Ventricular action potential
Ventricular Action Potential
The ventricular action potential is a complex electrical event that occurs in the ventricles of the heart. It is crucial for the initiation and propagation of the heartbeat, ensuring the coordinated contraction of the heart muscle. The action potential in ventricular myocytes is characterized by distinct phases that reflect the movement of ions across the cell membrane.
Phases of the Ventricular Action Potential
The ventricular action potential is typically divided into five phases, numbered 0 through 4:
Phase 0: Rapid Depolarization
Phase 0 is marked by a rapid influx of sodium ions (Na+) through voltage-gated sodium channels. This sudden increase in positive charge inside the cell causes the membrane potential to rise sharply, initiating the action potential.
Phase 1: Initial Repolarization
Following the peak of depolarization, there is a brief period of repolarization. This is due to the inactivation of sodium channels and the transient outward flow of potassium ions (K+) through specific potassium channels.
Phase 2: Plateau
Phase 2 is characterized by a plateau in the membrane potential. This phase is sustained by the balance between the inward flow of calcium ions (Ca2+) through L-type calcium channels and the outward flow of potassium ions. The plateau phase is crucial for the prolonged contraction of the cardiac muscle, allowing for effective pumping of blood.
Phase 3: Repolarization
During phase 3, the calcium channels close, and there is an increased outflow of potassium ions, leading to repolarization of the cell membrane. This phase returns the membrane potential to its resting state.
Phase 4: Resting Membrane Potential
Phase 4 is the resting phase, where the membrane potential is stable, maintained by the sodium-potassium pump and the selective permeability of the membrane to potassium ions. This phase prepares the cell for the next action potential.
Ionic Currents and Channels
The ventricular action potential is governed by various ionic currents, each mediated by specific ion channels. These include:
- INa: The fast sodium current responsible for the rapid depolarization in phase 0.
- ICa,L: The L-type calcium current that contributes to the plateau phase.
- Ito: The transient outward potassium current involved in phase 1.
- IK: The delayed rectifier potassium currents that facilitate repolarization in phase 3.
- IK1: The inward rectifier potassium current that stabilizes the resting membrane potential in phase 4.
Clinical Significance
Abnormalities in the ventricular action potential can lead to arrhythmias, which are disorders of the heart rhythm. Conditions such as long QT syndrome and Brugada syndrome are associated with alterations in the ionic currents that shape the action potential. Understanding these mechanisms is essential for developing treatments for cardiac arrhythmias.
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Contributors: Prab R. Tumpati, MD