation; TTM mitigates.
• Post-arrest multi-organ failure.
• ICD-related complications — inappropriate shocks (typically for AF with rapid rate, sinus tachycardia, or T-wave oversensing), pocket infection, lead fracture/failure, pneumothorax, cardiac tamponade from perforation, Twiddler's syndrome.
• Psychological morbidity from ICD shocks — depression, anxiety, post-traumatic stress.
• Amiodarone toxicity — pulmonary fibrosis, thyroid dysfunction, hepatic, corneal microdeposits, photosensitivity, peripheral neuropathy. [1]

Classic pitfalls (examiner favourites): [1]

• Treating a broad-complex tachycardia as 'SVT with aberrancy' and giving verapamil — in VT this causes haemodynamic collapse. Broad-complex = treat as VT unless you can prove otherwise.
• Misdiagnosing pre-excited AF in WPW as 'irregular broad-complex VT' — pre-excited AF needs flecainide/amiodarone or DC cardioversion, NOT AV-nodal blockers (which precipitate VF).
• Missing torsades as the cause of syncope in a patient on a QT-prolonging drug — measure the QT, give magnesium.
• Implanting an ICD within 40 days of acute MI — DINAMIT showed no mortality benefit and excess non-arrhythmic death; wait at least 40 days.[7]
• Using sotalol in heart failure or hypokalaemia — pro-arrhythmic (torsades); requires QT under 500 ms.
• Forgetting to look for digoxin toxicity in bidirectional VT — the answer is Digibind, not amiodarone.
• Forgetting that amiodarone itself prolongs the QT and can precipitate torsades in susceptible patients (especially with other QT drugs).
• Assuming 'electrocardiographic artefact' is VT — tremor, tooth-brushing, and Parkinsonian tremor can mimic polymorphic VT; check for a normal underlying QRS and a well patient.

Prognosis & Disposition

The prognosis is substrate-dependent.[1][2]

By substrate: [1]

• Idiopathic VT (structurally normal heart) — excellent prognosis; catheter ablation is curative; SCD risk is minimal.
• Scar-related VT (post-MI) — significant SCD risk; ICD reduces mortality by 23 to 60% (secondary prevention) and 28% (primary prevention, SCD-HeFT).[8]
• Cardiomyopathic VT — moderate-to-high SCD risk; ICD indicated if EF under 35%.
• Channelopathic VT/VF (LQTS, Brugada, CPVT) — variable; ICD in high-risk phenotypes.
• Electrical storm — in-hospital mortality 25 to 50%; one-year mortality after storm is high.

LV ejection fraction is the single most powerful predictor of SCD in structural heart disease, and the dominant ICD-implant criterion. [1]

Disposition after an acute episode: [1]

• Terminated, stable, no red flags, no structural heart disease — outpatient ECG, ambulatory ECG, cardiology referral.
• Sustained VT in structural heart disease — admission for SCD-risk stratification; ICD evaluation; consider ablation.
• Survivor of cardiac arrest — ITU admission, TTM, coronary angiography, work-up for cause, ICD before discharge if non-reversible.
• Electrical storm — ITU admission, sedation, urgent ablation, ICD therapy evaluation. [1]

Prognostic points: ICD reduces mortality by roughly 28% in primary prevention (SCD-HeFT)[8] and 23 to 60% in secondary prevention. Catheter ablation reduces VT recurrence and ICD shocks by ~75% but is adjunctive, not curative, in scar-related disease. Recurrence after successful idiopathic-VT ablation is under 10%.

