Treatment algorithm

Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups: see disclaimer

INITIAL

haemodynamically unstable ventricular tachycardia with a pulse

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synchronised cardioversion according to advanced cardiac life support protocol + treatment of reversible cause (if present)

Cardioversion is essential for the acute treatment of haemodynamically unstable ventricular tachycardia (VT) (symptomatic or severely hypotensive VT).[1]

Synchronised cardioversion should be considered before attempting anti-arrhythmic 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 haemodynamics.

Cardioversion may be repeated as needed until rhythm is controlled.

In patients with an identifiable reversible cause of VT (e.g., ischaemia, myocardial infarction, toxicity, drug overdose) management will also involve treatment of the reversible cause.[1]

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anti-arrhythmic medication

Additional treatment recommended for SOME patients in selected patient group

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 anti-arrhythmic drugs in these circumstances.[31]

Primary options

amiodarone: 300 mg intravenous push

Secondary options

lidocaine: 1 to 1.5 mg/kg intravenously as a single dose

torsades de pointes

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intravenous magnesium sulfate + withdraw offending drugs + correct electrolyte abnormalities

Torsades de pointes, a specific type of polymorphic ventricular tachycardia (VT) characterised by a twisting appearance around the baseline, occurs in the setting of QT prolongation due to either the congenital or the 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 hypokalaemia and hypomagnesaemia are frequently 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 Offending drugs should be withdrawn.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 centres. CredibleMeds: Arizona Center for Education and Research on Therapeutics Opens in new window Intravenous magnesium sulfate should be administered. Additionally, overdrive pacing and isoprenaline infusion may be useful in this arrhythmia as they reduce the QT interval.[31]

Primary options

magnesium sulfate: 1-2 g intravenously as a single dose

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isoprenaline infusion

Additional treatment recommended for SOME patients in selected patient group

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.[53]

It is important to be certain that the patient does not have acute ischaemia before administering isoprenaline.

Primary options

isoprenaline: 2 micrograms/minute intravenous infusion initially, dose titrated according to response, maximum 10 micrograms/minute

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temporary or permanent pacing

Additional treatment recommended for SOME patients in selected patient group

Indicated in recurrent torsades de pointes after acute therapy.

catecholaminergic polymorphic ventricular tachycardia

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beta-blockers

Medical therapy for catecholaminergic polymorphic ventricular tachycardia includes the use of beta-blockers for both acute and chronic treatment.[27][32]

High dose of beta-blockers is usually required.

Other treatment strategies have been proposed, including a stepwise addition of alternative 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]

Primary options

nadolol: consult specialist for guidance on dose

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implantable cardioverter defibrillator

Additional treatment recommended for SOME patients in selected patient group

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.[46] ICD shocks can be painful and if frequent may impair the patient's quality of life.[40][41][42][47]

ACUTE

haemodynamically stable non-idiopathic sustained ventricular tachycardia

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anti-arrhythmic medications + treatment of reversible cause (if present)

The group of patients discussed here as non-idiopathic 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 electrophysiological 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.

Anti-arrhythmic medications are useful in the acute management of haemodynamically stable VT. Before initiating anti-arrhythmic 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 haemodynamic 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.[31] Other anti-arrhythmic drugs may also be considered in the acute management of stable VT. The AHA recommends intravenous procainamide or intravenous amiodarone.[31] 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.[36] However, procainamide may be more pro-arrhythmic and should be used with caution in the setting of baseline QT prolongation.[31]

In patients with an identifiable reversible cause of VT (e.g., ischaemia, myocardial infarction, toxicity, drug overdose) management will also involve treatment of the reversible cause.[1]

Primary options

adenosine: 6 mg intravenously initially, followed by 12 mg every 1-2 minutes for up to 2 doses according to response

OR

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)

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

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synchronised cardioversion ± anti-arrhythmic medications

In patients who do not respond to the initial acute treatment with anti-arrhythmic therapy, synchronised electrical cardioversion is an important treatment for haemodynamically tolerated sustained (monomorphic) ventricular tachycardia (VT). Among patients who fail an initial attempt at synchronised cardioversion, anti-arrhythmic medications such as amiodarone or lidocaine may be administered prior to additional attempts at cardioversion.

Synchronised cardioversion should be considered before attempting anti-arrhythmic drug therapy in patients who are highly symptomatic (particularly those with symptoms of diminished cerebral perfusion), even if they have apparently stable haemodynamics.

Advanced cardiac life support guidelines recommend giving amiodarone or lidocaine, then synchronised cardioversion.[31]

In patients with an identifiable reversible cause of VT (e.g., ischaemia, myocardial infarction, toxicity, drug overdose) management will also involve ongoing treatment of the reversible cause.[1]

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

Secondary options

lidocaine: 1 to 1.5 mg/kg intravenously initially, followed by 1-4 mg/minute infusion

haemodynamically stable idiopathic sustained ventricular tachycardia

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intravenous anti-arrhythmic medications

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 electrophysiological 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 manoeuvres.

