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0:06
I'm engineer so in this video we're gonna talk about calcium channel blockers let's go and get started alright so let's go ahead an get started on calcium channel blockers the first thing that we have to talk about with these calcium channel blockers is their mechanism of action right and there's two different types of calcium channel blockers one is a group called non dihydropyridine calcium channel blockers what are the names of those two drugs well one of them is called verapamil so
0:32
it's called verapamil that is one of the non dihydropyridine calcium channel blockers so again this group that we're going to talk about here are called your non die hydro pyridine calcium channel blockers okay and it consists of verapamil and another one called diltiazem alright so how did these guys work and how are they different from the dihydropyridine calcium channel blockers well the nonde hydro pyridine worked primarily on the heart except for diltiazem del tiesm has both the effect
1:11
on the actual cardiac tissue as well on the vascular smooth muscle just minor it can also not just work on the heart tissue but it also can work on the vascular system okay that's important so we can work on the heart and the vascular system whereas verapamil is primarily going to work on the cardiac tissue now how do they work on the cardiac tissue they act on particular components of the heart you know within the heart you have two different types of cells right you have your intrinsic
1:40
kind of conduction system right so that basically consists of like your SA node which sends action potentials down to the AV node which goes to your bundle of hiss and the bundle of hiss sends things down into your bundle branches and then it's going to go down into your Purkinje system well that's all of your intrinsic conduction system what they do is they work primarily by inhibiting the SA node decreasing the heart rate that's pretty cool so one thing it can do
2:13
is it can decrease heart rate by decreasing the action potentials generated by the SA node I guess what else I can do it can also block the AV node what does the AV node do it helps with conducting action potentials from the atria to the ventricles if you block that you're gonna inhibit the AV conduction which is very important when it comes to certain arrhythmias all right so they can block the SA node and it can block the AV node so that's gonna decrease heart rate via the SA node and
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decrease AV conduction via the AV node but guess what else it can do it can act on the myocardial cells that are contractile not the pacemaker ones like these on the contractile ones the ones that have those myofilaments and it can work by blocking the calcium entry into those cells which induce contraction so I'm going to inhibit contractility so I'm gonna decrease contractility whoo that is pretty cool we're gonna go over the cellular activity of this in a
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second before we do that going into how it affects the pacemaker cells on the non pacemaker cells let's go quickly talk about the dihydropyridine calcium channel blockers so these are going to be your dye hydro pyridine calcium channel blockers that's these little suckers right now what are some of these little guys okay this is going to be things like amlodipine amlodipine is a very commonly utilized dihydropyridine calcium channel blocker another one is called Nakata
3:53
pean another one is called Nemoto pean and another one is called nifedipine so if you forget their names just remember that it ends in that i peen or the actually we could say de peen so it ends in that depend component right so I'm low to pain in the car to pain in the mode of pain of feda pain how did these guys work they work on your peripheral vasculature the arteriole smooth muscle within the vessels and it works to actually relax the smooth muscle within the tunic
4:26
Media which controls the tone of those vessels so if you inhibit constriction what do you get dilation so this is gonna promote vasodilation and that drop and vaso die of that actual initiation of vasodilation can help with dropping two things total peripheral resistance which is important for patients with high afterload you don't want to increase the after load right because I can put more stress on the heart and it also can decrease your overall pressure by decreasing the total peripheral
4:57
resistance so that's a beautiful thing about this drug okay or this drug class now how do these drugs actually work on the cellular level here we got two cells here we have a pacemaker cell which could be any one of these cells let's say okay and over here we're gonna have a non pacemaker cell and as you can see here it has that actin-myosin components okay and these are gonna be the contractile cells and then here connecting the two we're going to have just one gap Junction just one good old
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cute little gap Junction right how does this work well you know you have these things called funny sodium channels we're gonna fly through this right and funny sodium channels allow for a little bit of sodium to leak into the cell very small amount but enough to make the cell a little bit more positive if we make this cell more positive we're going to make the voltage okay less negative so it's going to be a less negative milah voltage as we cause the cell to
5:58
