Ventricular tachycardia

Ventricular tachycardia (VT) is a potentially life-threatening arrhythmia originating in the cardiac ventricles. VT usually results from underlying cardiac diseases, such as myocardial infarction or cardiomyopathy, but it can also be idiopathic or caused by drugs and electrolyte imbalances. Clinical manifestations range from palpitations and syncope to cardiogenic shock and sudden cardiac death (SCD). The characteristic ECG findings of VT are wide QRS complexes (> 120 ms), tachycardia (≥ 100/minute), and signs of AV dissociation. In the acute setting, management of VT may require immediate cardioversion, defibrillation, or administration of antiarrhythmic drugs. Most patients who develop symptomatic, recurrent VT require long-term therapy involving antiarrhythmic medication, automated implantable cardioverter-defibrillator (AICD) insertion, or catheter ablation of the arrhythmogenic focus. Torsades de pointes (TdP) is a type of polymorphic VT occurring in patients with a prolonged QT interval. Intravenous magnesium sulfate and correction of the underlying etiology of prolonged QTc are important aspects of TdP management.

Ventricular fibrillation is a type of ventricular tachyarrhythmia but is covered in a separate article (see “Ventricular fibrillation”).

• Ventricular tachycardia: ≥ 3 consecutive ventricular complexes (wide QRS complex) at a frequency of ≥ 100/minute
  • Classification by duration
    • Nonsustained ventricular tachycardia (NSVT): VT lasting < 30 seconds with spontaneous termination
    • Sustained ventricular tachycardia: VT lasting ≥ 30 seconds or VT causing hemodynamic instability within 30 seconds
  • Classification by morphology
    • Monomorphic VT: QRS morphology similar in all beats, indicating a single arrhythmogenic focus
    • Polymorphic VT: QRS morphology varies in each beat, indicating multiple arrhythmogenic foci
• Premature ventricular complex : ≤ 3 consecutive ventricular complexes often followed by a complete compensatory pause
  • Ventricular couplet: 2 consecutive ventricular complexes
  • Ventricular triplet: 3 consecutive ventricular complexes ^[1][2]

Reference: ^[3]

Cardiac causes ^[3][4]

• Cardiac scars: secondary to myocardial infarction or cardiac surgery
• Myocardial ischemia: secondary to angina
• Inflammatory causes: myocarditis, endocarditis, or rheumatic heart disease
• Idiopathic: areas of increased automaticity in a structurally normal heart
• Conduction disorders
  • Nonischemic cardiomyopathy (CM)
    • Inherited CM (e.g., HCM, DCM, arrhythmogenic right ventricular CM, progressive muscular dystrophies)
    • CM secondary to infiltrative disorders (e.g., sarcoidosis, hemochromatosis, or amyloidosis)
  • Inherited arrhythmia syndromes (channelopathies)
    • A group of genetic syndromes caused by mutations in genes that encode cardiac ion channels resulting in a predisposition for arrhythmias ^[5]
    • Can lead to sudden cardiac death if uncontrolled
    • Examples: Congenital long QT syndrome, Brugada syndrome, catecholaminergic polymorphic ventricular tachycardia (CPVT)

Ischemic heart disease is the most common cause of ventricular tachycardia. ^[3]

Extracardiac causes ^[4]

• Acquired long QT syndrome ^[6][7][8]
  • Drug-induced QT prolongation (e.g., class I and class III antiarrhythmics, macrolides, fluoroquinolones)
  • Electrolyte imbalances (hypokalemia, hypomagnesemia, hypocalcemia)
  • See “Acquired LQTS” for further detail.
• Certain drugs ; ^[9]
  • Digoxin toxicity
  • Antiarrhythmics
  • Recreational drugs such as cocaine

Drug-induced toxicity and electrolyte abnormalities are the most common extracardiac causes of ventricular tachycardia.

Mechanism

VT can result from an alteration in myocardial automaticity, electrical conduction, or ventricular repolarization secondary to several factors (see “Etiology” for details).

