Author: Tanner Marshall, MS
Editor: Rishi Desai, MD, MPH; Vincent Waldman, PhD
The heart has four chambers, two upper chambers—the left and right atrium, or together the atria, and two lower chambers—the left and right ventricles.
Atrial flutter is used to describe when the atria contract at really high rates—about 300 beats per minute, but sometimes as high as 400 beats per minute. Why flutter? Well there’s a wave of muscle contraction that flows through the atria that looks like its flapping or fluttering, hence the name. Normally, an electrical signal is sent out from the sinus node in the right atrium, but then propagates out through both atria super fast, causing the atria to contract. Usually, that signal moves in one direction from the atria to the ventricles through the AV node, it then moves down to the ventricles, and causes them to contract shortly after. After each ventricular contraction, the ventricle has to wait for another signal from the sinus node. With atrial flutter, a reentrant rhythm starts in either the right or left atrium. Reentrant signals loop back on themselves, overriding the sinus node and setting up an endless cycle that causes the atria to contract again and again and again—at really fast rates.
There are actually two types, type 1 or typical atrial flutter is more common and is caused by a single reentrant circuit that moves around the annulus, or the ring of the tricuspid valve of the right atrium, usually in a counterclockwise direction when viewed looking up through the tricuspid valve. Ok so imagine you’re this eyeball looking up through the valve, you’ll see the superior vena cava or SVC, the inferior vena cava or IVC, and the coronary sinus, or CS. In this case, a stretch of tissue along the pathway called the cavotricuspid isthmus propagates the signal more slowly than the surrounding tissue. Tissue that was just activated can’t be activated again until a certain amount of time has passed, which is called the refractory period; so that slow propagation gives the tissue enough time to be out of refractory, and therefore the circuit can loop on itself. Type 2 or atypical atrial flutter is where a re-entrant circuit develops in either the right or left atrium, but the exact location is less clearly defined. Again though we’ve got a similar setup where a wave of activated tissue, or depolarization hits a bit of tissue in such a way that it creates a loop of depolarization that keeps going around and around.
Alright, since everyone has a cavotricuspid isthmus, but not everyone has atrial flutter, there must be something else at play that causes a reentrant circuit. In most cases, there’s some underlying disease, like ischemia, that makes the heart cells more irritable, which can change the whole properties, like their refractory period, making it more likely reentrant circuits develop. In addition, usually the circuit is initiated by a premature atrial contraction or PAC, which is an electrical impulse that’s sent out early in the atrium, before you’d normally expect one. The exact cause of PACS generally isn’t known, and they can even happen in otherwise healthy people. So let’s just say tissue A has a short refractory period, and tissue B has a longer refractory period, if a PAC is timed just right, one tissue might depolarize and one might not, and this can propagate an abnormal wave of depolarization which can go through the atria and initiate a reentrant circuit.
In order for the ventricles to contract, though, that signal needs to move down through the AV node. Luckily, the AV node has a relatively long refractory period, meaning it can’t conduct every single impulse being sent from the atria, and typically maxes out at around 180 beats per minute, meaning it has to wait a minimum of about one-third of a second or 333 milliseconds until it can relay another signal. So if the atrial rate’s higher than 180 bpm, you’ll end up only getting a ratio of atrial beats to ventricular beats like 2:1 or 3:1 in this case. It might make a little more sense if we look at an ECG. Now, normally the depolarization wave originates in the SA node and produces what’s called a P-wave. The normal firing rate from the SA node is 60-100 beats per minute. But in atrial flutter the electrical signals are coming from a reentrant circuit which moves much faster, let’s say 350 beats per minute. In this case, there are no normal P-waves. Instead they are called flutter waves, or F waves, and they take on this sawtooth shape. Starting with this guy, it goes to the ventricles, and contracts the ventricle, causing this QRS complex. If the cells in the AV node need to wait about 330 ms, the next atrial contraction which happens in about 170 milliseconds, won’t be able to conduct to the ventricles. The next atrial event after that though, lands at 340 milliseconds from the first one, which means that the AV node’s out of refractory and ready to go, so it conducts this one. In this example, therefore, we’ve got a 2 to 1 atrial to ventricular rate because for every two atrial contractions, only one of them will lead to a ventricular contraction. So in this example there were 350 atrial beats per minute but only 175 ventricular beats per minute. Now let’s say the atria were going at 400 beats per minute, the first one conducts, then it’s 150 ms to the next one, then the next atrial beat would land at 300 milliseconds, and the av node still wouldn’t be ready yet, meaning the ventricle wouldn’t contract until the third atrial beat comes in at 450 milliseconds. In this case it’s a 3:1 atrial to ventricular rate, 400 atrial beats per minute to 133 ventricular beats per minute. Because the ventricles are contracting at a rate greater than 100 beats per minute, and because the source originates above the ventricles, this is considered a supraventricular tachycardia.
Alright, having a higher ventricular heart rates like 133 or 175 beats per minute isn’t usually life threatening, but if it’s happening at rest it generally isn’t something most people want to experience. If somebody has an underlying condition where they aren’t able to physically tolerate high ventricular rates like this, they might feel symptoms like shortness of breath, chest pain, dizziness, and nausea. Over time, from prolonged episodes of tachycardia, the ventricles can tire out and decompensate and people can develop heart failure. Also, since the atria aren’t contracting very effectively, blood tends to stagnate or pool in the atrium. And this can lead to the formation of blood clots that can embolize to the brain and cause a stroke.
Usually, because of the potential for embolism, people with atrial flutter are given anticoagulants, or blood thinners to reduce the chances of clot formation. They might also be given medications to control rates in the ventricles, like beta blockers or calcium channel blockers. Alternatively, an electrical cardioversion can be performed to stop the episode of flutter. These essentially depolarize all the atrial tissue at once and let the sinus node take control again. Finally, depending on the type of flutter—type 1 vs type 2, patients might be good candidates for a radiofrequency catheter ablation.
Essentially the cavotricuspid isthmus is destroyed such that no signals can propagate through it, and therefore no circuit can develop around the tricuspid valve.
All right, as a quick recap…. Atrial flutter is when the atria repeatedly contract at really high rates, usually due to an underlying condition combined with premature atrial contraction. Faster atrial contraction in turn increases the number of ventricular contraction, which can cause shortness of breath, chest pain, dizziness, and nausea in certain people. Over time, atrial flutter can lead to heart failure, blood clots, and strokes.
Sources edit
http://emedicine.medscape.com/article/151210-treatment#d14
http://lifeinthefastlane.com/ecg-library/atrial-flutter/