become a little bit more positive guess what that does it activates this voltage-gated calcium channel and this voltage-gated calcium channel is a T type of voltage-gated calcium channel and when he opens up he's gonna make the cell a little bit more positive and so if we talk about it becoming more positive it's gonna be even more or less or we should actually say less negative Milla voltage we're gonna start approaching positive voltage soon as that happens it activates this beautiful
6:28
channel this beautiful green channel here called the l-type calcium channels and when these open they allow for calcium to blast into the cell and really make the CEL super positive and as that happens it initiates what we call an action potential and this action potential we can propagate it to other pacemaker cells or non pacemaker cells right we can push some cations into the other nearby cells I have all these cations that I'm flushing into this non pacemaker cell what's that going to do
7:08
what's gonna make the inside of the cell positive right as we make the inside of the cell positive it's less negative milah voltage that's enough to activate these voltage-gated sodium channels that are on these non pacemaker cells and that allows for sodium to flush in very very powerfully and as sodium flushes into the cell it really makes that cell super positive and as that starts to happen it starts causing an action potential to be carried down the sarcolemma and even down these little
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components called T tubules and stimulates the sarcoplasmic reticulum on the sarcoplasmic reticulum we're gonna have all these different types of l-type calcium channels we're gonna zoom in to this and what happens is it's going to whenever the sodium crosses over this and depolarize the membrane it's just positive enough to stimulate the opening of these l-type calcium channels calcium rushes into the cell as it rushes into the cell what happens it eventually
8:15
activates the myosin right it binds to the triple myosin changes the I'm sorry binds to the troponin changes the shape of the tropomyosin and allows for my it's myosin to back binding to the actin and induce contraction so the overall result is muscle contraction now follow with me ready calcium channel blockers what do they do they blocked the l-type calcium channels if I block the l-type calcium channels right using my calcium channel blockers calcium can't come in there's less positive
8:47
charge in the cell then there is a decrease in the action potentials that means less positive ion's are getting shunted through gap junctions into pacemaker cells and non pacemaker cells that means that the cell isn't becoming less negative it's not gonna stimulate this voltage-gated sodium channels as well and there's going to be less sodium coming into the cell less sodium coming into the cell means less positive charge in the cell that's not going to generate that action
9:15
potential so that's gonna result in decreased influx of calcium if there's a decrease in flux of calcium through the l-type calcium channels in addition these bind also on that point and even make this pathway even more dropped we're gonna have even more low calcium levels that's going to result in less of this cross bridge interaction and decrease muscle contraction so we can decrease action potentials through SA node and AV node and inhibit contractility so cool the concept is the
9:48
exact same in the vascular smooth muscle here we have these l-type calcium channels and calcium flows into this actual smooth muscle cells so this is a smooth these were cardiac this is a smooth muscle cell of the tunica media within the vat the vessels that's in the vasculature calcium flushes in when calcium flushes into the cell when it's depolarized okay then what happens then calcium binds on to a protein called calmodulin and then calmodulin can activate this thing called cam kinase
10:23
and cam kinase can convert what's called myosin light-chain kinase into a phosphorylated myosin light-chain kinase which the hen can phosphorylate the heads of myosin when you phosphorylate the heads of myosin it creates such a way that it allows for that cross bridge formation to occur and what happens muscle contraction so as a result of that you get muscle contraction now follow with me we're going to use calcium channel blockers we're going to inhibit calcium entry less calcium comes
10:58
into the cell less calmodulin activation less cam kinase less phosphorylate myosin light-chain kinase and less phosphorylation of the myosin heads therefore there is a decrease in muscle contraction it's such a beautiful mechanism that's the mechanism of action of these drugs let's get it to the indications all right so let's get started on the indications why do we use these drugs what's the purpose of them what does it do remember we said the big thing is it drops the heart rate
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and it drops the AV conduction pathway right so it decreases that what would that be good and what kind of thing would we want to maybe slow down someone's heart rate what if they have afib and they have multiple reentrant circuits or multiple ectopic flow side that are sending these action potentials through that AV node what if we block it and we give it time to reset that'd be pretty helpful right so if someone has atrial fibrillation or if they have another condition where maybe they don't
