Atrial fibrillation is extraordinarily common, and I see it an insane number of times. I have organized a set “spiel” to explain to patients how we deal with this annoying arrhythmia, which I believe is quite useful for the student as well.
You can find a complete summary of the common arrhythmia in the Atrial Fibrillation ECG Review. And be sure to check out the Atrial Flutter ECG Review to learn about the similar, but slightly different, condition. But I suggest you read this blog first.
Me to the patient: Atrial fibrillation is an irregular, fast heartbeat that comes from the top of the heart. It can make the electricity in the top of the heart go as fast as 400 to 600 beats per minute (atrial rate); fortunately, not all of that electricity gets to the bottom of the heart (ventricles), which is the most important part of the heart. But usually the bottom does go quite fast ― around 120 to 170 bpm, if you are not taking medications that slow the heart rate down.
When a patient comes in with atrial fibrillation for the first time, we ask ourselves three questions: Why? What? and How?
Why did you develop atrial fibrillation?
- What do we do to relieve your symptoms?
- How do we prevent this from causing a stroke?
Question #1: Why did you develop atrial fibrillation?
This question addresses the causes of atrial fibrillation.
Me to the patient: While the most common cause is believed to be long-standing hypertension, obstructive sleep apnea is being recognized more and more as a trigger for atrial fibrillation. Also, we know that OSA causes hypertension. If you snore or have daytime somnolence, we should do a sleep test to look for sleep apnea. Two other common causes include hyperthyroidism and structural heart problems such as a leaky heart valve. So, we will check a thyroid stimulating hormone, or TSH, level and an echocardiogram to further evaluate for these.
Note for the student: The best way to remember the causes of atrial fibrillation is the mnemonic “PIRATES.”
Pulmonary embolus, pulmonary disease, post-operative, pericarditis
Ischemic heart disease, idiopathic (“lone AF”), intravenous central line (in right atrium)
Rheumatic valvular disease (specifically mitral stenosis or mitral regurgitation)
Anemia, alcohol (“holiday heart”), advanced age, autonomic tone (vagally-mediated AF)
Thyroid disease (hyperthyroidism)
Elevated blood pressure (hypertension), electrocution
Sleep apnea, sepsis, surgery
Question #2: What do we do to relieve the symptoms?
This question addresses the treatment of symptoms experienced with atrial fibrillation
Me to the patient: This is where atrial fibrillation can get complicated and frustrating sometimes. Because atrial fibrillation itself is different from patient to patient, the treatment for atrial fibrillation is also different from patient to patient. So, we have to take an individualized approach. Some atrial fibrillation comes and goes (paroxysmal), some comes and stays until we do something about it like shocking the heart (persistent), and sometimes people stay in atrial fibrillation for the rest of their life (permanent, the old term was “chronic atrial fibrillation”).
The fast heart rate during atrial fibrillation sometimes results in symptoms including heart racing (palpitations), dizziness, shortness of breath and fatigue. It is important to know that some people have absolutely no symptoms, despite very fast heart rates. Other people have dramatic symptoms such as passing out (syncope) and dramatic shortness of breath. Most people fall somewhere in the middle; they are aware of the atrial fibrillation and do not like the feeling, but it is not excruciating.
Note for the student: The symptoms of atrial fibrillation are either from fast heart rates or from the decreased cardiac output that occurs due to loss of atrial contraction, as depicted below:
Me to the patient: What we do is take a simple, step-wise approach to relieve symptoms. If that does not work, we intensify the therapy until you feel better. I can assure you that we can always relieve the symptoms of atrial fibrillation; it just sometimes takes some effort. We start with first step and proceed all the way to the final step if we have to. Here are the steps we usually follow:
Step 1: Try a heart rate control strategy.
Me to the patient: We will give you medication to slow the heart rate down. If it works and you feel good, that’s great! We are done! Some people require only one medication, whereas others require two or three. You will have “permanent atrial fibrillation” from here on out if we just stop here. If the heart rate control strategy does not work, if you still have symptoms even when the heart rate is controlled (< 100 bpm) or if you have significant side-effects to the medications, we will move to step 2.
Note for the student: We use beta-blockers (i.e. metoprolol), non-dihydropyridine calcium channel blockers (i.e. diltiazem) and sometimes digoxin to control the heart rate. It is important to know the ejection fraction before you give these medications. if you can. Review this atrial fibrillation case to understand why. Also, the table below can help guide you in which drug to use when the ejection fraction is normal or reduced.
If this is the first episode of atrial fibrillation in a somewhat healthy person with a structurally normal heart (normal chamber sizes, no heart valve issues) ― indicating a high chance for success in keeping the patient in normal sinus rhythm ― it is reasonable to go straight to step 2 (rhythm control with cardioversion) if the patient agrees.