• Monomorphic VT (similar QRS complexes)
  • Increased automaticity
  • Reentry circuit
    • Wide QRS complex (≥ 120 msec): usually caused by a slow ventricular activation outside the normal ventricular conduction system; tachycardia then originates below the AV node
• Polymorphic VT (dissimilar QRS complexes): abnormal ventricular repolarization (e.g., due to long QT syndrome, drug toxicity, electrolyte abnormalities)

Effect

• Asynchronous atrial and ventricular beats and rapid ventricular rhythm → ↓ blood flow into the ventricle during diastole → ↓ cardiac output
• Consequent hemodynamic compromise → symptoms of syncope, MI, angina

Reference ^[3]

• Often asymptomatic, especially in NSVT
• Cardiovascular features
  • Palpitations
  • Tachycardia (HR ≥100/min; typically regular)
  • Chest pain/pressure
  • Dyspnea, orthopnea
  • Symptoms of reduced cardiac output
    • Dizziness
    • Hypotension
    • Syncope
    • Cardiogenic shock and loss of consciousness
  • Cardiac arrest
• Symptoms may be unprovoked or exacerbated by physical and/or emotional triggers (e.g., exercise, anger). ^[10]

If sustained VT is suspected, immediately obtain an ECG to confirm the diagnosis and initiate treatment as it can rapidly progress to ventricular fibrillation and cause sudden cardiac death.

Reference: ^[3]

See “Approach to tachycardia” for details on the initial management of undifferentiated tachycardia.

All patients ^[3][11]

• Urgently consult cardiology.
• Bring a crash cart to the bedside and attach the defibrillator pads to the patient.
• Assess for hemodynamic stability and signs of unstable tachycardia.

Attach defibrillator pads to unstable patients and use a cardioverter-defibrillator or bedside monitor to obtain a rhythm strip for rapid assessment.

Hemodynamically unstable patients ^[3][11]

• Pulseless VT: Commence CPR while preparing to defibrillate and administer shock as soon as possible(see “ACLS” for details).
• VT with pulse: See “Management of unstable tachycardia with a pulse” for details.
  • Polymorphic VT: Defibrillate.
  • Monomorphic VT: Perform synchronized electrical cardioversion under procedural sedation .
  • Uncertain if monomorphic or polymorphic VT: Defibrillate.
• Refractory VT: Consider infusion of amiodarone or beta blockers (see “Electrical storm”).
• Deterioration to ventricular fibrillation: Defibrillation and CPR (managed the same as pulseless VT)

Pulseless VT and ventricular fibrillation are managed similarly with CPR and defibrillation.

Hemodynamically stable patients ^[3][11]

See also “Management of stable wide-complex tachycardia” (WCT) for an algorithm to diagnose and treat undifferentiated WCTs.

• Confirm the underlying rhythm
  • Differentiate VT from SVT with aberrancy if unclear (see “Diagnostics” for an approach).
  • If the diagnosis remains uncertain, treat as VT (∼ 80% of WCT is caused by VT).
  • Regular monomorphic WCT of unclear origin: Consider adenosine as a diagnostic and therapeutic measure for possible underlying SVT, unless an accessory pathway is suspected. ^[11][12]
• First-line treatment of VT: pharmacological cardioversion with antiarrhythmics
  • Patients with QT prolongation on baseline ECG: amiodarone
  • Patients without prolongation on baseline ECG: procainamide or sotalol
• Refractory VT: electrical cardioversion

A WCT may occur as a result of either VT or SVT with aberrancy. The Brugada criteria can help differentiate between the two.

Antiarrhythmics may precipitate acute hypotension and/or rhythm deterioration to TdP or ventricular fibrillation; be prepared to provide immediate defibrillation or hemodynamic support as required.

Avoid procainamide and sotalol in patients with QT prolongation on their baseline ECG, as this may precipitate TdP. ^[3]

Further management

• Once stabilized, evaluate for an underlying cause (see “Diagnostics”).
• Consider long-term management (see “Treatment”).
• Disposition ^[13]
  • High risk of recurrence or electrical storm: Admit to critical care unit.
  • Resolved sustained VT: Admit most patients to hospital for observation and further investigations.
  • Nonsustained VT: Admission for workup and risk stratification is typically required for all new cases of nonsustained VT; Discuss disposition of patients with known nonsustained VT with a specialist.

