Ventricular Tachycardia

• Reentry mechanism (most common, 70-80% of cases): Reentry requires three anatomic/electrophysiologic components: (1) two or more conduction pathways with unidirectional block in one pathway, (2) slow conduction in the unblocked pathway allowing time for recovery of the initially blocked pathway, and (3) reexcitation of tissue proximal to the site of unidirectional block. In the setting of myocardial infarction, scar tissue creates zones of slow conduction and areas of unidirectional block, establishing a reentry circuit. The circuit may involve surviving myocardial fibers interspersed within fibrotic tissue (anatomic reentry) or functional reentry without discrete anatomic barriers. The wavelength of the reentry circuit (conduction velocity × refractory period) determines circuit stability—shorter wavelengths allow multiple simultaneous circuits (polymorphic VT), while longer wavelengths favor monomorphic VT. This mechanism explains why VT in post-MI patients is typically monomorphic, reproducible, and mappable to discrete scar zones.

• Abnormal automaticity: Enhanced diastolic depolarization in ventricular myocytes results from increased intracellular calcium concentration, elevated sympathetic tone, myocardial ischemia, or electrolyte abnormalities (particularly hypokalemia and hypomagnesemia). Automaticity may arise from surviving Purkinje fibers in the subendocardium following infarction, fascicular tissues, or the outflow tracts. These automatic foci gradually depolarize during diastole until reaching threshold potential (-60 mV), triggering spontaneous action potentials independent of normal sinus rhythm. Characteristic of automatic VT is a warm-up period (gradual acceleration of rate after initiation) and failure to terminate with pacing maneuvers (overdrive suppression is ineffective). Automaticity is potentiated by catecholamines, explaining why beta-blockers and sedation are effective adjuncts.

• Triggered activity—Early Afterdepolarizations (EADs): EADs occur during phases 2-3 of the action potential (plateau phase) when repolarization is interrupted by abnormal depolarization. EADs are promoted by prolonged QT intervals (either congenital long QT syndromes or drug-induced via class IA/III antiarrhythmics, macrolides, antipsychotics, or electrolyte derangements). The mechanism involves reactivation of L-type calcium channels during the plateau phase when membrane potential hovers near -30 to -40 mV, allowing sufficient calcium current to trigger premature depolarizations. EAD-mediated VT characteristically exhibits pause-dependent initiation (longer preceding R-R intervals promote EAD occurrence) and is highly polymorphic, often degenerating into VF. This is the primary mechanism of torsades de pointes, a polymorphic VT with twisting QRS complex axis around the isoelectric line.

• Triggered activity—Delayed Afterdepolarizations (DADs): DADs occur after phase 3 repolarization is complete (phase 4), arising from spontaneous sarcoplasmic reticulum calcium release that activates the Na+/Ca2+ exchanger. The inward current from this exchanger (which normally extrudes calcium) paradoxically generates inward depolarizing current when operating in reverse, creating depolarizing oscillations in diastole. DADs are rate-dependent and suppressed by increased interval length (explaining why vagal maneuvers or beta-blockade may terminate DAD-mediated VT). Digitalis toxicity and catecholaminergic polymorphic ventricular tachycardia (CPVT) are classic causes. DAD-mediated VT shows a relatively constant rate and may be terminated by adenosine (which increases refractoriness) or verapamil (which suppresses sarcoplasmic reticulum calcium release).

• Substrate characteristics determining arrhythmia stability: The structural substrate profoundly influences VT phenotype. Post-MI scars with dense collagen and minimal viable myocardium create anatomically fixed reentry circuits producing monomorphic, hemodynamically tolerated VT. Conversely, acute ischemia or inflammatory cardiomyopathy with patchy, dynamic inflammation generates multiple overlapping circuits or focal automaticity, producing hemodynamically unstable, polymorphic VT prone to rapid degeneration. The fractional anisotropy of scar tissue (preferential longitudinal versus transverse conduction) further determines conduction velocity and circuit geometry. Fibrosis increases action potential duration and refractoriness, both stabilizing and predisposing to reentry depending on the spatial heterogeneity. Ion channel abnormalities underlying genetic arrhythmia syndromes (Brugada, long QT, catecholaminergic polymorphic VT) create regional electrophysiologic heterogeneity promoting abnormal automaticity or triggered activity without requiring structural scarring.

