Ventricular arrhythmias

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor: Cafer Zorkun, M.D., Ph.D. [2]

Causes of Ventricular Arrhythmias

Cardiac causes

Acute and chronic ischemic heart disease

Cardiomyopathy

Valvular heart disease

Mitral valve prolapse

Noncardiac causes

Stimulants: caffeine, cocaine, alcohol

Metabolic abnormalities: acidosis, hypoxemia, hyperkalemia, hypokalemia, hypomagnesemia

Drugs: digoxin (Lanoxin), theophylline, antipsychotics, tricyclic antidepressants, antiarrhythmics with proarrhythmic potential [e.g., flecainide (Tambocor), dofetilide (Tikosyn), sotalol (Betapace) and quinidine)

An overview of ventricular tachycardias, follow the wide complex tachycardia flowchart

	example	regularity	atrial frequency	ventricular frequency	origin (SVT/VT)	p-wave	effect of adenosine
Wide complex (QRS>0.12)
Ventricular Tachycardia		regular (mostly)	60-100 bpm	110-250 bpm	ventricle (VT)	AV-dissociation	no rate reduction (sometimes accelerates)
Ventricular Fibrillation		irregular	60-100 bpm	400-600 bpm	ventricle (VT)	AV-dissociation	none
Ventricular Flutter		regular	60-100 bpm	150-300 bpm	ventricle (VT)	AV-dissociation	none
Accelerated Idioventricular Rhythm		regular (mostly)	60-100 bpm	50-110 bpm	ventricle (VT)	AV-dissociation	no rate reduction (sometimes accelerates)
Torsade de Pointes		regular		150-300 bpm	ventricle (VT)	AV-dissociation	no rate reduction (sometimes accelerates)
Bundle-branch re-entrant tachycardia*		regular	60-100 bpm	150-300 bpm	ventricles (VT)	AV-dissociation	no rate reduction
(*) Bundle-branch re-entrant tachycardia is extremely rare

Premature Ventricular Complexes (PVCs)

A premature ventricular complex is characterized by the premature occurrence of a QRS complex that is bizarre in shape and lasts longer than 120 msec. The T wave is large and usually of opposite polarity to the QRS complex.

A premature ventricular complex is usually followed by a full compensatory pause. The term “ventricular bigeminy” refers to alternating normal sinus and premature ventricular complexes. Three or more successive premature ventricular complexes are arbitrarily defined as ventricular tachycardia. Premature ventricular complexes become more prevalent with increasing age and occur in association with a variety of stimuli.

It is important to determine whether underlying structural heart disease is present and left ventricular function is impaired.Other common causes include electrolyte abnormalities, stimulants, and some medications.

Management

Patients Without Heart Disease

In the absence of heart disease, PVCs are associated with little or no increased risk of developing a dangerous arrhythmia. In this situation, the risk-to-benefit ratio of antiarrhythmic drug therapy does not support routine treatment. It is important to review medications, determine if stimulants are being used, and correct electrolyte abnormalities. If no underlying cause is found, the optimal approach is patient reassurance. Patients should be made aware of the potential dangers of antiarrhythmic drug therapy as determined in the Cardiac Arrhythmia Suppression Trials (CAST and CAST II).

CAST showed that the risk of dying increased, rather than decreased, with successful long-term suppression of premature ventricular complexes after myocardial infarction in older patients. At best, CAST II showed no impact on long-term survival from drug treatment that successfully suppressed premature ventricular complexes. If patients with multiple premature ventricular complexes have severe, disabling symptoms, beta blockers are the safest initial choice.Referral to a cardiologist is indicated if beta-blocker therapy is not effective. In this situation, the next agents to be tried would be class I antiarrhythmic drugs, such as flecainide (Tambocor) and amiodarone (Cordarone), although radiofrequency ablation of an ectopic focus may also be an appropriate treatment.

Patients with Structural Heart Disease

The occurrence of premature ventricular complexes in patients with structural heart disease has been shown to significantly increase the risk of subsequent morbidity and mortality. Coronary heart disease, cardiomyopathy, and congestive heart failure are the major cardiac diseases associated with unfavorable outcomes in patients with premature ventricular complexes.

