What physiological mechanism primarily causes Torsades de Pointes?

Torsades de Pointes (TdP) is primarily associated with a specific type of arrhythmia that often results from an electrolyte imbalance, particularly abnormalities in potassium levels. When there is a deficiency of potassium (hypokalemia) or an excess of calcium (hypercalcemia), it can create conditions that disrupt the normal repolarization process of cardiac myocytes. This disruption leads to prolonged QT interval, which is a significant risk factor for TdP.

The altered ion concentrations affect myocardial action potentials, specifically prolonging the QT interval due to delayed repolarization. This prolongation can predispose the heart to the development of early afterdepolarizations, which may initiate TdP. Therefore, the physiological mechanism underlying TdP in these scenarios often stems from these ion imbalances rather than general structural issues, vagal influences, or simple reentrant circuits.

While structural heart diseases and reentrant circuits can contribute to various cardiac arrhythmias, they are not the primary mechanisms responsible for TdP. Increased vagal tone generally does not lead to TdP directly, making these options less relevant in this context. Thus, electrolyte imbalance is the most critical factor in the development of Torsades de Pointes.