Highlights & Basics
- ECG findings for sustained ventricular tachycardia (VT) include wide QRS complex (duration >120 milliseconds) at a rate greater than 100 bpm.
- Patients may have a normal cardiac output or may be hemodynamically compromised during episodes of VT. Presence or absence of symptoms does not reliably differentiate VT from supraventricular tachycardia.
- Torsades de pointes is a polymorphic VT with a characteristic twisting morphology occurring in the setting of QT interval prolongation.
- Sustained VT is usually observed in ischemic and nonischemic cardiomyopathy, but idiopathic VT may also be observed in patients without structural heart disease.
- Among patients with prior myocardial infarction or nonischemic cardiomyopathy, VT is usually due to reentry involving regions of slowed conduction adjacent to scar.
- Owing to the unpredictable and life-threatening nature of most etiologies of sustained VT, prophylactic implantable cardioverter defibrillator implantation is recommended in high-risk patients.
Quick Reference
History & Exam
Key Factors
coronary artery disease
tachycardia
hypotension
Other Factors
weak pulse
syncope
presyncope
airway compromise
impaired consciousness
lightheadedness
dizziness
diminished responsiveness
chest discomfort
dyspnea
asymptomatic
Diagnostics Tests
1st Tests to Order
ECG
transthoracic echocardiogram
electrolytes
troponin I
Other Tests to consider
cardiac catheterization
cardiac MRI
electrophysiologic (EP) study
genetic testing
Treatment Options
presumptive
hemodynamically unstable ventricular tachycardia with a pulse
synchronized cardioversion according to advanced cardiac life support protocol + treatment of reversible cause (if present)
antiarrhythmic medication
torsades de pointes
intravenous magnesium sulfate + withdraw offending drugs + correct electrolyte abnormalities
isoproterenol infusion
temporary or permanent pacing
Definition
Classifications
Ventricular tachycardia (VT)
Sustained VT
Nonsustained VT
Polymorphic VT
Monomorphic VT
Bidirectional VT
Hemodynamically stable VT
Hemodynamically unstable VT
Idiopathic VT
Torsades de pointes (TdP)
Catecholaminergic polymorphic VT
Outflow tract VT
Fascicular VT
Vignette
Common Vignette 1
Common Vignette 2
Other Presentations
Epidemiology
Etiology
Pathophysiology
Images
Diagnostic Approach
History
- Ischemic or nonischemic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤35%) and mild-to-moderate congestive heart failure symptoms (New York Heart Association class II or III symptoms). Those with severe heart failure (class IV) are at high risk as well, but have progressive heart failure as a competing mode of death, and thus should be considered for ICD only if they are candidates for cardiac resynchronization therapy
- Ischemic cardiomyopathy (LVEF ≤40%) with nonsustained VT and inducible sustained VT during electrophysiologic testing
- Ischemic cardiomyopathy (LVEF ≤30% and New York Heart Association class I symptoms)
- Hypertrophic cardiomyopathy (HCM) with high-risk features such as family history of sudden death from HCM; massive left ventricular hypertrophy (wall thickness ≥30 mm); unexplained syncope; left ventricular systolic dysfunction; left ventricular apical aneurysm; extensive late gadolinium enhancement on cardiovascular MRI; or frequent, longer, and faster runs of nonsustained VT.[8][9] Other clinical features that are utilized in calculating sudden cardiac death risk in HCM include age, left atrial diameter, left ventricular outflow tract obstruction, and exercise blood pressure response
- Congenital arrhythmia syndromes, including symptomatic patients with long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT with high-risk features.
Physical exam
ECG
- Preexisting preexcitation of a similar morphology to the wide complex arrhythmia; and/or
- Baseline bundle branch block that resembles the wide complex tachycardia.[22]
- 1. Absence of an RS complex in any precordial lead confirms diagnosis of VT
- 2. If RS complex is present in step 1, measure the QRS onset to nadir of S wave:
- a. R-to-S interval of >100 milliseconds confirms diagnosis of VT
- 3. If R-to-S interval is <100 milliseconds: examine ECG for atrioventricular (AV) dissociation. If present, diagnosis is VT.
- 4. If no AV dissociation, examine QRS complex in V1 and V6:
- a. with right bundle branch block QRS morphology:
- i. in lead V1: Monophasic R, QR, or RS favors VTii. in lead V6: R/S ratio of <1 favors VT; QS, QR, or monophasic R favors VT
- b. with left bundle branch block QRS morphology:
- i. in either lead V1 or V2: R >30 milliseconds, R-to-S (nadir) interval of >60 milliseconds or a notched S wave favors VTii. in lead V6: QR or QS favors VT
- c. note: both V1/V2 and V6 criteria need to favor VT for the diagnosis to be made using this step.
