Atrial fibrillation

Atrial fibrillation, sometimes called Afib for short, is the most common cardiac arrhythmia, which occurs when the atria contract way faster than expected and in a disorganized manner. As a result, the atria have a quivering or twitching movement that can’t pump blood into the ventricles efficiently.

Now, let’s cover some physiology of the cardiac conduction system. The cardiac conduction system is made up of specialized myocardial cells that can create and transport electrical potential, also called an action potential. These cells have many special features, including automaticity, meaning that they can generate an impulse; excitability, which is the ability to respond to a stimulus by creating an electrical impulse; conductivity meaning they can carry the impulse to other cells; and contractility, which is the ability to shorten the length of their fibers, causing a contraction.

Alright, now let’s look at the normal electrical conduction pathway in the heart on an ECG, which shows how the depolarization wave flows through the heart during each heartbeat. The normal electrical activity of the heart starts in the sinoatrial or SA node, which is considered the pacemaker of the heart.

Then, the impulse is conducted through the atria , causing depolarization and creating the P wave on an ECG. When the atrial muscle cells get depolarized, they contract, pushing blood from the atria into the ventricles.

From the atria, the impulse goes to the atrioventricular, or AV node, where the impulse propagation speed slows way down. The interval from the atrial depolarization to just before ventricular depolarization is the PR interval on an ECG. This delay allows the atria to

contract while the ventricles fill with blood.

From the AV node, the impulse goes through the Bundle of His, then to the right and left bundle branches, and finally through the Purkinje fibers, which deliver the impulse to the right and left

ventricles, causing them to depolarize, and is represented by the QRS complex on an ECG. This triggers simultaneous contraction of both ventricles, pushing blood into the systemic and pulmonary circulations. Finally, the ventricles repolarize to prepare for the next cycle, which allows them to relax and fill with blood, called diastole. And on ECG, ventricular repolarization will create a T wave, while the phase between ventricular depolarization and repolarization is represented by the ST segment. Sometimes, immediately after the T wave, there’s a U wave, which represents late repolarization of the ventricles.

Okay, now, atrial fibrillation is typically caused by any kind of structural damage to the heart or any damage to the heart's electrical conduction system. Often, these changes are strongly associated with several cardiovascular disorders and risk factors. For example, high blood pressure, coronary artery disease, valvular diseases, essentially anything that can create an inflammatory state or physically stretches the atria, may potentially damage the cells in the atria and lead to atrial fibrillation.

Other risk factors include older age, and a family history of heart disease or atrial fibrillation; as well as sleep apnea, obesity, diabetes, thyrotoxicosis, which means excess levels of thyroid hormones; and excessive alcohol consumption.

These factors likely stress and damage the cells in the atria, which can lead to tissue heterogeneity; in other words, cells start taking on different electrical properties, generating impulses from many foci in a totally disorganized manner,

which tends to override the sinoatrial node. So instead of one efficient atrial contraction, clients get all these mini contractions, usually between 350 and 600 per minute, that make it look like the atria are just quivering.

Sometimes, signals from one of these areas make it down to the ventricles and cause irregular ventricular contraction; these QRS complexes are interspersed at irregular intervals, though, and usually at high rates, between 100 and 150 beats per minute. As a result, the ventricular filling is also impaired, which reduces cardiac output.

Additionally, the inefficient emptying of the atria into the ventricles can cause blood to stay in the atria for longer than usual, allowing it to form atrial clots. This is especially concerning in the left atrium, which has a small pocket where the blood can collect, and clots are most likely to form. So, with atrial fibrillation, there’s a chance that one of these clots can get pumped from the atria into the ventricles, and from there, into the systemic circulation.

From there, the clot can get lodged in a cerebral artery, causing a stroke, or in other systemic arteries, blocking blood flow to areas such as the kidney, spleen, or extremities.

Often, people with atrial fibrillation start by experiencing paroxysmal events, which means AFib suddenly comes and goes, lasting less than a week at a time, probably because the tissue is still relatively healthy. Repeated paroxysmal events over extended periods stress the atrial cells even more. Over time, the cells in the atrium undergo progressive fibrosis or scarring, which means the AFib episodes didn’t terminate spontaneously in less than a week.

AFib episodes that last longer than one week are called persistent AFib; when it lasts for more than 12 months, it’s called long-standing persistent AFib. Finally, when long-standing persistent AFib is left untreated or doesn’t respond to treatment, that’s called permanent atrial fibrillation; in time, it can lead to heart failure.