Due to the competing micro-reentrant circuits, the ECG will not show distinct P wave or the saw tooth pattern but rather small amplitude oscillations. However, over time the atria of patients with AF remodel-atria dilate, undergo fibrosis and inflammation, and the electrical property of the atrial tissue becomes altered-thus paroxysmal AF becomes persistent AF. New onset AF is usually self-limiting and sinus rhythm is restored spontaneously. Once initiated, the fibrillation is maintained by multiple micro- reentrant circuits in the atria. In AF, the rapid atrial rate is initiated by a single focus of abnormal activity, most commonly near one of the pulmonary vein ostia in the LA. Those patients who are waiting for ablation may undergo electrical cardioversion. On the other hand, catheter ablation is highly successful in eliminating typical aflutter. Patients with AFL will choose watchful waiting as this arrhythmia may spontaneously revert to sinus. On ECG, AFL usually shows the typical sawtooth wave (atrial depolarization at around 300 bpm) with a regular ventricular response at a ratio of 1:2 or 1:4, although odd ratio or variable AV conduction is possible. In the absence of this ridge of tissue, it is called an “atypical” flutter, and the reentrant circuit can be elsewhere in the right atrium (RA) or infrequently left atrium (LA). So called “typical” flutter involves a region of cardiac tissue that connects the tricuspid valve annulus and the inferior vena cava (IVC), which is the main target in electrophysiologic study and catheter ablation. In AFL, the likely etiology is a single macro-reentrant atrial circuit. The use of transesophageal echocardiography can rule out any intracardiac thrombus, especially in the left atrial appendage, and facilitate earlier cardioversion.ĭISEASE BACKGROUND AND PROCEDURAL DESCRIPTION Thromboembolic disease is a major cause of morbidity and mortality in patients with AF or AFL.
In general, cardioversion is performed in those patients who are symptomatic. Lastly, both AF and AFL can occur after cardiac and thoracic surgeries. Common risk factors for developing AFL include male gender, advanced age, heart failure and chronic obstructive lung disease. Many diseases that cause AF can also cause AFL, and AFL can also be a side effect of anti-arrhythmic agents used to suppress AF. It is often associated with underlying heart disease. The association with hyperthyroidism, pulmonary embolism, obstructive pulmonary diseases, and heavy alcohol use are also well documented.Ītrial flutter (AFL) is rare in young adults with incidence rates range from 5 in 100,000 ( 80 years old). AF patients usually have some underlying heart disease such as hypertension, coronary artery disease, mitral valve disease (including rheumatic heart disease), or heart failure. In older population, the incidence of new cases ranges from 2 or population per year in the age group of 55-64 years to 35 in patients older than 85. The prevalence of atrial fibrillation (AF) increases with age and is rare in adults younger than 55 who do not have structural heart disease. Cardioversion (for atrial fibrillation or atrial flutter)