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Torsades de pointes

Created by Bianca Yoo.

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  • blobby green style avatar for user Krystle L
    at , education was mentioned as very important - what medications should the patient avoid to prevent them from going into Torsades?
    (4 votes)
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  • female robot grace style avatar for user Anna
    why doesn't V-fib correct itself like A-fib does?
    (1 vote)
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    • aqualine ultimate style avatar for user invictahog
      Atrial fibrillation does not always correct itself (see chronic a-fib). The problem with V-fib is that you die and it doesn't get a chance to correct itself. When you go into V-fib you don't get enough oxygen to the heart and it gets even more irritable and less likely to correct itself. Given that v-fib is often due to lack of oxygen in the first place (coronary ischemia/heart attack) it makes sense that v-fib only gets worse given that it is so disorganized that the heart cannot even pump.
      (6 votes)
  • blobby green style avatar for user sbrokaw
    So is someone that has prolonged QT Syndrome also considered to have Torsades de pointes? How do you differentiate between the two?
    (2 votes)
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    • leafers ultimate style avatar for user William H
      Long QT syndrome specifically relates to the QT phase, Torsades de pointes is a generalized abnormality in the hearts rhythm and a long QT is a common symptom although it is not always present. However, long QT syndrome can lead to TdP is left alone and unrecognized. To distinguish, one has to look at the EKG and determine the rhythm and which it corresponds to.
      (1 vote)
  • primosaur ultimate style avatar for user Swift Runner
    How come a-fib doesn't result in death but v-fib does? And is there any relation between atrial tachycardias and a-fib? And can a defliberator cause any damage to the heart or surrounding organs?
    (1 vote)
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    • leaf blue style avatar for user dysmnemonic
      A person in AF will typically have normal ventricular contractions, so they're mantaining cardiac output and perfusing their tissues. In VF, there's insufficient coordination of ventricular conduction, so the ventricular contractions are ineffective. This means that there's a loss of cardiac output and tissue perfusion, leading to cardiogenic shock and death.
      (3 votes)
  • blobby green style avatar for user Percy Jones
    Does standard V tachycardia and torsardes de pointes carry the same risks of resulting V fib? Is the only difference that torsardes is easily recognisable due to the polymorphinc R waves?
    (1 vote)
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  • blobby green style avatar for user Erfan Uddin
    I am a bit confused with the idea of QT interval and torsade de pointes. Since we know QT is inversely proportional to heart rate, and longer QT indicates slower heart rate (bradycardia). So, how could QT prolongation cause torsade de pointes which is also known as polymorphic ventricular tachycardia?
    (1 vote)
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    • blobby green style avatar for user Mel Whitney
      Prolonged QT interval generally "precedes" Torsades de Pointes. Since the QT is prolonged there is a "delay in repolarization and that delay affects the refractory periods, or the recovery times, of heart cells. The heart likes it when its cells work in unison. If there are differences in refractory times in neighboring heart cells, that can set you up to have a ventricular tachycardia". So if you learn about refractory periods you will have a better understanding
      (1 vote)
  • winston default style avatar for user Yunmo Chen
    I don't understand what QT is. Is it Q to the middle of T or Q to the end of T?
    (1 vote)
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  • blobby green style avatar for user subhi_miari
    why it's not possible to copy the transcript ! any idea
    (1 vote)
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  • orange juice squid orange style avatar for user Kutili
    Why does torsades de points turn into ventricular fibrilation?
    (1 vote)
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    • leafers ultimate style avatar for user jvspearman
      At she describes causes for abnormal circuits that can lead to v-fib. Some of these can also be explained by abnormal function of cardiac myocytes. For example certain abnormal ion channel openings can cause early depolarization, for example phase 3 interruptions are due to the aberrant opening of sodium channels. This can result in torsades de pointes, tachycardia, and other arrhythmias. Some drugs that prolong the QT interval, including class Ia and III antiarrhythmic agents can increase the likelihood.

      https://en.wikipedia.org/wiki/Afterdepolarization
      (1 vote)
  • leafers ultimate style avatar for user Sleuth
    What is the mechanism behind the high-low-high-low amplitude QRS complex creation?

    In the other dysrhythmia videos so far there was always a good drawing/explanation of the mechanical source for the EKG appearence of a arrhythmia.
    (0 votes)
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Video transcript

