Atrial flutter is defined as a regular but fast rhythm originating in the upper heart chambers known as the atria. The heart rate in the atria in this condition is typically about 300 beats per minute. The characteristic morphology on the electrocardiogram (EKG/ECG) is described as “sawtooth pattern.” This type of rhythm occurs most often in individuals with organic cardiac pathology such as pericarditis, coronary artery disease, and hypertrophic cardiomyopathy. Although the atrial flutter is described as a regular rhythm, it is not considered to be as a stable rhythm, and frequently degenerates to atrial fibrillation, an abnormal irregular rhythm.
In atrial flutter, generally the ventricles (lower heart chambers) do not beat as fast as the atria. This is due to the fact that the AV (atrioventricular node) acts as a safety valve in the event of any fast rhythm occurring at the atria such as atrial fibrillation and atrial flutter. The AV node is responsible for slowing down the conduction of the electrical activity, and if it receives the next electrical impulse before it is ready, then this impulse will be blocked at the AV node level thus, will never actually reach the ventricles.
There is usually a particular block pattern in atrial flutter e.g. 2:1 block, 4:1 block or varying block. In 2:1 block, the AV node will block every other electrical impulse so that while the atrial rate is around 300 beats per minute, then ventricular rate will be 150 beats per minute. If there are three out of four beats that are blocked, this is now known as 4:1 block wherein the atrial rate is 300 beats per minute while the ventricular rate will be 75 beats per minute. When the degree of block is variable at different times, this is called as varying block. Some of the factors affecting the varying degree of block includes catecholamine (epinephrine, norepinephrine) release and the use of any drugs that may block AV node conduction such as beta blockers, digitalis, and calcium channel blockers.
Atrial flutter sufferers can be sometimes asymptomatic and its onset is often presented by rapid thumping sensations and palpitations in the chest area. These sensations actually persist for the entire duration of the atrial flutter episode. Other accompanying manifestations are: shortness of breath, lightheadedness (“fainting” or “syncope”) or dizziness, nausea and in some cases, feelings of nervousness and impending death.
The complications of atrial fluttter are similar with atrial fibrillation namely clot formation and sudden cardiac death. The reason has something to do with ineffectual contraction of the atria just like in Afib, which lead to stasis of blood in the atria that may eventually result to formation of thrombus (clots) within the heart chamber most likely in the left atria. This is significant because the left side of the heart supplies blood to the entire body (systemic circulation) hence; any thrombus that dislodges from the left side of the heart can embolize to the brain, causing a stroke or cerebrovascular accident.
Typically, the atrial flutter should be treated the same as atrial fibrillation which is aiming the two major goals of therapy: to prevent control the ineffective contraction of the atria and to prevent thrombus formation. In order to achieve the aforementioned goals, the patient requires drugs that control the heart rate and rhythm (anti-arrhythmic agents) and some form of anticoagulants or anti-platelet agents. In addition, another consideration is the more invasive ablation treatment of the isthmus, a body of fibrous tissue that makes up a part of the reentrant loop pathway. If the catheter-based ablation of the isthmus is successful, this prevents reentry, and terminates atrial flutter.
In some cases of atrial flutter with an accessory pathway, the control of the ventricular rate may be more difficult because of one of the AV node properties known as concealed conduction. Therefore, in these cases, it may be easier to control the rate if patients are converted first from atrial flutter to atrial fibrillation. There is still no consensus at present with regard to a particular guideline to treatment but others made some attempts in the electrophysiology lab by pacing the atria at rates over 300 beats per minute.
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