Pathology fundamentals and hemodynamics
In atrial fibrillation, the atria lose the ability to contract effectively. Instead of a single ejection of blood, chaotic twitching of individual muscle bundles is observed. Electrical impulses are generated at an extreme rate of 350 to 700 per minute.
In this situation, the atrioventricular (AV) node acts as a filter. Since it is physiologically incapable of transmitting such a high number of signals to the ventricles, it blocks a portion of them. As a result, the ventricular rate (ventricular response) is typically 90–120 beats per minute, rarely reaching 150–200.
A key clinical sign of the tachy-systolic form is pulse deficit. Due to the shortened diastole, the ventricles do not have time to fill adequately with blood. The next contraction occurs "in vain": the cardiac output is so weak that the pulse wave does not reach the peripheral arteries. Upon auscultation, the true heart rate is higher than the pulse rate at the radial artery.
Causes (Etiology)
The pathogenetic basis of the arrhythmia is the re-entry mechanism—the formation of multiple re-entrant excitation circuits. The transition from a paroxysmal to a permanent form directly depends on the degree of left atrial enlargement.
Main groups of causes:
- Structural changes and left atrial overload: mitral valve disease and congenital defects (e.g., VSD), hypertension, heart failure, left ventricular hypertrophy, pulmonary embolism.
- Myocardial ischemia: myocardial infarction, coronary artery disease.
- Endocrine and metabolic disorders: thyrotoxicosis, potassium deficiency (hypokalemia).
- Toxic effects: alcohol ("holiday heart" syndrome), cardiac glycoside intoxication.
- Inflammation and iatrogenic causes: myopericarditis, pneumonia, consequences of thoracic surgery.
If no obvious causes can be identified, it is referred to as an idiopathic form.
ECG diagnostics
To establish a diagnosis, the electrocardiogram must exhibit three mandatory criteria:
- Absence of a normal P wave. It is completely replaced by pathological electrical activity.
- Appearance of fibrillation (f) waves. These are multiple small waves that constantly change in shape and amplitude. They are best visualized in leads V1, V2, II, III, and aVF.
- Absolute rhythm irregularity. The R-R intervals vary in duration, while the QRS complexes themselves remain normal (narrow) and undeformed.
Complications and management principles
Atrial fibrillation is dangerous due to two groups of complications:
- Hemodynamic: a high heart rate exhausts the myocardium, leading to the onset or rapid progression of heart failure.
- Thromboembolic: the lack of effective atrial systole causes blood stasis, especially in the atrial appendages. Thrombi form there and can migrate into the systemic circulation (causing stroke) or pulmonary circulation (causing pulmonary embolism).
Important: the highest risk of thrombus detachment occurs during cardioversion—the pharmacological or electrical restoration of normal sinus rhythm.
The primary objective for the physician in managing such a patient is to reduce the ventricular rate and eliminate the pulse deficit. Pharmacotherapy, specifically cardiac glycosides, is frequently used to control the rhythm.
Differences from atrial flutter
Atrial flutter (Flutter atriorum) is a related condition in which the atria contract regularly, but at a high rate (250–350 per minute).
Unlike fibrillation, the ECG shows distinct sawtooth F waves with no isoelectric line between them. The AV node transmits every second or third impulse (2:1 or 3:1 block). If the conduction ratio is stable, the ventricular rhythm will be regular. For better visualization of F waves on the ECG, a diagnostic maneuver—carotid sinus massage—is used, which temporarily slows down AV conduction.
Briefly: answers to topical questions
What scoring systems are used to assess the risk of thromboembolic complications and prescribe anticoagulants in atrial fibrillation?
The CHA2DS2-VASc score is used to assess the risk of thromboembolic complications in atrial fibrillation. It is employed to identify risk factors for ischemic stroke and systemic thromboembolism in patients diagnosed with atrial fibrillation or flutter.
Which specific classes of antiarrhythmic drugs are used for pharmacological cardioversion?
Class I and III antiarrhythmic drugs are used for pharmacological cardioversion and rhythm control. Most of them effectively restore sinus rhythm in recent-onset arrhythmia episodes lasting less than 48 hours. Class IC agents are also used for the management of symptomatic fibrillation.
What clinical symptoms and complaints, apart from pulse deficit, does a patient present with during an episode of atrial fibrillation?
In addition to pulse deficit, patients with atrial fibrillation may present with:
- palpitations, a feeling of irregular or racing rhythm;
- sensation of skipped beats or "heart flutters";
- shortness of breath;
- fatigue;
- chest discomfort.
What anticoagulant therapy strategy is used before elective cardioversion?
Mandatory anticoagulant therapy lasting at least three weeks is administered before elective cardioversion. This strategy is indicated when the episode duration is 48 hours or more, or of unknown duration, regardless of the CHA2DS2-VASc score.
Drugs used:
- Direct oral anticoagulants (DOACs) — apixaban, dabigatran etexilate, rivaroxaban, edoxaban.
- Vitamin K antagonists — warfarin, targeting an INR of 2.0–3.0.
For quick memorization of the atrial fibrillation ECG triad, use the rule: "No P, plus f, varying R-R". Meanwhile, the QRS complexes themselves remain unchanged.
Class and exam questions
Why does a pulse deficit occur in atrial fibrillation?
Due to the short diastole, the ventricles do not have time to fill with blood. Cardiac output drops, and the pulse wave simply fails to reach the peripheral arteries.
At what moment is the risk of thrombus detachment maximal?
The highest risk of thromboembolism occurs at the moment of sinus rhythm restoration (during pharmacological or electrical cardioversion).
How to distinguish atrial flutter from sinus rhythm without an ECG?
With a regular rhythm (stable AV conduction ratio) and absence of tachycardia, it is clinically impossible to distinguish flutter from sinus rhythm.
What else to study on this topic
- Atrial flutter: ECG criteria and sawtooth F waves
- Ventricular fibrillation and flutter as terminal states
- The role of left atrial remodeling and dilation in chronic arrhythmia
- Prognosis and recurrence risk in ventricular fibrillation depending on myocardial infarction
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