Approach

Obtain an ECG in all patients with suspected VT (ongoing or resolved). A narrow-complex tachycardia on ECG or rhythm strip excludes VT.

• Ongoing stable undifferentiated WCT (on presenting rhythm strip or 12-lead ECG)
  • High likelihood of VT (e.g., high clinical suspicion and clearly apparent ECG findings of VT): Presume VT diagnosis and begin initial management of VT prior to detailed diagnostics.
  • Uncertain likelihood of VT: Distinguish between VT and SVT with aberrancy if the patient remains stable.
    • Evaluate clinically and check 12-lead ECG in detail (see “VT vs. SVT with aberrancy”).
    • Consider using validated scores to differentiate VT from SVT with aberrancy based on ECG findings: e.g., Brugada criteria
    • Consider urgent cardiology consultation.
• Resolved confirmed VT (i.e., spontaneous resolution or successful cardioversion)
  • Obtain a new baseline ECG to identify signs of an underlying cardiac condition or conduction abnormality associated with episodic VT.
  • Consider further laboratory studies or imaging to identify underlying causes based on clinical suspicion and ECG findings.
• Resolved tachyarrhythmia of unclear origin: Consult cardiology for specialized studies, e.g., stress ECG, ambulatory ECG monitoring, EP study

If the patient becomes unstable at any time, presume a diagnosis of VT and proceed directly to treatment. Do not delay initial management of VT for detailed diagnostics.

ECG findings of VT ^[3]

• Rate: ≥ 100/minute, (most commonly 150–200/minute) ^[13]
• Rhythm: typically regular ^[14]
• QRS complexes
  • Duration: >120 ms; or > 3 small squares on the ECG (known as wide QRS complex)
  • Can be monomorphic VT or polymorphic VT
  • QRS morphology consistent with VT: The presence of any of the following is highly suggestive of VT. ^[13]
    • RBBB pattern
      • V6: R:S ratio < 1 (amplitude), QS wave (i.e., no R wave), or QR wave (i.e., no S wave)
      • V1: monophasic R wave, QR wave (i.e., no S wave), or RS wave (i.e., no Q wave)
    • LBBB pattern
      • V1 or V2: R wave duration > 0.03 seconds, S wave notched or slurred, or duration of Q wave to the lowest point of S wave > 0.07 seconds
      • V6: QR wave (i.e., no S wave) or QS wave (i.e., no R wave)
    • No RS complex in all precordial leads
    • RS duration > 100 ms in any precordial lead
  • QRS morphology reflects pathways of de- and repolarization and can indicate the origin of VT. ^[15]
• Signs of AV dissociation ^[16]
  • Dissociated P waves
    • No relationship between P waves and QRS complexes
    • Indicates that atrial and ventricular contractions are occurring independently
  • Fusion complexes
    • Mixed QRS morphology containing components of a ventricular complex and a normal sinus QRS complex
    • Caused by an atrial impulse transmitted to the ventricles colliding with the ventricular impulse
  • Capture beats (seen occasionally)
    • A normal sinus wave pattern interrupting wide-complex tachycardia
    • Capture beats have a normal QRS complex duration; a P wave may also be visible.
    • Caused by the occasional supraventricular impulse that passes through the AVN to cause ventricular depolarization
    • Indicates incomplete AV dissociation

≥ 3 consecutive wide QRS complexes at a frequency ≥ 100/minute and signs of AV dissociation confirm a diagnosis of VT. ^[16]

In wide-complex tachycardia (WCT), signs of AV dissociation help distinguish between VT (AV dissociation present) from SVT with aberrancy (AV dissociation absent). See “Brugada criteria” for further information.

