Ventricular Tachycardia

Ventricular tachycardia (VT) is a lethal cardiac arrhythmia that is very common after a heart attack. The risk of VT is highest in the first several hours after a heart attack. VT often degenerates into ventricular fibrillation (VF), which is 100 percent fatal if a defibrillator is not used to restore normal rhythm.

In the setting of an acute myocardial infarction, VT develops due to the injury of the muscle cells and an unstable electrical conduction pattern. Long after a heart attack that has resulted in major damage to the muscle and the pump function of the heart, a scar forms in the area of injury. The area becomes a source of electrical instability, which can develop into VT or VF. Medications in the first several hours after a heart attack can reduce the incidence of VT. The best way to prevent VT in the setting of a heart attack is to restore blood flow to the injured muscle and the administration of beta-blockers (metoprolol and carvedilol). The anti-arrhythmic lidocaine as a long history of use in the setting of heart attack and theoretically works better in the setting of a heart attack. Amiodarone is also commonly used to treat and prevent VT and is available in an oral form unlike lidocaine which is intravenous. Attempts to prevent VT after acute myocardial infarction (MI) with oral anti-arrhythmics like lidocaine was proven to be ineffective and more dangerous.

It is common to have a defibrillator placed to prevent VT in patients with low heart function and heart failure after a MI and in patients at risk of VT. Other conditions, such as hypertrophic cardiomyopathy, long QT syndrome and exercise, induced VT may require a defibrillator as well. If a patient is a survivor of a cardiac arrest, it is considered appropriate to place a defibrillator, as the cause of sudden death is likely to be VT.