Torsades de Pointes
Torsades de Pointes (TdP) is a special type of polymorphic VT characterized by periodic changes in the amplitude and peaks of the QRS complexes, appearing to twist around the isoelectric line, with a frequency of 200 - 250 bpm. It can be triggered when a premature ventricular contraction occurs late in diastole, falling on the terminal part of the preceding T wave (R-on-T), and may progress to ventricular fibrillation and sudden death. Causes include electrolyte imbalances (such as hypokalemia and hypomagnesemia), antiarrhythmic drugs (such as class Ia and III), phenothiazines, tricyclic antidepressants, intracranial lesions, and bradycardia (especially third-degree AV block). Some cases are congenital. Efforts should be made to identify and eliminate acquired causes of QT interval prolongation and discontinue drugs known or suspected to induce TdP. Treatment primarily involves intravenous magnesium sulfate. Class Ia or III drugs should be avoided as they may further prolong the QT interval.
Figure 1 R-on-T phenomenon and Torsades de Pointes
In lead II, the arrow indicates an R wave overlapping the preceding T wave (R-on-T phenomenon). The QT interval is prolonged to 0.64 seconds, and during the tachycardia episode, the main direction of the QRS complexes appears to twist continuously around the isoelectric line.
Accelerated idioventricular rhythm
Accelerated idioventricular rhythm (AIVR), also known as slow VT, is related to increased automaticity. The ECG shows 3 - 10 consecutive QRS complexes originating from the ventricles, with a heart rate typically between 60 - 110 bpm. The onset and termination of tachycardia are gradual, often following a ventricular premature beat or when the ventricular pacemaker accelerates beyond the sinus rate. Fusion beats are common at the onset and termination of the arrhythmia, and ventricular capture is frequent. It often occurs in patients with organic heart disease, particularly during reperfusion after acute myocardial infarction, cardiac surgery, cardiomyopathy, rheumatic fever, and digitalis toxicity. The episodes are brief or intermittent, and do not affect prognosis. Patients are generally asymptomatic, requiring no antiarrhythmic treatment.
Idiopathic ventricular tachycardia
Idiopathic ventricular tachycardia (IVT) is monomorphic VT occurring in patients without structural heart disease, often paroxysmal but also incessant. It is classified into outflow tract VT, annular VT, and fascicular VT based on the origin. Right ventricular outflow tract (RVOT) VT is the most common type of idiopathic VT, characterized by a late precordial transition (V3 or later) and narrow R waves in leads V1 and V2 on ECG. Paroxysmal VT is often triggered by exercise, stress, or other stimuli and can be suppressed with β-blockers, verapamil, or propafenone. Most patients have a good prognosis. For symptomatic patients, catheter ablation can be considered.
Figure 2 Accelerated idioventricular rhythm
In lead II, a series of wide, abnormal QRS complexes can be seen, with a ventricular rate of 79 - 88 bpm. Sinus P waves gradually overlap with the QRS complexes (indicated by arrows, showing AV dissociation).