Baseline ECG

• May be normal
• Features of the underlying cause may be seen, such as:
  • Signs of myocardial ischemia or previous infarction
  • Prolonged QT interval in acquired LQTS or congenital LQTS
  • Brugada pattern in patients with Brugada syndrome
  • Bundle branch blocks, reduced QRS voltage, or other signs of cardiomyopathies

Always obtain a 12-lead ECG following VT termination and patient stabilization to look for clues to help identify the underlying etiology.

Investigating the underlying cause

Laboratory studies ^[3]

• All patients: BMP and serum magnesium levels
• Further studies: to evaluate for the underlying cause
  • Toxicology screen
  • Drug levels (e.g., digoxin, lithium)
  • Troponin ^[17][18]
  • BNP or NT-proBNP ^[3]
  • Genetic testing for inherited arrhythmic syndromes ^[3]

Imaging ^[3]

• Indications: all patients with confirmed VT to assess LVEF and evaluate for structural cardiac defects ^[17]
• Modalities
  • Echocardiography: commonly used as first-line imaging
  • MRI: to assess for myocardial scarring and infiltrative diseases
  • Cardiac CT: alternative to MRI , and in the assessment of coronary arteries
• Findings: Variable; may include valvular defects, regional wall motion abnormalities, ↓ LVEF, and evidence of myocardial infiltration, scarring, or inflammation.

A bedside TTE may help identify regional wall motion abnormalities indicative of acute (or prior) myocardial infarction.

Further assessment of suspected arrhythmia ^[3][17]

• Exercise stress test: Consider if there is suspicion for VT provoked by stress/exertion (e.g., CPVT)
• Ambulatory ECG monitoring (Holter monitor or cardiac event recorder)
  • Evaluation of suspected intermittent VT
  • Assessment of response to antiarrhythmic treatment in confirmed VT
• Coronary angiography
  • Evaluation of unexplained cardiac arrest, VT with suspected MI, or recurrent polymorphic VT
  • Identification and treatment of coronary stenosis (PTCA) ^[3]
• Electrophysiological studies
  • Indications
    • Symptomatic patients with cardiomyopathy who do not meet AICD criteria to determine if sustained VT is the cause of the symptoms
    • Patients in whom catheter ablation is planned (see “Treatment”)
  • Can be used to provoke a VT or map ectopic foci, and can be combined with catheter ablation as a treatment

• Undifferentiated tachycardia: See “Differential diagnosis of tachycardia.”
• Wide-complex tachycardia: : Usually caused by VT, but can be due to supraventricular tachycardia with aberrancy in ∼ 20% of cases. ^[3][19]
  • Regular WCT: VT mimics include regular SVTs (e.g., AVNRT, atrial flutter) with aberrant conduction and pacemaker-related tachycardias.
  • Irregular WCT: VT mimics include irregular SVT with aberrancy, e.g., A-fib with WPW, MAT with LBBB
  • See also “Differential diagnosis of WCT.”

If uncertainty persists, assume a diagnosis of VT and treat accordingly.

The differential diagnoses listed here are not exhaustive.

Approach ^[3][11]

• Ongoing or sustained VT: Stabilize with pharmacological or electrical cardioversion (see “Initial management of VT”).
• Nonsustained VT or resolved sustained VT
  • Treat reversible causes if identified.
    • Correct any electrolyte imbalances
      • See the “Treatment” section in hypokalemia, hypomagnesemia, and/or hypocalcemia as needed.
      • Maintain serum potassium and magnesium levels within the physiologic range.
    • Stop drugs that prolong QTc.
    • Consider digoxin immune fab (fragment antigen-binding) for digoxin toxicity.
    • Treat underlying myocardial ischemia if present (see “Treatment of acute coronary syndrome” for details).
  • No identifiable reversible cause or recurrent VT
    • Consider long-term management with antiarrhythmics, AICD placement, or catheter ablation.
    • Optimize therapy in patients with heart failure.

Long-term management of patients with VT

Pharmacological therapy (antiarrhythmics) is often used alongside device therapy (e.g., AICD) to minimize symptoms, risk of recurrence, and risk of sudden cardiac death. Ablation of the arrhythmogenic foci is potentially curative.

