Extrasystole

Etiology and pathogenesis

Extrasystoles may occur against the background of organic myocardial lesions or functional regulatory disorders without structural changes.

Two leading mechanisms of premature impulse formation are distinguished:

1. The re-entry mechanism (circus movement of the excitation wave). This is considered the primary factor. It is based on the pathological circulation of an impulse due to electrical myocardial inhomogeneity—adjacent areas have different conduction velocities and refractoriness. This condition is provoked by ischemia, myocardial infarction (necrosis), dystrophy, sclerosis, or marked metabolic alterations.
2. Enhanced automaticity. It develops in ectopic foci, which are specific areas of the conduction system.

Supraventricular extrasystoles

This group includes atrial and atrioventricular (junctional) premature contractions. Their common feature is an incomplete compensatory pause. The ectopic impulse travels retrogradely, reaches the sinoatrial (SA) node, and resets it. As a result, the sum of the pre- and post-extrasystolic intervals is less than two normal cycles.

• Atrial. Characterized by the presence of a deformed (atypical) P wave preceding the complex. The QRS complex itself remains narrow and unchanged, as ventricular conduction is unimpaired.
• Atrioventricular. The QRS is also of normal morphology. The impulse travels antegrade to the ventricles and retrograde to the atria. The picture depends on timing: if the atria are depolarized earlier, an inverted P is visible before QRS (P-Q interval < 0.12 s); if simultaneously, the P wave merges with QRS and is invisible; if later, an inverted P is registered after QRS (on the ST segment or T wave).

Ventricular extrasystoles

The focus of automaticity is located directly in the ventricular myocardium (usually in the bundle of His branches). The impulse cannot pass retrogradely through the AV junction, so the SA node is not reset and generates its impulse on time. However, it catches the ventricles in a refractory state, causing one normal contraction to drop out. A full compensatory pause is formed (the sum of the intervals before and after the extrasystole equals two normal R-R intervals).

ECG criteria for ventricular extrasystole:

• The P wave preceding the complex is absent.
• The QRS complex is significantly widened (≥ 0.12 s), deformed, and often notched (excitation propagates atypically from one ventricle to the other).
• The ST segment and T wave are discordant, directed opposite to the main QRS deflection.

The topography of the focus is determined using chest leads:

• Left ventricular: resembles complete right bundle branch block (in $V_1$, the main deflection is upward—tall R).
• Right ventricular: resembles complete left bundle branch block (in $V_1$, the main deflection is downward—deep S).

Classification: rate, frequency, and rhythmicity

Several classifications are used to assess the severity of the condition.

By frequency (per hour):

• Rare (< 10).
• Moderate (10–29).
• Frequent (> 30).

By pattern/density:

• Couplets (two in a row).
• Runs or salvos (3 to 5 in a row).

Allorhythmias are regular alternations of extrasystoles with normal cycles:

• Bigeminy (1 normal : 1 extrasystole).
• Trigeminy (after every two normal complexes).
• Quadrigeminy (after every three normal complexes).

According to the number of foci, extrasystoles are classified as monotopic (identical QRS morphology, single focus) and polytopic (different QRS morphology, multiple foci).

Clinical significance and hemodynamics

Rare extrasystoles are detected in most healthy individuals and have no clinical significance. Patients may be asymptomatic or complain of 'skipped beats' and fluttering in the chest. Palpitation reveals a premature weak pulse wave, and in cases of hemodynamically ineffective contractions, a pulse deficit.

Arrhythmias occurring against the background of organic heart disease (especially myocardial infarction) warrant particular concern. Frequent, polytopic, paired, and early extrasystoles are prognostically extremely unfavorable. Early ventricular contractions (the 'R-on-T' phenomenon) fall on the T wave of the preceding cycle, impair diastolic filling, and can trigger ventricular fibrillation. Frequent bigeminy, in turn, can lead to a marked drop in cardiac output.

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• The Re-entry mechanism and the concept of electrical myocardial inhomogeneity
• Differential diagnosis of bundle branch blocks and ventricular extrasystoles
• Hemodynamic features of the 'R-on-T' phenomenon
• Wenckebach periodicity (Mobitz I) and progressive impairment of AV conduction
• Causes of polytopic extrasystoles in myocardial infarction

Other topics in the "Cardiovascular system" section

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