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have Ekta multiple ectopic foci but they have what's called a cave o tricuspid isthmus which is basically here around that tricuspid valve and it can generate reentrant circuits which is very common and atrial flutter we could also use this in atrial flutter in other words this is great for supraventricular tachycardias what's another one that can actually also kind of alter some of the activities that are kind of generated in the atria and have to go through the AV node
12:24
what if someone throws a lot of PA C's oh and it becomes to the point where they're actually symptomatic let's actually write this out for you guys called pre mature atrial contractions okay so we call these PA C's that's how they're abbreviated right if you're throwing tons and tons and tons of PA C's then you might start becoming symptomatic we could use calcium channel blockers in this sense but generally if someone has PA CS we don't necessarily have to give them medication they might
12:55
just be able to deal with it and they might be asymptomatic alright that's some of the things we can do so we can help with this process here good thing for arrhythmias what about decreasing that contractility let's go back to that effect if we decrease contractility what kind of situations would that be good for remember here's something I think about if you decrease contractility it does two things it decreases cardiac output and decreases blood pressure but it also does something else it
13:24
decreases oxygen demand Oh so this would be good if I decrease oxygen demand because I'm not consuming as much oxygen now because I'm not contracting all the time what would that be good for maybe someone who has angina pectoris but we got to be very careful because some of you you guys might realize we don't commonly use this for angina pectoris and it's not for acute coronary syndrome so we got to make sure that we specify this is not for ACS it's for someone who
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maybe has stable angina and they can't tolerate a beta-blocker well we go to if they can't tolerate a beta-blocker we might try calcium channel blocker another one that's commonly utilized because we can't give beta blockers in these patients is Prinze metals or vasospasm okay this one you can't give beta blockers to so if you can't give beta blockers to them what's another drug that could help you with this calcium channel blockers it drops blood pressure what kind of
14:27
conditions would that be helpful in hypertension so if someone has hyper tension now it's actually really important for us to remember that this can be used not just in hypertension but also in patients with hypertensive emergencies what is that whenever somebody has a blood pressure greater than 180 over 120 and they have end organ damage that would be another drug that we could give particularly like Anna carta pain okay or even nifedipine there's a lot of them
15:01
and then the other thing is it's also good in pregnancy so you can use this in patients who are hypertensive who are hypertensive and they're pregnant nifedipine is actually a very common one okay all right so what else does this do what does this remember whenever we use like things like dihydropyridine calcium channel blockers what do we say can do it can cause vaso dilation and what does that do well it does one thing right which is going to be it drops blood pressure another effect is it
15:38
actually decreases after load so it reduces after load okay so we can use this to help to reduce after load which reduces the stress on the heart so what would this be good for okay it could actually be good for someone if we want to drop blood pressure what if they have hypertension so this could be good in hyper tension here's something else that we can do you know there's a condition where certain patients who maybe have an underlying condition like scleroderma
16:11
right there's what's called cress syndrome where you can have calcine OSes rainouts phenomenon esophageal distillate II you can have scolaire dactyl II in tanjit LAN Jie Jie it's a type of scleroderma which is kind of an autoimmune disease and those situations patients might have go out into cold temperatures and whenever they go into these cold temperatures the vessels in their distal and the digits they undergo intense vasoconstriction and decrease the blood flow to those distal phalanges
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and they turn white then over time as they start to respond they go blue and then eventually they go back to red or to the normal skin cue what if we could use drugs that could reduce that vasospasm and cold temperatures and patients with rainouts phenomenon what would that be vasodilation mechanisms right that'd be good for calcium channel blockers which would be good for rainouts phenomenon all right cool now another thing you know what patients have subarachnoid hemorrhages whenever
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they have subarachnoid hemorrhages what's important to know about this is that this can promote spasming of the vessels that are going to be supplying that area of the brain so there can be vasospasm so there can be vaso spasms whenever someone has potentially maybe a subarachnoid hemorrhage so whenever someone has a subarachnoid hemorrhage this can promote vasospasm of the nearby vessels what can we do if that's spasming and contracting give a vasodilator a calcium channel blocker to