• Electrolyte and metabolic contributions: Hypokalemia decreases resting membrane potential, shortens action potential duration, and increases automaticity by increasing the slope of diastolic depolarization. Hypomagnesemia impairs Na-K-ATPase function and enhances calcium influx. Hypocalcemia prolongs the QT interval. Ischemic tissue exhibits intracellular acidosis, increased intracellular calcium, and elevated extracellular potassium (from ATP depletion and Na-K-ATPase failure), all creating a milieu favoring triggered activity and reentry. Catecholamine excess increases calcium influx and automaticity while shortening refractoriness, facilitating multiple competing foci characteristic of polymorphic VT.

• Structural heart disease (most common substrate): Prior myocardial infarction accounts for 80% of monomorphic VT cases in adult populations. Months to years after MI, dense scar tissue harbors slow conduction zones and unidirectional conduction block, creating reentry circuits typically located at the border zone between viable and scar tissue. The epicardial border zone is particularly proarrhythmic. Left ventricular ejection fraction (LVEF) ≤40% post-MI confers substantially elevated risk. Other structural heart diseases predisposing to VT include dilated cardiomyopathy (both ischemic and nonischemic), hypertrophic cardiomyopathy (HCM, where disorganized myocardial fibers and abnormal intramural branching of coronary arteries promote reentry), arrhythmogenic right ventricular cardiomyopathy (ARVC), infiltrative diseases (sarcoidosis, hemochromatosis, Chagas disease), and severe aortic/mitral valve disease. Reduced LVEF is perhaps the strongest independent predictor of VT occurrence, explaining why EF assessment is mandatory in VT evaluation.

• Acute coronary syndrome and ischemia: Acute transmural ischemia creates profound electrophysiologic heterogeneity—central necrotic zone, intermediate zone of injury with altered conduction and refractoriness, and peripheral normal zone. This heterogeneity strongly promotes reentry. VT in acute MI typically occurs within hours to days (distinguished from chronic post-MI VT) and frequently deteriorates into VF. Patients with acute anterior wall MI and cardiogenic shock face the highest risk. Importantly, VT in acute MI requires urgent reperfusion (percutaneous coronary intervention or fibrinolysis) as treatment is fundamentally different from chronic VT management.

• Long QT syndrome (congenital and acquired): Congenital forms result from loss-of-function mutations in potassium channel genes (KCNQ1 in LQT1, KCNH2 in LQT2) or gain-of-function mutations in sodium channel genes (SCN5A in LQT3). The prolonged QT interval reflects delayed repolarization, increasing susceptibility to EAD-mediated triggered activity. LQT1 episodes are typically exercise-induced; LQT2 episodes follow acoustic triggers or emotional stress; LQT3 episodes occur at rest or sleep. Acquired long QT occurs with class IA/III antiarrhythmics (particularly sotalol and dofetilide—quinidine is less commonly used today), macrolide antibiotics (azithromycin, erythromycin), fluoroquinolones, antipsychotics (haloperidol, ziprasidone), 5-HT3 antagonists, and electrolyte derangements. Torsades de pointes is the characteristic VT phenotype.

• Brugada syndrome: Autosomal dominant loss-of-function mutations in SCN5A (sodium channel gene) reduce inward sodium current, unmasking outward potassium current predominantly in epicardial right ventricular outflow tract. This creates marked ST-segment elevation in precordial leads (Type 1 Brugada pattern) and increased transmural voltage gradients favoring phase 2 reentry. VT/VF occurs typically at rest or during sleep, triggered by fever (which unmasks the phenotype), vagal stimulation, or spontaneously. Diagnosis relies on characteristic ECG findings; genetic testing and electrophysiology study may be warranted.

