Ventricular tachycardia overview
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1];Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2], Avirup Guha, M.B.B.S.[3]
Overview
Ventricular tachycardia is a tachycardia that originates in one of the ventricles of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation and sudden death. In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could be the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia since that time. Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified under three main categories; firstly, The morphology of the QRS complexes on the EKG (monomorphic ventricular tachycardia vs polymorphic ventricular tachycardia), secondly, the duration of the episode, thirdly the symptoms associated with the episode. The underlying mechanism of VT is due to automaticity arising in either the myocardium or in the distal conduction system. The most common underlying substrate for ventricular tachycardia is ischemic heart disease. The morphology of ventricular tachycardia often depends on its cause. Common causes of ventricular tachycardia include ischemic heart disease, illicit drugs (cocaine and methamphetamine), structural heart disease (including congenital heart diseases such as Tetralogy of Fallot), inherited channelopathies, drug toxicity (digoxin, drugs that prolong the QT interval) and electrolyte disturbances (such as hypokalemia, hypomagnesemia, and hypocalcemia). Ischemic heart disease is the most common cause of ventricular tachycardia in the US, followed by cardiomyopathy. VT causes approximately half of the 300,000 sudden deaths which occur out of hospital annually in the US. Brugada syndrome is thought to be the cause of half of the sudden cardiac deaths which occurs in young individuals without structural heart disease. The symptoms of ventricular tachycardia depends on the ventricular rate, the duration of tachycardia, and the presence of underlying disease. In general, the symptoms include shortness of breath, weakness, palpitations, fatigue, and syncope. Serial cardiac enzymes, serum electrolytes as well as calcium, magnesium and phosphate levels, should be obtained. A toxicology screen should also be obtained to assess for illicit drugs as the cause of the VT, as well as levels of medications that may have caused the VT. Therapy may be directed at either terminating an episode of the arrhythmia or for suppressing a future episode from occurring. The treatment is tailored to the specific patient, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. It is usually possible to terminate a VT episode with a direct current shock across the heart. This is ideally synchronized to the patient's heartbeat. As it is quite uncomfortable, shocks should be delivered only to an unconscious or sedated patient.
Historical Perspective
In 1906 Gallavardin discovered the reasons behind the cardiac instability which leads to ventricular tachycardia, and put forth the idea that VT could convert into ventricular fibrillation. Thomas Lewis gave the first electrocardiographic description of ventricular tachycardia in 1909. It was first suggested in 1921 that coronary occlusion could the main cause of ventricular tachycardia. Many advancements have been made in the diagnosis and management protocols of ventricular tachycardia since that time.
Classification
Ventricular tachycardia refers to a rhythm with a heart rate in excess of 100 (and in some definitions 120) beats per minute that arises distal to the bundle of His. Ventricular tachycardia can be classified under three main categories; firstly, The morphology of the QRS complexes on the EKG (monomorphic ventricular tachycardia vs polymorphic ventricular tachycardia), secondly, the duration of the episode, thirdly the symptoms associated with the episode.
Pathophysiology
The underlying mechanism of VT is due to automaticity arising in either the myocardium or in the distal conduction system. The most common underlying substrate for ventricular tachycardia is ischemic heart disease. The morphology of ventricular tachycardia often depends on its cause.
Causes
Common causes of ventricular tachycardia include ischemic heart disease, illicit drugs (cocaine and methamphetamine), structural heart disease (including congenital heart diseases such as Tetralogy of Fallot), inherited channelopathies, drug toxicity (digoxin, drugs that prolong the QT interval) and electrolyte disturbances (such as hypokalemia, hypomagnesemia, and hypocalcemia).
Differentiating Ventricular Tachycardia from other Disorders
Ventricular tachycardia must be distinguished from a variety of rhythm abnormalities which have similar appearance on electrocardiogram.
Epidemiology and Demographics
Ischemic heart disease is the most common cause of ventricular tachycardia in the US, followed by cardiomyopathy. VT is causes approximately of half of the 300,000 sudden deaths which occur out of hospital annually in the US. Brugada syndrome is thought to be the cause of half of the sudden cardiac deaths which occurs in young individuals without structural heart disease.
Risk Factors
Reversible/preventible risk factors for ventricular tachycardia include electrolyte disturbances such as hypokalemia, digitalis toxicity, antiarrhythmic use, pulmonary artery catheter placement and illicit drug use such as cocaine. Irreversible causes include structural heart disease and inherited channelopathies.
Screening
In a young patient with lone atrial fibrillation, short QT syndrome should be excluded. In a patient with a family history of sudden cardiac death a physical examination should be performed.
Natural History, Complications and Prognosis
Sustained ventricular tachycardia in general carries a poor prognosis due to an increased risk of sudden cardiac death.
Diagnosis
History and Symptoms
The symptoms of ventricular tachycardia will depend on the ventricular rate, the duration of tachycardia, and the presence of underlying disease. In general, the symptoms include shortness of breath, weakness, palpitations, fatigue, and syncope.
Physical Examination
Physical examination should consist of a thorough cardiac exam, lung exam, and close monitoring of vital signs. Jugular pulsation may be noted in the neck exam.
Laboratory Findings
Serial cardiac enzymes, serum electrolytes as well as calcium, magnesium and phosphate levels, should be obtained. A toxicology screen should also be obtained to assess for illicit drugs as the cause of the VT, as well as levels of medications that may have caused the VT.
Electrocardiogram
The diagnosis of ventricular tachycardia almost completely depends on EKG findings. The details are illustrated below. It is important to differentiate it from other wide complex tachycardias. The rate is > 100 beats per minute and is usually 150-200 beats per minute. The QRS complex is wide (>140 milliseconds). AV dissociation is always present, but is evident in only 20% of cases of VT.
Chest X Ray
Chest X ray is done only when ventricular tachycardia leads to congestive heart failure or if a secondary pathological disease is suspected as the cause of ventricular tachycardia.
Echocardiography
Echocardiography can be performed in the patient with ventricular tachycardia to rule out structural abnormalities such as a right ventricular cardiomyopathy and silent ischemia on stress testing. Coronary arteriography is often performed in the patient with ventricular tachycardia to rule out obstructive coronary artery disease.
Treatment
Electrical Cardioversion
Therapy may be directed at either terminating an episode of the arrhythmia or for suppressing a future episode from occurring. The treatment is tailored to the specific patient, with regard to how well the individual tolerates episodes of ventricular tachycardia, how frequently episodes occur, their comorbidities, and their wishes. It is usually possible to terminate a VT episode with a direct current shock across the heart. This is ideally synchronized to the patient's heartbeat. As it is quite uncomfortable, shocks should be delivered only to an unconscious or sedated patient.
Surgery
Surgery is not a mainstay or a preferred method of treatment for ventricular tachycardia. There are some specific scenarios however in which revascularization may be considered, and may help in preventing VT.