It is a common arrhythmia in cardiology clinics, often occurring in patients with rheumatic heart disease, coronary heart disease, hyperthyroidism, cardiomyopathy, hypertension, and can also occur in individuals without organic heart disease (idiopathic atrial fibrillation).

bubble_chart Diagnosis

(1) Medical history and symptoms: Clinical symptoms depend on the frequency of atrial flutter (AFL) and atrial fibrillation (AF) episodes, the ventricular rate during episodes, and the presence of underlying heart disease. Mild cases may be asymptomatic or present with grade I flusteredness and shortness of breath, while severe cases may exhibit significant cardiac insufficiency or colicky pain. The medical history should focus on the frequency and duration of AFL/AF episodes, medications used during each episode, current medications, and any history of thromboembolism.

(2) Physical examination findings: In addition to the clinical manifestations of the underlying heart disease, auscultation in AFL may reveal a regular or irregular rhythm (depending on the atrial-to-ventricular conduction ratio). In AF, auscultation shows an absolutely irregular rhythm with varying intensity of heart sounds, and the pulse rate is significantly lower than the heart rate. Blood pressure should be measured to rule out hypertension, and signs such as exophthalmos or fine hand tremors should be checked to exclude hyperthyroidism.

(3) Auxiliary examinations: Electrocardiography (ECG) not only confirms the diagnosis but also provides information on ventricular rate during AFL/AF, guiding treatment. In AFL, P waves are replaced by sawtooth-shaped flutter waves (F waves), with atrioventricular conduction ratios such as 2:1, 3:1, or 4:1, and QRS complexes are supraventricular. In AF, P waves are replaced by absolutely irregular fibrillation waves (f waves) in morphology, interval, and amplitude, and QRS intervals are absolutely irregular. A 24-hour Holter monitor aids in diagnosing paroxysmal AFL/AF and determines the highest and lowest ventricular rates during episodes. Echocardiography can detect structural heart changes and assess for the presence of atrial mural thrombi.

bubble_chart Treatment Measures

In addition to treating the disease cause and predisposing factors, the focus is on minimizing the patient's symptoms, reducing and preventing recurrence, and preventing the occurrence of thrombosis and embolism. Alleviating symptoms involves effectively controlling the ventricular rate during episodes. The preferred treatment is intravenous administration of 0.2–0.4 mg of Cedilanid diluted and injected slowly, which is contraindicated in cases of hypokalemia and drug poisoning disease. Alternatively, 150 mg of amiodarone or 70 mg of propafenone diluted and injected slowly can be used. For chronic atrial flutter or atrial fibrillation, oral digoxin 0.125–0.25 mg/day or amiodarone 200–600 mg/day can be administered to maintain the ventricular rate at 70–90 beats per minute. For recently occurring atrial flutter or atrial fibrillation (<3 months) or within 3 months after valve replacement surgery for rheumatic heart disease, pharmacological and/or direct current cardioversion can be performed. The method involves oral administration of 200 mg of amiodarone three times a day. If sinus rhythm is not restored after 3 days, direct current cardioversion with 100–200 joules is performed. Chronic atrial fibrillation, suspected sick sinus syndrome, or the presence of mural thrombi in the atria are contraindications for cardioversion. Currently, there are no effective drugs or methods to prevent the recurrence of atrial flutter or atrial fibrillation, but amiodarone or propafenone may be tried. To prevent thrombosis and embolism, enteric-coated aspirin 100–300 mg/day or warfarin can be used. When taking warfarin, prothrombin time should be monitored to maintain it at 1.5 times the normal value. A very small number of patients may experience fatal bleeding when taking these medications.