tors 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 tachyarrhythmias were handled by means of immediate resuscitation and defibrillation.
Ventricular tachycardia in acute coronary syndromes (myocardial infarction)
Acute coronary syndromes are subdivided into unstable angina (UA), ST elevation myocardial infarction (STEMI) and non ST elevation myocardial infarction (NSTEMI). The risk of VT is high in these conditions. Moreover, the risk is highly time-dependent, being highest in the hyperacute phase (the first minutes to hours after symptom onset). The vast majority of individuals who die in the acute phase of myocardial infarction actually die from ventricular tachyarrhythmias. Death due to pumping failure (i.e cardiogenic shock) is less common. Because the risk is highest in the first minutes to hours, most deaths occur outside of the hospital. The risk of VT (and thus ventricular fibrillation) diminishes gradually as time elapses. In addition to time, the major determinant of VT is the extent of the ischemia/infarction. The larger the ischemic are the greater the risk of arrhythmias.
ECG criteria for ventricular tachycardia
ECG features of ventricular tachycardia
- ≥3 consecutive ventricular beats with rate 100–250 beats per minute (in most cases >120 beats per minute). Ventricular tachycardia with rate 100 to 120 beats per minute is referred to as slow ventricular tachycardia. Ventricular tachycardia with rate >250 beats per minute is referred to as ventricular flutter.
- Wide QRS complexes (QRS duration ≥0,12 s).
Types of ventricular tachycardia
The ECG allows for subclassification of ventricular tachycardia. The discussion below may be perceived as advanced, but the reader should know that it is not required th-at all clinicians be able to classify ventricular tachycardias; merely being able to recognize it is sufficient. Therefore, the purpose of the discussion below is to present the reader with several types of ventricular tachycardia just for reference.
Sustained vs. Non-sustained ventricular tachycardia
Ventricular tachycardia with duration <30 seconds is classified a