- 1. Presence of an initial R wave
- 2. Width of an initial r or q wave >40 milliseconds
- 3. Notching on the initial downstroke of a predominantly negative QRS complex
- 4. Ventricular activation-velocity ratio (vi/vt), where v is the vertical excursion recorded during the initial (vi) and terminal (vt) 40 milliseconds of the QRS complex.
- QRS duration: >140 milliseconds with right bundle branch block morphology, or QRS duration >160 milliseconds with left bundle branch block morphology (these criteria do not apply to patients treated with antiarrhythmic drugs).
- The presence of a right superior axis or left bundle branch block morphology and any right axis. The absence of extreme axis deviation does not imply a supraventricular origin of the tachycardia.[25]
- QT interval prolongationImage
- Brugada syndrome: a disorder characterized by cardiac conduction abnormalities, which leads to a characteristic J-point elevation and downward-sloping ST segment elevation in the right precordial leads that can lead to sudden death due to polymorphic VT. A mutation in the SCN5A (sodium channel) gene has been implicated, but it is present in only a minority of patients. SCN10A has also been identified as a major susceptibility gene for Brugada syndrome.[12]
- Arrhythmogenic right ventricular cardiomyopathy (ARVC): a genetic disorder characterized by VT, sudden death, and progressive heart failure. In this disease, various regions of the right (and occasionally the left) ventricular muscle are replaced by deposition of fat and fibrotic tissue. Patients with ARVC frequently manifest right ventricular conduction delay on ECG; the finding of an epsilon wave in lead V1 is a specific, although not sensitive, sign for the disease. An epsilon wave represents late activation of a region of the ventricular myocardium, with delay being due to the presence of fatty infiltration and fibrosis.
Electrolytes and cardiac enzymes
Imaging studies
Stress testing and cardiac catheterization
Electrophysiologic (EP) testing
Genetic testing
Risk Factors
History & Exam
Tests
Differential Diagnosis
Differentiating Signs/Symptoms
- None.
Differentiating Tests
- ECG; electrophysiologic study: failure to meet criteria for ventricular tachycardia; absence of fusion or capture beats; absence of atrioventricular dissociation.
Differentiating Signs/Symptoms
- None.
Differentiating Tests
- ECG, electrophysiologic study: failure to meet criteria for ventricular tachycardia; absence of fusion or capture beats; absence of atrioventricular dissociation.
Differentiating Signs/Symptoms
- None.
Differentiating Tests
- Evidence of underlying sinus rhythm on ECG discernible through electrical noise (motion artifact).
- Evidence of arrhythmia isolated to specific leads on 12-lead ECG (tremor).
Sepsis or fever
Differentiating Signs/Symptoms
- Elevated temperature, malaise, rigors, symptoms of underlying infection.
Differentiating Tests
- ECG shows underlying sinus rhythm or sinus tachycardia.
- Appropriate cultures may show presence of infecting agent.
Panic/hyperventilation
Differentiating Signs/Symptoms
- Anxiety or panic, fear of imminent death, paresthesiae, chest pain, numbness, faintness, dizziness, sweating.
Differentiating Tests
- ECG shows underlying sinus rhythm.
- Hospital Anxiety and Depression Scale anxiety score >11.
Hyperthyroidism
Differentiating Signs/Symptoms
- Tremor, anxiety, weight loss but good appetite, diarrhea, eyelid retraction and lid lag, fatigue, heat intolerance, goiter.
Differentiating Tests
- ECG shows underlying sinus rhythm or atrial fibrillation.
- Elevated thyroxine/triiodothyronine and low thyroid-stimulating hormone levels.
Differentiating Signs/Symptoms
- Low blood pressure, abdominal pain with hematemesis and/or melena, hemorrhage from other sites, history of likely cause of blood loss: for example, trauma or postoperative.
Differentiating Tests
- ECG shows underlying sinus tachycardia.
- Ultrasound or CT may show internal bleeding source and/or collection of blood.
Pheochromocytoma
Differentiating Signs/Symptoms
- Headache, sweating, palpitations, fluctuating hypertension, anxiety, nausea, vomiting, weight loss, heat intolerance, tremors, chest and abdominal pain.
Differentiating Tests
- ECG shows underlying sinus tachycardia.
- Increased plasma and 24-hour urine epinephrine/norepinephrine/metanephrine levels.
- Glucagon stimulation test positive.
- Clonidine suppression test positive.
- CT, MRI, or m-iodobenzylguanidine scans show tumor in adrenal gland.
Pericarditis
Differentiating Signs/Symptoms
- Tachycardia and friction rub; jugular venous distention and pulsus paradoxus indicate pericardial effusion causing tamponade.
