Ventricular action potential: Difference between revisions

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'''Ventricular action potential''' is a term used in [[cardiac electrophysiology]] to describe the changes in [[membrane potential]] that occur during the [[cardiac cycle]] in the [[ventricular myocytes]]. This process is crucial for the proper functioning of the [[heart]], as it allows for the coordinated contraction of the heart muscle, which in turn enables the efficient pumping of blood throughout the body.
== Ventricular Action Potential ==


== Overview ==
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.


The ventricular action potential is initiated by an electrical impulse from the [[sinoatrial node]], the heart's natural pacemaker. This impulse travels through the [[atrioventricular node]] and the [[bundle of His]] before reaching the ventricular myocytes.
[[File:Action_potential_ventr_myocyte.gif|thumb|right|300px|Diagram of a ventricular action potential.]]


The ventricular action potential consists of five phases (0-4), each representing a different stage in the electrical activity of the ventricular myocytes.
== Phases of the Ventricular Action Potential ==


== Phases ==
The ventricular action potential is typically divided into five phases, numbered 0 through 4:


=== Phase 0 ===
=== 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 0, or the upstroke, is characterized by a rapid depolarization of the ventricular myocytes. This is caused by the opening of [[voltage-gated sodium channels]], which allows for a rapid influx of [[sodium ions]] into the cell.
=== 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 1 ===
=== 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 1, or the initial repolarization, is marked by the closure of the sodium channels and the opening of [[potassium channels]]. This allows for a brief efflux of potassium ions out of the cell, causing a slight decrease in the membrane potential.
=== 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 2 ===
=== 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.


Phase 2, or the plateau phase, is characterized by a balance between the influx of [[calcium ions]] through [[calcium channels]] and the efflux of potassium ions. This results in a prolonged period of depolarization.
== Ionic Currents and Channels ==


=== Phase 3 ===
The ventricular action potential is governed by various ionic currents, each mediated by specific ion channels. These include:


Phase 3, or the rapid repolarization, is marked by the closure of the calcium channels and the continued efflux of potassium ions. This causes the membrane potential to return to its resting state.
* '''I<sub>Na</sub>''': The fast sodium current responsible for the rapid depolarization in phase 0.
* '''I<sub>Ca,L</sub>''': The L-type calcium current that contributes to the plateau phase.
* '''I<sub>to</sub>''': The transient outward potassium current involved in phase 1.
* '''I<sub>K</sub>''': The delayed rectifier potassium currents that facilitate repolarization in phase 3.
* '''I<sub>K1</sub>''': The inward rectifier potassium current that stabilizes the resting membrane potential in phase 4.


=== Phase 4 ===
== Clinical Significance ==


Phase 4, or the resting phase, is the period between action potentials. During this phase, the membrane potential is maintained by the [[sodium-potassium pump]], which actively transports sodium ions out of the cell and potassium ions into the cell.
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.


== Clinical significance ==
== Related Pages ==


Abnormalities in the ventricular action potential can lead to various [[cardiac arrhythmias]], including [[ventricular tachycardia]] and [[ventricular fibrillation]]. These conditions can be life-threatening and require immediate medical attention.
* [[Action potential]]
* [[Cardiac electrophysiology]]
* [[Electrocardiography]]
* [[Heart]]
 
== References ==
 
{{Reflist}}


[[Category:Cardiac electrophysiology]]
[[Category:Cardiac electrophysiology]]
[[Category:Cardiology]]
[[Category:Cardiology]]
[[Category:Physiology]]
{{Cardiology-stub}}
{{Medicine-stub}}

Revision as of 16:14, 9 February 2025

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.

Diagram of a ventricular action potential.

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.

Related Pages

References

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