Special Populations

• Pregnancy — sustained VT in pregnancy is treated the same as in the non-pregnant patient. Synchronised DC cardioversion is safe in all trimesters. IV lidocaine is safe. IV amiodarone should be avoided in the first trimester (fetal thyroid goitre, hypothyroidism, neurotoxicity) but used if life-threatening; sotalol is generally avoided. Beta-blockers — metoprolol is preferred (limited placental transfer); avoid atenolol (fetal growth restriction). Verapamil is acceptable second-line. Catheter ablation with zero-fluoroscopy / lead-shielding can be performed if essential (best in the second trimester). New sustained VT in pregnancy should prompt work-up for peripartum cardiomyopathy (a structural substrate) and long QT syndrome (often first manifests in the postpartum period).[2]
• Paediatric VT — commonest substrates are post-operative tetralogy of Fallot (re-entry VT around the RVOT patch), congenital long QT syndrome, CPVT, myocarditis, and anomalous coronary artery. Weight-based dosing of all antiarrhythmics. ICD implantation is technically feasible even in small children; subcutaneous ICDs and epicardial systems expand options.
• Elderly — comorbidity-weighted decision to implant ICD (life-expectancy under 1 year is a contraindication). Drug-drug interactions and QT prolongation are common (multiple medications, renal impairment).
• Athletes — HCM, ARVC, long QT, Brugada, CPVT are the leading causes of SCD in young athletes; competitive sport is contraindicated in ICD recipients per ESC 2022 guidelines.[2]
• Renal failure — electrolyte derangement (hyperkalaemia from any cause) precipitates VT; dialysis-related fluid/electrolyte shifts are potent triggers. Amiodarone is not renally cleared (no dose adjustment); sotalol is renally cleared and accumulates in renal failure (dose-adjust or avoid); lidocaine is hepatically metabolised.
• Heart-transplant recipients — denervation hypersensitivity (adenosine causes prolonged asystole), graft vasculopathy (diffuse coronary disease predisposes to VF), and acute rejection all predispose to VT/VF. Avoid adenosine (prolonged asystole); use amiodarone for stable VT.
• Patients with congenital heart disease — post-repair tetralogy of Fallot has a high incidence of VT (re-entry around the RVOT patch); ICD and ablation are the mainstays.

Evidence, Guidelines & Regional Differences

Landmark trials

• MADIT-I (Moss et al., NEJM 1996)[3] — first major primary-prevention ICD trial. Post-MI, EF under 35%, NSVT, inducible VT not suppressible by IV procainamide → ICD vs conventional therapy. 54% relative reduction in mortality; established the role of ICD in high-risk primary prevention.
• MUSTT (Buxton et al., NEJM 1999)[5] — coronary disease, EF under 40%, NSVT, inducible VT. EPS-guided ICD therapy reduced arrhythmic death by 76% and overall mortality by 55% versus no antiarrhythmic therapy; EP-guided drug therapy alone was no better than no treatment.
• MADIT-II (Moss et al., NEJM 2002)[4] — post-MI, EF under 30% (no requirement for NSVT or inducibility) → ICD vs conventional therapy. 31% relative reduction in mortality. Established EF under 30% as a primary-prevention ICD criterion independent of arrhythmia markers.
• DEFINITE (Kadish et al., NEJM 2004)[6] — non-ischaemic DCM, EF under 36%, PVCs/NSVT → ICD vs no ICD. Significant reduction in arrhythmic death; all-cause mortality borderline significant (p=0.08). Established ICD role in non-ischaemic DCM.
• DINAMIT (Hohnloser et al., NEJM 2004)[7] — prophylactic ICD implanted 6 to 40 days after acute MI, EF under 35%, impaired HRV. Reduced arrhythmic death but no overall mortality benefit (excess non-arrhythmic death). Established the 'no ICD within 40 days of MI' rule.
• SCD-HeFT (Bardy et al., NEJM 2005)[8] — NYHA II–III HF, EF under 35% (ischaemic and non-ischaemic) → ICD vs amiodarone vs placebo. ICD reduced all-cause mortality by 23%; amiodarone showed no benefit (and possible harm in NYHA III). Anchored EF under 35% as the dominant primary-prevention criterion for both ischaemic and non-ischaemic aetiologies.
• CAMIAT (Cairns et al., Lancet 1997)[9] — amiodarone post-MI with frequent PVCs; reduced arrhythmic death but not all-cause mortality.
• EMIAT (Julian et al., Lancet 1997)[10] — amiodarone post-MI with LV dysfunction; reduced arrhythmic death but not all-cause mortality. Together CAMIAT and EMIAT established that amiodarone is adjunctive, not a substitute for ICD in structural-heart-disease VT.
• ALIVE (Dorian et al., NEJM 2002)[12] — amiodarone vs lidocaine for shock-resistant VF. Survival to hospital admission: amiodarone 22.8% vs lidocaine 12.0%. Established amiodarone as first-line antiarrhythmic in shockable-rhythm cardiac arrest.
• ROC-ALPS (Kudenchuk et al., NEJM 2016)[13] — amiodarone, lidocaine, or placebo in out-of-hospital cardiac arrest. No overall survival-to-discharge benefit, but a significant survival benefit in witnessed arrests (where the rhythm was shockable on EMS arrival). Cautioned against universal use of these drugs while supporting their use in witnessed shockable arrest.
• Vereckei aVR algorithm (Heart Rhythm 2008)[11] — single-lead (aVR) algorithm to differentiate VT from SVT-with-aberrancy in wide-complex tachycardia; sensitivity ~90%, simpler than Brugada.
• Banai & Tzivoni, 1993[14] and Keren & Tzivoni, 1991[15] — defined the magnesium-sulfate-first treatment of torsades de pointes that survives in every modern guideline.

