Cardiac Action Potential

The rapid increase and decrease of the membrane potential at a particular cell site is known as an action potential (AP). This depolarisation also causes adjacent areas to depolarise. Numerous animal cell types referred to as excitable cells, such as muscle cells, neurons, endocrine cells, and even plant cells, exhibit action potentials.

During the long plateau of the cardiac action potential, the membrane is kept at a high voltage for a few 100 ms, as opposed to the neural action potential. This plateau has developed due to slower calcium channels activating and maintaining the membrane voltage close to its equilibrium potential long after sodium channels have deactivated.

Table of Contents

• Cardiac Action Potential Meaning
• Phases of Cardiac Action Potential
• Frequently Asked Questions (FAQs)

Cardiac Action Potential Meaning

The cardiac action potential is a transient voltage change (membrane potential) across the membranes of the heart. This is brought on by the flow of charged ions (or atoms) through ion channel proteins from inside to outside cells. Action potentials in other electrically active cells, like nerves, differ from those in the heart. Due to the presence of various ion channels, action potentials also vary within the heart.

The cardiac action potential varies considerably in various parts of the heart. This distinction between the action potentials enables the various electrical properties of the different cardiac regions. A unique feature of the heart’s specialised conduction tissue is its ability to depolarise on its own, called automaticity.

The surface electrocardiogram (ECG) does not show electrical activity in the specialised conduction tissues because these tissues have a smaller mass than the myocardium.

Along with significant differences, cardiac muscle shares several characteristics with neurons and skeletal muscle. When at rest, a specific cardiac cell has a negative membrane potential, similar to a neuron. Voltage-gated ion channels open in response to stimulation above a threshold, allowing a stream of cations to enter the cell. An action potential begins when the threshold is reached. This results in the entry of positively charged ions into the cell, called depolarisation.

Phases of Cardiac Action Potential

The immediate activation of cardiac cells is required for the proper sequence and synchronised contraction of the ventricles and atria. An activation method must respond to variations in autonomic tone and fast changes in heart rate.

There are five major phases of cardiac action potential – phase 4, phase 0, phase 1, phase 2 and phase 3.

Phase 4

This is the resting membrane potential. The cell remains in this state until it receives an external electrical stimulus, usually from an adjacent cell. The diastole chamber of the heart is associated with phase 4 of the action potential. This indicates that both the calcium and sodium voltage-gated channels are closed.

The primary pacemaker cells of the heart that regulate heart rate are those that may spontaneously depolarise the fastest. Specific heart cells can spontaneously depolarise, generating an action potential without the involvement of adjacent cells. It is often referred to as “automaticity”.

Phase 0

When the rapid Na⁺ channels open, the membrane conductivity to Na⁺ (G_Na) rapidly increases, leading to a rapid inflow of Na⁺ ions (I_Na) into the heart cell and the onset of the rapid depolarisation phase. This is the rapid depolarisation phase. The phase 0 slope, or V_max, represents the highest cell depolarisation rate.

Whether the cell can open the rapid Na⁺ channels during phase 0 depends on the membrane potential at the stimulation time.

Phase 1

This is the phase of rapid repolarisation. The rapid Na⁺ channels are deactivated during phase 1 of the cardiac action potential. The flow of Cl^– and K⁺ ions causes the short net outward movement, generating the mild downward deviation of the action potential.

It has been proposed that the transport of Cl^– cell membranes during phase I results from a shift in membrane potential caused by K⁺ efflux and not from their involvement in the initial repolarisation (“notch”).

Phase 2

This is the longest phase, also called the “plateau” phase. This “plateau” phase is maintained by a balance between the outward movement of K⁺ ions through the delayed rectifier potassium channels, IKs, and the inward movement of Ca²⁺ ions (I_Ca) via L-type calcium channels.

Phase 2 also involves small contributions from the sodium-calcium exchanger current, I_Na,Ca and the sodium/potassium pump current, I_Na,K.

Phase 3

L-type Ca²⁺ channels close during phase 3 of the action potential, whereas slow delayed rectifier (IKs) K⁺ channels remain open. More types of K⁺ channels can open due to the net outward current that results from the negative change in the membrane potential. The cell repolarises due to this net outward, positive current, which is equivalent to the positive charge loss from the cell.

The cardiac units of the sinoatrial node provide the pacemaker potential that synchronises the heart. The cardiac action potential is essential for controlling the heart’s contraction. Human diseases, particularly arrhythmias, can result from abnormalities in the cardiac action potential, whether due to a hereditary mutation or injury.

Antiarrhythmic medicines, including lidocaine, quinidine, verapamil, and beta-blockers, influence the cardiac action potential.

Related Link:

• Skeletal Muscle Action Potential vs Cardiac Muscle Action Potential
• Cardiac Muscle

Main Page: BYJU’S NEET