- [Voiceover] Torsades de pointes is type of ventricular tachycardia, or V-tach. Specifically, it's a polymorphic ventricular tachycardia. The polymorphic V-tach in torsades always follows long QT intervals. In torsades you have a long QT that's followed by a polymorphic V-tach. What does all that mean? This is a lot to swallow, so let's break this down. Morphic refers to the QRS intervals. Poly just implies that there are multiple, that there are multiple QRS intervals. Torsades de pointes is actually French for twisting of the points. What does that mean? Imagine you have a party streamer. Say you take the ends of that streamer and you twist them. What you'll get is a twisted party streamer that's going to look a lot like this. You'll notice the dips and waves in the twist. This is what a polymorphic V-tach looks like on EKG. It looks like this twisted party streamer, where you have high amplitude QRS waves, and low amplitude, high amplitude, low amplitude, high amplitude, and it keeps on going back and forth. The QRSs appear to flip around a horizontal axis. Remember in torsades, the polymorphic V-tach is always preceded by a long QT. Let's go over QT. Here we have a single beat on EKG. We're going to have the P wave and the QRS interval and the T wave. The QT interval is from the beginning of the Q all the way to the end of the T wave. That's the QT interval. It represents when the ventricles are depolarizing and when they're repolarizing. The QT interval represents the length of time or the interval when the ventricles depolarize and repolarize. People with a long QT typically have some sort of delay in repolarization. This delay could be due to either genetic mutations in ion channels or from certain medications. For whatever reason, they have a delay in repolarization and that delay affects the refractory periods, or the recovery times, of heart cells. The heart likes it when its cells work in unison. If there are differences in refractory times in neighboring heart cells, that can set you up to have a ventricular tachycardia because you're messing with the conduction system when you're messing with the repolarization and the refractory periods. Something else to note is that the QT interval is rate dependent. What does that mean? Let's say you have a heart rate and it's going very fast. You can imagine that the QT interval here is going to be pretty short because the heart is beating so fast. On the other hand, if you have a heart rate that's going really slowly, you can imagine that your QT interval might be long and drawn out. The rate of the heart affects how long the QT is. Given that there's some rate dependence, there are formulas created that adjust the QT interval. You can calculate what's called the QTC, where the C stands for corrected. This is just the corrected QT. The QTC, in certain situations, is considered to be more accurate than the regular QT. The only reason I bring this up is just in case you're looking at an EKG and you see that there's the QT and a QTC. I want you to know what the difference is between the two. What's normal for a QT interval? In adults, females typically have a slightly longer QT interval than males. In a normal adult male, the QT should be less than 0.43 seconds. In a normal adult female, it should be less than 0.45 seconds. A QT interval is considered to be prolonged in an adult male if it's greater than 0.45 seconds, and prolonged in a female if it's greater than 0.47 seconds. If you're just eyeballing an EKG, it's impossible to tell the difference between 0.43 seconds and 0.45 seconds. Again, if you're just eyeballing an EKG, here's something good to know. Every large box represents 0.2 seconds. If the QTC is longer than two large boxes, or larger than 0.4 seconds, then you want to take a closer look at the QT or the QTC. Typically, the machine itself will calculate it for you, or you can even take out calipers, which are these little measuring tools, and you can measure it yourself. Remember, on EKG in someone with torsades you're going to have the long QT syndrome, or you have a prolonged QT, and you're also going to have this polymorphic ventricular tachycardia. You'll have the long QT and the polymorphic V-tach. Having a long QT doesn't usually give you symptoms to come into the hospital. However, people who are experiencing a ventricular tachycardia might have symptoms where they want to come into the hospital. Often they present in V-tach and you're not going to see the long QT on EKG. What you can do, though, is look at old EKGs. You can look at the old EKG and see if you notice a prolonged QT interval, which has now turned into this polymorphic V-tach. Here's and EKG of someone with polymorphic V-tach. You have these short amplitude waves, followed by these large amplitude QRSs, and then short again, and then large amplitude. You notice that the QRSs are wide complexes. And, because this is a tachycardia, the heart rate's greater than 100. People with torsades who are in a polymorphic V-tach can have heart rates up to 250, even 300 beats per minute, which is dangerously high. These people might not be able to circulate blood effectively to their body because their heart's beating so fast, there's not enough time for the heart to fill with blood and pump that to the rest of the body. Also, V-tach can turn into another deadly heart rhythm called ventricular fibrillation, also called V-fib. In V-fib, the heart doesn't even beat. Instead, the walls are spasming and blood can't circulate through the rest of the body. Why would someone have a prolonged QT interval or a long QT syndrome? A person can have a prolonged QT for a couple of reasons. There's congenital long QT syndrome. Congenital means that you're born with it. These people are born with a genetic mutation where they have abnormal ion channels. These abnormal ion channels will prolong their QT. There's also acquired long QT, meaning it comes from some sort of outside source. The most popular culprit for long QT? That's medications. Different medications can make you more likely to develop long QT. It's not all medications, but there is definitely a certain list of medications that will do this. Ironically, certain types of anti-arrhythmics will put you at increased risk for developing long QT. That seems kind of funny. The medications we use to prevent arrhythmias can cause them. When you think about the mechanism, it makes sense. Certain anti-arrhythmics will delay repolarization of ventricular cells. Like we said earlier, this can set up an environment for a heart to go into V-tach. Since people with congenital long QT are always at a higher risk of developing torsades, it's good to know about this condition, and to think about it if they develop an abnormal rhythm. Also in this group of people, education is really important. You can advise people on what meds to avoid to prevent going into torsades. And, depending on the patient and their circumstances, the patient may opt for the implantation of an internal defibrillator. An internal defibrillator is a machine that's implanted into the heart, and it will shock the heart back into a normal rhythm if it develops or disintegrates into a deadly rhythm. Remember we said that torsades is a type of V-tach. V-tach is dangerous because it can turn into ventricular fibrillation, or V-fib. If that's not reversed immediately, then the result is rapid death. Why does V-tach turn into V-fib? In V-tach, there's either an irritated area of the ventricles, or some sort of abnormal circuit that's going around in circles firing away, making the heart beat really fast. However, V-tach is still an organized rhythm. However, in some patients, usually patients with a sick heart or a heart that's irritated due to either electrolyte abnormalities or medications, this organized rhythm can disintegrate into random chaotic electric wavelets. These wavelets don't generate unifying attraction of the ventricles, and instead the ventricular walls just spasm and blood can't circulate If no blood circulates in the body, that's what causes death.