Step 2: Try a heart rhythm control strategy with a “cardioversion.”
Me to the patient: If step 1 doesn’t work, or to be more aggressive, we can perform a “cardioversion” ― meaning give you a shock (electrical cardioversion) or a strong medication (chemical cardioversion) that can put the heart back into normal rhythm. I know this sounds scary, but it is a simple procedure. For a shock of the heart, an anesthesiologist will provide sedation for just a few minutes; no breathing tube is needed. We then deliver a shock, and you wake up with a normal heartbeat. That’s it! The risk is low, and complication is mostly related to the anesthesia involved. The risk for stroke or actually inducing serious arrhythmia as a complication of the procedure is significantly less than 1%.
We sometimes may have to prove that you do not have a blood clot in the heart before doing a cardioversion by doing a test called a transesophageal echocardiogram, or TEE ― that is, taking a detailed picture of your heart by having you swallow a camera and looking from behind your heart (not as scary as it sounds). If your symptoms have definitely been apparent for less than 48 hours, we will not need to do a TEE. If your symptoms have been apparent for more than 48 hours, or if we are not sure, we will have to do this test to prove there is no clot before we shock you. Alternatively, we can thin your blood for 3 to 4 weeks before doing the shock, thereby avoiding the TEE. By thinning the blood for this long, the chance of a clot being present is very very low.
If the atrial fibrillation returns despite the cardioversion, we move to step 3 (antiarrhythmic drug therapy).
Note for the student: The AFFIRM trial compared patient outcomes with a rate control strategy (step 1) vs. a rhythm control strategy (step 2 and step 3). There was no difference in mortality between the two groups; therefore, we individualize the therapy based on a patient’s symptoms, as above (if no symptoms once rate controlled, no need to pursue a rhythm control strategy).
Step 3: Try stronger medications called antiarrhythmic drugs.
Me to the patient: If the cardioversion fails, we can try stronger medications called antiarrhythmic drugs, or AADs, which work to actually stabilize the electricity in the atrium rather than just slowing down the heart rate. These medications can sometimes by themselves convert your heartbeat to normal and keep it there ― essentially eliminating the atrial fibrillation. You may be wondering “Doc, if you can just give me a medication and make the atrial fibrillation go away, why the heck bother with step 1 and step 2?” The answer is this: Antiarrhythmic drugs have their own risks and potential side-effects. They are quite complex and sometimes can actually induce worse arrhythmia in some people, so we don’t just go giving these drugs to everyone.
If we choose to start an antiarrhytmic drug and your heartbeat does not convert back to normal with the medication itself, we will attempt a cardioversion again with a shock while on the new medication. If this does not work, we can either try a different antiarrhyhmic drug or move to step 4 (atrial fibrillation ablation).
Note for the student: First, I usually don’t go into details about atrial fibrillation ablation on first encounter with the patient, but briefly mention that if the medications fail, there are procedures such as atrial fibrillation ablation (a.k.a. pulmonary vein isolation or PVI) and devices such as pacemakers (with AV node ablation) that can relieve the symptoms and are used as a last resort. The above is a ton of information to hit a patient with the first time around, and you can imagine it can be overwhelming. Second, you can find an in-depth look at the various classes of drugs that act upon the electrical conduction system in the Antiarrhythmic Drugs Topic Review.
Step 4: Atrial fibrillation ablation or AV node ablation.
Me to the patient: As a very last resort, there is a procedure in which an electrophysiologist can find the location from where the atrial fibrillation is originating and actually eliminate it; this is called atrial fibrillation ablation. Doing an ablation for atrial fibrillation is not a major surgery, but it certainly is not simple. The procedure is invasive and takes at least a couple hours. There is no guarantee, as success rates vary, and there is, of course, risk for complications (although somewhat low). Some people need the procedure twice before it works; this is why it is a last resort.
Note for the student: Atrial fibrillation usually originates from the pulmonary veins, which drain blood from the lungs into the left atrium. To do an atrial fibrillation ablation, the pulmonary veins are electrically isolated from the rest of the heart. This means the atrial fibrillation continues in the pulmonary veins, but the atrium and ventricles have no clue. Atrial flutter, a similar arrhythmia, is much easier to ablate than atrial fibrillation; thus, we are more aggressive proceeding right to ablation for atrial flutter.
Me to the patient: On very rare occasions, medications and antiarrhythmic drugs may not work to slow the heart rate down and someone may not be a good candidate for atrial fibrillation ablation. In this instance, we can disconnect the electricity that comes from the top of the heart (atrium) from the bottom (ventricles) with a procedure called an “AV node ablation.” This way the atrial fibrillation keeps going fast in the atrium, but the ventricles have no clue because they are electrically disconnected. The problem with this procedure is that the heart rate in the ventricles will go very slow, usually around 30 to 40 bpm, which is way too low; thus, a pacemaker must be inserted to keep the heart rate up.
