The heart’s consistent beating relies on precise electrical signals generated by individual heart muscle cells, known as cardiomyocytes. These electrical impulses, called cardiomyocyte action potentials, are rapid changes in the electrical charge across the cell membrane. This electrical activity is fundamental to how the heart functions as a pump, ensuring coordinated contractions that move blood throughout the body.
The Heart’s Electrical Beat
The cardiomyocyte action potential unfolds in distinct phases, each contributing to the heart’s rhythmic contraction and relaxation. The process begins with a resting state, where the inside of the cell is negatively charged compared to the outside, around -90 millivolts (mV). This resting potential is primarily maintained by the movement of potassium ions.
The first phase, rapid depolarization (Phase 0), occurs when an electrical signal from a neighboring cell reaches a threshold. This triggers a swift influx of positively charged sodium ions into the cell, causing the membrane potential to rapidly become positive.
Following depolarization, a brief initial repolarization (Phase 1) occurs, marked by a slight decrease in the positive charge. This is followed by the plateau phase (Phase 2). During this phase, the membrane potential remains relatively stable for several hundreds of milliseconds.
The action potential then enters the repolarization phase (Phase 3), where the cell’s electrical charge returns to its negative resting state. This involves a significant outflow of positive ions from the cell, making the inside of the cell more negative again. Finally, the cell returns to its resting state (Phase 4).
Key Players in Electrical Signals
The precise choreography of the cardiomyocyte action potential is governed by specialized protein channels embedded within the cell membrane, which regulate the flow of charged particles called ions. These “voltage-gated” channels open and close in response to changes in the cell’s electrical potential, allowing specific ions to cross the membrane. The main players are sodium, calcium, and potassium ions.
During the initial rapid depolarization (Phase 0), voltage-gated sodium channels open quickly, allowing a large number of positively charged sodium ions to rush into the cell. These channels then quickly inactivate, limiting the sodium influx.
As sodium channels inactivate, transient outward potassium channels open briefly, allowing some potassium ions to leave the cell, contributing to the initial repolarization (Phase 1). Following this, L-type calcium channels open, allowing calcium ions to slowly enter the cell during the plateau phase (Phase 2). This inward calcium current balances the outward potassium currents, maintaining the prolonged depolarized state.
The repolarization phase (Phase 3) is driven primarily by the closing of calcium channels and the sustained opening of various types of potassium channels. This allows a steady outflow of potassium ions, restoring the negative charge inside the cell. Once the cell returns to its resting potential (Phase 4), specific potassium channels maintain this negative charge.
Why These Electrical Signals Matter
The cardiomyocyte action potential directly orchestrates the mechanical function of the heart. The precise sequence of electrical changes within each heart muscle cell triggers its contraction, leading to the efficient pumping of blood. This link between electrical excitation and mechanical contraction is known as excitation-contraction coupling.
When an action potential spreads across a cardiomyocyte, the influx of calcium ions during the plateau phase acts as a trigger. This initial influx of calcium, though small, prompts a much larger release of calcium from internal stores within the cell. This significant rise in intracellular calcium concentration is the direct signal for the contractile proteins, actin and myosin, to interact.
The interaction of actin and myosin filaments causes the muscle cell to shorten, generating force. Because all cardiac muscle cells are electrically connected through specialized junctions, the action potential spreads rapidly from cell to cell, ensuring that all cells in a chamber contract together. This synchronized contraction of the atria and then the ventricles allows the heart to effectively eject blood into the circulatory system.
When the Heart’s Electrical Rhythm Falters
Disruptions to the normal cardiomyocyte action potential can lead to various heart rhythm disorders, collectively known as arrhythmias. These irregularities arise when there are problems with how the electrical impulses are generated or how they spread throughout the heart. The delicate balance of ion movement across the cell membrane is easily disturbed, leading to abnormal electrical activity.
For instance, issues with the opening or closing of specific ion channels can alter the duration or shape of the action potential. A prolonged action potential, for example, might allow for unwanted electrical activity to spontaneously arise, leading to irregular beats. Changes in the resting membrane potential or the cell’s ability to spontaneously depolarize can also contribute to abnormal rhythms.
These cellular-level disruptions can manifest as a heart beating too fast, too slow, or with an irregular pattern. While the underlying mechanisms are complex, the core issue traces back to a deviation from the normal sequence of ion flows that define the cardiomyocyte action potential.