Guidelines

• 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death[1] — North American standard.
• 2022 ESC Guidelines for the Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death[2] — European standard; harmonises with 2017 AHA/ACC/HRS in most respects.

Regional / examination deltas

[17] [27]

• US (ACC/AHA/HRS 2017)[1] — primary-prevention ICD at LVEF 35% or less (SCD-HeFT) and EF 30% or less post-MI (MADIT-II)[4][8]; secondary-prevention ICD in survivors of VT/VF; for the stable wide-complex tachycardia the randomised evidence favours IV procainamide 10 mg/kg over amiodarone 5 mg/kg over 20 minutes (PROCAMIO: fewer major cardiac adverse events and higher termination).[18]
• Europe (ESC 2022)[2] — broadly aligned with AHA/ACC/HRS; catheter ablation has a prominent role in scar-related VT and electrical storm, where it interrupts refractory storms.[19]
• India (NEET-PG / INICET focus) — algorithm-driven questions dominate: identify the rhythm, apply the Vereckei aVR criteria (initial R wave in aVR, initial r or q wave over 40 ms, downstroke notching, vi/vt of 1 or less)[11], know the ICD criteria (EF 35% or less; EF 30% or less post-MI)[8][4], recognise torsades (IV magnesium sulfate[14]), and recognise bidirectional VT (digoxin toxicity[23]).

Exam Pearls

• Treat any broad-complex tachycardia in a structurally abnormal heart as VT until proven otherwise.[29]
• Vereckei aVR algorithm: initial R wave in aVR, initial r or q wave over 40 ms, notching on the initial downstroke, or vi/vt of 1 or less = VT — superior accuracy to the Brugada criteria.[11][29]
• Pulseless VT = treat as VF — immediate unsynchronised defibrillation plus high-quality CPR.[17][22]
• Sustained VT with pulse + stable → IV procainamide 10 mg/kg or amiodarone 5 mg/kg over 20 min (PROCAMIO: adverse events 9% vs 41%; termination 67% vs 38%).[18]
• Sustained VT with pulse + unstable → synchronised DC cardioversion without delay for drugs.[18]
• Amiodarone 300 mg IV for VF/pulseless VT unresponsive to three or more shocks — survival to admission 44% vs 34% (Kudenchuk RCT); lidocaine is inferior (ALIVE: 22.8% vs 12.0% survival to admission).[17][12]
• Epinephrine in cardiac arrest — increases 30-day survival (3.2% vs 2.4%) but with more severe neurologic impairment in survivors (PARAMEDIC-2).[27]
• Torsades de pointes: polymorphic VT + long QT — stop the QT drug, IV magnesium sulfate (treatment of choice), accelerate the heart rate with isoprenaline or pacing (isoprenaline contraindicated in ischaemic heart disease).[14][15]
• Bidirectional VT in a patient on digoxin = digoxin toxicity — magnesium abolished digitalis-toxic ventricular arrhythmias; check the digoxin level and potassium.[23]
• Idiopathic VT (apparently normal heart): RVOT VT (adenosine-sensitive, cAMP-mediated triggered activity) vs fascicular VT (verapamil-sensitive re-entry) — both amenable to catheter ablation.[25][24]
• ICD primary prevention: LVEF 35% or less NYHA II–III (SCD-HeFT: 23% mortality reduction) and EF 30% or less post-MI (MADIT-II: HR 0.69); non-ischaemic DCM with EF under 36% and PVCs/NSVT (DEFINITE: arrhythmic death HR 0.20).[8][4][6]
• ICD NOT implanted early post-MI — DINAMIT (implant 6 to 40 days post-MI) showed no overall mortality benefit.[7]
• Electrical storm = three or more distinct episodes of VT/VF within 24 h requiring defibrillator intervention — medical therapy first, catheter ablation for refractory storms.[19]
• CPVT = exercise- and stress-induced sudden death in the young; beta-blockers mainstay, a third still arrhythmic on them — flecainide and left cardiac sympathetic denervation are options.[28]
• Brugada syndrome = RBBB + persistent ST-segment elevation V1–V3 + sudden death, SCN5A mutations; coved-type ST elevation carries the higher VT/VF/sudden-death risk.[26]
• Targeted temperature management: HACA used 32 to 34 °C for 24 h (favourable neurologic outcome 55% vs 39%); TTM trial showed 33 °C and 36 °C targets are equivalent.[20][21]
• High-quality CPR: minimise interruptions, adequate rate and depth, allow full recoil, avoid leaning, avoid excessive ventilation.[22]

