Cardiac contraction

Contraction occurs via the same sliding filament mechanism as in skeletal muscle: Action potentials conducted along T tubules are associated with opening of the voltage-gated Ca2+ channels and entry of extracellular Ca2+ into the cells. 

Relaxation of cardiac muscle depends on the removal of cytosolic Ca2+.

Five phases of the ventricular muscle action potential, 0 through 4: 

Typical cardiomyocyte action potential

Phase 4 = stable resting membrane potential; phase 0 = rapid depolarization upon stimulation; phase 1 = partial repolarization; phase 2 = plateau phase; and phase 3 = repolarization.

Action potential, phases of excitability and contraction of a cardiomyocyte

There is the special mechanism of cardiomyocyte's action potential. The phase of rapid depolarization is due to the entrance of Na + ions through the so-called fast sodium channels. 

Then, after a short phase of early rapid repolarization, the phase of slow depolarization or plateau phase occurs. It is due to the simultaneous entry of Ca2+ though the slow calcium channels and the outflow of K+ ions. The phase of the last fast repolarization is due to the prevailing outflow of K+ ions. Finally, there is the phase of a resting potential.

During contractions of the cardiac muscle (systole) phase changes in excitability can be observed in it. Immediately after the beginning of excitation, cardiac muscle loses its excitability (absolute refractory period). Following this phase, excitability is gradually recovering, but remains below normal - relative refractory period. After a relative refractory phase a transient phase of hyperexcitability of the cardiac muscle occurs, and then excitability returns to its initial level.

The normal mechanical pumping cycle of the heart requires a single excitation event. 

Ventricular muscle cells have a long, effective (absolute) refractory period. This protects against circular (reentry) conduction.

Any additional action potentials spread rapidly through coupled myocardial cells and produce additional contraction (it is extrasystole=arrhythmias=inappropriate heart beats). 

There is loss of control by the pacemaker fails and each spread of excitation through the ventricles triggers the next. If the ventricular rate is excessive, there is insufficient time between beats for the ventricles to fill.

Notations: 

1 - time of electric stimulus application, 

2 - time of pulses from the sinus node, 

3 - extrasystole, 

4 -compensatory pause, 

5 - precipitated contraction.

When applying external stimulation on the heart at different phases of its cycle, it turns out that regardless of the magnitude of stimulation the heart does not respond, if stimulation is applied during the systole, that is, during the absolute refractory period. With the development of the diastole heart's excitability starts to recover and the phase of relative refractoriness occurs. Application of an intense stimuli at this time can cause an extraordinary contraction of the heart - extrasystole. The pause, which follows the extrasystole, lasts longer than usual, this is so-called compensatory pause.