• Catecholaminergic polymorphic ventricular tachycardia (CPVT): Autosomal dominant mutations in RYR2 (ryanodine receptor) or CASQ2 (calsequestrin) genes cause abnormal sarcoplasmic reticulum calcium release with exaggerated diastolic calcium oscillations triggering DADs. VT is stress-induced (exercise or emotional arousal) and manifests as bidirectional VT (alternating QRS axis beat-to-beat) or polymorphic VT. Diagnosis requires exercise stress testing demonstrating induced VT; treatment centers on beta-blockers and flecainide (which stabilizes calcium handling). Genetic testing confirms diagnosis.

• Infiltrative and inflammatory diseases: Cardiac sarcoidosis causes granulomatous infiltration creating patchy fibrosis and electrical heterogeneity, particularly affecting basal septal region. Chagas disease (Trypanosoma cruzi) causes myocardial inflammation progressing to fibrotic cardiomyopathy with VT typical of dilated cardiomyopathy phenotype. Giant cell myocarditis and acute fulminant myocarditis present with acute polymorphic VT. Hemochromatosis and amyloidosis cause restrictive/dilated cardiomyopathy with VT risk. Tuberculous pericarditis and viral myocarditis may transiently promote VT during acute phase.

• Idiopathic VT (normal heart): Approximately 5-10% of VT occurs in patients without structural heart disease. Outflow tract VT (RVOT or LVOT VT) originates from enhanced automaticity in fascicular tissues or Purkinje fibers near the outflow tracts. RVOT VT typically shows left bundle branch block (LBBB) morphology with inferior axis (arising from free wall) or right axis deviation (arising from septum). LVOT VT usually shows RBBB morphology. These typically occur in young patients and are often exercise-induced or catecholamine-sensitive. Fascicular VT arises from left anterior or left posterior fascicles (showing RBBB + right axis morphology when anterior fascicle involved, or RBBB + left axis when posterior fascicle involved). Fascicular VT is characteristically sensitive to verapamil. Idiopathic polymorphic VT without QT prolongation is rare and may represent milder phenotype of genetic syndromes or focal automaticity.

• Drug-induced and electrolyte abnormalities: Class IA antiarrhythmics (quinidine, procainamide, disopyramide), class III agents (amiodarone, sotalol, dofetilide, ibutilide), fluoroquinolones, macrolides, tricyclic antidepressants, and antipsychotics prolong QT and increase EAD susceptibility, particularly when combined or with baseline electrolyte derangements. Severe hypokalemia (K+ <3.0 mEq/L) and hypomagnesemia (Mg2+ <1.5 mg/dL) are critical—even in normal hearts—promoting both automaticity and triggered activity. Cocaine and amphetamines increase catecholamines driving automaticity and DADs. Theophylline and digoxin toxicity promote automaticity and DADs.

• Genetic predisposition and channelopathies: Beyond the syndromic conditions above, common variants in ion channel genes and repolarization genes (identified in genome-wide association studies) modestly increase VT risk, particularly in the setting of structural heart disease or electrolyte derangements. Family history of sudden cardiac death should prompt genetic evaluation.

• Palpitations: Conscious awareness of abnormal heartbeat is common during VT. Patients describe rapid fluttering, racing sensation, or pounding in the chest. The sensation depends on VT rate and individual perception threshold. With slower VT (rate 120-150 bpm), symptoms may be minimal or absent. Faster VT (>200 bpm) typically causes severe symptoms. The regular rhythm of monomorphic VT may be distinguished from the irregular sensation of atrial fibrillation by patient history, though distinguishing clinically is unreliable.

