Ventricular tachycardia: mechanisms, diagnosis and slow post-infarction rhythms
THE CONTEXT
Ventricular tachycardia (VT) usually occurs with significant ventricular disease, although it can occasionally arise in an otherwise healthy heart.
Associations and mechanisms
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VT most commonly occurs with acute myocardial infarction, chronic coronary artery disease or cardiomyopathy. It is associated with extensive ventricular disease, impaired left ventricular function and ventricular aneurysm.
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In these settings, VT may cause haemodynamic compromise or degenerate into ventricular fibrillation.
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The usual mechanism is re-entry within scarred ventricular tissue. Abnormal automaticity or triggered activity in ischaemic tissue is less common.
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VT in an otherwise healthy heart usually results from abnormal automaticity in the right ventricular outflow tract or a fascicle of the left bundle branch.
Clinical findings and diagnostic uncertainty
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Symptoms include palpitation, dyspnoea, lightheadedness and syncope. The ECG shows tachycardia above 120/min with broad, abnormal QRS complexes.
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VT can be difficult to distinguish from supraventricular tachycardia with bundle branch block or pre-excitation. A 12-lead ECG or electrophysiology study may help.
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When the diagnosis remains uncertain, it is safer to manage the rhythm as VT.
Idioventricular rhythm after myocardial infarction
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During recovery from myocardial infarction, idioventricular rhythm or slow VT may occur at a rate slightly above the preceding sinus rate but below 120/min.
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These episodes often reflect reperfusion of the infarct territory and may be a favourable sign. They are usually asymptomatic, self-limiting and require no treatment.
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Other forms of sustained VT require treatment, often as an emergency.