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reduce those vasospasm so this would be good in helping to reduce vasospasm in sub arachnoid hemorrhage patients pretty cool right and also on top of that we can control their blood pressure we don't want to drop their blood pressure too much but we don't want to continue to keep allowing for more hemorrhage to occur so it can help to control the BP and reduce vasospasm okay now the next thing that's really interesting is that there's some drugs that actually some of
18:21
these calcium channel blockers could potentially be used in patients who have cluster headaches so cluster headaches are basically described as this stabbing lancinating pain that you can sometimes feel behind the eye and it's usually unilateral they also could have rhinorrhea they could potentially have nasal congestion they could even have what's called Horner's syndrome which is when they might have ptosis they might have facial anhidrosis as well as the meiosis of the actual pupil and so
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sometimes we can use calcium channel blockers in the treatment of cluster headaches so they could be used not in the initial setting because usually initially when someone has a cluster headache the best thing to do is to give high flow oxygen 10 to 12 liters but usually if you want to try to prevent these recurrences there's a potential of using calcium channel blockers for patients who have cluster headaches okay last thing here remember calcium is also not just important to vascular smooth
19:23
muscle it's also important within the smooth muscle of the GI T and they can inhibit calcium entry into those actual smooth muscle cells which can initially cause relaxation okay of particular points of the GI T you know there's a condition called achalasia so it's called achalasia and basically what happens with achalasia in this situation what we're worried about is right at what's called the lower esophageal sphincter right your lower esophageal sphincter it's super tight okay let's
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use that word tight in other words it doesn't want to relax if we could potentially give a drug that could relax that lower esophageal sphincter what could we then do we can allow for the food bowls which is in our esophagus to enter into the stomach so then we could actually help to move this thing into the stomach because some of the symptoms particularly of achalasia is they could have potentially regurgitation they could have halitosis they can have dysphasia okay so if we
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can relax that actual lower esophageal sphincter we could potentially allow for the food to go from the esophagus and nicely into the stomach unfortunately it's not the best for achalasia but it's something that we can do to potentially help them alright so now let's go ahead and talk about potential side effects or adverse drug reactions that could potentially happen if you're on a calcium channel blocker because yes you should know how they work you should
20:57
know the names of them you should know what they're used for but you should also know what's something that I have to watch out for if I put someone on this medication one of the potential things here is you got to go back to the overall mechanism of action right what does it do to the heart that can drop the heart rate a decent amount and what happens if you drop the heart rate that could potentially maybe lead to severe bradycardia potentially even a heart
21:22
block look at heart blocks too they can decrease perfusion to the potentially the brain what could that lead to syncope okay so that's something we have to be careful of another thing is remember you reduce contractility so maybe if you give too much of this drug or you give it to someone who has already maybe a potentially a weak heart or maybe even like aortic stenosis or something like that then you can reduce their contractility right this generally reduces contractility
21:48
but if maybe you give too much of it or they're a little bit more sensitive what does that do well that drops their cardiac output if you drop someone's cardiac output all right so you reduce contractility reduce cardiac output then that can potentially reduce their blood pressure and what does that do if you reduce cardiac output you can reduce blood pressure and this can be leading to hypotension so a potential side effect is bradycardia potentially heart block as
22:18
well as hypotension alright it's acting on the peripheral vasculature right and again what does it do to the peripheral vasculature it relaxes the vascular smooth muscle right so with you causing vaso dilation what can that do well here let's think about this vasodilation can drop blood pressure you know what happens we need to drop blood pressure remember you stimulate these specific sinuses you know within the aorta you have the carotid sinus and you also have
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what's called the aortic sinus at the aortic arch what do they do they send action potentials to your central nervous system and activate your cardiac accelerator what does that do it increase your sympathetic nervous system activity which leads to an increase in heart rate what is that called if you give this drug if vaso dilates and then leads to them having a reflex tachycardia that's a potential symptom so reflex tachycardia also your face so dilating you're dropping blood pressure