• Syncope and presyncope: Results from rapid VT causing critically reduced cardiac output and cerebral perfusion. Monomorphic VT in patients with reduced LVEF frequently causes hemodynamic collapse because the abnormal ventricular activation sequence is electromechanically inefficient—the ventricles contract in an uncoordinated fashion with reduced force generation despite high electrical rate. Polymorphic VT nearly always causes hemodynamic compromise, often degenerating to VF. Syncope during VT episode is ominous and indicates defibrillator requirement. Presyncope (impending syncope) may represent brief periods of VT or rapid non-sustained VT.

• Dyspnea: Acute pulmonary congestion results from rapid VT causing acute left ventricular dysfunction and pulmonary capillary wedge pressure elevation. In patients with chronic cardiomyopathy, acute VT may precipitate acute decompensated heart failure. The dyspnea occurs secondary to reduced cardiac output and pulmonary edema.

• Chest pain/discomfort: May represent true myocardial ischemia if VT occurs during acute coronary syndrome, or may be nonspecific discomfort from rapid palpitations. High-rate VT increases myocardial oxygen demand while reducing perfusion time (shortened diastole), potentially precipitating ischemia even in coronary disease-free patients.

• Sudden cardiac death: Degeneration of VT into ventricular fibrillation results in loss of organized electrical activity and complete loss of mechanical function (cardiac output drops to zero). Without prompt defibrillation within 3-5 minutes, irreversible brain injury and death result. Approximately 50% of first VT episodes in patients without prior VT history progress to VF. This is why VT is categorized as a life-threatening arrhythmia.

• Physical examination findings during VT:
• Cannon A waves (prominent CV waves) in jugular venous pulse result from atrioventricular dissociation—when the atrium contracts against a closed tricuspid valve during ventricular systole, pressure increases sharply in the right atrium
• Loss of carotid pulse relationship to heart sounds: During VT with AV dissociation, occasional "capture beats" (supraventricular impulses that conduct to ventricles, resetting the VT cycle) or "fusion beats" (simultaneous activation by both VT and sinus impulse) may be detected; these produce palpable pulses irregularly interspersed among VT beats

Initial test — the 12-lead ECG

• Wide-complex tachycardia (WCT): rate >100 bpm with QRS ≥120 ms. Per the 2017 AHA/ACC/HRS ventricular arrhythmia guideline, any WCT should be assumed to be VT until proven otherwise, particularly in a patient with prior MI or reduced LVEF — where the pretest probability of VT exceeds 90%. Obtain a 12-lead if the patient is stable; never delay therapy in an unstable patient to obtain one.
• Findings that clinch VT: AV dissociation (P waves marching independently), capture beats, and fusion beats (Dressler beats) are essentially diagnostic because they prove the ventricle is being driven independently of the atrium. Other supportive features: QRS >140 ms with RBBB morphology or >160 ms with LBBB morphology, northwest (extreme) axis, precordial concordance (all-positive or all-negative QRS V1–V6), and absence of any RS complex in the precordium.
• Named algorithms: the Brugada criteria (four sequential questions ending with morphology criteria in V1 and V6) and the Vereckei aVR algorithm (initial R wave in aVR favors VT) are the two systems examiners cite. Compare with an old ECG — a QRS identical to the patient's baseline bundle branch block favors SVT with aberrancy.
• Morphology as substrate clue: LBBB pattern with inferior axis suggests RVOT VT; RBBB with left axis suggests posterior fascicular VT; polymorphic QRS twisting about the baseline with a long QTc is torsades de pointes.

Confirmatory and substrate workup

• Laboratory: potassium, magnesium, calcium, troponin, and drug levels (digoxin) — reversible triggers must be excluded before attributing VT to fixed scar.
• Transthoracic echocardiography: mandatory to define LVEF and structural disease; LVEF drives ICD eligibility.
• Ischemia evaluation: coronary angiography when ischemic substrate is plausible.
• Cardiac MRI with late gadolinium enhancement: identifies scar, sarcoidosis, ARVC, and myocarditis when echo is unrevealing.
• Ambulatory/event monitoring, exercise testing (unmasks CPVT and exercise-induced outflow tract VT), and electrophysiology study with programmed stimulation for inducibility, mapping, and ablation planning.