Ventricular Tachycardia

Ventricular tachycardia refers to a rhythm originating from a ventricular ectopic focus at a rate >100 bpm. The electrocardiogram shows a wide complex tachycardia with no associated P waves.

In patients with bundle branch block,Wolff-Parkinson-White syndrome, or aberrant conduction, supraventricular tachycardia can resemble ventricular tachycardia. Because of the morbidity and mortality associated with untreated ventricular tachycardia, any wide-complex tachycardia should be assumed to be ventricular tachycardia until proved otherwise. Physicians should keep in mind that patients with ventricular tachycardia can have minimal symptoms.

Management of Ventricular Tachycardia

The mortality rate within two years is reported to be higher than 30% in patients with non sustained ventricular tachycardia on Holter monitoring and impaired left ventricular function. Two large multicenter trials showed a clear advantage for automatic cardioverter defibrillator implantation over drug therapy in patients who had a malignant ventricular arrhythmia or who had been resuscitated from sudden cardiac death. The selection of high-risk patients for defibrillator implantation should be based on left ventricular function and the findings of electrophysiologic studies.

Implantable defibrillators appear to be most beneficial in patients with a low ejection fraction who are noted to have frequent premature ventricular complexes, non sustained ventricular tachycardia on Holter monitoring, and a history of syncope or nearsyncope. It is critical to rule out coronary heart disease and to optimize the treatment of congestive heart failure in these patients. When ventricular tachycardia is diagnosed in relatively asymptomatic patients, medical treatment should be attempted. New recommendations from the American Heart Association emphasize the initial use of 300 mg of iv. administered amiodarone, followed by repeated 150 mg iv. doses every 8-10 minutes, in patients with pulseless VT.

Patients with stable ventricular tachycardia should be given 150 mg of amiodarone intravenously over 10 minutes, followed by an infusion at 1 mg/minute for 6 hours and then at 0.5 mg/minute until the VT converts to sinus rhythm or another less dangerous rhythm. The alternative treatment is intravenously administered lidocaine (Xylocaine), given first in a 100 mg bolus (or 1 mg/kg) and then in an infusion at 1-4 mg/minute.

In hemodynamically unstable patients, electrical cardioversion should be attempted in accordance with the recently revised advanced cardiac life support (ACLS) protocols.

Automatic implantable cardioverter defibrillators (ICD) are considered the most effective treatment for patients with life-threatening VT or VF. According to expert recommendations, implantation of an automatic cardioverter defibrillator should be considered in these situations:

1. Cardiac arrest resulting from ventricular fibrillation or tachycardia not caused by a transient or reversible cause

2. Spontaneous, sustained ventricular tachycardia

3. Syncope of undetermined origin and sustained VT or ventricular fibrillation (VF) induced during electrophysiologic studies

4. Non sustained VT with coronary artery disease and LV dysfunction if VT or VF is induced during electrophysiologic studies.

ACC/AHA/ESC 2006 Guidelines for Management of Patients With Ventricular Arrhythmias (DO NOT EDIT)

Resting Electrocardiogram Recommendations

Class I

"* Resting 12-lead ECG is indicated in all patients who are evaluated for ventricular arrhythmias. (Level of Evidence: A). "

Exercise Testing Recommendations

Class I

"1 Exercise testing is recommended in adult patients with ventricular arrhythmias who have an intermediate or greater probability of having CHD by age, gender, and symptoms* to provoke ischemic changes or ventricular arrhythmias. (Level of Evidence: B) *See Table 4 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for further explanation of CHD probability."

"2 Exercise testing, regardless of age, is useful in patients with known or suspected exercise-induced ventricular arrhythmias, including catecholaminergic VT, to provoke the arrhythmia, achieve a diagnosis, and determine the patient’s response to tachycardia. (Level of Evidence: B)"

Class III

"1 See Table 1 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for contraindications. (Level of Evidence: C)"

Class IIa

"1 Exercise testing can be useful in evaluating response to medical or ablation therapy in patients with known exercise-induced ventricular arrhythmias. (Level of Evidence: B)"

Class IIb

"1 Exercise testing may be useful in patients with ventricular arrhythmias and a low probability of CHD by age, gender, and symptoms.* (Level of Evidence: C) *See Table 4 in the ACC/AHA 2002 Guideline Update for Exercise Testing (141) for further explanation of CHD probability."

