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Health and medicine
Course: Health and medicine > Unit 3
Lesson 10: Cardiac dysrhythmias and tachycardias- Electrical conduction in heart cells
- Normal sinus rhythm on an EKG
- Supraventricular tachycardia (SVT)
- Atrial fibrillation (Afib)
- Atrial flutter (AFL)
- Multifocal atrial tachycardia (MAT)
- Atrioventricular reentrant tachycardia (AVRT) & AV nodal reentrant tachycardia (AVNRT)
- Ventricular tachycardia (Vtach)
- Torsades de pointes
- What is ventricle fibrillation (Vfib)?
- Pulseless electrical activity (PEA) and asystole
- Electrocardioversion
- Pacemakers
- Antiarrhythmics
- Ablation
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Multifocal atrial tachycardia (MAT)
Created by Bianca Yoo.
Want to join the conversation?
- As discussed at, if the automaticity foci do not fire in an organized enough manner to stimulate a viable ventricular contraction what purpose do they serve/under what circumstances would they spur an effective contraction? 1:20(2 votes)
- The automaticity foci individually do actually stimulate a ventricular contraction. This acts as a sort of back-up plan in case the SA node misses a beat or two, they will then fire and the ventricles will contract. The issue in MAT is that all/multiple of the automaticity foci are firing their own individual rhythm and consequently the ventricles are receiving signals irregularly from the bundle of His so, whilst the foci are allowing the heart to pump (and the ventricles to contract), it is less efficient than the normal conduction of the heart.(2 votes)
- Can an intake of too much calcium (e.g.: too much dairy) lead to this condition even though none of the causes listed are present in the patient?(2 votes)
- high levels of intracellular calcium is also linked to prinzmetal angina, which is spasms of the coronary vessels(1 vote)
- Is this also referred to as Wandering Atrial Pacemaker?(1 vote)
- Wait, the narrow QRS makes it an SVT, along with the elevated HR.(1 vote)
- Why is there hyperpolarization from R-S?(1 vote)
- Wait. Do you feel 'lub dub' when your ventricles contract or when the mitral and tricuspid valves close?? Rishi said the latter but now she is saying that it's when the ventricles contract (). 1:22
Thanks in advance(1 vote)- Ventricular contraction causes the valve closure. The valves open one way, so when the ventricles squeeze the pressure inside is pushing back on the leaflets to close the valves.(1 vote)
- Why would untimely Ca release from the cell cause depolarization? Wouldn't that have a polarizing effect?(1 vote)
- that is depolarization when the cell becomes more positive than its environment. Since calcium has 2x as much positive charge as sodium or potassium, calcium release into the muscle to inactivate tropomyosin and start a contraction causes the cell to become more positive than a neuron would with the same amount of ions. It also becomes more positive than the environment. This positive charge gets passed on cell to cell to synchronize ventricular contraction.(1 vote)
- why is there constantly volume changes between each section?
the volume keeps getting lower!(1 vote)- Well, she just recorded it like that. Better to wear headphones.(1 vote)
- So, in this case (MAT), Calcium Channel Blockers would work as a treatment?(0 votes)
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.