Transmission Mechanism and Functional Syncytium
The propagation of the impulse from the sinuatrial node to the working myocardium occurs exclusively via an electrical pathway. Local currents arising between excited and resting cardiomyocytes play the primary role in this process.
A key structural feature of cardiac tissue is the presence of gap junctions (nexus), which are specialized tight contacts between cell membrane regions. These zones are penetrated by specific channels that ensure extremely high permeability to ions. It is precisely due to gap junctions that the myocardium forms a false syncytial structure:
- Anatotomically, each muscle cell is isolated by its own membrane.
- Physiologically, gap junctions bind all cardiomyocytes into a single, continuous functional system.
This integration ensures the fulfillment of the "all-or-none" law: a newly generated electrical signal passes unimpeded to all cells, causing the entire organ to respond to the stimulus as a whole.
Sequence of Cardiac Excitation
The signal always moves in a strictly unidirectional manner: from the atria to the ventricles. The process starts in the sinuatrial node, from which the wave diffuses first through the right atrium and then engulfs the left atrium, moving at a speed of 1 m/s until it reaches the atrioventricular node.
Propagation through the ventricles follows a strict sequence:
- First priority. Papillary muscles and trabeculae attached to the valve cusps are activated. This is of critical importance: the tensioning of chordae tendineae prevents the inversion (prolapse) of the valve cusps into the atrial cavity during powerful ventricular systole.
- Second priority. Excitation encompasses the interventricular septum and descends toward the apex of the heart.
- Third priority. The lateral walls and the base of the ventricles are involved in the process.
Within the muscle wall itself, the conduction vector is directed from specialized atypical conducting cells to typical working cardiomyocytes, and further toward the endocardium and epicardium.
Conduction Velocity and AV Delay
The specialized conduction system has the capacity to transmit signals significantly faster than typical fibers. The most rapid conduction is recorded in the His-Purkinje system, where velocities reach 3 m/s. In the ventricular working myocardium, the velocity is approximately 1 m/s.
An diametrically opposite situation is observed in the atrioventricular (AV) node, where velocity drops to a minimum of 0.05 m/s. This physiological slowing is termed atrioventricular delay. Its occurrence is due to several structural factors:
- Absence of gap junctions between cells of this segment.
- Inherently lowered excitability of AV nodal tissue.
- Slowed "hopping" of the impulse across intercellular membranes.
- Anatomical orientation: atypical cardiomyocytes are oriented transversely relative to the conduction vector, which physically impedes the signal.
The hemodynamic significance of this phenomenon lies in ensuring the correct working sequence of the chambers. The delay guarantees that the ventricles begin systole only after the atria complete their contraction and pump a portion of blood into them.
Prevention of Backflow and Repolarization
The heart works in a coordinated fashion thanks to mechanisms that block the backward travel of the electrical wave (re-entry). The primary defense is refractoriness (inexcitability) of areas that have already generated an action potential. Additionally, in atypical ventricular pathways and the region above the AV node, excitation lasts significantly longer, forming a reliable block against retrograde impulses.
The process of excitation decay (repolarization) is also strictly ordered:
- In the atria, this stage occurs at the time when the impulse is actively moving through the ventricular tissue.
- In the ventricles, the process fades in a direction from the apex to the base of the organ.
- Last of all, excitation disappears in the papillary muscles and trabeculae supporting the valvular apparatus.