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Pathology
Atrioventricular block
Bundle branch block
Pulseless electrical activity
Atrial fibrillation
Atrial flutter
Atrioventricular nodal reentrant tachycardia (AVNRT)
Premature atrial contraction
Wolff-Parkinson-White syndrome
Brugada syndrome
Long QT syndrome and Torsade de pointes
Premature ventricular contraction
Ventricular fibrillation
Ventricular tachycardia
Cardiac tumors
Shock
Arterial disease
Aneurysms
Aortic dissection
Angina pectoris
Coronary steal syndrome
Myocardial infarction
Prinzmetal angina
Stable angina
Unstable angina
Abetalipoproteinemia
Familial hypercholesterolemia
Hyperlipidemia
Hypertriglyceridemia
Coarctation of the aorta
Conn syndrome
Cushing syndrome
Hypertension
Hypertensive emergency
Pheochromocytoma
Polycystic kidney disease
Renal artery stenosis
Hypotension
Orthostatic hypotension
Lymphangioma
Lymphedema
Peripheral artery disease
Subclavian steal syndrome
Nutcracker syndrome
Superior mesenteric artery syndrome
Angiosarcomas
Human herpesvirus 8 (Kaposi sarcoma)
Vascular tumors
Behcet's disease
Kawasaki disease
Vasculitis
Chronic venous insufficiency
Deep vein thrombosis
Thrombophlebitis
Acyanotic congenital heart defects: Pathology review
Aortic dissections and aneurysms: Pathology review
Atherosclerosis and arteriosclerosis: Pathology review
Cardiac and vascular tumors: Pathology review
Cardiomyopathies: Pathology review
Coronary artery disease: Pathology review
Cyanotic congenital heart defects: Pathology review
Dyslipidemias: Pathology review
Endocarditis: Pathology review
Heart blocks: Pathology review
Heart failure: Pathology review
Hypertension: Pathology review
Pericardial disease: Pathology review
Peripheral artery disease: Pathology review
Shock: Pathology review
Supraventricular arrhythmias: Pathology review
Valvular heart disease: Pathology review
Vasculitis: Pathology review
Ventricular arrhythmias: Pathology review
Atrial fibrillation
0 / 15 complete
0 / 3 complete
of complete
of complete
2022
2021
2020
2019
2018
2017
2016
atrial fibrillation p. 300
atrial fibrillation p. 728
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
atrial fibrillation and p. 300
atrial fibrillation p. 300
atrial fibrillation and p. 298
atrial fibrillation and p. 300
atrial fibrillation p. 300
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.
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