VENTRICULAR TACHYCARDIA

✓ Medically ReviewedDISEASEID: MDBT0165🚨 TRIAGE: EMERGENCYICD-10: I47.2

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Definition

CLINICAL DEFINITION

Ventricular tachycardia (VT) is defined as three or more consecutive ventricular premature beats at a rate of >100 beats per minute (typically 120–250 bpm), originating below the bundle of His. It is characterised by wide QRS complexes (>120 ms) and atrioventricular dissociation, and is classified as non-sustained (lasting <30 seconds) or sustained (lasting ≥30 seconds or requiring intervention due to haemodynamic compromise).

IN PLAIN ENGLISH

Ventricular tachycardia is a fast heart rhythm that starts in the lower chambers of the heart (the ventricles). It prevents the heart from pumping blood effectively and can be life-threatening if it does not stop on its own or requires emergency treatment.

COMMON MISCONCEPTION / WHAT IT DOES NOT MEAN

Ventricular tachycardia is NOT a supraventricular tachycardia (SVT) with aberrant conduction, although wide-complex tachycardias of supraventricular origin can mimic VT on an ECG. It is also distinct from ventricular fibrillation, which is a chaotic, disorganised rhythm without effective cardiac output.

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Word Breakdown

ventricul- / cardi-

=ventricle (Latin 'ventriculus', small cavity) and heart (Greek 'kardia')

-tachy

=fast or rapid (from Greek 'tachys')

Literal Meaning: A rapid heart rhythm originating in the ventricles

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Abbreviations

VT=Ventricular Tachycardia — rapid heart rhythm originating from the ventricles

NSVT=Non-Sustained Ventricular Tachycardia — runs of VT lasting less than 30 seconds

SMVT=Sustained Monomorphic Ventricular Tachycardia — continuous VT with a single QRS morphology

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Synonyms & Variants

V-Tach›Ventricular tachyarrhythmia›

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Category-Specific Context

As a cardiac arrhythmia, ventricular tachycardia represents a disorder of the heart's electrical conduction system where the ventricles depolarise rapidly and independently of the sinoatrial node. It is classified by duration (non-sustained vs sustained), morphology (monomorphic vs polymorphic), and aetiology (ischaemic, non-ischaemic, or idiopathic).

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Clinical Context & Usage

CLINICAL SETTINGS

Emergency DepartmentCoronary Care UnitIntensive Care UnitCardiology WardElectrophysiology Laboratory

USAGE & DOCUMENTATION NOTES

In clinical documentation, VT is typically documented by its duration and morphology (e.g., 'runs of NSVT' or 'sustained monomorphic VT'). ECG reports often describe the QRS axis, presence of AV dissociation, fusion beats, or capture beats to confirm the ventricular origin. Clinicians frequently use the term 'V-tach' in verbal handovers.

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Primary Causes & Pathophysiology

PATHOPHYSIOLOGY

Ventricular tachycardia arises from abnormal automaticity, triggered activity, or re-entry circuits within the ventricular myocardium. The most common mechanism in structural heart disease is scar-mediated macro-re-entry, often following a myocardial infarction, where areas of slow conduction bordering fibrotic tissue create a continuous electrical loop. Triggered activity, mediated by early or delayed afterdepolarisations, is more common in electrolyte imbalances, drug toxicity (e.g., long QT syndromes), or catecholaminergic states. The rapid ventricular rate compromises diastolic filling time, leading to decreased stroke volume, reduced cardiac output, and potential haemodynamic collapse or degeneration into ventricular fibrillation.

PRIMARY CAUSES

Coronary Artery Disease / Prior Myocardial Infarction

Myocardial scarring creates zones of slow conduction that facilitate macro-re-entrant circuits, the most common cause of sustained monomorphic VT.

Non-ischaemic Cardiomyopathy (e.g., Dilated, Hypertrophic, ARVC)

Myocardial fibrosis and structural remodelling disrupt normal electrical propagation, promoting re-entry or abnormal automaticity.

Acute Myocardial Ischaemia

Ischaemic injury alters resting membrane potentials and creates electrical heterogeneity, triggering polymorphic VT or ventricular fibrillation.

Electrolyte Derangements (Hypokalaemia, Hypomagnesaemia)

Prolongs repolarisation and promotes early afterdepolarisations, predisposing to polymorphic VT such as Torsades de Pointes.

Idiopathic Outflow Tract VT

Occurs in structurally normal hearts, typically arising from the right or left ventricular outflow tract via cAMP-mediated triggered activity.

