Health and medicine
- 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
Created by Bianca Yoo.
Want to join the conversation?
- I appreciate you using classes of drug and their use, but I wish you would mention typical drugs in each class?!(7 votes)
- Typical drugs for each class include:
Class 1: None. This class of drug is normally only prescribed when the other drugs are ineffective.
Class 2: Metoprolol (most common), carvedilol, bisoprololl, sotalol (also considered a class 3 drug)
Class 3: Amiodarone and sotalol
Class 4: Amlodipine, diltiazem, and verapamil(9 votes)
- Are you talking about the voltage potential inside the cell relative to the potential on the outside of the cell?
Which ions are flooding into the cell and which are being pumped out?(1 vote)
- This might be a helpful graphic to give a good idea. http://mcat-review.org/action-potential.gif Most action potentials use Sodium and Potassium through the body, except for the heart which also uses Calcium ions(6 votes)
- Can you give a more detailed introduction to the different types of Class I abtiarrhythmatics? That is, type Ia, Ib and Ic?(3 votes)
- One website I have found about the different types of antiarrhythmics is http://www.cvpharmacology.com/ such as http://www.cvpharmacology.com/antiarrhy/sodium-blockers. Some other sources that might go more in-depth might be actual nursing textbooks.
Let me know if this helps or not.(1 vote)
- Class IB drugs like Lidocaine decrease the AP duration which makes the EFP shorter. How does this help? I must be missing something.(1 vote)
- The refractory period is often shortened,, yes, but it exhibits a use-dependent block of the Na channel. What I mean by this is that it has a greater effect in ischemic cells, so patients who have had a heart attach. Class 1B drugs are very rapid acting so they are mainly for emergencies like AFIB/MI patients.(2 votes)
- 4:38Why is it called refractory period? I mean, isn't refraction something else?(1 vote)
- Refractory - stubborn or resistant to change.
Refractory period - unresponsive to additional neural stimulation
Refraction - relating to wave-lengths of light. "Refraction is the change in direction of propagation of a wave due to a change in its transmission medium. The phenomenon is explained by the conservation of energy and conservation of momentum. Due to change of medium, the phase velocity of the wave is changed but its frequency remains constant." Wikipedia(2 votes)
- how can a super ventricular tachycardia happen when the rate of the heart goes down?(1 vote)
Arrhythmias are typically treated with either medications or with electric shock therapy. Now on the medication side of things there are different types of medications that treat arrhythmias, but before we get into that, let's quickly review the cardiac action potentials. So I'm going to draw them out right here. So we have two different types of action potentials for cardiac cells. We have our nodal action potentials and that means that they work at the SA and the AV node, and we also have our non-nodal action potentials. These work on the non-nodal cells meaning your cardiac myelocytes. And I'm going to write that down because that's an important concept. So they work on the cardiac myelocytes as well as the cells that make up the His-Purkinje system. and cardiac action potentials share similar characteristics as action potentials in other parts of the body. So we have the rapid depolorization phase in both of these. We also have the rapid repolarization phase and it repolarizes down into baseline. And the change in voltage is due to different ion channels being opened during different phases of the action potentials. So let's talk about the non-nodal action potential first. What's going on here. Well we have phase zero. And phase zero is this rapid depolarization and this is because we have an opening of sodium channels. So sodium channels open, sodium pours into the cell, and gives this rapid spike in voltage. At some point these sodium channels close, potassium channels open, so sodium no longer goes into the cell and as potassium now leaves the cell, we're going to enter something called phase one, which again is mediated by potassium channels and we're going to get this slight dip in voltage which brings us into phase two. And in phase two, we have calcium channels that open while the potassium channels are still open. So what's going on here? Calcium is entering the cell as potassium leaves the cell and the charges sort of balance each other out. So therefore you get this plateau period where there's no change in voltage. Eventually these calcium channels start closing and you have a lot of open potassium channels and this brings you to phase three which is your repolarization phase. So phase three is this decline in voltage and is a repolarization phase caused by a lot of potassium channels being opened which brings us down to baseline and that's phase four. And this is your resting membrane potential and this is mediated by the cell being freely permeable or open to potassium. So that's the action potential for a non-nodal cell, and again this is the action potential for a cardiac myelocyte or a cardiac muscle cell. What about the nodal cells? Well at first glance you'll notice that the action potential for the nodal cell looks a lot different than the non-nodal action potential. For one thing you don't have phase one or phase two. All you have is phase zero, phase three, which is again your repolarization phase, and phase four. Now let's talk about what's going on in this action potential. So in phase four, we have this slow rise in voltage because of open sodium channels. And at the tail end of the phase four period, calcium channels start opening. We hit threshold and a bunch of calcium channels open and we get this large spike in voltage. This is phase zero and again this is because calcium channels are opening. There's no phase one and phase two. So we go automatically into phase three which is this repolarization phase and this is mediated by a bunch of opening potassium channels and eventually we're back down to phase four where we have the sodium channels again, opening slowly. So again, these two action potentials not only look different because there's no phase one and phase two in the nodal action potential, different ion channels are open during different phases. Another important piece to point out is that your area between phase zero and phase three this is known as your effective refractory period. It's a window of time when you can't trigger another phase zero action potential and I'm going to call it ERP for short. Again, during your ERP, you can't trigger another phase zero action potential. So basically it's like a built-in mechanism to prevent this all