Ischemic injury can contribute to arrhythmia by promoting what mechanism?

Ischemic injury can contribute to arrhythmia by promoting what mechanism?

• A. Afterdepolarizations
• B. Decreased conduction velocity
• C. Reduced heart rate
• D. Improved perfusion

Answer: (A)

Ischemia creates a chaotic ionic and energy state in heart cells, with ATP depletion, acidosis, and Ca2+ overload. This environment fosters afterdepolarizations, which are abnormal depolarizations that occur after the main repolarization of the action potential and can trigger extra beats. Early afterdepolarizations arise when the action potential duration is prolonged and L-type calcium channels reactivate during repolarization, potentially triggering another heartbeat. Delayed afterdepolarizations occur because intracellular Ca2+ overload drives a transient inward current via the Na+/Ca2+ exchanger during phase 4, also generating a trigger for a new impulse. These afterdepolarizations can initiate arrhythmias in ischemic tissue. While reduced conduction velocity from ischemia can support reentry as a substrate, the direct mechanism most linked to triggering arrhythmias in this context is afterdepolarizations. Reduced heart rate or improved perfusion are not mechanisms that promote arrhythmias.

Ischemia creates a chaotic ionic and energy state in heart cells, with ATP depletion, acidosis, and Ca2+ overload. This environment fosters afterdepolarizations, which are abnormal depolarizations that occur after the main repolarization of the action potential and can trigger extra beats. Early afterdepolarizations arise when the action potential duration is prolonged and L-type calcium channels reactivate during repolarization, potentially triggering another heartbeat. Delayed afterdepolarizations occur because intracellular Ca2+ overload drives a transient inward current via the Na+/Ca2+ exchanger during phase 4, also generating a trigger for a new impulse. These afterdepolarizations can initiate arrhythmias in ischemic tissue. While reduced conduction velocity from ischemia can support reentry as a substrate, the direct mechanism most linked to triggering arrhythmias in this context is afterdepolarizations. Reduced heart rate or improved perfusion are not mechanisms that promote arrhythmias.