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Drug-Induced Causes

💊 Class IA and IC Antiarrhythmics (e.g., Flecainide, Procainamide) ↗

Mechanism: Sodium channel blockade slows conduction velocity, potentially provoking proarrhythmia and re-entrant VT, especially in structural heart disease.

→ Discontinue the offending agent immediately; avoid Class IC agents in patients with ischaemic or structural heart disease.

💊 QT-Prolonging Drugs (e.g., Macrolides, Fluoroquinolones, Haloperidol, Methadone) ↗

Mechanism: Blockade of the hERG potassium channel delays ventricular repolarisation, increasing the risk of early afterdepolarisations and Torsades de Pointes.

→ Stop the offending drug, correct electrolytes (IV magnesium), and consider overdrive pacing or isoprenaline if bradycardia-dependent.

💊 Sympathomimetics (e.g., Adrenaline, Dobutamine, Cocaine) ↗

Mechanism: Excessive beta-adrenergic stimulation increases intracellular calcium, promoting delayed afterdepolarisations and triggered activity.

→ Withdraw the agent; manage with beta-blockers if haemodynamically tolerated and not contraindicated.

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Epidemiology

Prevalence:The prevalence of non-sustained VT increases with age and the presence of structural heart disease, occurring in up to 10% of patients post-myocardial infarction and frequently detected on ambulatory monitoring in patients with heart failure. Sustained VT is less common but carries a high risk of sudden cardiac death.

Age Group:Older adults (secondary to ischaemic heart disease and cardiomyopathies), though younger individuals may be affected if they have inherited channelopathies (e.g., Long QT syndrome, Brugada syndrome) or ARVC.

Sex Predilection:Male

Geographic Distribution:Globally distributed, but prevalence correlates with regional rates of ischaemic heart disease and access to post-infarction care. Inherited channelopathies may show founder effects in specific populations.

Red Flags & Triage ★

TRIAGE LEVEL

🚨 EMERGENCY

DO NOT MISS — LIFE-THREATENING PRESENTATIONS

Wide-complex tachycardia in a patient with prior myocardial infarction — highly predictive of VT; do not administer AV nodal blockers (e.g., verapamil) as this may cause haemodynamic collapse.
Polymorphic VT with a prolonged QT interval (Torsades de Pointes) — requires IV magnesium sulphate and withdrawal of QT-prolonging agents; standard antiarrhythmics like amiodarone may worsen the condition.

URGENT EVALUATION TRIGGERS

Haemodynamic instability (hypotension, altered mental status, acute heart failure, chest pain) accompanying wide-complex tachycardia — requires immediate synchronised DC cardioversion.
Runs of NSVT in the setting of acute chest pain or recent myocardial infarction — indicates ongoing ischaemia or electrical instability requiring urgent evaluation.
Syncope or pre-syncope in a patient with known structural heart disease or documented VT — high risk for sudden cardiac death.

Contraindications & Precautions

CONTRAINDICATIONS

AV nodal blocking agents (e.g.
Verapamil
Diltiazem) in wide-complex tachycardia of unknown origin — can cause profound hypotension and cardiovascular collapse if the rhythm is actually VT.
Flecainide and Propafenone in patients with structural heart disease or prior myocardial infarction — contraindicated due to high risk of proarrhythmia and increased mortality.

SPECIAL PRECAUTIONS

Always assume a wide-complex tachycardia is VT in patients with a history of structural heart disease or prior MI.
Correct underlying hypokalaemia and hypomagnesaemia aggressively before or during antiarrhythmic therapy to prevent proarrhythmia.
Ensure resuscitation equipment and defibrillator are immediately available when administering IV antiarrhythmics like Amiodarone or Procainamide.

Complications

DOWNSTREAM CLINICAL COMPLICATIONS

Haemodynamic collapse and cardiogenic shock — rapid ventricular rates severely impair cardiac output and systemic perfusion.
Degeneration into Ventricular Fibrillation (VF) — disorganised electrical activity leading to sudden cardiac arrest and death if not immediately defibrillated.
Thromboembolism — prolonged episodes with severe ventricular dysfunction may promote intracardiac stasis
though less common than in atrial fibrillation.
Tachycardia-induced cardiomyopathy — chronic frequent runs of VT can lead to reversible left ventricular systolic dysfunction.

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Confused With (LASA & DDx) ★

LEXICAL (LASA) — SIMILAR NAMES

Supraventricular Tachycardia (SVT) with aberrancy

Both present as wide-complex tachycardias on ECG. Misdiagnosing VT as SVT with aberrancy and administering AV nodal blockers can be fatal.