Differentiating Tests
- ECG shows diffuse concave-up ST-elevation, associated PR depression.
- Chest x-ray may show enlarged cardiac silhouette (globular heart) if pericardial effusion present.
- Echocardiogram may show pericardial effusion.
Differentiating Signs/Symptoms
- History of recent use or high intake.
- Tremor, agitation, signs of intoxication.
Differentiating Tests
- ECG shows underlying sinus tachycardia.
Criteria
- Hemodynamically unstable: patient unconscious with hypotension and undetectable pulse.
- Hemodynamically stable/well: an alert patient with normal blood pressure.
- Hemodynamically unstable/ill: patient with weak pulse and hypotension, signs of diminished cerebral perfusion (lightheadedness, dizziness, diminished responsiveness, or unconsciousness) or diminished coronary perfusion (chest discomfort, dyspnea).
Screening
Treatment Approach
Treatment for identifiable reversible cause of VT such as ischemia, MI, toxicity, drug overdose
Hemodynamically unstable sustained VT
Torsades de pointes
Catecholaminergic polymorphic VT
Hemodynamically stable nonidiopathic sustained VT
- Synchronized electrical cardioversion is another important treatment for hemodynamically tolerated sustained (monomorphic) VT. Among patients who fail an initial attempt at synchronized cardioversion, antiarrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion
- Synchronized cardioversion should be considered before attempting antiarrhythmic drug therapy in patients who have syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable hemodynamic parameters.
Initial management of hemodynamically stable idiopathic VT
Subsequent management of hemodynamically stable idiopathic VT
Patients at high risk for VT or with history of sustained VT/cardiac arrest without identifiable reversible cause: ICD
- Ischemic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤35%) and mild-to-moderate congestive heart failure symptoms (New York Heart Association class II or III symptoms)
- Ischemic cardiomyopathy with LVEF ≤30%
- Ischemic cardiomyopathy (LVEF ≤40%) with nonsustained VT and inducible sustained VT during EP testing
- Nonischemic cardiomyopathy (LVEF ≤35% and New York Heart Association class II or III symptoms)
- Hypertrophic cardiomyopathy (HCM) with high-risk features such as family history of sudden death from HCM; massive left ventricular hypertrophy (wall thickness ≥30 mm); unexplained syncope; left ventricular systolic dysfunction; left ventricular apical aneurysm; extensive late gadolinium enhancement on cardiovascular magnetic resonance imaging; or frequent, longer, and faster runs of nonsustained VT.[8][9] Other clinical features that are utilized in calculating sudden cardiac death risk in HCM include age, left atrial diameter, left ventricular outflow tract obstruction, and exercise blood pressure response.
- Congenital arrhythmia syndromes, including symptomatic patients with long QT syndrome and Brugada syndrome.
Adjunctive therapies for high-risk patients already implanted with an ICD or for whom ICD therapy is not an option
Treatment Options
hemodynamically unstable ventricular tachycardia with a pulse
synchronized cardioversion according to advanced cardiac life support protocol + treatment of reversible cause (if present)
Comments
- Cardioversion is essential for the acute treatment of hemodynamically unstable ventricular tachycardia (VT) (symptomatic or severely hypotensive VT).[1]
- Synchronized cardioversion should be considered before attempting antiarrhythmic drug therapy in patients who have syncope, presyncope, frequent palpitations, or hypotension (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable hemodynamics.
- Cardioversion may be repeated as needed until rhythm is controlled.
- In patients with an identifiable reversible cause of VT (e.g., ischemia, myocardial infarction, toxicity, drug overdose) management will also involve treatment of the reversible cause.[1]
antiarrhythmic medication
Primary Options
- amiodarone
300 mg intravenous push
- amiodarone
Secondary Options
- lidocaine
1 to 1.5 mg/kg intravenously as a single dose
- lidocaine
Comments
- Medical therapy provides an important adjunctive therapy to emergency cardiovascular care, based on the advanced cardiac life support protocol. Amiodarone and/or lidocaine are considered useful antiarrhythmic drugs in these circumstances.[34]
torsades de pointes
intravenous magnesium sulfate + withdraw offending drugs + correct electrolyte abnormalities
Primary Options
- magnesium sulfate
1-2 g intravenously as a single dose
- magnesium sulfate
Comments
- Torsades de pointes, a specific type of polymorphic ventricular tachycardia (VT) characterized by a twisting appearance around the baseline, occurs in the setting of QT prolongation due to either the congenital or acquired forms of the long QT syndrome. Torsades de pointes should be treated as any other form of VT according to the advanced cardiac life support protocol, with special recognition of the fact that hypokalemia and hypomagnesemia frequently are associated with torsades. Electrolyte deficiencies should be replenished aggressively. Offending drugs should be withdrawn. An up-to-date list of drugs is available through research centers.CredibleMeds: Arizona Center for Education and Research on Therapeutics Intravenous magnesium sulfate should be administered. Additionally, overdrive pacing and isoproterenol infusion may be useful in this arrhythmia as they reduce the QT interval.[34]
isoproterenol infusion
Primary Options
- isoproterenol
2 micrograms/minute intravenous infusion initially, dose titrated according to response, maximum 10 micrograms/minute
- isoproterenol
Comments
- Indicated in patients who present with recurrent torsades de pointes after initial acute therapy.
