Main phases of the electrical cycle
The electrical activity of a typical ventricular cardiomyocyte differs significantly from that of nerve cells and consists of five sequential stages:
- Phase 4 (Resting potential). The cell is polarized, the membrane potential is stable and remains at -90...-100 mV. This level is maintained due to high permeability to K⁺ ions, the concentration of which inside the cell is significantly higher than outside.
- Phase 0 (Depolarization). A sharp change in charge occurs. The potential rises rapidly from negative values, passing the zero mark (overshoot reaches +20 mV).
- Phase 1 (Rapid initial repolarization). Immediately after the peak (spike), a brief and small drop in voltage is observed.
- Phase 2 (Plateau — slow repolarization). The most specific part of the cycle. The potential is held near the zero mark for a long time. It is this phase that prolongs the excitation process; its duration practically coincides with the time of mechanical contraction of the cell.
- Phase 3 (Rapid final repolarization). The membrane potential drops steeply, returning to the initial resting level (-100 mV).
Ionic currents
Each stage of membrane potential change is driven by the movement of specific ions through specialized channels:
- During depolarization, fast sodium channels open in an avalanche-like manner. Na⁺ ions rush massively into the cell down their concentration gradient.
- At the onset of repolarization, the inward sodium current inactivates, and simultaneously the outward current of K⁺ from the cell is activated.
- During the plateau, a dynamic equilibrium is established. The outward potassium current is balanced by a powerful counter-flow of Ca²⁺ ions entering through slow L-type channels (as well as a small residual sodium current). Calcium influx at this stage is critically necessary for subsequent electromechanical coupling—the physical contraction of the myocyte.
- During final repolarization, calcium and sodium channels close completely, and a massive outward flow of K⁺ rapidly restores the initial negative charge inside the cell.
Change in excitability and heart protection
The ability of a cardiomyocyte to respond to new stimuli is strictly tied to the phases of the action potential. A prolonged electrical response guarantees long refractoriness.
- Absolute refractory period (ARP). Encompasses the phases of depolarization, initial repolarization, plateau, and the beginning of final repolarization. In the ventricles, this period lasts 270 ms. Excitability drops to zero: no stimulus, even the strongest one, can trigger a new impulse. The main physiological significance of ARP is the protection of the myocardium from summation of contractions and tetanus. This guarantees that the heart has time to relax (enter diastole) and fill with blood.
- Relative refractory period. Occurs at the end of rapid repolarization. Excitability gradually recovers to 100%. Triggering a new action potential at this moment is possible, but only with a suprathreshold (very strong) stimulus.
- Supernormal excitability. A short period of time immediately after returning to the resting potential when the cell responds even to subthreshold stimuli. At this moment, the risk of extrasystoles increases.
Mechanism of excitation propagation
The generation of an action potential in one area of the myocardium inevitably leads to its propagation. The outer surface of the excited area becomes negatively charged, while adjacent, still resting membrane zones retain a positive charge.
Local electrical currents arise between these regions. Their strength first increases and then decreases, causing depolarization of adjacent areas. The repolarization process works similarly: zones that have restored their initial charge become positive on the outside, while still-excited ones remain negative. The potential difference arising on the surface of the organ forms a vortex electromagnetic field that can be recorded on the body surface.
Briefly: answers to topical questions
How does the action potential of a typical cardiomyocyte differ from that of sinus node (atypical) cells?
The action potential of a typical ventricular cardiomyocyte is described in sources as an AP with a stable resting potential and a plateau phase; sinus node cells lack a stable resting potential, and slow diastolic depolarization (SDD) develops between action potentials.
| Characteristic | Typical ventricular cardiomyocyte | Sinus node cells |
|---|---|---|
| Resting potential / maximum diastolic potential | Phase 4 — resting potential approximately –90...–100 mV | Stable resting potential is absent; SDD starts from a maximum diastolic potential of about –60 mV |
| Phases | 5 phases: 0 — depolarization, 1 — initial rapid repolarization, 2 — slow repolarization (plateau), 3 — final rapid repolarization, 4 — resting potential | SDD; phase 0 — depolarization; phase 3 — repolarization |
| Depolarization | Driven by a rapid, massive influx of Na+ into the cell | Primarily calcium-mediated via slow L-type channels; Na+ influx is also indicated |
| Plateau | Phase 2 — slow repolarization (plateau); Ca2+ influx slows repolarization and prolongs excitation | Phase 0 and phase 3 are indicated in the description of the sinus node cell AP |
| Automaticity | AP phases and resting potential are described for the typical ventricular cardiomyocyte in sources | SDD provides the property of automaticity — the ability to self-excite |
What role does the sodium-potassium pump play in establishing the resting potential of a cardiomyocyte?
The sodium-potassium pump (Na+/K+-ATPase) maintains and restores the ionic gradients that preserve the resting membrane potential.
- Na+/K+-ATPase uses ATP energy to transport ions against their concentration gradient.
- Na+ ions are actively pumped out of the cell, while K+ ions are pumped into the cell.
- At rest, the concentration of K+ is higher inside the cell, and Na+ is higher outside; membrane permeability to K+ and K+ efflux from the cell contribute to the formation of the potassium equilibrium potential and the resting potential.
- Following the action potential, the activity of Na+/K+-ATPase restores the ionic balance/ionic gradients.
Class and exam questions
Why is the heart muscle incapable of tetanic contraction?
Due to the presence of the plateau phase, the absolute refractory period of cardiomyocytes is very prolonged (about 270 ms in the ventricles). The cell remains unexcitable for almost the entire duration of its mechanical contraction, making wave summation impossible.
Which ion maintains the action potential plateau?
The plateau phase is maintained by the inward current of calcium (Ca²⁺) ions through slow L-type channels, which balances the outward potassium current.
What happens during supernormal excitability?
Immediately after the restoration of the resting potential, cell excitability briefly exceeds 100%. During this phase, even a weak (subthreshold) stimulus is capable of causing a premature myocardial contraction.
What else to study on this topic
- Features of the action potential of sinoatrial node pacemaker cells
- Slow diastolic depolarization (SDD) and the nature of automaticity
- Differences between sodium depolarization in working myocytes and calcium depolarization in nodal cells
- The role of chloride (Cl⁻) ions and Na⁺/K⁺-ATPase in pacemaker cells
- Temporal parameters of refractoriness in the cardiac conduction system
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