Ventricular tachycardia (VT): types, causes, ECG features and management
This chapter deals with ventricular tachycardia from a clinical perspective, with emphasis on ECG diagnosis, definitions, management and clinical characteristics. Ventricular tachycardia is a highly nuanced arrhythmia which originates in the ventricles. A wide range of conditions may cause ventricular tachycardia and the ECG is as nuanced as are those conditions. Regardless of etiology and ECG, ventricular tachycardia is always a potentially life-threatening arrhythmia which requires immediate attention. The ventricular rate is typically very high (100–250 beats per minute) and cardiac output is affected (i.e reduced) in virtually all cases. Ventricular tachycardia cause immense strain on the ventricular myocardium, simultaneously as the cause of the arrhythmia already affects cellular function. This results in electrical instability which explains why ventricular tachycardia may progress to ventricular fibrillation. Left untreated, ventricular fibrillation leads to asystole and cardiac arrest. All health care providers, regardless of profession, must be able to diagnose ventricular tachycardia.
Causes of ventricular tachycardia
Patients with ventricular tachycardia almost invariably have significant underlying heart disease. The most common causes are coronary heart disease (acute coronary syndromes or ischemic heart disease), heart failure, cardiomyopathy (dilated cardiomyopathy, hypertrophic obstructive cardiomyopathy), valvular disease. Less common causes are arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/ARVD), Brugada syndrome, long QT syndrome, sarcoidosis, Prinzmetal’s angina (coronary vasospasm), electrolyte disorders, congenital heart disease and catecholamine induced ventricular tachycardia.
The vast majority of patients with ventricular tachycardia either have coronary artery disease (ischemic heart disease), heart failure, cardiomyopathy or valvular heart disease. In these populations one of the strongest predictors of sudden cardiac death is left ventricular function. Individuals with reduced left ventricular function (e.g defined as ejection fraction <40 %) are at high risk of sudden cardiac arrest.
Idiopathic ventricular tachycardia (IVT)
Ventricular tachycardia may be classified as idiopathic if no cause can be identified. Idiopathic ventricular tachycardia has a more favorable prognosis, as compared with other forms of ventricular tachycardia.
Mechanisms of ventricular tachycardia
Ventricular tachycardia (VT) may emerge due to increased/abnormal automaticity, re-entry or triggered activity. All types of myocardial cells may be engaged in initiation and maintenance of this arrhythmia. As mentioned above VT causes hemodynamic compromise. The rapid ventricular rate, which may be accompanied by already impaired ventricular function, does not allow for adequate filling of the ventricles, which results in reduced stroke volume and reduced cardiac output.
Most patients experience presyncope or syncope if the arrhythmia is sustained. In its fulminant course, VT degenerates to ventricular fibrillation, which then degenerates into asystole and cardiac arrest. Importantly, the progress from VT to cardiac arrest may be aborted either spontaneously or by means of treatment. Interestingly, treatment of VT is considered one of the greatest advances in cardiology. Until 1961, patients with acute myocardial infarction were placed in beds located far away from physicians’ and nurses’ stations in order to not disturb the patients’ rest. It was believed that the mere presence of physicians and nurses caused harmful stress. Approximately 30% of patients died in the hospital and fatal tachyarrhythmias was presumably the leading cause. Animal studies conducted in the late 1950s, 1960 and 1961 showed that VT could be terminated by delivering an electrical shock. This prompted physicians to construct coronary care units, in which all patients with acute myocardial infarction were monitored with continuous ECG and ventricular tachyarrhythmi