If you're seeing this message, it means we're having trouble loading external resources on our website.

If you're behind a web filter, please make sure that the domains *.kastatic.org and *.kasandbox.org are unblocked.

Main content
Current time:0:00Total duration:12:08

Video transcript

arrhythmias are typically treated with either medications or with electroshock therapy now in the medication side of things there are different types of medications that treat arrhythmias but before we get to that let's quickly review the cardiac acts 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 acts 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 in the non nodal cells meaning your cardiac myocytes and I'm going to write that down because that's an important concept so they work in the cardiac myocytes as well as the cells that make up the his Purkinje system and cardiac action potentials share similar characteristics as acts potentials and other parts of the body so we have the rapid depolarization phase and 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 you get this rapid spike in voltage at some point these sodium channels closed potassium channels open so sodium no longer goes into the cell and as potassium now leave the cell we're going to enter something called phase one which again is mediated by potassium channels and we're gonna get this slight dip and 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 if we 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 3 which is your repolarization phase so phase 3 is this decline in voltage as the repolarization phase caused by a lot of potassium channels being opened which brings us down to baseline and that's phase 4 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 exponential for a cardiac myocyte or a cardiac muscle cell what about the nodal cells well at first glance you'll notice that the acts potential for the nodal cell looks a lot different than the non nodal select potential for one thing you don't have phase one or phase two all you have is phase zero phase 3 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 it opens 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 and voltage this is phase zero and again it's 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 accidentals not only look different because there's no phase 1 in phase 2 and the nodal acts potential different ion channels are opened during different phases another important piece to point out is that your area between phase zero and phase 3 this is known as your effective refractory period it's a window of time when you can't trigger another phase zero active potential and I'm going to call it ERP for short again during your ERP you can't trigger another phase zero acts potential so basically it's like a built-in mechanism to prevent the self from over firing it's kind of like the cells recovery period so what would happen if we increase our ERP well you would increase amount of time between depolarizations they're free to increase amount of time between heartbeats or when this myocyte contract if you're increasing amount of time between heartbeats you're decreasing the heart rate I just wanted to point that out because that's how some antiarrhythmics work and we'll revisit this in a couple seconds so we're going to talk about four different types of anterior things starting with class one and these are our sodium channel blockers so remember and the non-nodal act 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 lot of time between depolarizations meaning of a longer time between heartbeats meaning that you're slowing down the heart rate and that's why sodium channel blockers are great for trading super ventricular tachycardias which we sometimes call SVT s for short examples of s DTS 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 SDGs that are treated by sodium channel blockers so the next class we're going talk about our class two antiarrhythmics and these are beta blockers beta blockers work because they decrease sympathetic stimulation they block the beta 1 receptors at the SA and the AV node just want to draw out a couple nodal X potentials now how does sympathetics work to increase heart rate well sympathetics work by increasing the slope of phase four so basically you're hitting thresholds sooner and if you hit threshold sooner you're going to have more frequent depolarizations okay so I want to race this so we can see how beta blockers work beta blockers work by blocking sympathetics and if sympathetics increase your face.4 slope beta blocker is going to work by decreasing your phase four slope so actually it's going to take you longer to hit threshold once you get threshold the actions 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 svt's again like a fib and even atrial flutter beta blockers can also be used for ventricular tachycardias also known as v-tach so some of the 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 three antiarrhythmics and these are your potassium channel blockers these work primarily at non nodal cells and we're in the non nodal action potential is potassium important it's important here at phase three so when the tasking channel blockers are on board we're going to get an elongated Phase three period because we're blocking potassium channels now what does that do well where we once had an ERP this long our effective refractory period is now this song just like with class one drugs when we increase our effective refractory period there's more time between depolarizations meaning there's more time between heartbeats meaning you are slowing down the heart rate and potassium channel blockers are great for treating svt's and v-tach but something important to note is that your phase 3 of the action potential corresponds to your QT interval and EKG since potassium channel blockers elongate your phase 3 you're going to be elongated your QT interval an elongated 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 B fib and v-fib the bottom chambers of the heart are spasming and nothing's 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 are taking or 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 for antiarrhythmics and these are your calcium channel blockers calcium channel blockers come in two types you have your dihydropyridine which it's abbreviated D H P for short and you have your non dihydropyridine calcium channel blockers your nonde hide repeating calcium channel blockers work at your essay and your AV nodes so they work at the heart we are dihydropyridine calcium channel blockers these work at blood vessels sometimes to remember this I will erase this Oh now John a heart and place the oh so that I remember that the non dihydropyridine calcium channel blockers work at the heart and again the dihydropyridine calcium channel blockers these work blood vessels they have little to no effect at the SA AV node so where and the nodal a potential our calcium channel is 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 take you longer to go through your phase zero therefore you're going to decrease firing at the SA node because it's taking you 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 at the SA node since they also work at the AV node we're going to slow down conduction through 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 SVT's now you might be wondering why don't they work for tachycardia is like v-tach well that's because in studies they found 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