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This structure, located in the left atrium, is the place where a blood clot forms in more than 90% of cases in non-valvular (or non-rheumatic) atrial fibrillation. [79] [80] TEE has a high sensitivity for locating thrombi in this area and can also detect sluggish blood flow in this area that is suggestive of blood clot formation. [78]
However, atrial flutter is more resistant to correction with such medications than atrial fibrillation. [1] For example, although the class III antiarrhythmic agent ibutilide is an effective treatment for atrial flutter, rates of recurrence after treatment are quite high (70–90%). [ 1 ]
The cardiac etiologies of palpitations are the most life-threatening and include ventricular sources (premature ventricular contractions (PVC), ventricular tachycardia and ventricular fibrillation), atrial sources (atrial fibrillation, atrial flutter) high output states (anemia, AV fistula, Paget's disease of bone or pregnancy), structural ...
There are two major classes of cardiac fibrillation: atrial fibrillation and ventricular fibrillation. Atrial fibrillation is an irregular and uncoordinated contraction of the cardiac muscle of atria. It can be a chronic condition, usually treated with anticoagulation and sometimes with conversion to normal sinus rhythm.
The CHADS 2 score and its updated version, the CHA 2 DS 2-VASc score, are clinical prediction rules for estimating the risk of stroke in people with non-rheumatic atrial fibrillation (AF), a common and serious heart arrhythmia associated with thromboembolic stroke.
Atrial flutter is when the atria repeatedly contract at really high rates, usually due to an underlying condition combined with premature atrial contraction. Faster atrial contraction in turn increases the number of ventricular contraction, which can cause shortness of breath, chest pain, dizziness, and nausea in certain people.
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