Ventricular Fibrillation (VF)

Both are life-threatening ventricular arrhythmias, but VF is chaotic without discernible QRS complexes and requires immediate defibrillation, whereas VT may have organised complexes and can sometimes be managed with medications or synchronised cardioversion.

CLINICAL DIFFERENTIAL DIAGNOSES (DDx)

SVT with Aberrant Conduction (e.g., bundle branch block)

Key Distinguishing Feature: Presence of typical bundle branch block morphology, absence of AV dissociation, and response to vagal manoeuvres or adenosine.

Antidromic AVRT (WPW syndrome)

Key Distinguishing Feature: Wide-complex tachycardia conducting down the accessory pathway; often seen in younger patients without structural heart disease, with delta waves on baseline ECG.

Hyperkalaemia-induced wide-complex rhythm

Key Distinguishing Feature: Sine-wave appearance, extremely wide QRS, absent P waves, and clinical context of renal failure or potassium-sparing drug use; does not respond to standard antiarrhythmics.

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Clinical Pearls

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The presence of AV dissociation, fusion beats, or capture beats on a 12-lead ECG is virtually diagnostic of ventricular tachycardia and confirms the ventricular origin of the wide-complex rhythm.

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In any patient with a wide-complex tachycardia and a history of structural heart disease or prior MI, the rhythm is VT in the vast majority of cases; treat as VT until proven otherwise.

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Torsades de Pointes is a specific form of polymorphic VT associated with QT prolongation; it is treated with IV magnesium sulphate and overdrive pacing, whereas amiodarone is contraindicated as it further prolongs the QT interval.

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Haemodynamically stable monomorphic VT can often be terminated with IV amiodarone or procainamide, but electrical cardioversion should be performed immediately if the patient shows any signs of clinical deterioration.

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Example Usage & SOAP

CLINICAL SENTENCE

"Telemetry showed a 15-beat run of non-sustained monomorphic ventricular tachycardia at 140 bpm, which self-terminated without haemodynamic compromise."

IN A SOAP NOTE

S: 65-year-old male with a history of ischaemic cardiomyopathy (LVEF 25%) reports mild palpitations but denies chest pain, dyspnoea, or syncope. O: BP 110/70 mmHg, HR 88 bpm (sinus rhythm). Telemetry review reveals a 12-beat run of NSVT (rate 150 bpm, LBBB morphology, superior axis). Serum K+ 4.1 mmol/L, Mg2+ 0.85 mmol/L. A: Asymptomatic NSVT in the setting of known ischaemic cardiomyopathy. High risk for future sustained ventricular arrhythmias. P: Optimise guideline-directed medical therapy for heart failure. Check amiodarone levels (currently on low-dose). Refer to electrophysiology for ICD optimisation and consideration of VT ablation if runs increase in frequency.

DIFFERENTIAL DIAGNOSIS CONTEXT

Differential for wide-complex tachycardia: (1) Ventricular tachycardia (look for AV dissociation, positive/negative precordial concordance, Brugada criteria); (2) SVT with aberrant conduction (look for typical RBBB/LBBB morphology, response to adenosine); (3) Antidromic AVRT via accessory pathway (look for delta waves on baseline ECG, younger patient); (4) Hyperkalaemia (look for sine-wave pattern, peaked T waves, clinical context of renal failure).

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Prognosis

SHORT-TERM OUTCOME

Highly dependent on the underlying aetiology and haemodynamic stability. Unstable sustained VT requires immediate cardioversion and carries a high short-term mortality if not treated promptly. NSVT in a structurally normal heart generally has a benign short-term prognosis.

LONG-TERM PROGNOSIS

Patients with sustained VT and structural heart disease have a high long-term risk of recurrent arrhythmias and sudden cardiac death, often requiring an implantable cardioverter-defibrillator (ICD) or catheter ablation. Prognosis is closely tied to the underlying left ventricular ejection fraction.

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References & Coding

ICD-10 DIAGNOSTIC CODE

I47.2

LITERATURE CITATIONS & GUIDELINES

[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. J Am Coll Cardiol. 2018;72(14):e91-e220.

[2]Priori SG, Blomström-Lundqvist C, Mazzanti A, et al. 2015 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Europace. 2015;17(10):1467-1507.

MEDICAL DISCLAIMER — This content is intended for educational purposes and qualified healthcare professionals only. Always refer to current clinical diagnostic criteria, institutional protocols, and official guidelines. Medobo is not responsible for clinical decisions made based on this content.