Transmission mechanism and functional syncytium
The spread of the impulse from the sinoatrial node to the working myocardium is carried out exclusively by electrical means. The main role in this process is played by local currents arising between excited and yet resting cardiomyocytes.
A key structural feature of cardiac tissue is the presence of nexus junctions — specialized tight contacts between cell membrane areas. These zones are penetrated by special channels that guarantee the highest permeability for ions. It is thanks to nexus junctions that the pseudo-syncytial structure of the myocardium is formed:
- Anatomically each muscle cell is isolated by its own membrane.
- Physiologically nexus junctions bind all cardiomyocytes into a single and inseparable functional system.
This integration ensures the fulfillment of the "all-or-none" law: the generated electrical signal passes unimpeded to all cells, forcing the entire organ to respond to the stimulus as a whole.
Sequence of cardiac excitation spread
The signal always moves strictly unidirectionally: from the atria to the ventricles. The process starts in the sinus node, from where the wave diffuses first through the right atrium and then captures the left atrium, moving at a speed of 1 m/s until it reaches the atrioventricular node.
Spreading through the ventricles has a strict sequence:
- First priority. Papillary muscles and trabeculae attached to the valve cusps are activated. This is of critical importance: the tension of the chordae tendineae prevents the prolapse of the valve cusps into the atrial cavity at the moment of powerful ventricular systole.
- Second priority. Excitation encompasses the interventricular septum and descends to the apex of the heart.
- Third priority. The lateral walls and the base of the ventricles are involved in the process.
Within the thickness of the muscle wall itself, the conduction vector is directed from specialized atypical conducting cells to typical working cardiomyocytes, and further towards the endocardium and epicardium.
Conduction velocity and AV delay
The specialized conduction system has the ability to transmit signals much faster than typical fibers. The most rapid conduction is recorded in the His-Purkinje system — here the velocity reaches 3 m/s. In the working myocardium of the ventricles, the velocity is about 1 m/s.
The diametrically opposite situation is observed in the atrioventricular (AV) node, where the velocity drops to a minimum of 0.05 m/s. This physiological deceleration is called the atrioventricular delay. Its occurrence is due to several structural factors:
- Absence of nexus junctions (gap junctions) between cells of this segment.
- Initially reduced excitability of the AV node tissue.
- Delayed "jumping" of the impulse across intercellular membranes.
- Anatomical arrangement: atypical cardiomyocytes are oriented transversely relative to the conduction vector, which physically slows down the signal.
The hemodynamic meaning of this phenomenon is to ensure the correct sequence of chamber operation. The delay guarantees that the ventricles begin their 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 manner thanks to mechanisms that block the return of the electrical wave (re-entry). The main defense is refractoriness (non-excitability) of areas that have already generated an action potential. Additionally, in the atypical pathways of the ventricles and in the region above the AV node, excitation lasts significantly longer, forming a reliable block for return impulses.
The process of excitation decay (repolarization) is also strictly ordered:
- In the atria this stage occurs at the moment when the impulse is actively moving through the ventricular tissue.
- In the ventricles the process decays in the 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.
Briefly: answers to topical questions
What is the conduction velocity of the electrical impulse in various parts of the cardiac conduction system?
The conduction velocity of the electrical impulse varies across different parts of the heart.
- Atria — 1 m/s; in interatrial pathways, the velocity is indicated as 0.3 m/s.
- Atrioventricular node — 0.05 m/s; in the penetrating fibers of the AV junction — 0.02–0.05 m/s.
- His-Purkinje system — 3 m/s; for the bundle of His, the maximum velocity in the heart is also indicated as 1.5–5 m/s.
- Ventricular myocardium / ventricular working cardiomyocytes — 1 m/s; 0.6–1.0 m/s is also indicated.
What ionic currents form the action potential in atypical cardiomyocytes of the sinus node?
The sources detail the ionic mechanisms of phase 4 — slow diastolic depolarization — in sinus node cells.
- Potassium mechanism: during diastole, the membrane permeability for K+ ions gradually decreases; this leads to a decrease in the potassium equilibrium potential and depolarization of the membrane potential.
- Inward sodium and calcium currents: during the interspike period, there is a constant slow inward current of Na+ ions and, to a lesser extent, Ca2+.
- Calcium channels: in phase 4, high permeability for Ca2+ is observed through open slow calcium channels.
- End of SDD: the inward current of Na+ and Ca2+ additionally increases, which accelerates spontaneous depolarization.
What effects does the autonomic nervous system have regarding the cardiac excitation conduction velocity?
The sources indicate the following influences of the autonomic nervous system on excitation conduction in the heart.
- Sympathetic nervous system — causes a positive dromotropic effect. Mechanisms include acceleration of slow diastolic depolarization in sinus node cells, increased excitability of typical and atypical cardiomyocytes, and increased entry of Ca2+ ions into cardiomyocytes.
- Vagus nerves (n. vagus) — cause a negative dromotropic effect. They reduce the excitability of sinoatrial and atrioventricular node cells, decrease the permeability of cardiomyocyte cell membranes for Ca2+, and reduce the rate of slow diastolic depolarization.
To remember the order of ventricular excitation spread, use the acronym PMB: P — Papillary muscles, M — Interventricular septum and apex, B — Lateral walls and base.
Class and exam questions
What is the hemodynamic significance of the atrioventricular delay?
The conduction delay in the AV node is necessary to allow the atria to contract fully and pump blood into the ventricles strictly before the onset of ventricular systole.
Why do the papillary muscles of the ventricles depolarize and contract first?
Their early contraction ensures the tension of the trabeculae, which prevents prolapse (turning inside out) of the atrioventricular valve cusps during a sharp increase in ventricular pressure.
How is retrograde impulse conduction (re-entry) normally prevented?
Backflow is prevented by the refractoriness of already excited tissue. In addition, a prolonged state of excitation in atypical cells above the AV node creates a physiological block for the return wave.
What is the maximum impulse conduction velocity in the heart, and where is it recorded?
The maximum velocity is 3 m/s. It is recorded in atypical ventricular cardiomyocytes — the His bundle and Purkinje fiber system.
What else to study on this topic
- Mechanism of impulse generation in the sinus node (automatism)
- Ionic nature of the cardiomyocyte action potential
- Histological structure of nexuses and myocardial cell membranes
- Phases of cardiac muscle refractoriness
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