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what's a potential effect of this if there's a potential of hypotension next thing there's also something you have to watch out for is that when you give this drug right not only can it cause reflex tachycardia hypotension but with vasodilation there's a risk of increased capillary permeability and this can lead to increased fluid in the interstitial space and what is that call whenever you have a lot of fluid in the interstitial space edema and this a commonly occurs in the peripheral lower
24:12
extremities so there's also the risk of peripheral edema the other thing that you have to remember is if you vaso dilate blood vessels that are close to the skin so if these vessels dilate and they're closed to the skin what can that make it look like or what can to make it feel like if those vessels dial it on the skin it can feel like you're flushing right so it can have this sensation of flushing so that is another potential side effect of being on these dihydropyridine calcium
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channel blockers so this is for dihydropyridine calcium channel blockers whereas the effect on the heart is primarily by non dihydropyridine calcium channel blockers so again another potential side effect is flushing because of vasodilation are the vessels close to the skin and not only you'd have to worry about hypotension in general but you should also worry about orthostatic hypotension right which is basically whenever you come for maybe a seeded to a standing position and the
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blood doesn't return to the heart enough you don't get enough blood volume in the heart to pump to the brain and you start to get dizzy pretty syncopal and potentially pass out so that's something else you want to watch out for all right next one super weird one but they love to ask this on the exams and they don't really know why this happens but calcium channel blockers have the potential to cause thickening of the gingiva they make it thick right so what is that
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called if you thicken up that gingiva that's called gingival hyperplasia so they increase the production of the epithelial tissue of the gingiva and this is called gingival hyperplasia and surprising enough the most common one that causes this is M lode of pain so they see it most common in and Load of pain all right now let's go back to this now remember what we did on the actual smooth muscle of the GI T what could it potentially do to the smooth muscle of the GI T for achalasia it relax that
26:19
lower esophageal sphincter but what if you relax the smooth muscle that's helping to propel food contents or feces towards the rectum decrease GI motility if you decrease Gianni Mota leti that gut ain't gon work right and because of that it can potentially lead to constipation right and nobody wants that alright so this last side-effect are 80-yard that we have to watch out for with calcium channel blockers actually more particularly is with thus one of the calcium channel blockers called
26:55
verapamil right if you guys remember verapamil was one of those non dihydropyridine calcium channel blockers this side effect is a little odd but it's something I wanted to mention because it could come up on an exam if you guys go back to a little bit your endocrinology you have the hypothalamus right which is a kind of a piece of gray matter located within what's part of your called your diencephalon and in the hypothalamus you have these particular neurons these dopamine producing note
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neurons right so here's my dopamine-producing neurons what happens is these axons come all the way down and they secrete a specific type of hormone called dopamine and that dopamine acts particularly on this lacto troph right which is the cell that produces prolactin let's zoom in and take a look at how verapamil affects this before we do that though you guys remember that dopamine right dopamine does what it actually acts on these lac d'oo tropes and inhibits prolactin production so now
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dopamine inhibits these actual lac d'oo tropes right and if you inhibit the lactose troves now they're not going to release prolactin all right so there's going to be a decrease in prolactin production generally whenever there's dopamine okay so whenever there's normal dopamine production this dopamine is going to inhibit prolactin production by the lactose now take into consideration verapamil verapamil actually works by inhibiting dopamine release if you inhibit dopamine
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release that's going to be decreased dopamine in the synapses now you have less inhibition on the lacto Truths and if there's less inhibition there's going to be stimulation of these lacto tropes and now the prolactin production will start to increase what do we call this whenever someone has elevated prolactin levels it's called hyper Pro lacked in amia all right like i spelt that right hyperprolactinemia now that can produce different types of clinical manifestations in the different sexes
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right so for example in the male it can cause enlargement or accumulation more of the actual male breast tissue okay and that's called gynecomastia so gynecomastia all right that's moobs okay that's that's moobs the other one is going to be in females it can actually cause milk production okay increase milk production and that could potentially lead to galacto Rhea on top of that it also can affect the normal FSH and LH activity as well as estrogen levels and that could potentially lead