- It may be useful in this arrhythmia as it reduces the QT interval.[56]
- It is important to be certain that the patient does not have acute ischemia before administering isoproterenol.
temporary or permanent pacing
Comments
- Indicated in recurrent torsades de pointes after acute therapy.
catecholaminergic polymorphic ventricular tachycardia
beta-blockers
Primary Options
- nadolol
consult specialist for guidance on dose
- nadolol
Comments
- High dose of beta-blockers is usually required.
- Other treatment strategies have been proposed, including a stepwise addition of alternate treatment options, such as calcium-channel blockers and flecainide, to beta-blockers in patients who do not respond sufficiently or who cannot tolerate beta-blockers. Left cardiac sympathetic denervation appears to be effective, but has only been tested on small cohorts, and is not universally available.[27]
implantable cardioverter defibrillator
Comments
- Implantable cardioverter defibrillator (ICD) insertion is needed in patients with recurrent syncope despite beta-blockers, or those who are survivors of cardiac arrest, especially in the setting of coronary artery disease. ICDs should not be implanted without concomitant beta-blocker therapy, as ICD shocks will increase catecholamine surge, potentially leading to a vicious cycle of ventricular arrhythmias and ICD shocks.
- ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating ventricular tachycardia by overdrive pacing and/or cardioversion defibrillation.
- ICD implant requires surgery and is associated with a small risk of procedural mortality. The long-term risks of ICD therapy include device malfunction, infection, and/or inappropriate shocks. Risk factors for infection include comorbid conditions such as diabetes and chronic obstructive pulmonary disease, as well as oral anticoagulation therapy and corticosteroid use. Measures such as antibiotic prophylaxis and good patient education on wound care can help reduce risk.[49] ICD shocks can be painful and if frequent may impair the patient's quality of life.[43] [44] [45] [50]
hemodynamically stable nonidiopathic sustained ventricular tachycardia
antiarrhythmic medications + treatment of reversible cause (if present)
Primary Options
- adenosine
6 mg intravenously initially, followed by 12 mg every 1-2 minutes for up to 2 doses according to response
- adenosine
- procainamide
10-17 mg/kg (20-30 mg/minute) intravenous infusion initially (or 100 mg intravenously every 5 minutes), followed by 1-4 mg/minute infusion, adjust dose according to response, maximum 9 g/day (maintenance)
- procainamide
Secondary Options
- amiodarone
150 mg intravenous infusion given over 10 minutes initially, followed by 1 mg/minute for 6 hours, followed by 0.5 mg/minute for 18 hours
- amiodarone
Comments
- The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for ventricular tachycardia (VT) as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiologic testing and response to certain medications. Therefore, in the case of VTs, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable.
- Antiarrhythmic medications are useful in the acute management of hemodynamically stable VT. Before initiating antiarrhythmic drug therapy for a wide complex tachycardia, it is important to be confident in the diagnosis and to make sure that the patient is not experiencing supraventricular tachycardia (SVT) with aberrant conduction. Conversely, the diagnosis of SVT with aberrancy should also be made carefully, as certain medications (e.g., verapamil, diltiazem) can exacerbate the clinical situation by worsening the patient's hemodynamic status if the actual arrhythmia is VT.
- According to the American Heart Association (AHA), intravenous adenosine can be considered to aid in treatment and diagnosis when the cause of the regular, monomorphic rhythm cannot be determined.[34] Other antiarrhythmic drugs may also be considered in the acute management of stable VT. The AHA recommends intravenous procainamide or intravenous amiodarone.[34] Intravenous procainamide has been shown to be more efficacious than intravenous amiodarone in terminating wide complex tachycardia (67% vs. 38%, respectively; P = 0.026), and was associated with fewer adverse events.[39] However, procainamide may be more proarrhythmic and should be used with caution in the setting of baseline QT prolongation.[34]
- In patients with an identifiable reversible cause of VT (e.g., ischemia, myocardial infarction, toxicity, drug overdose) management will also involve treatment of the reversible cause.[1]
synchronized cardioversion ± antiarrhythmic medications
Primary Options
- amiodarone
150 mg intravenous infusion given over 10 minutes initially, followed by 1 mg/minute for 6 hours, followed by 0.5 mg/minute for 18 hours
- amiodarone
Secondary Options
- lidocaine
1 to 1.5 mg/kg intravenously initially, followed by 1-4 mg/minute infusion
- lidocaine
Comments
- In patients who do not respond to the initial acute treatment with antiarrhythmic therapy, synchronized electrical cardioversion is an important treatment for hemodynamically tolerated sustained (monomorphic) ventricular tachycardia (VT). Among patients who fail an initial attempt at synchronized cardioversion, antiarrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion.