"2 Exercise testing may be useful in the investigation of isolated premature ventricular complexes (PVCs) in middle-aged or older patients without other evidence of CHD. (Level of Evidence: C)"

Ambulatory Electrocardiography Recommendations

Class I

"1 Ambulatory ECG is indicated when there is a need to clarify the diagnosis by detecting arrhythmias, QTinterval changes, T-wave alternans (TWA), or ST changes, to evaluate risk, or to judge therapy. (Level of Evidence: A) "

"2 Event monitors are indicated when symptoms are sporadic to establish whether or not they are caused by transient arrhythmias. (Level of Evidence: B) "

"3 Implantable recorders are useful in patients with sporadic symptoms suspected to be related to arrhythmias such as syncope when a symptom-rhythm correlation cannot be established by conventional diagnostic techniques. (Level of Evidence: B) "

Electrocardiographic Techniques and Measurements Recommendations

Class IIa "1 It is reasonable to use TWA to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or who are at risk for developing lifethreatening ventricular arrhythmias. (Level of Evidence: A) "

Class IIb "1 ECG techniques such as signal-averaged ECG (SAECG), heart rate variability (HRV), baroflex sensitivity, and heart rate turbulence may be useful to improve the diagnosis and risk stratification of patients with ventricular arrhythmias or who are at risk of developing life-threatening ventricular arrhythmias. (Level of Evidence: B) "

Left Ventricular Function and Imaging Recommendations

Class I

"1 Echocardiography is recommended in patients with ventricular arrhythmias who are suspected of having structural heart disease. (Level of Evidence: B) "

"2 Echocardiography is recommended for the subset of patients at high risk for the development of serious ventricular arrhythmias or SCD, such as those with dilated, hypertrophic, or RV cardiomyopathies, AMI survivors, or relatives of patients with inherited disorders associated with SCD. (Level of Evidence: B) "

"3 Exercise testing with an imaging modality (echocardiography or nuclear perfusion [single-photon emission computed tomography (SPECT)]) is recommended to detect silent ischemia in patients with ventricular arrhythmias who have an intermediate probability of having CHD by age, symptoms, and gender and in whom ECG assessment is less reliable because of digoxin use, LVH, greater than 1-mm ST-segment depression at rest, WPW syndrome, or LBBB. (Level of Evidence: B) "

"4 Pharmacological stress testing with an imaging modality (echocardiography or myocardial perfusion SPECT) is recommended to detect silent ischemia in patients with ventricular arrhythmias who have an intermediate probability of having CHD by age, symptoms, and gender and are physically unable to perform a symptomlimited exercise test. (Level of Evidence: B) "

Class IIa

"1 MRI, cardiac computed tomography (CT), or radionuclide angiography can be useful in patients with ventricular arrhythmias when echocardiography does not provide accurate assessment of LV and RV function and/or evaluation of structural changes. (Level of Evidence: B)"

"2 Coronary angiography can be useful in establishing or excluding the presence of significant obstructive CHD in patients with life-threatening ventricular arrhythmias or in survivors of SCD, who have an intermediate or greater probability of having CHD by age, symptoms, and gender. (Level of Evidence: C)"

"3 LF imaging can be useful in patients undergoing biventricular pacing. (Level of Evidence: C) "

Electrophysiological Testing in Patients With Coronary Heart Disease Recommendations

Class I

"1 EP testing is recommended for diagnostic evaluation of patients with remote MI with symptoms suggestive of ventricular tachyarrhythmias, including palpitations, presyncope, and syncope. (Level of Evidence: B) "

"2 EP testing is recommended in patients with CHD to guide and assess the efficacy of VT ablation. (Level of Evidence: B) "

"3 EP testing is useful in patients with CHD for the diagnostic evaluation of wide-QRS-complex tachycardias of unclear mechanism. (Level of Evidence: C) "

