Specific conduction syndromes
Some rhythm disorders have unique genetic and electrocardiographic characteristics, as well as specific risks for the patient. The prognosis in ventricular pre-excitation syndromes is often unfavorable as they provoke paroxysmal arrhythmias, with atrial fibrillation being particularly dangerous in this regard.
- Clerk-Levy-Cristesco (CLC) syndrome: Characterized by an isolated shortening of the P-Q interval (less than 0.12 s). The QRS complex remains normal and unchanged.
- Brugada syndrome: Has a familial pattern and is associated with a genetic mutation of sodium channels (the SCN5A gene). Organic myocardial lesions are absent; however, there is a tremendous risk of sudden nocturnal death, predominantly among young men. The ECG reveals ST-segment elevation in leads V1–V3, sometimes presenting with a right bundle branch block pattern. The only reliable method to prevent a fatal outcome is the implantation of a cardioverter-defibrillator.
For precise topical diagnosis of accessory pathways, intracardiac electrophysiological study (EPS) is used, involving the insertion of catheters into the heart chambers. Once the pathway is localized, radical treatment is performed via destruction (ablation) using transvenous electrocoagulation or laser.
Sinoatrial (SA) block
In SA block, impulse formation or its conduction from the sinoatrial node to the atrial myocardium is impaired.
Electrocardiographic features: Against the background of a completely regular sinus rhythm, a pause suddenly occurs. The essence of this pause lies in the complete dropout of one or several cardiac cycles—both the P wave and the QRST complex are absent on the ECG. Mathematically, the duration of such a pause is usually a multiple of the normal P-P distance (e.g., equal to two normal cycles). During a prolonged standstill, replacement beats, such as atrial or junctional extrasystoles, may appear.
Clinical presentation: During auscultation, heart sounds are not heard during the pause, and pulse palpation reveals the dropping of a pulse wave (pulse deficit).
Atrioventricular (AV) block
This pathology is caused by impaired signal transmission from the atria to the ventricles. AV blocks can be dynamic (transient) or permanent. Mild degrees are even found in healthy individuals, whereas severe forms usually accompany serious diseases (coronary artery disease, myocarditis).
- First-degree AV block: All atrial impulses reach the ventricles, but conduction is delayed. It is detected solely by instrumental methods. The main ECG criterion is prolongation of the P-Q interval beyond 0.21 s (e.g., up to 0.34 s). The rhythm remains regular, with no QRS dropouts.
- Second-degree AV block: Characterized by periodic blocking of the impulse. On the ECG, this manifests as the dropout of individual ventricular complexes (QRST). It is subdivided into Mobitz type I and Mobitz type II.
- Third-degree (complete) AV block: Impulse conduction ceases entirely, resulting in AV dissociation. The atria contract at their own sinus rhythm (e.g., 100–110 bpm), while the ventricles beat at a slower rate driven by an ectopic pacemaker (escape rhythm). On the ECG, P waves are registered regularly, but completely independently of the QRS complexes, sometimes overlapping with them or with T waves.
The morphology of the ventricular complex depends on the level of the block. In the proximal form (originating from the AV junction), QRS complexes are narrow, and the heart rate is about 40 bpm. In the distal form (obstruction below the AV node, in the bundle branches), QRS complexes become wide and deformed, and the rate drops below 30 bpm (idioventricular rhythm).
Etiology and complications
AV conduction disorders are caused by multiple factors:
- Organic: Acute ischemia (myocardial infarction).
- Infectious-inflammatory: Rheumatic fever, myocarditis, diphtheria, infective endocarditis.
- Iatrogenic (drug-induced): Overdose of cardiac glycosides, $\beta$-blockers, calcium channel antagonists (verapamil), and class I antiarrhythmics.
- Functional: Marked parasympathicotonia (carotid sinus syndrome, "athlete's heart").
The most formidable complication is Stokes-Adams syndrome. It develops at the moment of transition from incomplete block to complete block. A pre-automatic pause occurs—the period before the escape pacemaker activates. The cessation of cardiac contractions causes acute cerebral hypoxia, leading to severe dizziness and syncope. With the long-term presence of complete AV block and a slow heart rate, the risk of severe heart failure increases significantly.
Briefly: answers to topical questions
What is the difference between Mobitz type I and Mobitz type II in second-degree AV block?
The main difference lies in the presence or absence of progressive prolongation of the P-Q interval prior to the dropout of the ventricular complex.
| Characteristic | Mobitz I | Mobitz II |
|---|---|---|
| Mechanism | Impulse blocking with preceding progressive slowing of conduction from the atria to the ventricles | Impulse blocking without preceding prolongation of atrioventricular conduction time |
| ECG presentation | Gradual prolongation of the P-Q interval over a series of several cardiac cycles followed by dropout of the QRS complex; after the pause, the cycle repeats | Impulse blocking without preceding prolongation of atrioventricular conduction time |
To remember the degrees of AV block, imagine the connection between the atria and ventricles: 1st degree—they "talk" slowly (all impulses pass with a delay); 2nd degree—the ventricles sometimes "ignore" the atria (dropout of complexes); 3rd degree—complete "disconnection", each works on its own (AV dissociation).
Class and exam questions
In 1st degree, absolutely all atrial impulses reach the ventricles, and only conduction delay occurs (P-Q interval > 0.21 s). QRST complex dropouts are absent, so the block is clinically asymptomatic and visible only on the ECG.
In 1st degree, absolutely all atrial impulses reach the ventricles, and only conduction delay occurs (P-Q interval > 0.21 s). QRST complex dropouts are absent, so the block is clinically asymptomatic and visible only on the ECG.
The main sign is the sudden dropout of an entire cardiac cycle against the background of a regular rhythm. The ECG records a straight line without a P wave and QRST complex, and the length of this pause is mathematically a multiple of the normal P-P interval.
The main sign is the sudden dropout of an entire cardiac cycle against the background of a regular rhythm. The ECG records a straight line without a P wave and QRST complex, and the length of this pause is mathematically a multiple of the normal P-P interval.
Widening and deformation of the QRS complex (regardless of the degree of AV block) indicates a distal level of the lesion. This means that the conduction obstacle is located below the AV node—in the bundle branches.
Widening and deformation of the QRS complex (regardless of the degree of AV block) indicates a distal level of the lesion. This means that the conduction obstacle is located below the AV node—in the bundle branches.
What else to study on this topic
- Diagnostic criteria for Mobitz type I and Mobitz type II in second-degree AV block.
- Principles of ectopic pacemaker operation during AV dissociation.
- Indications for pacemaker insertion in Stokes-Adams syndrome.
- Features of intracardiac EPS procedure.
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