Pharmacological therapy ^[3][17]

• β-blockers are typically used as first-line therapy because they reduce the risk of sudden cardiac death.
• Other medications (e.g., class Ic antiarrhythmics or class III antiarrhythmics) may be combined with β-blockers if symptoms persist.

AICD for VT ^[3]

• Overview
  • Used to terminate episodes of VT in order to prevent sudden cardiac death.
  • Typically combined with pharmacological therapy
  • May be used for primary or secondary VT prevention
• Indications for AICD : all of the following criteria are met ^[22]
  • Expected survival > 1 year
  • Recurrent VT despite treatment of reversible causes
  • One or more of the following:
    • Previous sudden cardiac arrest, sustained VT, or unstable VT
    • Select patients with HFrEF (See “AICDs in heart failure” for more information.)
    • LVEF ≤ 40% with NSVT or recent myocardial infarction if EP study shows inducible sustained VT

Ablation ^[3][23]

• Overview
  • Potential curative treatment for VT
  • Most patients do not subsequently require an AICD or further antiarrhythmic therapy. ^[24][25]
  • Following an EP study, the arrhythmogenic focus is ablated.
• Indications
  • Recurrent VT despite optimal therapy
  • Antiarrhythmics are not tolerated
  • Patient preference
• Options
  • Radiofrequency catheter ablation
  • Surgical ablation

Torsades de pointes (TdP) ^[3][8]

• Definition: a type of polymorphic VT occurring in patients with a prolonged QT interval
• Etiology
  • Congenital LQTS
  • Acquired LQTS (e.g., drug-induced LQTS, electrolyte abnormalities, heart disease)
• Clinical features: similar to clinical features of VT
• Diagnostics
  • Laboratory and imaging studies: same as for VT (see “Diagnostics”)
  • Characteristic ECG findings include: ^[26]
    • Polymorphic VT with QRS complexes that typically appear to twist around the isoelectric line, usually in self-limiting bursts
    • Often preceded by bigeminy and followed by several premature ventricular contractions
    • R-on-T phenomenon may also be seen.
• Acute management
  • Hemodynamically unstable patients: Defibrillation plus CPR.
  • Hemodynamically stable patients: Administer IV magnesium sulfate . ^[3]
  • Identify and treat the underlying etiology of QT prolongation.
    • Restrict or withdraw QT-prolonging drugs. ^[3]
    • Maintain electrolyte balance.^[3]
      • Acute potassium repletion to bring serum K+ ≥ 4.0 mEq/L
      • Maintaining serum K⁺ level between 4.5 mEq/L and 5 mEq/L may help prevent recurrent TdP.
      • Magnesium repletion to bring serum magnesium ≥ 2.0 mmol/L, then maintain within physiological range
      • Calcium repletion for hypocalcemia as needed
    • Chronic hypoxia (e.g. COPD): Supplement O₂.
    • Hypothyroidism: screen with serum TSH and treat with L-thyroxine replacement as needed ^[27][28]
  • TdP refractory to magnesium sulfate: Consider overdrive pacing with pacemaker or isoproterenol infusion. ^[3]
• Long-term management ^[3]
  • Consult cardiology.
  • Consider β-blockers to minimize the risk of sudden cardiac death (see “Long-term pharmacotherapy in VT” for details).
  • Persistent prolonged QT interval despite β-blocker therapy: Consider AICD insertion (with pharmacotherapy) or left cardiac sympathetic denervation.
  • Congenital LQTS: See “Treatment” in “Long QT syndrome.”
• Complications: can progress to life-threatening ventricular fibrillation ^[29]

Electrical storm ^[30][31]

