Ventricular repolarization is the process where the heart’s muscle cells in the ventricles restore their electrical balance after a contraction. This process is similar to recharging a battery, preparing the cells for the next electrical impulse that triggers the subsequent heartbeat. Without this recovery, the heart cannot contract efficiently or consistently, compromising its ability to pump blood throughout the body.
The Cellular Basis of Repolarization
The electrical activity in a ventricular muscle cell is described by the cardiac action potential, a sequence of ion movement across the cell membrane. Repolarization is primarily governed by Phase 3, the rapid repolarization phase, which immediately follows the plateau of contraction. This restoration is driven by the coordinated opening and closing of microscopic channels.
The cell returns to its negative resting potential primarily through the swift outflow of potassium ions (\(\text{K}^+\)) from the cell’s interior. As the cell enters Phase 3, \(\text{Ca}^{2+}\) channels close, halting the influx of positive calcium ions. Simultaneously, voltage-gated potassium channels open, creating a strong outward current of \(\text{K}^+\) that rapidly restores the negative charge inside the cell.
Phase 4 represents the final stage, the resting potential, where the cell is fully recovered and stable. Potassium channels remain open, maintaining a stable, highly negative membrane potential. This negative charge ensures the cell is not spontaneously excitable and can only be activated by a strong signal from the heart’s conduction system.
Measuring Ventricular Repolarization
Clinicians use the non-invasive Electrocardiogram (\(\text{ECG}\)) to monitor ventricular repolarization. On an \(\text{ECG}\), the \(\text{T}\) wave represents the final, rapid repolarization of the ventricles. The \(\text{ST}\) segment, immediately preceding the \(\text{T}\) wave, corresponds to the plateau phase where the ventricles are fully contracted.
The most important measurement is the \(\text{QT}\) interval, which measures the duration from the start of the \(\text{QRS}\) complex (ventricular depolarization) to the end of the \(\text{T}\) wave. This interval reflects the total time required for the ventricles to contract and fully recover their electrical state. The \(\text{QT}\) interval length indicates heart health and correlates with the stability of the heart’s rhythm.
The \(\text{QT}\) interval changes with heart rate, so it must be mathematically corrected, yielding the corrected \(\text{QT}\) interval (\(\text{QTc}\)). A \(\text{QTc}\) value above 450 milliseconds in men or 460 milliseconds in women is considered prolonged and warrants investigation. The \(\text{QTc}\) serves as a standardized metric for identifying individuals at risk for dangerous heart rhythms.
Risks Associated with Abnormal Repolarization
When ventricular repolarization is abnormally prolonged, the primary danger is life-threatening arrhythmias. The delay creates a period of electrical vulnerability where ventricular cells can be prematurely re-excited. This vulnerability can be triggered by an Early Afterdepolarization (\(\text{EAD}\)), a secondary depolarization occurring during the prolonged repolarization phase.
If an \(\text{EAD}\) reaches a critical threshold, it can trigger a premature ventricular beat that falls directly onto the \(\text{T}\) wave (R-on-T phenomenon). This timing can initiate Torsades de Pointes (\(\text{TdP}\)), a dangerous polymorphic ventricular tachycardia. \(\text{TdP}\) is characterized by a “twisting” pattern on the \(\text{ECG}\) and can quickly degenerate into ventricular fibrillation, leading to sudden cardiac death.
Abnormal repolarization stems from inherited and acquired causes, often involving malfunctioning potassium channels. Genetic causes include Long \(\text{QT}\) Syndrome, where mutations slow the repolarization process, affecting the rapid delayed rectifier potassium current (\(\text{I}_{Kr}\)). Acquired causes are more common, including electrolyte imbalances like low potassium (\(\text{hypokalemia}\)). Many medications, such as antiarrhythmics and macrolide antibiotics, can block the \(\text{I}_{Kr}\) channel, increasing the risk of \(\text{TdP}\).