- Ventricular tachycardia (VT) is a series of three or more repetitive beats originating from the ventricle at a rate faster than the upper limit of normal for age. The QRS complex is always different from sinus rhythm and is usually wide but can appear narrow in infants. VT may, but not always, have atrioventricular (AV) dissociation; nonsustained VT: >3 beats and <30 seconds
- Sustained VT: lasts >30 seconds
- VT may be monomorphic or polymorphic.
- Torsades de pointes: a polymorphic variant
- The QRS complexes gradually change shape and axis throughout the tachycardia.
- Associated with congenital long QT syndrome (LQTS), acquired long QT, and Brugada syndrome
- Metabolic disturbances (hypoxia, acidosis, hypo/hyperkalemia, hypomagnesemia, hypothermia)
- Drug toxicity (e.g., digitalis toxicity, antiarrhythmic agents)
- Substance abuse (cocaine, methamphetamine)
- Myocardial ischemia (e.g., Kawasaki disease, congenital coronary anomalies)
- Invasive lines or catheters
- Pericardial effusion
- LQTS may be inherited in an autosomal recessive or autosomal dominant pattern. It is mostly commonly associated with potassium cardiac ion channel defects and may be associated with hearing loss and/or a family history of sudden death.
- Brugada syndrome may be inherited in an autosomal dominant pattern. It is most commonly associated with a defect in the cardiac sodium channel (SCN5A) and appears to be inherited in an autosomal dominant pattern.
VT may result from a reentrant, triggered, or abnormal automaticity mechanism.
- Diverse and often overlapping
- Brugada syndrome
- Catecholaminergic polymorphic VT
- Dilated cardiomyopathy
- Hypertrophic cardiomyopathy
- Arrhythmogenic right ventricular cardiomyopathy
- Before and after surgery for congenital heart disease (CHD) (e.g., tetralogy of Fallot, transposition of the great arteries, aortic stenosis, Ebstein anomaly, and pulmonary vascular occlusive disease)
- Myocardial tumors
- Heart failure
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