- Synchronized cardioversion should be considered before attempting antiarrhythmic drug therapy in patients who are highly symptomatic (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable hemodynamics.
- Advanced cardiac life support guidelines recommend giving amiodarone or lidocaine, then synchronized cardioversion.[34]
- In patients with an identifiable reversible cause of VT (e.g., ischemia, myocardial infarction, toxicity, drug overdose) management will also involve ongoing treatment of the reversible cause.[1]
hemodynamically stable idiopathic sustained ventricular tachycardia
intravenous antiarrhythmic medications
Primary Options
Outflow tract VT
adenosine6 mg intravenously initially, followed by 12 mg every 1-2 minutes for up to 2 doses according to response
Fascicular VT
verapamil5-10 mg intravenously initially, followed by 10 mg after 30 minutes if no adequate response seen, maximum 20 mg total dose
Outflow tract VT
metoprolol tartrate5 mg intravenously initially, repeat every 2 minutes according to response, maximum 15 mg total dose
Secondary Options
- amiodarone
150 mg intravenous infusion given over 10 minutes, followed by 1 mg/minute for 6 hours, followed by 0.5 mg/minute for 18 hours
- amiodarone
- lidocaine
1 to 1.5 mg/kg intravenously as a single dose
- lidocaine
Comments
- Idiopathic ventricular tachycardias (VTs) are several distinct entities of VT that occur in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance, but are identifiable by electrophysiologic testing and response to certain medications. Therefore, in the case of VTs, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. These conditions require specific treatment, and seeking specialist help is recommended.
- Specific types of idiopathic VT characteristically respond to specific medications, a feature that is useful for diagnostic as well as therapeutic purposes in the acute setting. Idiopathic outflow tract VT can be terminated with a bolus of adenosine. Outflow tract tachycardias may also respond to beta-blockade or to vagal maneuvers.
- Fascicular VT characteristically responds to verapamil, but the drug should be used with extreme caution due to the risk of hypotension and hemodynamic collapse if given to other forms of VT.
- In cases refractory to adenosine or verapamil, idiopathic VT can be treated with antiarrhythmic medications (lidocaine, amiodarone); if necessary, synchronized electrical cardioversion may be performed.[34]
- If the patient is not already being managed by a specialist, following successful termination of the tachycardia and stabilization, he or she should be referred to a specialist (electrophysiologist) for further management.
synchronized cardioversion
Comments
- In patients with idiopathic ventricular tachycardia who have failed to respond to antiarrhythmic drug therapy, synchronized electrical cardioversion should be considered. Earlier use of cardioversion may be warranted in patients who are highly symptomatic (particularly with symptoms of diminished cerebral perfusion) despite apparently stable hemodynamics.
- If the patient is not already being managed by a specialist, following successful termination of the tachycardia and stabilization, he or she should be referred to a specialist (electrophysiologist) for further management.
nonidiopathic: at high risk for ventricular tachycardia or history of sustained ventricular tachycardia/cardiac arrest without identifiable reversible cause
implantable cardioverter defibrillator
Comments
- The group of patients discussed here as nonidiopathic include those with identifiable reversible causes for ventricular tachycardia (VT) as well as those in whom there are no identifiable causes. Idiopathic VT (although defined as occurring in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance) is identifiable by electrophysiologic (EP) testing and response to certain medications. Therefore, in the case of VTs, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. This is different from tachycardias with no identifiable cause, in which the patient would have no signs of a definitive cause for the VT or signs of an idiopathic VT.
