Tachyarrhythmias originating in the ventricles are most often associated with ischaemic heart disease and primary or secondary heart failure (i.e. dilated cardiomyopathies). They are common during and up to 24 h after acute myocardial infarction (MI), when increases in sympathetic activity and extracellular [K⁺] as well as slowed conduction favour their initiation. Such peri-infarction arrhythmias may be immediately life-threatening, and indeed the vast majority of deaths associated with MI are caused by ventricular fibrillation occurring before the individual reaches the hospital. If survived, these arrhythmias generally do not recur and are not associated with a subsequent increased risk over and above that conferred by the MI itself. Subsequently, however, the border zone of the healed infarct scar may serve as a substrate for the development of dangerous re-entrant ventricular tachyarrhythmias which can recur or become incessant weeks to years after the MI. Their seriousness and prognostic significance are related to the extent of cardiac damage and impairment of ventricular function that has been sustained. These late arrhythmias themselves confer an additional risk of death, and must be treated either with drugs or with an implantable defibrillator (see below). Ventricular tachyarrhythmias can also be associated with cardiomyopathy, and valvular and congenital heart disease, although idiopathic varieties may occur in structurally normal hearts.

Specific Ventricular Tachyarrhythmias

Premature ventricular contractions (PVCs) are caused by a ventricular ectopic focus and can occur randomly or following every (bigeminy; Figure 50a) or every second (trigeminy) normal beat. Because depolarization is initiated at a site within ventricular muscle, it spreads throughout the ventricles more slowly than normal impulses which are distributed rapidly by the specialized His–Purkinje conduction system. Thus, the QRS complex is broad and abnormally shaped. PVCs may be of no prognostic consequence, but can predispose to more serious arrhythmias if they develop during or after MI, and/or occur during the T wave of the preceding beat.

Ventricular tachycardia (VT) originates in the ventricles, and is defined as a run of successive ventricular ectopic beats occurring at a rate of >100 beats/min (usually 120–200 beats/min). VT is classified as non-sustained or sustained based on whether it lasts for >30 s. Depending on the heart rate, VT can cause symptoms such as syncope, angina and shortness of breath, and if sustained can compromise cardiac pumping, leading to heart failure and death. VT can also deteriorate into ventricular fibrillation (see below), particularly with a heart rate of >200 beats/min.

The ECG in VT demonstrates high frequency, bizarrely shaped QRS complexes which are abnormally broadened (>120 ms in duration). Normal atrial activation may continue to be driven by the SAN (Figure 50b), or the abnormal ventricular pacemaker may cause atrial tachycardia via retrograde impulses traversing the AVN. The configuration of the QRS complex can be used to classify VT into two broad categories. In monomorphic VT (Figure 50b), the QRS complexes all have a similar configuration and the heart rate is generally constant, whereas in polymorphic

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