Repolarization is the phase that follows depolarization in the cardiac action potential, restoring the electrical balance across the cell membrane. This process prepares each cardiac cell for the next heartbeat by returning the membrane potential to its negative resting state.
Understanding what happens during repolarization helps explain how the heart maintains a steady rhythm and why precise timing of this phase is critical for effective pumping function.
| Phase | Main Event | Ion Movement | Effect on Membrane Potential |
|---|---|---|---|
| Resting | Polarized state | High K+ inside, Na+ outside | Negative inside relative to outside |
| Depolarization | Rapid Na+ influx | Na+ channels open | Rapid shift to positive inside |
| Repolarization | K+ efflux increases, Na+ channels inactivate | K+ channels open, Na+ channels close | Return to negative resting potential |
| Plateau | Balanced Ca2+ and K+ currents | Ca2+ enters, K+ exits | Sustained partial depolarization |
Cardiac Action Potential Repolarization Dynamics
During repolarization, voltage-gated potassium channels open more widely while inactivated sodium channels recover. This shift allows potassium ions to exit the cell, making the interior more negative again.
The movement of potassium outward counteracts the earlier sodium influx and gradually brings the membrane potential back toward the resting level without overshooting in a healthy heart.
Ion Channel Roles in Repolarization
Potassium Channels and Efflux
Potassium channels are the primary mediators of repolarization, increasing conductance to allow K+ to leave the cell along its concentration gradient. The rising phase of potassium current helps restore the negative resting membrane potential and reduces excitability.
Calcium Current and Sodium Inactivation
In certain cardiac regions, a slower calcium current through L-type calcium channels partially offsets the potassium efflux, prolonging the plateau and influencing the duration of repolarization. Sodium channels enter an inactivated state during this phase and cannot reopen until the membrane potential recovers.
ECG Relationship to Repolarization
On an ECG, the T wave reflects the net repolarization of the ventricles, representing the recovery of the myocardium after each contraction. Changes in the shape, height, or timing of the T wave can signal alterations in ion channel function or electrolyte status.
Pharmacologic and Metabolic Influence
Drugs that block potassium channels can prolong repolarization and extend the QT interval on an ECG, while some medications that enhance potassium current may shorten repolarization. Metabolic factors such as potassium concentration and autonomic tone also modify how quickly repolarization occurs in different regions of the heart.
Key Takeaways on Repolarization
- Repolarization restores the negative resting membrane potential after depolarization.
- Potassium efflux through specialized channels is the main driver of this phase.
- Inactivated sodium channels temporarily prevent renewed depolarization.
- The ECG T wave reflects whole-ventricle repolarization in the intact heart.
- Drugs and metabolic factors can shorten or prolong repolarization, affecting rhythm stability.
FAQ
Reader questions
Why does the T wave on an ECG correspond to ventricular repolarization?
The T wave represents the recovery phase of the ventricles as they return to their resting electrical state, which is visually captured by the ECG after the QRS complex.
How can medications alter repolarization duration and ECG intervals?
Certain drugs that block potassium channels slow repolarization and lengthen the QT interval, while other medications that enhance repolarizing currents can shorten it, affecting cardiac safety.
What role does extracellular potassium play in the repolarization process?
Changes in extracellular potassium concentration shift the driving force on potassium channels, which can either accelerate or delay repolarization and modify the shape of the action potential.
What happens if sodium channels fail to recover properly during repolarization?
Impaired recovery of sodium channels can reduce the heart's ability to fire reliably and may contribute to abnormal repolarization patterns and conduction issues.