Class IIa

"1 EP testing is reasonable for risk stratification in patients with remote MI, NSVT, and LVEF equal to or less than 40%. (Level of Evidence: B)"

Electrophysiological Testing in Patients With Syncope Recommendations

Class I

"1 EP testing is recommended in patients with syncope of unknown cause with impaired LV function or structural heart disease. (Level of Evidence: B) "

Class IIa

"1 EP testing can be useful in patients with syncope when bradyarrhythmias or tachyarrhythmias are suspected and in whom noninvasive diagnostic studies are not conclusive. (Level of Evidence: B)"

Ablation Recommendations

“

Class I Ablation is indicated in patients who are otherwise at low risk for SCD and have sustained predominantly monomorphic VT that is drug resistant, who are drug intolerant, or who do not wish long-term drug therapy. (Level of Evidence: C) Ablation is indicated in patients with bundle-branch reentrant VT. (Level of Evidence: C) Ablation is indicated as adjunctive therapy in patients with an ICD who are receiving multiple shocks as a result of sustained VT that is not manageable by reprogramming or changing drug therapy or who do not wish long-term drug therapy (206,278). (Level of Evidence: C) Ablation is indicated in patients with WPW syndrome resuscitated from sudden cardiac arrest due to AF and rapid conduction over the accessory pathway causing VF (279). (Level of Evidence: B) Class III Ablation of asymptomatic relatively infrequent PVCs is not indicated. (Level of Evidence: C) Class IIa Ablation can be useful therapy in patients who are otherwise at low risk for SCD and have symptomatic nonsustained monomorphic VT that is drug resistant, who are drug intolerant or who do not wish long-term drug therapy. (Level of Evidence: C) Ablation can be useful therapy in patients who are otherwise at low risk for SCD and have frequent symptomatic predominantly monomorphic PVCs that are drug resistant or who are drug intolerant or who do not wish long-term drug therapy. (Level of Evidence: C) Ablation can be useful in symptomatic patients with WPW syndrome who have accessory pathways with refractory periods less than 240 ms in duration (279). (Level of Evidence: B) Class IIb Ablation of Purkinje fiber potentials may be considered in patients with ventricular arrhythmia storm consistently provoked by PVCs of similar morphology(280). (Level of Evidence: C) Ablation of asymptomatic PVCs may be considered when the PVCs are very frequent to avoid or treat tachycardia-induced cardiomyopathy (281). (Level of Evidence: C)

”

Management of Cardiac Arrest Recommendations

“

Class I After establishing the presence of definite, suspected, or impending cardiac arrest, the first priority should be activation of a response team capable of identifying the specific mechanism and carrying out prompt intervention. (Level of Evidence: B) Cardiopulmonary resuscitation (CPR) should be implemented immediately after contacting a response team. (Level of Evidence: A) In an out-of-hospital setting, if an AED is available, it should be applied immediately and shock therapy administered according to the algorithms contained in the documents on CPR (334,335) developed by the AHA in association with the International Liaison Committee on Resuscitation (ILCOR) and/or the European Resuscitation Council (ERC). (Level of Evidence: C) For victims with ventricular tachyarrhythmic mechanisms of cardiac arrest, when recurrences occur after a maximally defibrillating shock (generally 360 J for monophasic defibrillators), intravenous amiodarone should be the preferred antiarrhythmic drug for attempting a stable rhythm after further defibrillations. (Level of Evidence: B) For recurrent ventricular tachyarrhythmias or nontachyarrhythmic mechanisms of cardiac arrest, it is recommended to follow the algorithms contained in the documents on CPR (334,335) developed by the AHA in association with ILCOR and/or the ERC. (Level of Evidence: C) Reversible causes and factors contributing to cardiac arrest should be managed during advanced life support, including management of hypoxia, electrolyte disturbances, mechanical factors, and volume depletion. (Level of Evidence: C) Class IIa For response times greater than or equal to 5 min, a brief (less than 90 to 180 s) period of CPR is reasonable prior to attempting defibrillation. (Level of Evidence: B) Class IIb A single precordial thump may be considered by health care professional providers when responding to a witnessed cardiac arrest. (Level of Evidence: C)

