Conduction system and its regulation
The heart functions in a coordinated manner thanks to a strict hierarchy of pacemakers. The sinus node sets the normal rate, while the atrioventricular (AV) node acts as a secondary pacemaker (generating 40–60 impulses per minute).
The AV junction performs a crucial filter function. Conduction velocity in its penetrating fibers drops to 0.02–0.05 m/s. This allows the impulse to pass in only one direction (antegrade) and protects the ventricles from overload during high atrial excitation rates. Fibrous tissue between the chambers acts as an electrical insulator, preventing retrograde return of the impulse.
Next, the signal travels along the bundle of His, where velocity is maximal (1.5–5 m/s), and spreads through the Purkinje fibers. These terminal branches contain myosin and are capable of contracting along with the working myocardium, providing a powerful systole.
Nervous regulation is carried out by the autonomic nervous system:
- Parasympathetic (n. vagus): via $M_2$-cholinergic receptors, it suppresses automaticity and conduction. The right branch controls the sinus node, the left — the AV node. The ventricles are not innervated by the vagus nerve.
- Sympathetic: via $\beta_1$-adrenergic receptors, it increases automaticity and accelerates conduction, affecting the entire myocardium.
Action potential of a Purkinje fiber
The electrophysiological model of a conduction system cell includes five phases, each of which depends on the movement of specific ions:
- Phase 0 (Rapid depolarization): Upon reaching the threshold potential (–60 mV), rapid sodium channels open. An avalanche-like influx of $Na^+$ changes the membrane charge to +35 mV. The duration of this phase determines conduction.
- Phase 1 (Early repolarization): Brief efflux of $K^+$.
- Phase 2 (Plateau): Slow influx of $Ca^{2+}$ maintains the positive membrane charge, preventing rapid repolarization.
- Phase 3 (Final repolarization): Massive efflux of $K^+$ returns the cell to the resting potential (–90 mV).
- Phase 4 (Spontaneous diastolic depolarization): Slow influx of $Na^+$ and $K^+$. The rate of this process determines the cell's automaticity.
Features of the nodes and refractoriness
In the cells of the sinus and AV nodes, the mechanisms of impulse generation are different. The resting potential here is about –55 mV, which causes most rapid sodium channels to be inactivated. Phases 0 and 4 are provided by the inward calcium current. This current is initiated by a preliminary sodium influx through specific non-selective cationic channels — If-channels (funny channels), the operation of which forms the basis of normal automaticity.
To protect the heart from tetanic contraction and pathological impulse circulation (reentry), an effective refractory period (ERP) exists. It encompasses phases 0, 1, 2, and the beginning of phase 3. During this time, the cell is absolutely non-excitable and cannot conduct another full-fledged impulse.
Pathogenesis and pharmacotherapy of arrhythmias
Arrhythmias arise against the background of hypoxia, metabolic disorders, or endocrine failures (e.g., in thyrotoxicosis). According to their developmental mechanism, they are divided into blocks (decreased conduction), extrasystoles (increased automaticity), and re-entry arrhythmias — reentry (impaired conduction).
To treat tachyarrhythmias, 4 main classes of drugs are used:
- Class I: Sodium channel blockers (affect phases 0 and 4, reduce conduction).
- Class II: $\beta$-blockers (have a non-competitive effect, inhibit adenylyl cyclase).
- Class III: Potassium channel blockers (prolong phase 3 and ERP).
- Class IV: Slow calcium channel blockers (reduce automaticity in the nodes).
For bradyarrhythmias and heart blocks, rate-accelerating agents are used: M- anticholinergics and $\beta$-agonists.
Briefly: answers to topical questions
What subclasses are distinguished within Class I antiarrhythmic drugs and which specific medications belong to them?
Within Class I antiarrhythmic drugs (sodium channel blockers), three subclasses are distinguished: IA, IB, and IC. The division is based on the nuances of channel binding, effects on cardiac electrophysiological parameters, and clinical application. Specific medications belonging to each of the subclasses are not listed in the provided materials.
What is the exact electrophysiological mechanism behind the formation of a re-entry excitation loop?
The mechanism of formation of a re-entry excitation loop (reentry) is based on the occurrence of a unilateral conduction block.
- Orthodromic conduction — the impulse cannot pass through the damaged refractory fiber, but passes through an adjacent healthy pathway.
- Antidromic return — upon reaching the distal regions, the impulse returns retrogradely to the damaged area.
- Circuit closure — by the time of return, the damaged tissue exits refractoriness and conducts the impulse in the reverse direction.
As a result, the impulse re-enters the undamaged fiber, forming a closed loop of circulation.
What is the mechanism of the proarrhythmic action of antiarrhythmic drugs?
The mechanism of the proarrhythmic action of antiarrhythmic drugs lies in their ability to paradoxically provoke rhythm disorders. Two main pathways are distinguished:
- Vagolytic mechanism — blockade of the vagus nerve increases sinus node automaticity and facilitates conduction through the AV junction, which enhances ventricular arrhythmia.
- Effect on reentry — conduction suppression can paradoxically shorten the impulse movement trajectory. Movement along the "short circle" occurs faster, causing acceleration of the re-entry rhythm.
A risk factor is the combination of structural heart changes and electrical instability.
Relationship between AP phases and ions: 0 — Sodium (inward, conduction), 2 — Calcium (inward, plateau), 3 — Potassium (outward, repolarization). Phase 4 (automaticity) — function of If-channels.
Class and exam questions
Why is the AV node called a "filter"?
Conduction velocity in its penetrating fibers is minimal (0.02–0.05 m/s). This delays extra impulses during atrial tachycardia, transmitting them only antegrade and protecting the ventricles from overload.
What is the effective refractory period (ERP)?
This is the time (phases 0, 1, 2, and early 3) during which a cell cannot generate a new full-fledged action potential. Prolongation of ERP protects the myocardium from extrasystoles and circus movement waves of excitation (reentry).
What is the difference between the action potential of the sinus node and Purkinje fibers?
In pacemaker cells, the resting potential is higher (–55 mV), rapid sodium channels do not function, and depolarization and automaticity are provided by the calcium ion current and the operation of If-channels.
What else to study on this topic
- Detailed mechanism of action of each of the 4 classes of antiarrhythmic drugs
- Use of additional agents in arrhythmias (adenosine, cardiac glycosides, potassium and magnesium preparations)
- The role of fibrous tissue in the electrical isolation of the atria from the ventricles
- Clinical-pathogenetic correlation: the relationship between the developmental mechanism and the form of arrhythmia
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