Immediate stabilisation (2020 AHA ACLS)

• Pulseless VT or ventricular fibrillation — the two shockable rhythms: immediate unsynchronized defibrillation with high-quality CPR, epinephrine 1 mg IV/IO every 3–5 minutes, and an antiarrhythmic after the shock — amiodarone 300 mg IV bolus (repeat 150 mg) or lidocaine as the alternative.
• VT with a pulse but unstable (hypotension, ischemic chest pain, altered mentation, pulmonary edema) — the choice of shock depends on morphology:
• **Unstable monomorphic VT → synchronized cardioversion** with sedation; synchronization avoids an R-on-T shock that would induce VF.
• **Unstable polymorphic VT, including torsades with a pulse → immediate high-energy unsynchronized defibrillation**, treated as VF: the beat-to-beat change in QRS morphology means the device often cannot sense an R wave and will simply fail to discharge. Do not waste time trying to synchronize.

Stable sustained monomorphic VT — pharmacologic first line

• Class IA antiarrhythmic — procainamide IV: favored for stable monomorphic VT in the 2017 AHA/ACC/HRS guideline; watch for hypotension and QRS widening.
• Class III — amiodarone IV: preferred when LV function is poor or ischemia is ongoing.
• Class IB — lidocaine IV: most useful in ischemia-driven VT (binds inactivated sodium channels in depolarized tissue).
• Failure of drug therapy → proceed to synchronized cardioversion.

Special phenotypes

• Torsades de pointes: IV magnesium sulfate (typically 2 g) even if the magnesium level is normal; withdraw QT-prolonging drugs, replete potassium (keep K+ in the high-normal range, roughly 4.5–5.0 mEq/L), and treat pause dependence with overdrive pacing or isoproterenol. If the patient becomes hemodynamically unstable or pulseless, deliver unsynchronized defibrillation — synchronized cardioversion may be impossible.
• Polymorphic VT with a normal QT: assume acute ischemia — urgent revascularization plus beta blockade.
• Idiopathic fascicular VT: verapamil-sensitive. Outflow tract VT: beta blockers, then ablation.

Definitive management

• ICD: secondary prevention after arrest or hemodynamically significant sustained VT not from a reversible cause; primary prevention per the 2022 AHA/ACC/HFSA heart failure guideline for LVEF ≤35% with NYHA class II–III symptoms (or LVEF ≤30% in NYHA class I), on ≥3 months of optimized GDMT — ARNI (or ACEI/ARB), beta blocker, MRA, and SGLT2 inhibitor — at least 40 days post-MI, with expected meaningful survival >1 year.
• Catheter ablation for recurrent monomorphic VT, ICD shocks, or electrical storm; cardiac sympathetic denervation in refractory cases.

Contraindicated

• Verapamil and diltiazem in any undifferentiated WCT — AV nodal blockade may precipitate hemodynamic collapse. Adenosine is contraindicated in irregular or polymorphic WCT and in suspected pre-excited AF (it can accelerate accessory-pathway conduction), but may be used diagnostically in a regular, monomorphic, hemodynamically stable WCT.
• Class IC agents (flecainide) in structural heart disease/post-MI — proarrhythmic mortality signal from CAST.
• Antiarrhythmics as a substitute for an ICD: they reduce shocks, not mortality.

Complications of the arrhythmia

• Degeneration to ventricular fibrillation and sudden cardiac death — emergency. Rapid or polymorphic VT loses organized activation; the ECG shows chaotic undulation with no discernible QRS and the patient is pulseless. Survival falls with every minute of delayed defibrillation.
• Cardiogenic shock and acute pulmonary edema — emergency. Dyssynchronous ventricular activation plus loss of atrial kick and shortened diastolic filling collapse stroke volume; signaled by hypotension, cool extremities, and rising lactate.
• Electrical storm (three or more separate sustained VT/VF episodes or appropriate ICD therapies in 24 hours) — emergency; mandates search for ischemia, electrolyte derangement, or decompensated heart failure, with beta blockade, sedation, and urgent ablation.
• Tachycardia-induced cardiomyopathy: chronic incessant or frequent VT causes calcium handling failure and LV dilation with a falling EF that improves after rhythm control.
• Anoxic brain injury and post-cardiac arrest syndrome after resuscitated arrest; signaled by absent motor response and myoclonus off sedation.

