Atrial fibrillation (AFib) is the most common heart rhythm disorder, defined by rapid and chaotic electrical signals in the heart’s upper chambers, the atria. This disorganized activity causes the atria to quiver instead of contracting effectively, leading to an irregular and often fast heartbeat. The prevalence of AFib increases with age, affecting millions in the United States, and it is a major contributor to stroke and can impair quality of life.
The Heart’s Normal Electrical System
The heart’s electrical system ensures it beats in a coordinated manner. The process begins in the sinoatrial (SA) node, a cluster of specialized cells in the right atrium that acts as the heart’s natural pacemaker. Under normal resting conditions, the SA node generates an electrical impulse 60 to 100 times per minute.
This initial signal spreads across both atria, causing the atrial muscle to contract and push blood into the heart’s lower chambers, the ventricles. The electrical impulse then travels to the atrioventricular (AV) node, situated near the center of the heart, where the signal is briefly delayed.
This pause at the AV node acts as a gatekeeper, ensuring the atria have finished emptying blood into the ventricles before they contract. After this delay, the impulse continues down a specialized pathway known as the bundle of His, which splits into right and left bundle branches. These branches distribute the signal throughout the ventricles, causing them to contract forcefully and pump blood to the lungs and the rest of the body in a sequence known as normal sinus rhythm.
Atrial Remodeling as the Source of AFib
Atrial fibrillation arises from long-term changes to the atria known as remodeling. This process alters the physical structure and electrical properties of the atrial tissue, creating an environment where AFib can begin and sustain itself. These changes are often driven by chronic conditions like high blood pressure, heart failure, obesity, and diabetes.
Structural remodeling involves physical alterations to the atria. Persistent strain from conditions like hypertension causes the atrial chambers to stretch and enlarge (atrial dilation). Over time, this stress also triggers fibrosis, where healthy heart muscle is replaced by stiff, scar-like tissue. This fibrotic tissue does not conduct electricity properly, creating roadblocks and detours that promote disorganized, reentrant circuits.
Electrical remodeling also occurs at a cellular level. The ion channels that control the flow of electrical charge in and out of heart cells become dysfunctional. These changes can make the atrial cells more excitable and shorten their refractory period—the brief rest they need between beats. This allows the cells to fire more rapidly, contributing to the chaotic signaling in AFib.
Within this remodeled tissue, a trigger is often needed to initiate an AFib episode. These triggers are rapid, erratic electrical impulses that can originate from specific areas, most commonly the pulmonary veins. In a healthy heart, such an impulse might have no effect, but in a remodeled atrium, it can act as a spark that ignites the unstable tissue and starts the episode.
Autonomic Nervous System Influence
The autonomic nervous system, which regulates functions like heart rate, also plays a part in triggering AFib. This system’s two branches can have distinct effects on the heart’s rhythm. The balance between these branches can influence the irritability of remodeled atrial tissue.
The sympathetic nervous system is responsible for the “fight-or-flight” response. When activated by stress or illness, it releases adrenaline, which increases heart rate and the force of contraction. This surge can make vulnerable atrial cells more prone to firing erratically, triggering an AFib episode.
Conversely, the parasympathetic nervous system governs “rest-and-digest” functions, and its primary nerve, the vagus nerve, can slow the heart rate. In some individuals, high vagal nerve activity—which can occur during sleep or after a large meal—can also provoke AFib. This demonstrates that both overstimulation and certain calming inputs from the nervous system can disturb atrial rhythm.
Consequences of Atrial Dysfunction
The primary issue in AFib stems from the loss of coordinated atrial contraction. This contraction, known as the “atrial kick,” is responsible for pushing the final volume of blood into the ventricles, accounting for up to 30% of their filling.
When the atria quiver during AFib, this atrial kick is lost. As a result, the ventricles do not fill as effectively, which reduces the heart’s overall efficiency and cardiac output—the amount of blood pumped to the body each minute. This reduction in blood flow can lead to common AFib symptoms such as fatigue, dizziness, weakness, and shortness of breath.
A more serious consequence arises from blood stasis within the atria. Because the atria are not contracting forcefully, blood can become sluggish and pool, particularly within a pouch in the left atrium called the left atrial appendage (LAA). Stagnant blood has a high tendency to form clots.
If a piece of a clot breaks free, it can travel through the bloodstream. Should this embolus lodge in an artery supplying the brain, it blocks blood flow and causes an ischemic stroke, the most serious complication of AFib. This mechanism explains why individuals with AFib have a significantly higher risk of stroke.