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As you can see, I love medicine and have no trouble talking about anything and everything related to the human body. There will be more to come about atrial fibrillation as it is highly important and one of the main causes of stroke in the united states. The others being carotid disease and hypertension, or high blood pressure. Keep in mind, I am trying to keep this website fun yet informative. There is literally so much to learn about medicine and no possible way you can know everything about everything. Anyway. I hope you’re having a good time checking out my site! see you next time.



Lets Talk About A-fib

Background of Atrial Fibrillation:

Atrial fibrillation is the most common chronic arrhythmia (irregular heart rhythm) with an incidence and prevalence that increase with age, affecting 10% of people over 80. It may occur alone or concomitantly with other forms of heart disease that cause enlargement of the atira (valvular heart disease, dilated cardiomyopthay, arial septal defect, hypertension, and coronary artery disease). It may be the initial presenting sign in thyrotoxicosis (hyperthyroidism). Conditions such as pericarditis, chest trauma, cardiac surgery, thyroid disorders, and pulmonary disease may predispose a patient to afib. Acute alcohol withdrawl or alcohol excess may also precipitate afib. I am covering this topic because my father had suffered a stroke caused by a fib while working on his roof. Click here to check his business.


The way I think about afib is that any disease that will cause an enlargment of the atria of the heart will predispode a patient to atrial fibrillation. For some reason, the larger the atria, the more likely it is that afib will occur. Valvular heart disease causes atrial enlargement because if a valve is stenotic (stiff and doesn’t open as easily or as widely as it should), it causes blood to back up into the atria. The larger the volume of blood in the atria, the more the walls will stretch (like filling a balloon with water). The other cardiac disease listed above cause the same problem by different means. I will explain this more tomorrow if you have questions. The enlargement of the atria along with the irregularity of the heart rhythm results in more blood pooling in the atria and remaining there, unable to be fully ejected into the ventricles. Virchow’s triad describes the 3 characteristics that are thought to lead to thrombosis or clotting of the blood. The 2 characteristics are blood STASIS (or pooling), hypercoaguability, and vessel injury. Clearly in afib, there is blood stasis and when blood is just “hanging around” and not moving, it is more likely to form blood clots or thrombi. Theses clots are then floating around the atria and free to leave the heart through the aorta and travel through the carotid arteries up to the smaller blood vessels in the brain and block them. When this occurs, part of the brain is starved of blood supply and thus oxygen, we know all tissues need oxygen to survive, so without oxygen, part of the brain dies. This is what a stroke is. 


The heart rhythm in atrial fibrillation is always irregular, but the ventricular rate may range from slow to fast. The EKG demonstrates erratic, disorganized atrial activity between discrete QRS complexes (signify ventricular depolarization and contraction) that occur in an irregular pattern. Atrial fibrillation often occurs paroxysmally (transiently) before becoming the established rhythm.


The are three types of atrial fibrillation presentations: first is paroxysmal atrial fibrialltion which means simply that the atrial fibrillation comes and goes on its own, without the assistance of antiarrhythmic drugs or cardioversion to convert the patient out of atrial fibrillation. Second is persistent atrial fibrillation, this generally means that the patient needs antiarrhythmis drugs, cardioversion or surgical ablation to convert them out of atrial fibrillation. Lastly, there is permanent atrial fibrillation, which is usually treated with “rate control and rat poison” meaning that we attempt to control the heart rate with a beta blocker thus reducing the patient symptoms and we use coumadin, an antocoagulant to reduce the risk of thrombus or clot formation in the left atrium and subsequent embolization or “travel” to the blood vessels of the brain causing a stroke.


There are also three types of atrial fibrillation electrically speaking, first is atrial fibrillation rate controlled, meaning that the venricular response is controlled or between 60-100 beats per minute. Second is atrial fibrillation with a slow ventricular response, meaning that the ventricular response or heart rate is less that 60 beats per minute. Lastly is atrial firbrillation with a fast ventricular response, meaning that the ventricular response or heart rate is over 100 beats per minute.


Up to 2/3 of patients with a first episode atrial fibrillation will convert back to sinus rhythm spontaneously in 24 hours. If atrial fibrillation persists for longer than a week, it is unlikely to spontaneously revert to sinus rhythm and will require some type of treatment or intervention.

The most serious consequence of atrial fibrillation is thrombus formation and subsequent embolization of the thrombus to the cerebral circulation, causing a CVA (cerebrovascular accident or stroke) or TIA (transient ischemic attack). The “CHADS2” score is used to determine what patients would benefit from anticoagulation with COUMADIN. CHADS2 is an acronym that stands for C-congestive heart failure, H-hypertension (high blood pressure), A-age >75, D-diabetes, S-stroke gets 2 points. One point is assigned for each condition that the patient has, except that stroke gets 2 points. If the total points are over 2, the patient will most likely benefit from therapy with coumadin which will reduce the risk of thombus (clot) formation in the left atrium and this embolization (movement) of the thrombus to the cerebral circulation.