Exam application bank (NEET-PG / INICET)

One-line answer

Ventricular tachyarrhythmias are rapid rhythms originating below the bundle of His that produce a broad QRS complex and span a continuum from monomorphic ventricular tachycardia (VT) through polymorphic VT (including torsades de pointes) to ventricular fibrillation (VF).[11][29] Sustained VT with pulse is treated with IV procainamide 10 mg/kg or amiodarone 5 mg/kg over 20 minutes if stable (PROCAMIO[18]), or synchronised DC cardioversion if unstable; pulseless VT and VF are shockable rhythms managed by the ALS algorithm — immediate unsynchronised defibrillation, high-quality CPR[22], epinephrine (PARAMEDIC-2[27]), and amiodarone 300 mg IV after three or more failed shocks (Kudenchuk RCT[17]). Long-term management is the implantable cardioverter-defibrillator (ICD): primary prevention at LVEF 35% or less in NYHA II–III heart failure (SCD-HeFT: 23% mortality reduction[8]) or EF 30% or less post-MI (MADIT-II: HR 0.69[4]), but not within 40 days of MI (DINAMIT: no overall benefit[7]); DEFINITE extended the benefit to non-ischaemic dilated cardiomyopathy with EF under 36% plus PVCs/NSVT.[6] Torsades de pointes is treated by stopping the offending drug and giving IV magnesium sulfate, the treatment of choice.[14][15] The Vereckei aVR algorithm (initial R wave, initial r or q over 40 ms, downstroke notching, vi/vt of 1 or less) distinguishes VT from SVT with aberrancy.[11]

Worked stems (answer without another resource)

Stem 1 — Classic presentation. Map symptoms to mechanism; name the first investigation and first treatment step with dose/route if drug therapy is standard. [1]

Stem 2 — Unstable / complicated. List red flags that force immediate resuscitation, theatre, ICU, antidote, or reperfusion — and what you do in the first 15 minutes. [1]

Stem 3 — Atypical group. Elderly, pregnancy, child, or immunocompromised: how presentation and thresholds change. [1]

Stem 4 — Differential trap. Name the three closest mimics and one discriminator for each. [1]

Stem 5 — Disposition. Who goes home with safety-netting, who is admitted, who needs HDU/ICU/theatre, and what follow-up is mandatory. [1]

Rapid viva checklist

1. Definition + classification
2. Pathophysiology chain
3. Bedside signs / criteria
4. Score with exact components (if any)
5. Emergency bundle
6. Definitive therapy with doses
7. Complications of disease and of treatment
8. Special populations
9. Guideline/trial name if classic
10. Three exam traps

Coverage self-check

If you cannot answer any stem above from this page alone, re-read the matching section — the page is intended to be self-sufficient for final-prof and NEET-PG/INICET questions on Ventricular Tachyarrhythmias.

