Myocardial Conduction Disturbances

Causes of Impaired Impulse Conduction

Pathology never develops in isolation. The ability of the heart muscle to properly conduct an impulse is impaired by a variety of factors. The etiology of these disorders can be divided into several main groups:

• Congenital heart defects: anatomical defects of the atrial or ventricular septum, as well as combined anomalies (e.g., tetralogy of Fallot).
• Direct myocardial damage: inflammatory diseases (myocarditis), structural remodeling (myocardial dystrophy), and cardiomyopathies (both dilated and hypertrophic forms).
• Vascular and tissue damage: local hemorrhages directly within the conduction pathways, as well as systemic vascular inflammation (vasculitis).
• Severe infections: pronounced intoxication in tonsillitis, diphtheria, or sepsis.
• Regulatory and endocrine disorders: thyroid pathology (thyrotoxicosis or hypothyroidism), vegetative-vascular dystonia, and severe emotional stress.

Classification of Conduction Disturbances

Depending on the nature of the damage, impulse conduction disorders can be functional or organic. For accurate diagnosis and understanding of pathogenesis, disturbances are classified according to three key parameters:

1. By change in conduction velocity: pathological acceleration of the signal, as well as its slowing. The extreme degree of slowing is complete conduction block.
2. By duration: disorders are divided into temporary (transient) and permanent.
3. By localization (site of block origin):
4. Sinoatrial — at the level of the sinus node and its exit to the atria.
5. Intraatrial — within the atria.
6. Atrioventricular — between atria and ventricles.
7. Intraventricular — intraventricular conduction defects.

Hemodynamic Consequences

Any significant conduction problems inevitably affect the pumping function of the heart. With the development of tachycardia, atrial fibrillation, or atrial flutter, the duration of diastole is critically shortened.

Because of this, the heart chambers do not have time to adequately fill with blood, which triggers a cascade of hemodynamic problems:

• Drop in stroke volume (SV) and cardiac output (CO): the heart pumps less blood per contraction and per minute overall.
• Decrease in blood pressure: both systolic and diastolic pressure fall. The pathogenesis of this condition is associated not only with low cardiac output, but also with a decrease in total peripheral vascular resistance (TPVR).
• Impaired coronary blood flow: the blood supply to the myocardium itself generally decreases to some degree. The main consequence of this is a high risk of developing acute coronary insufficiency, which may manifest as an anginal attack or myocardial infarction.

Allorhythmias and Cellular Mechanisms

A specific manifestation of rhythm and conduction disorders is allorhythmia — a condition in which normal (timely) impulses alternate in a certain sequence with premature contractions (extrasystoles).

Two forms are most common:

• Bigeminy: an extrasystole follows strictly after every single normal regular impulse.
• Trigeminy: a premature impulse occurs after two normal contractions.

The progression of disorders into severe, life-threatening forms does not happen by chance. It is typically characterized by a simultaneous combination of several pathological shifts in cardiomyocytes and the surrounding interstitium:

1. Increase in potassium ion ($K^+$) concentration in the extracellular environment (interstitial hyperkalemia).
2. Increased accumulation of free fatty acids inside cardiomyocytes.
3. Development of pronounced acidosis (decreased pH) — both inside muscle cells and in the extracellular fluid.
4. Sharp increase in the intracellular concentration of cyclic adenosine monophosphate (cAMP).