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.