The mantra, and the ward-round test

[1] [2]

The mantra: pulse decides the shock, the QRS decides the diagnosis, the ejection fraction decides the device — and the broad complex in a sick heart is always VT until you can prove it is not.[1][2]

Ward-round test — three stems, thirty seconds each

Stem 1 — the man from the top of the topic, now pulseless (answer)

The post-MI patient's eyes roll back and he has no pulse. The monitor still shows the broad-complex tachycardia at 190 bpm. What is the rhythm and what do you do in the next minute? Model: This is pulseless VT — a shockable rhythm, treated identically to VF. Do not wait for synchronisation. Deliver an immediate unsynchronised shock and start high-quality CPR (minimise interruptions, adequate rate and depth)[22], run the ALS algorithm with IV epinephrine (PARAMEDIC-2 evidence)[27] and amiodarone 300 mg IV after three or more failed shocks (survival to admission 44% vs 34%).[17] Reversibility comes after ROSC — coronary assessment, electrolytes, and targeted temperature management if he stays comatose (HACA: 32 to 34 °C for 24 h).[20]

Stem 2 — broad-complex at 170 bpm, conscious, BP 100 (answer)

A 70-year-old with a prior inferior MI is in a regular broad-complex tachycardia at 170 bpm, QRS 150 ms, blood pressure 100/60, alert but breathless. The registrar suggests verapamil for "SVT with aberrancy". What is the right call? Model: A broad-complex tachycardia in a patient with prior MI is VT until proven otherwise — the classic error is treating it as "SVT with aberrancy"; AV nodal blockers have no proven role before VT is excluded. Apply the Vereckei aVR criteria (initial R wave, initial r or q over 40 ms, downstroke notching, vi/vt of 1 or less) and look for AV dissociation to confirm VT.[11][29] He is stable (perfusing, alert), so give IV procainamide 10 mg/kg over 20 minutes — or amiodarone 5 mg/kg — per PROCAMIO.[18] If he destabilises — hypotension, syncope, ischaemic pain — move straight to synchronised DC cardioversion.[18]

Stem 3 — the patient on erythromycin who starts twisting (answer)

A 68-year-old woman on oral erythromycin for cellulitis, with chronic kidney disease, develops a polymorphic tachycardia with a QRS axis that twists around the baseline. The QTc is 540 ms. What is the rhythm, and what is the first drug? Model: This is torsades de pointes — a life-threatening ventricular tachycardia occurring with a prolonged QT, most frequently related to administration of QT-prolonging drugs, with renal-failure electrolyte disturbance adding risk.[15] The first drug is IV magnesium sulfate — the treatment of choice for torsades, which suppresses the early after-depolarisations and triggered activity driving the rhythm.[14][23] Stop the erythromycin, correct the electrolyte disturbance (hypokalaemia with or without hypomagnesaemia)[14], and if the rhythm recurs, accelerate the heart rate with isoprenaline or cardiac pacing.[15] Defibrillate if it becomes sustained or pulseless.[17]