Fascicular VT characteristically responds to verapamil, but the drug should be used with extreme caution due to the risk of hypotension and haemodynamic collapse if given to other forms of VT.

In cases refractory to adenosine or verapamil, idiopathic VT can be treated with anti-arrhythmic medications (lidocaine, amiodarone); if necessary, synchronised electrical cardioversion may be performed.[31]

If the patient is not already being managed by a specialist, following successful termination of the tachycardia and stabilisation, patients should referred to a specialist (electrophysiologist) for further management.

Primary options

Outflow tract VT

adenosine: 6 mg intravenously initially, followed by 12 mg every 1-2 minutes for up to 2 doses according to response

OR

Fascicular VT

verapamil: 5-10 mg intravenously initially, followed by 10 mg after 30 minutes if no adequate response seen, maximum 20 mg total dose

OR

Outflow tract VT

metoprolol: 5 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

OR

lidocaine: 1 to 1.5 mg/kg intravenously as a single dose

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synchronised cardioversion

In patients with idiopathic ventricular tachycardia who have failed to respond to anti-arrhythmic drug therapy, synchronised 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 haemodynamics.

If the patient is not already being managed by a specialist, following successful termination of the tachycardia and stabilisation, patients should referred to a specialist (electrophysiologist) for further management.

ONGOING

non-idiopathic: at high risk for ventricular tachycardia or history of sustained ventricular tachycardia/cardiac arrest without identifiable reversible cause

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implantable cardioverter defibrillator

The group of patients discussed here as non-idiopathic 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 electrophysiological (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: ischaemic cardiomyopathy (left ventricular ejection fraction [LVEF] ≤35%, or ≤40% with non-sustained VT and inducible VT during EP); non-ischaemic 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 non-sustained 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 anti-arrhythmic 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 ischaemia. ICD implantation is contra-indicated 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.[46] ICD shocks can be painful and if frequent may impair the patient's quality of life.[40][41][42][47]

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Consider – 

anti-arrhythmic medication

Additional treatment recommended for SOME patients in selected patient group

Anti-arrhythmic 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, randomised trials have shown that currently available oral anti-arrhythmic 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 anti-arrhythmic 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.[50]

Primary options

mexiletine: 200 mg orally every 8 hours

OR

flecainide: 100-150 mg orally twice daily

OR

propafenone: 150-300 mg orally (immediate-release) every 8 hours; or 225-425 mg orally (extended-release) every 12 hours

OR

sotalol: 80-160 mg orally twice daily

OR

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

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anti-arrhythmic monotherapy

Anti-arrhythmic 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, randomised trials have shown that currently available oral anti-arrhythmic drugs, other than beta-blockers, do not prolong life when used chronically in the treatment of life-threatening ventricular arrhythmias and sudden death.[7] Anti-arrhythmic 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.[50]

Primary options

mexiletine: 200 mg orally every 8 hours

OR

flecainide: 100-150 mg orally twice daily

OR

propafenone: 150-300 mg orally (immediate-release) every 8 hours

OR

sotalol: 80-160 mg orally twice daily

OR

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

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catheter ablation

Treatment recommended for ALL patients in selected patient group

Catheter ablation may also be used as a palliative measure in patients with structural heart disease experiencing recurrent episodes of ventricular tachycardia.[37][51]

idiopathic ventricular tachycardia

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specialist referral for ongoing anti-arrhythmic treatment

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 electrophysiological 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.

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beta-blockers or calcium-channel blockers or catheter ablation

Treatment recommended for ALL patients in selected patient group

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.[37]

Primary options

metoprolol: 50-200 mg/day orally (immediate-release) given in 2 divided doses

OR

atenolol: 25 to 100 mg orally once daily

OR

verapamil: 180-240 mg/day orally (immediate-release) given in 3-4 divided doses; 180-240 mg orally (extended-release) once daily

OR

diltiazem: 90-360 mg/day orally (immediate-release) given in 3-4 divided doses; 90-360 mg orally (extended-release) once daily

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catheter ablation

Treatment recommended for ALL patients in selected patient group

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.[37]

It is also reasonable as first-line therapy in patients with mild-to-moderate symptoms who prefer not to take medications.

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class I or class III anti-arrhythmic medications

Treatment recommended for ALL patients in selected patient group

In ongoing therapy, anti-arrhythmic 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.[37][38]

Medication choice is usually based on individual patient/physician preference.

Primary options

mexiletine: 200 mg orally every 8 hours

OR

flecainide: 100-200 mg orally twice daily

OR

propafenone: 150 to 350 mg orally (immediate-release) every 8 hours

OR

sotalol: 80-160 mg orally twice daily

Secondary options

amiodarone: 200 mg/day orally given in single or divided doses

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Please note that formulations/routes and doses may differ between drug names and brands, drug formularies, or locations. Treatment recommendations are specific to patient groups. See disclaimer

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