- Patients at high risk for VT for which implantable cardioverter defibrillator (ICD) implantation is the recommended initial treatment/preventive measure include those with: ischemic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤35%, or ≤40% with nonsustained VT and inducible VT during EP); nonischemic cardiomyopathy (LVEF ≤35% and New York Heart Association class II or III symptoms); hypertrophic cardiomyopathy (HCM) with one or more of the following high-risk features: 1) family history of sudden death from HCM; 2) massive left ventricular hypertrophy (wall thickness ≥30 mm); 3) unexplained syncope; 4) left ventricular systolic dysfunction; 5) left ventricular apical aneurysm; 6) extensive late gadolinium enhancement on cardiovascular magnetic resonance imaging; 7) frequent, longer, and faster runs of nonsustained VT; or congenital arrhythmia syndromes, including long QT syndrome and Brugada syndrome with high-risk features.[8][9]
- ICD therapy provides a continuous monitor for the cardiac rhythm and the capability of terminating VT by overdrive pacing and/or cardioversion defibrillation.
- ICD therapy has become the most important treatment to reduce mortality among high-risk patients, with a 30% to 40% relative risk reduction in cardiac death with ICD therapy. Medications have been shown to be less efficacious than ICDs in reducing the burden of malignant ventricular arrhythmias in high-risk patients and are considered adjunctive therapy for managing these conditions.
- ICDs have been shown to be more effective than antiarrhythmic medications in reducing overall mortality in cardiac arrest survivors who did not have reversible causes of cardiac arrest, including toxic/metabolic abnormalities, trauma, and acute ischemia. ICD implantation is contraindicated in such cases when correction of the disorder is considered feasible and likely to substantially reduce the risk of recurrence.
- ICD implant requires surgery and is associated with a small risk of procedural mortality. The long-term risks of ICD therapy include device malfunction, infection, and/or inappropriate shocks. Risk factors for infection include comorbid conditions such as diabetes and chronic obstructive pulmonary disease, as well as oral anticoagulation therapy and corticosteroid use. Measures such as antibiotic prophylaxis and good patient education on wound care can help reduce risk.[49] ICD shocks can be painful and if frequent may impair the patient's quality of life.[43] [44] [45] [50]
antiarrhythmic medication
Primary Options
- mexiletine
200 mg orally every 8 hours
- mexiletine
- flecainide
100-150 mg orally twice daily
- flecainide
- propafenone
150-300 mg orally (immediate-release) every 8 hours; or 225-425 mg orally (extended-release) every 12 hours
- propafenone
- sotalol
80-160 mg orally twice daily
- sotalol
- amiodarone
800-1600 mg/day orally given in single or divided doses for 1-3 weeks, followed by 600-800 mg/day given in single or divided doses for 4 weeks, followed by 200-400 mg/day given in single or divided doses
- amiodarone
Comments
- Antiarrhythmic drugs may be useful as adjunctive therapies for high-risk patients already implanted with an implantable cardioverter defibrillator (ICD) or for whom ICD therapy is not an option.[7] However, randomized trials have shown that currently available oral antiarrhythmic drugs, other than beta-blockers, do not prolong life when used chronically in the treatment of life-threatening ventricular arrhythmias and sudden death.[7] Some antiarrhythmic medications may be inappropriate for patients with structural heart disease because of their negative inotropic properties and increased risk of causing ventricular tachycardia. Amiodarone can increase defibrillation thresholds and, therefore, potentially impair ICD function.[53]
antiarrhythmic monotherapy
Primary Options
- mexiletine
200 mg orally every 8 hours
- mexiletine
- flecainide
100-150 mg orally twice daily
- flecainide
- propafenone
150-300 mg orally (immediate-release) every 8 hours
- propafenone
- sotalol
80-160 mg orally twice daily
- sotalol
- amiodarone
800-1600 mg/day orally given in single or divided doses for 1-3 weeks, followed by 600-800 mg/day given in single or divided doses for 4 weeks, followed by 200-400 mg/day given in single or divided doses
- amiodarone
Comments
- Antiarrhythmic drugs may be useful as adjunctive therapies for high-risk patients already implanted with an implantable cardioverter defibrillator (ICD) or for whom ICD therapy is not an option.[7] However, randomized trials have shown that currently available oral antiarrhythmic drugs, other than beta-blockers, do not prolong life when used chronically in the treatment of life-threatening ventricular arrhythmias and sudden death.[7] Antiarrhythmic medications may be inappropriate for patients with structural heart disease because of their negative inotropic properties and increased risk of causing ventricular tachycardia. Amiodarone can increase defibrillator thresholds and, therefore, potentially impair ICD function.[53]
structural heart disease with recurrent episodes of ventricular tachycardia
idiopathic ventricular tachycardia
specialist referral for ongoing antiarrhythmic treatment
Comments
- Idiopathic ventricular tachycardias (VTs) are several distinct entities of VT that occur in the absence of structural heart disease, known genetic disorder, drug toxicity, or electrolyte imbalance, but are identifiable by electrophysiologic testing and response to certain medications. Therefore, in the case of VTs, idiopathic VT refers to a specific subtype of tachycardias that are defined and identifiable. These conditions require specific treatment, and seeking specialist help is recommended.