”

Ventricular Tachycardia Associated With Low Troponin Myocardial Infarction Recommendations

“

Class I Patients presenting with sustained VT in whom lowlevel elevations in cardiac biomarkers of myocyte injury/necrosis are documented should be treated similarly to patients who have sustained VT and in whom no biomarker rise is documented. (Level of Evidence: C)

”

Sustained Monomorphic Ventricular Tachycardia Recommendations

“

Class I Wide-QRS tachycardia should be presumed to be VT if the diagnosis is unclear. (Level of Evidence: C) Direct current cardioversion with appropriate sedation is recommended at any point in the treatment cascade in patients with suspected sustained monomorphic VT with hemodynamic compromise. (Level of Evidence: C) Class III Calcium channel blockers such as verapamil and diltiazem should not be used in patients to terminate wide-QRS-complex tachycardia of unknown origin, especially in patients with a history of myocardial dysfunction. (Level of Evidence: C) Class IIa Intravenous procainamide (or ajmaline in some European countries) is reasonable for initial treatment of patients with stable sustained monomorphic VT. (Level of Evidence: B) Intravenous amiodarone is reasonable in patients with sustained monomorphic VT that is hemodynamically unstable, refractory to conversion with countershock, or recurrent despite procainamide or other agents. (Level of Evidence: C) Transvenous catheter pace termination can be useful to treat patients with sustained monomorphic VT that is refractory to cardioversion or is frequently recurrent despite antiarrhythmic medication. (Level of Evidence: C) Class IIb Intravenous lidocaine might be reasonable for the initial treatment of patients with stable sustained monomorphic VT specifically associated with acute myocardial ischemia or infarction. (Level of Evidence: C)

”

Repetitive Monomorphic Ventricular Tachycardia Recommendations

“

Class IIa Intravenous amiodarone, beta blockers, and intravenous procainamide (or sotalol or ajmaline in Europe) can be useful for treating repetitive monomorphic VT in the context of coronary disease (375) and idiopathic VT. (Level of Evidence: C)

”

Polymorphic VT Recommendations

“

Class I Direct current cardioversion with appropriate sedation as necessary is recommended for patients with sustained polymorphic VT with hemodynamic compromise and is reasonable at any point in the treatment cascade. (Level of Evidence: B) Intravenous beta blockers are useful for patients with recurrent polymorphic VT, especially if ischemia is suspected or cannot be excluded. (Level of Evidence: B) Intravenous loading with amiodarone is useful for patients with recurrent polymorphic VT in the absence absence of abnormal repolarization related to congenital or acquired LQTS. (Level of Evidence: C) Urgent angiography with a view to revascularization should be considered for patients with polymorphic VT when myocardial ischemia cannot be excluded. (Level of Evidence: C) Class IIb Intravenous lidocaine may be reasonable for treatment of polymorphic VT specifically associated with acute myocardial ischemia or infarction. (Level of Evidence: C)

”

Torsades de Pointes Recommendations

“

Class I Withdrawal of any offending drugs and correction of electrolyte abnormalities are recommended in patients presenting with torsades de pointes. (Level of Evidence: A) Acute and long-term pacing is recommended for patients presenting with torsades de pointes due to heart block and symptomatic bradycardia. (Level of Evidence: A) Class IIa Management with intravenous magnesium sulfate is reasonable for patients who present with LQTS and few episodes of torsades de pointes. Magnesium is not likely to be effective in patients with a normal QT interval. (Level of Evidence: B) Acute and long-term pacing is reasonable for patients who present with recurrent pause-dependent torsades de pointes. (Level of Evidence: B) Beta blockade combined with pacing is reasonable acute therapy for patients who present with torsades de pointes and sinus bradycardia. (Level of Evidence: C) Isoproterenol is reasonable as temporary treatment in acute patients who present with recurrent pausedependent torsades de pointes who do not have congenital LQTS. (Level of Evidence: B) Class IIb Potassium repletion to 4.5 to 5 mmol/L may be considered for patients who present with torsades de pointes. (Level of Evidence: B) Intravenous lidocaine or oral mexiletine may be considered in patients who present with LQT3 and torsades de pointes. (Level of Evidence: C)

