Overview of atrial fibrillation (AFib)
Atrial fibrillation (AFib) is the most common treated chronic arrhythmia, with a lifetime risk of around 1 in 4 people older than 40.1 In AFib, rapid and disorganized electrical activity in the atria causes them to contract erratically (“fibrillate”) and ineffectively. This electrical activity bombards the AV node with inputs, prompting irregular ventricular contractions. Thus, AFib promotes atrio-ventricular asynchrony and generally results in an irregular heartbeat. AFib can be intermittent (“paroxysmal”) but can also become permanent, especially if left untreated. The major complications are tachycardia and intra-cardiac blood clots, which can travel to the brain and cause a stroke.2
Though well studied, the mechanisms that cause AFib are still poorly understood. Many AFib drivers have been identified such as cellular level changes (calcium handling and automaticity) and abnormal cardiac physiology (atrial pressures and structure). AFib is associated with abnormal atria due to underlying cardiac diseases, such as ischemic heart disease, hypertension, valvular heart disease, and cardiomyopathies. It can also be driven by non-cardiac causes such as electrolyte disturbances, pulmonary embolism, toxic substances, and acute infections. These factors can also interact to drive feedback loops. For example, fibrosis and inflammation that cause morphological changes to the atria can alter the refractory period and promote a continuously running electrical circuit within the atrial tissue known as “re-entry.”
Sound recorded by Eko digital stethoscope technology:
When present, AFib produces an “irregularly irregular” heart rhythm. The erratic electrical activity in the atria results in contractions of varying strength, which causes S1 to vary in intensity (heard best at the cardiac apex).
In AFib, the focus of atrial depolarization moves continuously around the atrium and is not fixed, resulting in an ECG with no clear P waves. Instead, irregular, low-amplitude fibrillatory waves may be seen, though these may be difficult to identify. The spontaneous electrical activity in the atria causes irregular ventricular depolarizations, which can be seen on the ECG as inconsistently spaced QRS complexes. The variable time between ventricular depolarizations also means that the strength of each ventricular contraction can vary. Some QRS complexes are associated with contractions that are so weak that they do not produce an audible heart sound. This is known as “electrical-mechanical dissociation.”
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