mild-to-moderate symptoms (rare palpitations that do not interfere with daily activities)
beta-blockers or calcium-channel blockers or catheter ablation
Primary Options
- metoprolol tartrate
50-200 mg/day orally (immediate-release) given in 2 divided doses
- metoprolol tartrate
- atenolol
25 to 100 mg orally once daily
- atenolol
- verapamil
180-240 mg/day orally (immediate-release) given in 3-4 divided doses; 180-240 mg orally (extended-release) once daily
- verapamil
- diltiazem
90-360 mg/day orally (immediate-release) given in 3-4 divided doses; 90-360 mg orally (extended-release) once daily
- diltiazem
Comments
- In ongoing therapy for patients with idiopathic ventricular tachycardia and mild-to-moderate symptoms, beta-blockers or calcium-channel blockers usually provide sufficient treatment.
- In terms of the choice of calcium-channel blockers, verapamil is usually used, with diltiazem as another option.
- It is a matter of physician and patient preference in deciding between medications and ablation in this setting.[40]
moderate-to-severe symptoms (syncope, presyncope, or frequent, disabling palpitations) or associated cardiomyopathy
catheter ablation
Comments
- In ongoing therapy for patients with moderate-to-severe symptoms or with associated cardiomyopathy, catheter ablation of ventricular tachycardia should be considered as first line. Catheter ablation is also indicated in patients in whom beta-blockers and/or calcium-channel blockers are ineffective or poorly tolerated.[40]
- It is also reasonable as first-line therapy in patients with mild-to-moderate symptoms who prefer not to take medications.
failure of beta-blockers, calcium-channel blockers, or catheter ablation, or noncandidates for catheter ablation
class I or class III antiarrhythmic medications
Primary Options
- mexiletine
200 mg orally every 8 hours
- mexiletine
- flecainide
100-200 mg orally twice daily
- flecainide
- propafenone
150 to 350 mg orally (immediate-release) every 8 hours
- propafenone
- sotalol
80-160 mg orally twice daily
- sotalol
Secondary Options
- amiodarone
200 mg/day orally given in single or divided doses
- amiodarone
Comments
- In ongoing therapy, antiarrhythmic agents, including class I drugs (mexiletine, flecainide, and propafenone) and class III agents (amiodarone and sotalol), may be used in patients who fail therapy with beta-blockers and/or calcium-channel blockers and who are not candidates for catheter ablation or in whom catheter ablation is ineffective.[40] [41]
- Medication choice is usually based on individual patient/physician preference.
Emerging Tx
Remote magnetic navigation
Stereotactic radioablation
Prevention
Primary Prevention
- Ischemic or nonischemic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤35%) and mild-to-moderate congestive heart failure symptoms (New York Heart Association class II or III symptoms). Those with severe heart failure (class IV) are at high risk as well, but have progressive heart failure as a competing mode of death, and thus should be considered for ICD only if they are candidates for cardiac resynchronization therapy
- Ischemic cardiomyopathy (LVEF ≤40%) with nonsustained VT and inducible sustained VT during electrophysiologic testing
- Ischemic cardiomyopathy (LVEF ≤30% and New York Heart Association class I symptoms)
- Hypertrophic cardiomyopathy (HCM) with high-risk features such as family history of sudden death from HCM; massive left ventricular hypertrophy (wall thickness ≥30 mm); unexplained syncope; left ventricular systolic dysfunction; left ventricular apical aneurysm; extensive late gadolinium enhancement on cardiovascular magnetic resonance imaging; or frequent, longer, and faster runs of nonsustained VT.[8][9] Other clinical features that are utilized in calculating sudden cardiac death risk in HCM include age, left atrial diameter, left ventricular outflow tract obstruction, and exercise blood pressure response
- Congenital arrhythmia syndromes, including symptomatic patients with long QT syndrome, Brugada syndrome, and catecholaminergic polymorphic VT with high-risk features.