Complications of therapy

• Amiodarone: pulmonary toxicity/fibrosis (new dyspnea with a restrictive pattern and reduced DLCO), hypo- or hyperthyroidism from its iodine load, transaminitis, corneal microdeposits, and blue-gray skin discoloration. Requires baseline and periodic PFTs, TSH, and LFTs.
• Sotalol, dofetilide, procainamide: QT prolongation with proarrhythmic torsades — emergency; procainamide additionally causes hypotension, drug-induced lupus (anti-histone antibodies), and agranulocytosis.
• Lidocaine: dose-dependent CNS toxicity — perioral numbness, tremor, then seizures, exaggerated in hepatic dysfunction or low output states.
• ICD: inappropriate shocks (usually from atrial fibrillation with rapid conduction or lead noise), lead fracture or dislodgement, pocket infection and device-related endocarditis (emergency — requires complete system extraction), pneumothorax at implant, and psychological distress.
• Catheter ablation: pericardial tamponade (emergency — hypotension with pulsus paradoxus and distended neck veins), stroke, complete heart block, and vascular access injury.

• Wide-complex tachycardia in a patient with prior MI is VT until proven otherwise. The single most tested error is treating it as SVT with aberrancy and giving an AV nodal blocker — verapamil or diltiazem in any undifferentiated WCT can precipitate hemodynamic collapse. Adenosine is reasonable only for a regular, monomorphic, hemodynamically stable WCT that is diagnostically ambiguous; it is contraindicated in irregular or polymorphic WCT and in suspected pre-excited AF, where it can accelerate accessory-pathway conduction.
• **AV dissociation, capture beats, and fusion beats are the pathognomonic triad.** If the stem describes independent P waves or an intermittent narrow beat interrupting the tachycardia, the answer is VT. On exam, the corresponding sign is cannon A waves.
• Best next step is dictated by the pulse, the blood pressure, and the QRS morphology — not the rhythm's name: pulseless VT or VF → unsynchronized defibrillation (these are the two shockable rhythms); unstable monomorphic VT with a pulse → synchronized cardioversion; unstable polymorphic VT or torsades with a pulse → unsynchronized defibrillation, because the device may be unable to synchronize to the changing QRS; stable → IV antiarrhythmic (procainamide or amiodarone).
• Polymorphic VT with a long QT is torsades — the answer is IV magnesium, plus stopping the offending QT-prolonging drug and repleting potassium. Polymorphic VT with a normal QT means acute ischemia; the answer there is revascularization, not magnesium.
• Bidirectional VT (beat-to-beat QRS axis alternation) points to digoxin toxicity or CPVT. In digoxin toxicity the associated findings are nausea, xanthopsia, and hyperkalemia in acute overdose; the treatment is digoxin immune Fab.
• The classic ICD association: per the 2022 AHA/ACC/HFSA heart failure guideline, primary prevention requires LVEF ≤35% with NYHA class II–III symptoms (or LVEF ≤30% in NYHA class I), ≥3 months of optimized four-pillar GDMT (ARNI or ACEI/ARB, beta blocker, MRA, SGLT2 inhibitor), >40 days after MI, and expected survival >1 year — implanting immediately post-MI is the distractor.
• Verapamil is the answer only for idiopathic fascicular VT in a structurally normal heart (RBBB plus axis deviation, young patient) — the exception that proves the AV-nodal-blocker rule.
• Class IC agents (flecainide) are contraindicated in structural heart disease or prior MI because of the excess mortality seen in CAST.