The heart has four chambers, two upper chambers—the
right and left atrium, and two lower chambers—the right and left ventricles. Fibrillation describes when the muscle fibers
are all contracting at different times, so the end result is this quivering, or twitching
movement. Normally, an electrical signal is sent out
from the sinus node in the right atrium, it then propagates out through both atria super
fast, which allows them to depolarize at about the same time, and you end up with a nice,
coordinated contraction. That signal then moves down to the ventricles
and causes them to contract shortly after. With Atrial fibrillation, or A-fib or AF,
signals move around the atria in a completely disorganized way that tends to override the
sinus node. Instead of a one big contraction then, all
these mini contractions make it just look like the atria are just quivering.

On an electrocardiogram, or ECG, normally
the “P wave” corresponds to the atrial contraction, which is followed shortly after
by the “QRS complex”—which is the ventricular contraction. During AF, all these small areas are contracting
at different times so you end up with this scribble sort of looking ECG, each little
peak corresponding to one spot in the atria twitching. Sometimes a signal from one of these areas
makes it down to the ventricles and cause ventricular contraction, these QRS complexes
are interspersed at irregular intervals though, and usually at fairly high rates between 100
and 175 beats per minute. In the normal heartbeat, a well-coordinated
atrial contraction does contributes a small amount of blood that’s called the “atrial
kick”, people with AF lose this atrial kick, although this loss isn’t life-threatening. Okay but how or why does this happen to the
atrium? Why do the cells start depolarizing in a totally
uncoordinated way? Well, the answer isn’t super cut-and-dry. There are a ton of risk factors that predispose
someone to developing AF, and the exact mechanisms aren’t well understood.

AF often happens alongside other cardiovascular
diseases, like high blood pressure, coronary artery disease, valvular diseases—essentially
anything that can create an inflammatory state or physically stretch out the atria and potentially
damage the cells in the atria. Other, non-cardiovascular risk factors include
obesity, diabetes, and excessive alcohol consumption. Adding to all this, there also seems to be
a genetic component as well. These factors likely stress the cells in the
atria, which can lead to tissue heterogeneity, which means that cells start taking on different
electrical properties.

For example, this cell might start conducting
signals faster than it’s neighbor, and that cell might develop a shorter refractory period,
which is the time following a depolarization that they can’t conduct another signal. These different tissue properties can ultimately
cause the conduction in the atria to become unpredictable. Normally, with tissue that’s the same, you’ll
get essentially one wavefront of conduction that moves through the atria. With different tissue properties, multiple
wavelets are thought to develop, called the multiple wavelet theory.

These wavelets conduct randomly around the
atria, sometimes colliding and creating new “daughter wavelets”. Along with this multiple wavelet theory, there’s
also an automatic focus theory, where there’s a specific origin that is thought to initiate
AF by rapid firing of electrical impulses that overtake the sinus node, and combined
with the risk factors and tissue heterogeneity, this can promote AF. It’s thought that focus of cells are conducting
cells in the cardiac muscle around pulmonary veins – yeah, pulmonary veins! Remember these veins physically enter the
left atrium, and where the pulmonary veins enter there is tissue that has really unique
electrical properties.

Oftentimes, people with AF start with what
are called paroxysmal events, which means AF suddenly comes and goes, lasting less than
a week at a time, probably because the tissue is still relatively healthy. Repeated paroxysmal events that occur over
longer periods of time, though, tend to stress the atrial cells even more. There are probably a number of mechanisms
explaining how a burst of rapid beats from one of these paroxysmal events leads to stress,
with one potential mechanism being through calcium overload. Nonetheless, over time, the cells in the atrium
seem to undergo progressive fibrosis or scarring from this stress. When this happens, the AF episode isn’t
able to spontaneously terminate, and patients have persistent AF, defined as lasting more
than a week without self-terminating. Persistent AF episodes can last for quite
a long time – weeks to months, and when the AF episodes last beyond 12 months, it’s
known as long-standing persistent AF, and “permanent AF” is what’s it’s called
when the patient and clinician make a joint decision to not attempt to stop the rhythm.

Common symptoms of AF are feelings of general
fatigue, since the heart rate isn’t being governed by the sinus node anymore, and contracts
at irregular intervals, delivering blood less effectively to the tissues. Other related symptoms include dizziness,
shortness of breath, and weakness. Patients might also feel palpitations or “thumping”
in their chest. One potential complication of AF is stroke. When the atria don’t contract as a single
unit, but just sort of quiver, the blood that sits in the atria becomes more stagnant.

When blood stays still, it tends to form clots. With AF, it’s possible that blood clots
form, which then travel into the ventricle and are pumped off to the body, and potentailly
to the brain, where they can lodge. This cuts off blood flow to that part of the
brain – which is a type of stroke. Diagnosis of persistent AF is done by ECG,
although if the episodes are paroxysmal, but they’re suspected, then someone might have
a holter monitor, which is a portable device placed on the chest that monitors their rhythm
over longer periods of time and records potential AF events to be viewed later.

Since AF is caused by such a diverse range
of issues, treatment is generally different from patient to patient. Certain medications that help control the
heart rate might be given, or medications that reduce the likelihood of of blood clot
formation and therefore prevent stroke. Also, patients may receive an implantable
cardiac pacemaker, which, by constantly pacing the atrium, can reduce the chance of an AF
episode. Finally, some patients may have a radiofrequency
catheter ablation, where certain areas of tissue are destroyed such that the electrical
signal doesn’t propagate any more. One type of procedure is the “maze procedure”
where a maze of new pathways are created to help electrical impulses move in more consistent,
predictable patterns.

Sometimes patients will have the ablation
of the AV node separating the upper and lower chambers, essentially cutting off any communication
between the two. Since the ventricles aren’t getting any
input anymore, these patients need an implantable pacemaker to make sure the ventricles contract
at high enough rates..



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