Myocardial conduction disorders: etiology and types

Why is impulse conduction impaired?

Pathology never occurs in isolation. The ability of the heart muscle to conduct impulses adequately is impaired by a number 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 lesions: inflammatory diseases (myocarditis), structural remodeling (myocardial dystrophy), and cardiomyopathies (both dilated and hypertrophic forms).
Vascular and tissue damage: local hemorrhages directly in the areas of conduction pathways, as well as systemic vascular inflammation (vasculitis).
Severe infections: marked intoxication in tonsillitis, diphtheria, or the development of sepsis.
Regulatory and endocrine disorders: thyroid pathologies (thyrotoxicosis or hypothyroidism), vegetative-vascular dystonia, and severe emotional stress.

Classification of disorders

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

By change in conduction velocity: pathological acceleration of the signal, as well as its slowing, are distinguished. The extreme degree of slowing is complete conduction blockade.
By duration: disorders are divided into temporary (transient) and permanent.
By localization (level of block):
Sinoatrial — at the level of the sinus node and its exit to the atria.
Intraatrial — intra-atrial disorders.
Atrioventricular — atrioventricular blocks.
Intraventricular — intraventricular conduction defects.

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Hemodynamic consequences

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

Because of this, the heart chambers do not have time to fill properly with blood, triggering 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).
Impairment of coronary blood flow: blood supply to the myocardium itself generally decreases to one degree or another. The main consequence of this is a high risk of acute coronary insufficiency (CI), which can manifest as an attack of angina pectoris or myocardial infarction.

Allorhythmias and cellular mechanisms

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

The two most common forms are:

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

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

Increase in the concentration of potassium ions ($K^+$) in the extracellular environment (interstitial hyperkalemia).
Increased accumulation of higher fatty acids inside the cardiomyocytes themselves.
Development of marked acidosis (decrease in pH level) — both inside muscle cells and in the intercellular fluid.
Sharp increase in the concentration of cyclic adenosine monophosphate (cAMP) in the intracellular environment.

Briefly: answers to topical questions

What ECG signs are characteristic of first-degree atrioventricular block?

First-degree atrioventricular block is characterized by slowed impulse conduction from the atria to the ventricles with mandatory conduction of every impulse. When the disorder is functional, narrow QRS complexes are recorded on the electrocardiogram. An additional ECG sign is the disappearance of the block during physical exertion or an atropine test.

What degrees of atrioventricular block are distinguished in clinical practice?

In clinical practice, the following degrees of atrioventricular block are distinguished:

First-degree AV block — slowing of impulse conduction from the atria to the ventricles with conduction of every impulse.
Second-degree AV block — periodic interruption of atrial impulse conduction to the ventricles. It has three variants: Mobitz type I (Wenckebach periodicity), Mobitz type II, and advanced second-degree AV block.
Third-degree AV block; sources also refer to it as complete atrioventricular block.

How to memorize

To avoid confusing types of allorhythmia, focus on the prefixes: BIgeminy — a 2-beat cycle (1 normal + 1 extrasystole), TRIgeminy — a 3-beat cycle (2 normal + 1 extrasystole).

Class and exam questions

Why does blood pressure drop during conduction disorders?

Due to shortened diastole, the ventricles do not have time to fill with blood. This reduces cardiac output, which, together with a drop in total peripheral vascular resistance, leads to hypotension.

Why are impulse conduction failures dangerous for the heart itself?

They cause a decrease in coronary blood flow. Under conditions of myocardial oxygen starvation, the risk of developing coronary insufficiency — angina or infarction — increases sharply.

What cellular changes provoke severe arrhythmias?

Intra- and extracellular acidosis, potassium accumulation in the interstitium, as well as an excess of higher fatty acids and cAMP inside cardiomyocytes, play a key role.

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What else to study on this topic

Pathogenesis of the decrease in total peripheral vascular resistance (TPVR) in arrhythmias.
Mechanisms of extrasystole formation in bigeminy and trigeminy.
Effect of interstitial hyperkalemia and acidosis on the action potential of the cardiomyocyte.
The role of cAMP and higher fatty acids in impairing cardiac electrophysiology.
Hemodynamic features in atrial fibrillation and atrial flutter.

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Myocardial Conduction Disorders