as 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 as non-sustained ventricular tachycardia. Sustained ventricular tachycardia has duration >30 seconds.
Monomorphic ventricular tachycardia
In monomorphic ventricular tachycardia all QRS complexes display the same morphology (minor differences are allowed). This indicates that the impulses originate in the same ectopic focus. In structural heart disease (coronary heart disease, heart failure, cardiomyopathy, valvular disease etc) monomorphic ventricular tachycardia is typically caused by re-entry. Refer to Figure 1.
The Purkinje fibers in the interventricular septum appear to have an important role in ventricular tachycardia among patients with coronary heart disease. These Purkinje fibers appear to be highly arrhythmogenic in the setting of myocardial ischemia, particularly re-ischemia. Because any impulse arising in the interventricular septum will enter the Purkinje network (to some degree) the QRS complexes tend to be shorter than arrhythmias originating in the free ventricular walls. QRS duration is generally 120 to 145 ms in ventricular tachycardias arising in the septum.
Fascicular ventricular tachycardia is an idiopathic form of VT. It is caused by re-entry in the fascicles of the left bundle branch (i.e in the Purkinje fibers). Fascicular ventricular tachycardia occurs in people aged less than 50 years of age, and predominantly in males. The QRS complexes display morphology similar to right bundle branch block and there is left axis deviation.
Right ventricular outflow tract (RVOT) ventricular tachycardia is a monomorphic VT originating in the outflow tract of the right ventricle. The arrhythmia is mostly idiopathic but some patients may have ARVC (arrhythmogenic right ventricular cardiomyopathy). Because the impulses originate in the right ventricle, the QRS complexes have left bundle branch appearance and the electrical axis is around 90°. Refer to Figure 2.
Polymorphic ventricular tachycardia
A ventricular tachycardia with varying QRS morphology or varying electrical axis is classified as polymorphic. Th