Atrial Fibrillation (Afib) is a widespread type of irregular heartbeat. This condition causes the heart’s upper chambers (atria) to beat rapidly and chaotically instead of in a coordinated manner. Understanding its pathophysiology involves exploring the physiological processes that lead to and sustain this irregular rhythm.
The Heart’s Electrical Symphony
The human heart relies on a precise electrical system to pump blood effectively. The sinoatrial (SA) node, located in the right upper chamber, acts as the natural pacemaker. This specialized tissue spontaneously generates electrical impulses at a regular rate, between 60 and 100 times per minute.
These electrical signals then spread across both the right and left atria, causing the atria to contract synchronously. The impulse then reaches the atrioventricular (AV) node, situated between the atria and ventricles. The AV node briefly slows the electrical signal, allowing the atria to fully contract and pump blood into the ventricles before they contract. After this short delay, the impulse travels rapidly through the bundle of His, bundle branches, and Purkinje fibers, leading to the coordinated contraction of the ventricles.
Disrupted Electrical Signals
In atrial fibrillation, the normal electrical activity of the atria becomes chaotic. Instead of a single, regular impulse from the SA node, multiple, disorganized electrical impulses fire rapidly and erratically. These abnormal impulses often originate from areas outside the SA node, particularly in the muscle sleeves extending into the pulmonary veins. These “ectopic foci” can fire at very high frequencies, sometimes as rapidly as 340 beats per minute, overwhelming the normal pacemaker.
The rapid and uncoordinated firing of these ectopic foci can initiate “re-entrant wavelets.” This occurs when electrical impulses circle within the atrial tissue, creating multiple circulating electrical pathways. These re-entrant circuits prevent the atria from contracting effectively, causing them to quiver or “fibrillate” instead of contracting in a synchronized manner. This chaotic electrical activity prevents the atria from efficiently pushing blood into the ventricles, impacting the heart’s pumping efficiency.
Remodeling of the Atria
Over time, sustained abnormal electrical activity and underlying conditions lead to structural and cellular changes within the atrial tissue, creating a substrate that perpetuates atrial fibrillation. This process is known as atrial remodeling. Atrial enlargement or dilation, where the atrial chambers expand, is a common change. This enlargement can increase the pathways available for re-entrant wavelets, making the arrhythmia more likely to persist.
Fibrosis, involving the deposition of scar tissue and stiffening of the atrial walls, is another alteration. This fibrous tissue disrupts the normal electrical communication between heart muscle cells, slowing electrical conduction and creating areas where impulses can become trapped and re-enter. Changes in ion channels also occur, affecting the heart’s electrical conductivity and making it more prone to abnormal rhythms. Inflammation and oxidative stress contribute to these structural changes, promoting collagen deposition and exacerbating atrial remodeling.
Underlying Contributing Factors
Various underlying conditions and lifestyle factors contribute to the electrical and structural changes seen in atrial fibrillation. High blood pressure, or hypertension, is a common factor, increasing the risk of Afib by 40-50% and accounting for approximately 20% of new cases. Chronic hypertension can lead to increased pressure within the heart, causing atrial dilation and promoting fibrosis.
Conditions like heart failure and coronary artery disease also increase Afib risk by placing stress on the heart and promoting remodeling. Obesity is another strong contributor, with each unit increase in body mass index (BMI) raising the risk of Afib by about 3%. Obesity is associated with left atrial enlargement, chronic inflammation, and increased epicardial adipose tissue, all of which contribute to a pro-arrhythmic environment.
Diabetes mellitus and sleep apnea also heighten the risk of Afib. Patients with obstructive sleep apnea, for instance, face a four-fold higher risk of developing Afib compared to those without the condition. Excessive alcohol consumption can directly trigger Afib episodes and, over time, alter the atria’s physical structure and electrical properties. Advanced age is also a prominent risk factor, with the incidence rate of Afib rising significantly with age.