Causes (Etiology)
Rhythm disorders do not occur out of nowhere. There are several groups of factors capable of triggering an arrhythmia:
- Organic myocardial damage. This group includes coronary artery disease (CAD), various heart defects, cardiomyopathies, heart failure development, and hypertensive crises.
- Extracardiac disorders. Problems not directly related to the heart structure but affecting its function: metabolic shifts, endocrine pathologies, and autonomic disorders.
- Intoxications. Alcohol abuse takes first place here.
- Iatrogenic (drug-induced) factors. Arrhythmia can be caused by cardiac glycosides, antidepressants, diuretics, sympathomimetics, and, paradoxically, antiarrhythmic agents themselves (proarrhythmic effect).
Electrophysiology and mechanisms
The core of any arrhythmia is an alteration in the basic properties of the heart muscle: automaticity, conduction, and excitability.
Normal impulse pathway
To understand the pathology, one must recall the normal sequence of excitation:
- Sinoatrial node (the primary rhythm generator with maximal automaticity).
- Spread of the wave across the atria.
- Atrioventricular junction (atrioventricular node and the beginning of the bundle of His), where the impulse undergoes physiological deceleration.
- His-Purkinje system (bundle of His, its branches, and Purkinje fibers).
- Working contractile myocardium.
Pathophysiological Mechanisms
Arrhythmias develop according to three main scenarios:
- Disorder of automaticity. An ectopic focus with increased automaticity becomes active in the conduction system. If it generates impulses more frequently than the sinoatrial node, the primary pacemaker is suppressed. The result is a non-sinus accelerated ectopic rhythm.
- Disorder of conduction. The propagation velocity of the excitation wave drops, or conduction is completely blocked. This leads to heart blocks, the appearance of ectopic escape rhythms, or even asystole (cardiac arrest).
- Re-entry mechanism (Re-entry). Occurs due to electrical heterogeneity of tissues caused by myocardial damage. The impulse encounters a zone where forward (antegrade) conduction is blocked. It is forced to bypass this zone, reaches distal areas, and returns retrogradely to the starting point, which has already emerged from the refractory period. This forms a pathological closed loop of circulation, clinically manifesting as extrasystoles or tachycardias.
Clinical presentation and hemodynamics
The symptoms of arrhythmias are extremely diverse: from a complete lack of complaints (the patient does not feel missed beats or tachycardia at all) to severe life-threatening conditions.
Main manifestations:
- Subjective sensations: a feeling of skipped beats, strong palpitations, or heart fluttering.
- Myocardial ischemia: due to the arrhythmia, myocardial oxygen demand exceeds delivery, which provokes angina pectoris attacks (retrosternal pain).
- Heart failure: can be acute (with abrupt hemodynamic disturbance) or chronic (gradually progressing with persistent rhythm disorders).
- Cerebral symptoms: occur due to impaired blood supply to the brain. In a mild form, these are dizziness and presyncope.
Adams-Stokes-Morgagni attack This is a severe manifestation of cerebral ischemia against the background of a sharp drop in cardiac output. It is characterized by sudden loss of consciousness and seizures. The patient's skin first turns pale, then cyanosis develops. Blood pressure is unmeasurable, heart sounds are absent, and breathing is disrupted. There is a very high risk of sudden cardiac death.
Diagnostic Principles
The diagnosis is established based on instrumental data, as subjective complaints are too variable.
- Standard ECG: a baseline method that sometimes allows for an accurate diagnosis even from a single-lead recording.
- Long-term monitoring (Holter monitoring): continuous ECG recording for 24 hours during the patient's normal daily life. This method is essential for:
- Detecting transient arrhythmias.
- Searching for triggers of the attacks.
- Monitoring the effectiveness of prescribed treatment.
Briefly: answers to topical questions
What ECG features are characteristic of ventricular extrasystole?
Ventricular extrasystole is characterized by specific changes in the ventricular complex and a compensatory pause following it.
Key ECG criteria:
- QRS width — the complex is significantly widened ($\ge$ 0.12 s), deformed, and notched.
- Amplitude — increased in chest leads.
- Atrial relation — absence of a preceding P wave, since the impulse originates distally to the AV node.
- Repolarization — the ST segment and T wave are discordant (directed oppositely to the main deflection of the QRS complex).
- Pause — a full compensatory pause is recorded.
- Morphology — fusion complexes may be present.
How are antiarrhythmic drugs classified according to the Vaughan-Williams classification?
Antiarrhythmic drugs are classified into four main classes based on their mechanism of action.
- Class I drugs — sodium channel blockers (quinidine, procainamide, disopyramide, ajmaline, lidocaine, moracizine). They slow down conduction.
- Class II drugs — $\beta$-blockers (propranolol). Effective for supraventricular arrhythmias.
- Class III drugs — potassium channel blockers (amiodarone). Universal for all types of arrhythmias.
- Class IV drugs — calcium channel blockers (verapamil, diltiazem). Used for atrial pathologies.
What are the ECG criteria for atrial fibrillation?
The diagnosis of atrial fibrillation is confirmed in the presence of three key electrocardiographic signs.
- Absence of P waves — they are completely replaced by fibrillation waves.
- Presence of f (fibrillation) waves — multiple small waves of varying shape and amplitude. They are best visualized in leads V1, V2, II, III, aVF.
- Ventricular complexes (QRS) — have normal, unchanged morphology, yet R-R intervals vary, indicating absolute rhythm irregularity.
What ECG changes are characteristic of first-degree AV block?
First-degree atrioventricular block is characterized by slowed conduction, in which all atrial impulses reach the ventricles.
Main ECG criteria:
- Prolongation of the P-Q interval exceeding 0.21 s (it may be transient).
- Regular rhythm.
- Complete absence of dropped QRS complexes.
To remember the normal impulse conduction pathway: SA-Atria-AV-His-Purkinje (Sinoatrial node → Atria → AV junction → His-Purkinje system).
Class and exam questions
What is the essence of the re-entry mechanism?
This is a pathological process in which the excitation wave encounters a block, bypasses the damaged area, and returns to the starting point. A closed electrical loop is formed, causing the heart to contract abnormally.
Why does angina pectoris occur in arrhythmia?
Due to the rhythm disturbance, oxygen delivery to the myocardium decreases, while its demand may increase. This mismatch causes ischemic retrosternal chest pain.
Why is a Stokes-Adams attack dangerous?
During this attack, the heart stops pumping blood adequately, causing acute cerebral ischemia. The patient loses consciousness, pulse and blood pressure disappear, which can result in sudden cardiac death.
Can an arrhythmia be detected if the ECG is normal during a doctor's appointment?
Yes, Holter monitoring is used for this. The device records the ECG for 24 hours, which makes it possible to "catch" rhythm disturbances that occur periodically.
What else to study on this topic
- Features of ECG signs in automatism disorders.
- Classification and types of heart blocks.
- Detailed analysis of the proarrhythmic action of drugs.
- Differences between acute and chronic heart failure in the setting of arrhythmia.
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