Note for the student: In my few years of clinical practice, there’s been only a handful of times I've had a patient who needed an AV node ablation with a pacemaker for atrial fibrillation. This is an extreme measure to take to control the heart rate, but sometimes it is the only thing that works.
Question #3: How do we stop atrial fibrillation from causing a stroke?
This question addresses the prevention of a life-threatening condition that can result from the interrupted blood flow with atrial fibrillation.
Me to the patient: This is the most important thing. The symptoms of atrial fibrillation can be annoying and decrease your quality of life, but stroke can be devastating and life-threatening. Atrial fibrillation causes the top chambers to simply “quiver” and not squeeze blood down to the bottom adequately. This results in blood flowing a bit less in those top chambers. There is a little pouch of the atrium called the atrial appendage, and if the blood does not flow good through there, it can result in a blood clot as the blood cells stick together. If that clot decides to break loose, it can travel to the brain and cause a stroke.
Your risk for stroke from atrial fibrillation is calculated based on various factors. We use a point-scoring system: Age > 65 (1 point) or age > 75 (2 points), female gender, hypertension, diabetes, heart failure, vascular disease (including aneurysm and prior heart attack) or a prior mini stroke (TIA) or stroke (2 points). Based on your situation, your annual risk for a stroke from atrial fibrillation is (fill in the blank); see below for point to stroke risk conversion.
Guidelines from the American Heart Association recommend no thinning of the blood if you score 0 points on this stroke risk scale. A score of 1 could go with either blood thinning or not (based on the individual). However, if you score 2 or more on this scale, then a full blood thinner is recommended. Aspirin in general is not thought to be strong enough to thin the blood and prevent stroke from atrial fibrillation.
In general, we always think about the benefits of the blood thinner to prevent stroke as well as the risks, which include serious bleeding. If your score is 2 or higher on this scale, and you have no major bleeding risk, then the benefits of blood thinning to prevent stroke are thought to be more than the risks.
There are four different blood thinners that are FDA approved to prevent stroke in the setting of atrial fibrillation. These are warfarin (Coumadin), dabigatran (Pradaxa), rivaroxaban (Xarelto) and apixaban (Eliquis). The choice of which to chose is complex and depends not only on the cause of your atrial fibrillation (i.e. valvular atrial fibrillation requires warfarin) but also on your kidney function and insurance coverage for the drugs, as they can be expensive.
Note for the student: In the AFFIRM trial, the risk for thromboembolism including stroke was the same regardless of using a rate control strategy (step 1) or a rhythm control strategy (step 2 and step 3). Thus, even if a patient is kept in normal sinus rhythm with an antiarrhythmic drug, the risk for thromboembolism is believed to be the same as a patient with permanent atrial fibrillation on a rate control strategy. This is likely due to “breakthrough” episodes of atrial fibrillation, which may or may not be symptomatic, but can result in thromboembolism; for this reason, it’s important to stress to patients that the degree of symptoms they feel from atrial fibrillation (such as palpitations) does not correlate with their risk for stroke. Many patients want to call 911 with every palpitation from atrial fibrillation they feel for fear of having a stroke. However, in reality, as long as they are on adequate thromboembolic prophylaxis with the appropriate blood thinner, their risk for stroke is generally no different during symptoms than it is when they are symptom free.
Lastly, the point-scoring system we use is called the CHA2DS2 VASc score and is explained here. Below are the statistics regarding annual risk for thromboembolism that you can offer patients based on their score.
1 point = 1.3%
- 2 points = 2.2%
- 3 points = 3.2%
- 4 points = 4.0 %
- 5 points = 6.7 %
- 6 points = 9.8%
- 7 points = 9.6% (study had small sample size with this score, leading to more variability)
- 8 points = 6.7% (study had very small sample size)
- 9 points = 15.2%
That’s a long spiel! But there you have it! Hope these three important questions help guide you to take an organized approach in explaining the complexities of atrial fibrillation to patients. It is extraordinarily important the ensure a patient understands his or her disease ― and I plan on referring some of my patients to this article to further educate them about this annoying arrhythmia.
A few last things to remember. There are sometimes exceptions to these above treatment steps, and unusual situations such as atrial fibrillation with Wolff-Parkinson-White Syndrome or Hypertrophic Cardiomyomapthy can occur. You can find an entire summary, from pathophysiology to special situations, by visiting the Atrial Fibrillation Topic Review.
- by Steven Lome
Links for patients:
- Cleveland Clinic Atrial Fibrillation Information
- Mayo Clinic Atrial Fibrillation Information
- WebMD Atrial Fibrillation Information