”

Incessant Ventricular Tachycardia Recommendations

“

Class I Revascularization and beta blockade followed by intravenous antiarrythmic drugs such as procainamide or amiodarone are recommended for patients with recurrent or incessant polymorphic VT due to acute myocardial ischemia. (Level of Evidence: C) Class IIa Intravenous amiodarone or procainamide followed by VT ablation can be effective in the management of patients with frequently recurring or incessant monomorphic VT. '(Level of Evidence: B) Class IIb Intravenous amiodarone and intravenous beta blockers separately or together may be reasonable in patients with VT storm.(Level of Evidence: C) Overdrive pacing or general anesthesia may be considered for patients with frequently recurring or incessant VT. (Level of Evidence: C) Spinal cord modulation may be considered for some patients with frequently recurring or incessant VT. (Level of Evidence: C)

”

Left Ventricular Dysfunction Due to Prior Myocardial Infarction Recommendations

“

Class I Aggressive attempts should be made to treat HF that may be present in some patients with LV dysfunction due to prior MI and ventricular tachyarrhythmias. (Level of Evidence: C) Aggressive attempts should be made to treat myocardial ischemia that may be present in some patients with ventricular tachyarrhythmias. (Level of Evidence: C) Coronary revascularization is indicated to reduce the risk of SCD in patients with VF when direct, clear evidence of acute myocardial ischemia is documented to immediately precede the onset of VF. (Level of Evidence: B) If coronary revascularization cannot be carried out and there is evidence of prior MI and significant LV dysfunction, the primary therapy of patients resuscitated from VF should be the ICD in patients who are receiving chronic optimal medical therapy and those who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: A) ICD therapy is recommended for primary prevention to reduce total mortality by a reduction in SCD in patients with LV dysfunction due to prior MI who are at least 40 d post-MI, have an LVEF less than or equal to 30% to 40%, are NYHA functional class II or III, are receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: A) (See Section 1.2.) The ICD is effective therapy to reduce mortality by a reduction in SCD in patients with LV dysfunction due to prior MI who present with hemodynamically unstable sustained VT, are receiving chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: A) Class IIa Implantation of an ICD is reasonable in patients with LV dysfunction due to prior MI who are at least 40 d post-MI, have an LVEF of less than or equal to 30% to 35%, are NYHA functional class I on chronic optimal medical therapy, and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: B) (See Section 1.2.) Amiodarone, often in combination with beta blockers, can be useful for patients with LV dysfunction due to prior MI and symptoms due to VT unresponsive to beta-adrenergic– blocking agents. (Level of Evidence: B) Sotalol is reasonable therapy to reduce symptoms resulting from VT for patients with LV dysfunction due to prior MI unresponsive to beta-blocking agents. (Level of Evidence: C) Adjunctive therapies to the ICD, including catheter ablation or surgical resection, and pharmacological therapy with agents such as amiodarone or sotalol are reasonable to improve symptoms due to frequent episodes of sustained VT or VF in patients with LV dysfunction due to prior MI. (Level of Evidence: C) Amiodarone is reasonable therapy to reduce symptoms due to recurrent hemodynamically stable VT for patients with LV dysfunction due to prior MI who cannot or refuse to have an ICD implanted. (Level of Evidence: C) Implantation is reasonable for treatment of recurrent ventricular tachycardia in patients post-MI with normal or near normal ventricular function who are receiving chronic optimal medical therapy and who have reasonable expectation of survival with a good functional status for more than 1 y. (Level of Evidence: C)

”

Resources

1. Zipes DP, Camm AJ, Borggrefe M, et al., ACC/AHA/ESC 2006 Guidelines 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 and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death)Circulation 2006;114;e385-e484

2. Kesh Hebbar A, Hueston WJ, Management of Common Arrhythmias: Part II.Ventricular Arrhythmias and Arrhythmias in Special Populations Am Fam Physician 2002;65:2491-6.