• Definition: ≥ 3 episodes of sustained VT, V-fib, or appropriate shocks delivered by an AICD within a 24-hour period
• Causes
  • Structural heart disease, e.g., MI, cardiomyopathy
  • Nonstructural cardiac dysrhythmias: e.g., short QT interval, Brugada syndrome, congenital long QT syndrome
  • Cardiotoxic substances: e.g., QT-prolonging drugs, cardiac glycoside toxicity
  • Metabolic disturbances: e.g., thyrotoxicosis, electrolyte imbalances
• Management
  • Follow ACLS.
  • Treat reversible causes, e.g., correction of electrolyte imbalances, Digoxin immune fab for cardiac glycoside toxicity, definitive therapy for thyrotoxicosis, PCI for ACS, antipyretics for patients with Brugada syndrome and fever.
  • Consider IV antiarrhythmic infusions under specialist guidance for pharmacological cardioversion. ^[3][31]
    • Beta blockers (e.g., propranolol) and amiodarone are most commonly used. ^[31]
    • Other antiarrhythmics are indicated for specific underlying disorders.
  • Consult cardiology for definitive treatment.

Aggressively treat electrical storm as it has high morbidity and mortality.

ARVC-associated VT ^[3][12]

Young adults with arrhythmogenic right ventricular cardiomyopathy (ARVC) can present with life-threatening VT.

• Suggestive baseline ECG: may show RBBB, Epsilon waves
• Pharmacological cardioversion (preferred agents) ^[32][33][34]
  • Amiodarone OR sotalol
  • With or without other β-blockers, e.g., atenolol
• Further management: Cardiology consult to consider EP study, beta blockers, and AICD placement (See “ARVC” for details).

Urgently refer patients with suspected ARVC to cardiology for confirmation of diagnosis and definitive treatment as it can cause sudden cardiac death.

VT in patients with AICDs ^[13][30]

Multiple appropriate shocks

• Clinical features of shock may be present between shocks delivered by AICD
• ECG shows VT
• Treat as electrical storm and consider pharmacological cardioversion if electrical cardioversion is ineffective.

Lack of appropriate shocks

• Clinical features of shock are typically present without shocks delivered by AICD
• ECG shows VT
• Management
  • Begin initial management of VT.
  • Urgently consult cardiology for CIED interrogation
  • See “Overview of acute AICD complications” for further information.

Inappropriate shocks

• Typically presents with multiple AICD shocks without intervening clinical features of shock
• ECG may be normal, show atrial arrhythmias, or other artifacts that cause oversensing
• Management
  • Urgent cardiology consult for CIED interrogation
  • Consider magnet placement in select cases.
  • See “Overview of acute AICD complications” for further information.

• Progression to ventricular fibrillation
• Sudden cardiac death
• Arrhythmia-induced cardiomyopathy ^[35]

We list the most important complications. The selection is not exhaustive.

• Perform ABCDE survey, checking for signs of hemodynamic instability.
• Attach defibrillator pads and cardiac monitor.
• Obtain 12-lead ECG or rhythm strip.
• Establish IV access.
• Urgently consult cardiology.
• Pulseless patients: Perform CPR and defibrillation.
• Unstable patients: Presume VT diagnosis and perform electrical cardioversion or defibrillation under procedural sedation based on VT morphology.
  • Monomorphic VT likely: synchronized cardioversion
  • Polymorphic VT likely or unclear: unsynchronized cardioversion (i.e., defibrillation)
• Electrical storm: Follow ACLS, start antiarrhythmic infusion (e.g., amiodarone, beta blockers), and admit to critical care unit.
• Stable patients: Treat based on likelihood of VT vs. SVT with aberrancy, using clinical evaluation and ECG findings, e.g., Brugada criteria.
  • VT likely: Attempt pharmacological cardioversion (e.g., with amiodarone, procainamide, or sotalol) first; electrical cardioversion if unsuccessful.
  • Torsades de pointes: Administer IV magnesium sulfate.
  • SVT with aberrancy likely: Treatment depends on underlying rhythm and likelihood of underlying accessory pathway (see “SVT” and “Management of stable WCT”).
  • Unclear diagnosis: Treat as VT.
• Repeat ECG once VT terminated.
• Evaluate and treat underlying causes once stable (see “Etiology”)
• Admit to hospital for further investigations and observation.