Secondary Prevention
Follow-Up Overview
Prognosis
Idiopathic ventricular tachycardia
Nonidiopathic VT
Monitoring
Complications
Citations
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 Oct 21;43(40):3997-4126.[Abstract][Full Text]
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 Oct 2;72(14):e91-220.[Abstract]
Pedersen CT, Kay GN, Kalman J, et al. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm. 2014 Oct;11(10):e166-96.[Abstract][Full Text]
Panchal AR, Bartos JA, Cabañas JG, et al; Adult Basic and Advanced Life Support Writing Group. Part 3: adult basic and advanced life support: 2020 American Heart Association guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Circulation. 2020 Oct 20;142(16_suppl_2):S366-468.[Abstract][Full Text]
Cronin EM, Bogun FM, Maury P, et al. 2019 HRS/EHRA/APHRS/LAHRS expert consensus statement on catheter ablation of ventricular arrhythmias. J Arrhythm. 2019 May 10;35(3):323-484.[Abstract][Full Text]
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Key Articles
Other Online Resources
Referenced Articles
Guidelines
Diagnostic
Summary
Provides comprehensive guidance on the evaluation and management of adults and children with hypertrophic cardiomyopathy.Published by
American Heart Association; American College of Cardiology
Published
2020
Summary
Provides clinical guidance on the diagnosis and management of sustained VT and ventricular fibrillation in patients with structural heart disease including previous myocardial infarction, dilated cardiomyopathy, and other forms of nonischemic cardiomyopathy.Published by
Canadian Cardiovascular Society; Canadian Heart Rhythm Society
Published
2020
Summary
Comprehensive recommendations on the management of adults who have ventricular arrhythmias (VA) or who are at risk for sudden cardiac death (SCD), including diseases and syndromes associated with a risk of SCD from VA.Published by
American College of Cardiology; American Heart Association; Heart Rhythm Society
Published
2017
Summary
Provides clinical guidance on the diagnosis and management of patients with ventricular arrhythmias, including sustained VT.Published by
European Heart Rhythm Association; Heart Rhythm Society; Asia Pacific Heart Rhythm Society
Published
2014
Summary
Provides clinical guidance for diagnosis and risk stratification of patients affected by inherited primary arrhythmia syndromes.Published by
Heart Rhythm Society; European Heart Rhythm Association; Asia Pacific Heart Rhythm Society
Published
2013
Summary
Provides clinical guidance for diagnosis and risk stratification of patients with hypertrophic cardiomyopathy.Published by
European Society of Cardiology
Published
2023
Summary
Provides clinical guidance for the diagnosis and management of patients with ventricular arrhythmias, with a focus on the prevention of sudden cardiac death.Published by
European Society of Cardiology
Published
2022
Treatment
Summary
Provides comprehensive guidance on the evaluation and management of adults and children with hypertrophic cardiomyopathy.Published by
American Heart Association; American College of Cardiology
Published
2020
Summary
Part 3 of the American Heart Association guidelines for CPR and emergency cardiovascular care covers basic life support and advanced life support for adult patients, including those with life-threatening conditions in whom cardiac arrest is imminent, and after successful resuscitation from cardiac arrest.Published by
American Heart Association
Published
2020
Summary
Comprehensive recommendations on the management of adults who have ventricular arrhythmias (VA) or who are at risk for sudden cardiac death (SCD), including diseases and syndromes associated with a risk of SCD from VA.Published by
American College of Cardiology; American Heart Association; Heart Rhythm Society
Published
2017
Summary
These guidelines provide guidance on the management of adults with all types of supraventricular tachycardia other than atrial fibrillation. The guidelines include several algorithms for the management of supraventricular arrhythmias.Published by
American College of Cardiology; American Heart Association Task Force on Clinical Practice Guidelines; Heart Rhythm Society
Published
2015
Summary
Provides clinical guidance for cardiac pacing, including for hemodynamic indications, cardiac resynchronization therapy, and pacemaker follow-up.Published by
American College of Cardiology; American Heart Association; Heart Rhythm Society
Published
2012
Summary
Provides clinical guidance on the diagnosis and management of sustained VT and ventricular fibrillation in patients with structural heart disease including previous myocardial infarction, dilated cardiomyopathy, and other forms of nonischemic cardiomyopathy.Published by
Canadian Cardiovascular Society; Canadian Heart Rhythm Society
Published
2020
Summary
Provides clinical guidance for diagnosis and risk stratification of patients affected by inherited primary arrhythmia syndromes.Published by
Heart Rhythm Society; European Heart Rhythm Association; Asia Pacific Heart Rhythm Society
Published
2013
Summary
Consensus recommendations on indications, techniques, and outcomes for catheter ablation.Published by
Heart Rhythm Society; European Heart Rhythm Association; Asia Pacific Heart Rhythm Society; Latin American Heart Rhythm Society
Published
2019
Summary
Provides clinical guidance for the diagnosis and management of patients with ventricular arrhythmias, with a focus on the prevention of sudden cardiac death.Published by
European Society of Cardiology
Published
2022
Summary
Provides general recommendations for the management of adults with supraventricular tachycardia based on the principles of evidence-based medicine.Published by
European Society of Cardiology
Published
2019
Summary
Provides clinical guidance for management of patients with hypertrophic cardiomyopathy.Published by
European Society of Cardiology
Published
2023