What is Atrial Fibrillation (AFIB)?

What is Atrial Fibrillation (AFIB)?

Atrial fibrillation is a supraventricular tachyarrhythmia characterized by uncoordinated atrial activation with consequent deterioration of atrial mechanical function, resulting in an irregular ventricular response on electrocardiogram. 1

Electrocardiographic Definition

AFIB is defined by three key ECG characteristics that distinguish it from other arrhythmias:

• Absolutely irregular RR intervals that do not follow any repetitive pattern (sometimes called "arrhythmia absoluta") 1
• Absence of distinct P waves on the surface ECG, replaced by rapid oscillations or fibrillatory waves that vary in amplitude, shape, and timing 1
• Atrial cycle length (when visible) is usually variable and less than 200 ms, corresponding to an atrial rate of ≥300 beats per minute 1

Pathophysiology and Mechanisms

The irregular ventricular response in AFIB depends on several factors:

• Electrophysiological properties of the AV node and other conducting tissues determine how many atrial impulses are transmitted to the ventricles 1, 2
• Autonomic tone balance between vagal and sympathetic activity modulates AV nodal conduction 1, 2
• Presence of accessory pathways can lead to extremely rapid ventricular rates exceeding 200 beats per minute, which is a medical emergency 1, 2
• Drug effects on AV nodal conduction alter the ventricular response rate 1, 2

Hemodynamic Consequences

AFIB causes significant cardiovascular compromise through multiple mechanisms:

• Loss of atrial contraction reduces cardiac output by 5-15% acutely, with more pronounced effects in patients with reduced ventricular compliance who depend on atrial kick for adequate filling 1, 2
• Rapid ventricular rates limit diastolic filling time and can cause rate-related interventricular or intraventricular conduction delays 1, 2
• Irregular ventricular response creates beat-to-beat variability in stroke volume due to force-interval relationships, often resulting in pulse deficit 1
• Persistent tachycardia above 120-130 bpm can produce ventricular tachycardiomyopathy, which may be reversible with rate control 1, 2

Clinical Significance and Complications

AFIB is the most common sustained cardiac arrhythmia with serious implications:

• Stroke risk increases substantially due to atrial thrombus formation and subsequent cerebral or systemic emboli 3, 4
• Heart failure can develop or worsen due to loss of atrial contribution to ventricular filling and tachycardia-induced cardiomyopathy 2, 5
• Increased mortality from all causes is associated with AFIB 3
• Lifetime risk of developing AFIB is approximately 25% in patients older than 40 years, with incidence increasing significantly with age 6, 3

Diagnostic Approach

An ECG recording during the arrhythmia is essential for diagnosis:

• 12-lead ECG is the gold standard for confirming AFIB and should be of sufficient duration and quality to evaluate atrial activity 1
• Minimum duration of 30 seconds on a rhythm strip with characteristic ECG features is required to diagnose an AFIB episode 1
• Irregular pulse should always raise suspicion, but ECG confirmation is mandatory 1
• Provocative maneuvers such as Valsalva, carotid massage, or intravenous adenosine can help unmask atrial activity when ventricular rate is very rapid 1

Common Diagnostic Pitfalls

Several conditions can mimic AFIB and must be differentiated:

• Atrial flutter with variable conduction may appear irregular but typically shows longer atrial cycle lengths ≥200 ms and saw-tooth flutter waves, particularly in leads II, III, aVF, and V1 1, 2
• Regular RR intervals can occur in AFIB when AV block or ventricular/junctional tachycardia is present, potentially causing diagnostic confusion 1, 2
• Frequent ventricular extrasystoles can create irregular rhythms that superficially resemble AFIB 1
• Pacemaker patients may require temporary pacemaker inhibition to expose underlying atrial fibrillatory activity 1
• Wide-QRS-complex tachycardia that is rapid, irregular, and sustained strongly suggests AFIB with either accessory pathway conduction or underlying bundle-branch block 1