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Video transcript

- [Voiceover] Multifocal atrail tachycardia, otherwise known as MAT for short, is a type of supraventricular tachycardia. It's classically associated with elderly people with chronic lung disease, specifically COPD, and in conjunction with old hearts that are predisposed to conduction abnormalities. Before we talk about what causes MAT, let's take a look at the heart. Here we're looking at a cross-section of the heart. Imagine the heart, and we slice it down the middle, so we're looking at the inside of the heart. Over here we have the right atrium, and then on this side we have the left atrium. Because we're looking at the patient's heart, the right side is over here, and the left side is over here. We're looking at the patient. The heart's right atrium contains the heart's dominant pacemaker, the SA node. Near the SA node and the atria lie multiple automaticity foci, which serve as backup pacers in the event that the dominant SA node fails. In a normal heart, the heartbeat originates from the SA node. The signal travels to the structure here called the AV node, and then the signal carries down through the ventricles. This signal causes the ventricles to contract, and that's when you feel your heartbeat. However, in MAT, pacemaker activity no longer originates from the SA node, but rather from multiple automaticity foci. Each automaticity focus paces at its own rate. As a result, multiple pacing centers, or foci, fire at the same time, but in no organized fashion, so they're all sending signals to the ventricles to contract. Since the ventricles are getting signals from multiple pacing centers, this is going to cause a tachycardia, or a heart rate of greater than 100 beats per minute. On EKG, MAT can be identified and diagnosed based on three main criteria. One, is that the heart rate is greater than 100, because MAT is a tachycardia. You'll also see greater than or equal to three different P wave morphologies, which is a fancy word for shapes. And, you'll have variation in the PR intervals, meaning that they'll be different lengths. Let's look at an EKG with someone in MAT. You'll notice that this person is in a tachycardia. We count heart rate by looking at the boxes. We start at an R interval, and we go one box, that stands for 300. The next box is 150 beats per minute. The next box is 100 beats per minute. A person would have a heart rate of 100 if the next R interval was somewhere over here. You'll notice that the RR interval is always less than three boxes. This person is definitely in a tachycardia. Just like classic MAT, there are at least three different shapes of P waves. Notice how each P wave looks slightly different, and there's variation in the PR interval. This PR interval is about four boxes, and this one's about five. Also, MAT has an irregular rhythm. The way I like to look for this is by drawing a dot above the R interval. You can notice, after you draw the dots above all of these, that there isn't even spacing between each dot, so this represents an irregular rhythm. Finally, MAT has narrow QRS complexes. That means that the QRS complex is less than or equal to 0.12 seconds, or three small boxes. Narrow QRS complexes signify that the abnormality is coming from the atria. Why is MAT commonly seen in people with heart and lung disease? It's thought that what makes people particularly vulnerable to MAT is atrial distortion, where the atria become pathologically enlarged. Here I'm drawing enlarged atria. This can be due to years of COPD, coronary artery disease, and heart failure. It's speculated that this atrial distention is a possible underlying mechanism of MAT. However, it can't be the only mechanism because we definitely see MAT in people without pathologically enlarged atria. Also know that you can see pathological enlargement in the left or the right atria, or even both, with MAT. An enlarged atrium makes someone more vulnerable to the risk factors of MAT. What are MAT risk factors? Anything that increases intracellular calcium in the cardiac myelocyte. This increase in intracellular calcium leads to spontaneous calcium release during a window time when calcium typically isn't released. This causes untimely depolarization, meaning that the myelocyte will depolarize during a time when it shouldn't, such as a refractory period. Several things cause increases in intracellular calcium such as hypokalemia, which is a low level of potassium. Similarly, hypomagnesemia can also cause an increase in intracellular calcium. Hypomagnesemia can actually promote hypokalemia through potassium wasting in the kidney. Hypoxia is another common risk factor that we see in MAT. Again, this is seen in a lot of our patients that have COPD. Another risk factor is acidemia, which is a pathologically low pH. Again, we see this in patients with COPD who have chronic hypoxia, as well as people who just suffered a heart attack or myocardial infarction, otherwise known as an MI. When the heart's compromised, it can't circulate blood to the tissue, and so people become acidotic. Finally, people with severe infections leading to sepsis, can also have acidemia.