Atrial fibrillation
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If left untreated, this patient is at greatest risk for which of the following complications?
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Anticoagulant drugs p. 420
atrial fibrillation p. 300
Arrhythmias
atrial fibrillation p. 728
Atrial fibrillation
β -blockers for p. 329
calcium channel blockers for p. 363
cardiac glycosides for p. NaN
ECG tracing of p. 300
embolic risk with p. 728
embolic stroke p. 529
hypertension as cause p. 306
jugular venous pulse in p. 294
potassium channel blockers for p. 329
sleep apnea p. 703
Coronary artery disease
atrial fibrillation and p. 300
Emboli
atrial fibrillation p. 300
Hypertension p. 306
atrial fibrillation and p. 298
Stroke p. 529
atrial fibrillation and p. 300
Thromboembolic event
atrial fibrillation p. 300
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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 a quivering, or twitching movement.
Normally, an electrical signal is sent out from the sinus node in the right atrium. The signal then propagates out through both atria super fast, which allows them to depolarize at about the same time, so that you end up with a nice, coordinated contraction of the atria. 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 one big contraction, you get all these mini contractions that make it look like the atria are just quivering.
On an electrocardiogram, or ECG, normally the “P wave” corresponds to the atrial contraction. The “QRS complex,” which is the ventricular contraction, follows shortly after. During AF, all these small areas contract at different times so that you end up with an electrocardiogram that looks like scribbles, where each little peak corresponds 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 contributes a small amount of blood that’s called the “atrial kick.” People with AF lose this atrial kick; however, this loss isn’t life-threatening.
Okay, but how or why does this happen in 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, including 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. Additionally, there also seems to be a genetic component.
Sources
- "Robbins Basic Pathology" Elsevier (2017)
- "Harrison's Principles of Internal Medicine, Twentieth Edition (Vol.1 & Vol.2)" McGraw-Hill Education / Medical (2018)
- "Pathophysiology of Disease: An Introduction to Clinical Medicine 8E" McGraw-Hill Education / Medical (2018)
- "Atrial Fibrillation" Annals of Internal Medicine (2017)
- "Atrial fibrillation" Journal of Biomedical Research (2014)
- "Risk Factors and Genetics of Atrial Fibrillation" Cardiology Clinics (2014)
- "Atrial Fibrillation" Circulation Research (2017)
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