References

1. [1]Al-Khatib SM, Stevenson WG, Ackerman MJ, et al. 2017 AHA/ACC/HRS Guideline for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society J Am Coll Cardiol, 2018.PMID 29097296
2. [2]Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death Eur Heart J, 2022.PMID 36017572
3. [3]Moss AJ, Hall WJ, Cannom DS, et al. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. Multicenter Automatic Defibrillator Implantation Trial Investigators N Engl J Med, 1996.PMID 8960472
4. [4]Moss AJ, Zareba W, Hall WJ, et al. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction N Engl J Med, 2002.PMID 11907286
5. [5]Buxton AE, Lee KL, Fisher JD, et al. A randomized study of the prevention of sudden death in patients with coronary artery disease. Multicenter Unsustained Tachycardia Trial Investigators N Engl J Med, 1999.PMID 10601507
6. [6]Kadish A, Dyer A, Daubert JP, et al. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy N Engl J Med, 2004.PMID 15152060
7. [7]Hohnloser SH, Kuck KH, Dorian P, et al. Prophylactic use of an implantable cardioverter-defibrillator after acute myocardial infarction N Engl J Med, 2004.PMID 15590950
8. [8]Bardy GH, Lee KL, Mark DB, et al. Amiodarone or an implantable cardioverter-defibrillator for congestive heart failure N Engl J Med, 2005.PMID 15659722
9. [9]Cairns JA, Connolly SJ, Roberts R, et al. Randomised trial of outcome after myocardial infarction in patients with frequent or repetitive ventricular premature depolarisations: CAMIAT. Canadian Amiodarone Myocardial Infarction Arrhythmia Trial Investigators Lancet, 1997.PMID 9078198
10. [10]Julian DG, Camm AJ, Frangin G, et al. Randomised trial of effect of amiodarone on mortality in patients with left-ventricular dysfunction after recent myocardial infarction: EMIAT. European Myocardial Infarct Amiodarone Trial Investigators Lancet, 1997.PMID 9078197
11. [11]Vereckei A, Duray G, Szénási G, et al. New algorithm using only lead aVR for differential diagnosis of wide QRS complex tachycardia Heart Rhythm, 2008.PMID 18180024
12. [12]Dorian P, Cass D, Schwartz B, et al. Amiodarone as compared with lidocaine for shock-resistant ventricular fibrillation N Engl J Med, 2002.PMID 11907287
13. [13]Kudenchuk PJ, Daya M, Dorian P Amiodarone, Lidocaine, or Placebo in Out-of-Hospital Cardiac Arrest N Engl J Med, 2016.PMID 27557314
14. [14]Banai S, Tzivoni D. Drug therapy for torsade de pointes J Cardiovasc Electrophysiol, 1993.PMID 8269292
15. [15]Keren A, Tzivoni D. Torsades de pointes: prevention and therapy Cardiovasc Drugs Ther, 1991.PMID 1854660
16. [16]Antzelevitch C, Nof E Brugada syndrome: recent advances and controversies Curr Cardiol Rep, 2008.PMID 18715534
17. [17]Kudenchuk PJ, Cobb LA, Copass MK, et al. Amiodarone for resuscitation after out-of-hospital cardiac arrest due to ventricular fibrillation N Engl J Med, 1999.PMID 10486418
18. [18]Ortiz M, Martín A, Arribas F, et al. Randomized comparison of intravenous procainamide vs. intravenous amiodarone for the acute treatment of tolerated wide QRS tachycardia: the PROCAMIO study Eur Heart J, 2017.PMID 27354046
19. [19]Proietti R, Sagone A. Electrical storm: Incidence, Prognosis and Therapy Indian Pacing Electrophysiol J, 2011.PMID 21468247
20. [20]Hypothermia after Cardiac Arrest Study Group. Mild therapeutic hypothermia to improve the neurologic outcome after cardiac arrest N Engl J Med, 2002.PMID 11856793
21. [21]Nielsen N, Wetterslev J, Cronberg T, et al. Targeted temperature management at 33°C versus 36°C after cardiac arrest N Engl J Med, 2013.PMID 24237006
22. [22]Meaney PA, Bobrow BJ, Mancini ME, et al. Cardiopulmonary resuscitation quality: improving cardiac resuscitation outcomes both inside and outside the hospital: a consensus statement from the American Heart Association Circulation, 2013.PMID 23801105
23. [23]Keren A, Tzivoni D. Magnesium therapy in ventricular arrhythmias Pacing Clin Electrophysiol, 1990.PMID 1695751
24. [24]Michowitz Y, Belhassen B. New Insights on Verapamil-Sensitive Idiopathic Left Fascicular Tachycardia J Electrocardiol, 2018.PMID 30177332
25. [25]Markowitz SM, Litvak BL, Ramirez de Arellano EA, et al. Adenosine-sensitive ventricular tachycardia: right ventricular abnormalities delineated by magnetic resonance imaging Circulation, 1997.PMID 9286949
26. [26]Escárcega RO, Jiménez-Hernández M, Garcia-Carrasco M, et al. The Brugada syndrome Acta Cardiol, 2009.PMID 20128157
27. [27]Perkins GD, Ji C, Deakin CD, et al. A Randomized Trial of Epinephrine in Out-of-Hospital Cardiac Arrest N Engl J Med, 2018.PMID 30021076
28. [28]Imberti JF, Underwood K, Mazzanti A, Priori SG. Clinical Challenges in Catecholaminergic Polymorphic Ventricular Tachycardia Heart Lung Circ, 2016.PMID 26948768
29. [29]Vereckei A, Duray G, Szénási G, et al. Application of a new algorithm in the differential diagnosis of wide QRS complex tachycardia Eur Heart J, 2007.PMID 17272358