from over firing and it's kind of like the cell's recovery period. So what would happen if we increase our ERP? Well you would increase the amount of time between depolarizations. Therefore you'd increase the amount of time between heartbeats or when this myelocyte can contract and if you're increasing the amount of time between heartbeats, you're decreasing the heart rate. And I just wanted to point that out, because that's how some anti-arrhythmics work and we'll revisit this in a couple seconds. So we're going to talk about four different types of anti-arrhythmics starting with class I, and these are our sodium channel blockers. So remember in the non-nodal action potential, sodium channels are really important for phase zero. So if you block sodium channels, it takes you a longer time to get through phase zero. So what's happened? Well before when we had an ERP this long our ERP is now this long. We've extended the effective refractory period and like we said before, when you extend the effective refractory period, you're going to have a longer time between depolarizations, meaning you have a longer time between heartbeats, meaning that you're slowing down the heart rate. And that's why sodium channel blockers are great for treating supraventricular tachycardias, which we sometimes call SVTs for short. Examples of SVTs are atrial fibrillation, also known as A-fib, and this is a condition where the top chambers of the heart are spasming. You can also use a sodium channel blocker to treat an SVT caused by Wolff-Parkinson-White syndrome which causes a certain type of reentrant tachycardia. And again, these are just a couple of examples of SVTs that are treated by sodium channel blockers So the next class we're going to talk about are Class II anti-arrhythmics and these are beta blockers. Beta blockers work because they decrease sympathetic stimulation. They block the beta I receptors at the SA and the AV node. I just want to draw out a couple nodal action potentials. Now how do sympathetics work to increase heart rate? Well sympathetics work by increasing the slope of phase IV. So basically you're hitting thresholds sooner. And if you hit thresholds sooner, you're going to have more frequent depolarizations. Okay, so I'm going to erase this so we can see how beta blockers work. Beta blockers work by blocking sympathetics and if sympathetics increase your phase four slope, beta blockers are going to work by decreasing your phase four slope. So actually it's going to take you longer to hit threshold. Once you hit threshold the action potential will be the same. But it takes you longer to hit that threshold. So again, by decreasing the rise of phase four, you're going to decrease the frequency of SA node firing and since beta blockers work at the AV node as well, you're going to slow conduction through the AV node. So both of these things are going to work to decrease heart rate. And that's why beta blockers are great at treating SVTs. Again like A-fib and even atrial flutter. Beta blockers can also be used for ventricular tachycardias, also known as V-tach. So someone with a history of an SVT or V-tach, might be put on a beta blocker to help control their heart rate. Okay, so the next class we're going to talk about are class III anti-arrhythmics, and these are your potassium channel blockers. These work primarily at non-nodal cells and where in the non-nodal action potential is potassium important? It's important here at phase three. So when potassium channel blockers are on board, we're going to get an elongated phase three period because we're blocking potassium channels. And what does that do? Well where we once had an ERP this long, our effective refractory period is now this long. Just like with class I drugs, when we increase our effective refractory period, there's more time between depolarizations, meaning there's more time between heart beats, meaning you are slowing down the heart rate. And potassium channel blockers are great for treating SVTs and V-tach. But something important to note is that you're phase three of the action potential corresponds to your QT interval on EKG. Since potassium channel blockers elongate your phase three, you're going to be elongating your QT interval. And elongating your QT interval is dangerous because it can lead to a dangerous rhythm called torsades and this is a type of V-tach. Torsades is also dangerous because it can disintegrate into something called ventricular fibrillation. Also called V-fib. In V-fib the bottom chambers of the heart are spasming and nothing is contracting, so you're not pumping blood to the rest of the body. That's why V-fib is deadly if it's not treated immediately. So anyone that has a long QT, whether it be from medications they're taking of from a genetic mutation that they're born with, anyone who has a long QT, they stay away from potassium channel blockers because we don't want to throw them into V-fib. Okay, so let's talk about class IV anti-arrhythmics. And these are your calcium channel blockers. Calcium channel blockers come in two types. You have your dihydropyridine which is abbreviated DHP for short, and you have your non-dihydropyridine calcium channel blockers. Your non-dihydropyridine calcium channel blockers work at your SA and your AV nodes. So they work at the heart. Where dihydropyridine calcium channel blockers these work at blood vessels. Sometimes to remember this I will erase this O, and I'll draw in a heart in place of the O, so that I remember that the non-dihydropyridine calcium channel blockers work at the heart. And again, the dihydropyridine calcium channel blockers these work at blood vessels. They have little to no effect at the SA and AV node. So where in the nodal action potential are calcium channels important? Well they're important at phase zero. So when you have a calcium channel on board, you're going to hit threshold just as fast, but it's going to take you longer to go through your phase zero. Therefore, you're going to decrease firing at the SA node, because it's taking longer to get through phase zero. So again, because we're decreasing or delaying the slope of the phase zero period at the SA node, we're going to decrease firing of the SA node. Since they also work at the AV node, we're going to slow down conduction to the AV node. and again, both of these will lead to a slower heart rate. And since we're slowing heart rate, calcium channel blockers work great for SVTs. Now you might be wondering, why don't they work for tachycardias like V-tach. Well that's because in studies they found out that potassium channel blockers do a better job at treating V-tach than calcium channel blockers. So that's why if somebody has V-tach, they're not going to reach for a calcium channel blocker first.