Why Doesn't the Heart Cramp?
Unlike skeletal muscle, where the period of unexcitability (refractoriness) is significantly shorter than the contraction itself, cardiomyocytes function differently. In skeletal muscles, a short refractory period allows impulses to overlap, causing summation and prolonged spasm — tetanus.
In the myocardium, the absolute refractory period covers the entire contraction period. This means that until the muscle fiber has fully contracted and begun to relax, it is fundamentally unable to respond to a new electrical stimulus. It is this protective mechanism that prevents spastic circulatory arrest and ensures normal pump function.
Time Relationships in Heart Chambers
To understand how the heart works, it is important to compare the duration of the action potential (AP) and mechanical contraction in its different structures:
- Atria. The duration of the AP here is about 180 ms, whereas the mechanical response takes only 100–110 ms. Since the electrical process lasts longer than the muscular one, a new excitation can only envelop the tissue after complete relaxation of the fibers.
- Ventricles. In the working ventricular myocardium, the AP duration is practically equal to the duration of systole and is 330 ms.
- Atypical Cardiomyocytes. In the cells of the cardiac conduction system, the AP is the longest at 450 ms, with the absolute unexcitability period accounting for 400 ms.
Response to Ultra-Frequent Stimulation
If abnormally frequent impulses begin to emanate from the sinus node, the heart goes through several stages of adaptation. Initially, a simple increase in heart rate occurs. However, when the critical stimulation frequency is reached, tetanus still does not occur.
Instead, fibrillation develops — a dangerous condition in which synchrony is disrupted. Individual cardiomyocytes begin to contract disjointedly and chaotically. Normally, each subsequent myocardial contraction can be triggered strictly after the previous cardiac cycle is fully completed.
Intracellular Calcium Dynamics
$Ca^{2+}$ ions play a key role in the mechanisms of contraction and its strength. Upon excitation of the cardiomyocyte, calcium is directed from the T-tubules to the contractile proteins (actin-myosin complex). The feature of the myocardium is that far from all of this calcium is consumed in the current contraction.
A significant portion of the ions is stored in the sarcoplasmic reticulum (endoplasmic reticulum). This 'stored' volume will be used only during the subsequent cycle. Thus, the ionic shifts of the previous cardiac cycle directly dictate the strength of the next one: the more $Ca^{2+}$ has accumulated in the cell, the more powerful the response will be.
Clinical Significance: Paired Stimulation
The dependence described above is actively used in modern cardiology. Knowing the features of calcium dynamics and chronoinotropic dependence, physicians use the method of paired coupled pacing.
The essence of the method is that a special device (cardiosynchronizer) delivers an additional stimulus precisely at the moment of natural excitation. This provokes a massive additional release of $Ca^{2+}$ from the T-tubules. The result is a potentiated (manifold enhanced) contraction of the cardiac muscle, which is important for correcting a number of pathologies.