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to certain types of menstrual irregularities okay so that's something that you need to be aware of with verapamil is that it can potentially produce hyperprolactinemia causing gynecomastia and males Galacta Rhea and menstrual irregularities in female okay so what are some of these things that we have to watch out for remember what does it do to the AV node it blocks that AV node right so it decreases AV node conduction and on top of that it also drops your heart rate as
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well right so there's the combo of dropping the heart rate by decreasing the impulses generated by the SA node and blocking that AV node if we block that AV node in a particular condition called wolff-parkinson-white syndrome that is potentially dangerous why wolff-parkinson-white Center has this accessory pathway called the bundle of Kent which is this accessory pathway which is able to conduct electrical potentials just like the AV node but what did you do with giving it a calcium
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channel blocker maybe too much of it you inhibited the AV node conduction now the electrical potentials only have one way to go through and that is the bundle of Kent the risk of that is that that can lead to potentially v-tach or v-fib that is why this is dangerous you do not want to give this drug to patients with wolff-parkinson-white syndrome plus it can even be worse if they have a corresponding a-fib that's actually one-to-one okay the other thing is you
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want your inhibiting the AV node right what if you give another drug that also inhibits that AV node even more that's a problem so another thing that you do not want to give this with is also if someone is on a beta blocker okay so you do not give this if they're on a beta blocker you don't want to combine those two the last thing is if you decrease the action potentials or you decrease the conduction from the atria to the ventricles are you gonna have a proper
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connection between the atria ventricle now know what's that call whenever you either have partial interaction or complete loss of interaction between the atria and the ventricles that's called a heart block so another potential contraindication that you want to watch out for in this is heart block you don't want to give this to a patient who has a heart block maybe second maybe third degree because you potentially could block that heart block the AV conduction
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and make their heart block even worse potentially causing them to become sinkable all right last thing here it also can reduce contractility of the heart right so if you reduce contractility what do we say that does remember we said that it can cause two things drop drop your cardiac output and drop your blood pressure but it also decreases oxygen demand well here's the situation when you got to be careful what if somebody already has a weak damaged heart like what someone has
32:52
congestive heart failure particularly someone has maybe decompensated heart failure maybe they have decompensated heart failure or just in general a really weak heart okay decompensated heart failure are you gonna want to give this drug to someone who has a really weak heart as it is no that can make it much much much much worse right because you're technically inhibiting the inotropic activity with an already presently weak heart what if you have something where the
33:24
aortic valve is super-super stenotic and normally if someone has a or textin oasiz what's the problem with aortic stenosis you're getting less blood flow across that a ordered valve into the actual aorta and where does the order get deliver blood to to the brain right if you have a or --tx the gnosis which is reducing blood flow to the brain what is that going to result in potentially syncope and you're also not getting enough blood flow going through the coronary vessels so there could also be
34:00
decreased blood flow through the coronary arteries which could potentially lead to and Jinan that's a problem so if you decrease the contractility what are you gonna do you're gonna drop the blood flow even more which is gonna exacerbate syncope and exacerbate blood flow to the coronary system which can lead to potentially a myocardial infarction and the last thing that we also want to be careful of this with is someone who's already hypotensive if they're
34:33
hypotensive you give them this drug what are you gonna do even more you're gonna drop their blood pressure even more and that's not something that we want okay last but not least something you have to remember if you give someone a calcium channel blocker you better know how to reverse it if you need to so what is the antidote we can kind of say if someone is on a calcium channel blocker the antidote that you should remember is very simple you're giving a calcium
35:04
channel blocker that's blocking calcium entry right in a kind of a competitive way what happens if you increase the substrate concentration in a biochemical reaction you could potentially knock that competitive inhibitor out of that actual binding site so if I give them more calcium I could potentially knock that calcium channel blocker off and allow for calcium to get into those cells so what do I got to give them give them a lot of calcium so the antidote is
35:30
actually pretty simple you can give them calcium in the form of their calcium gluconate or calcium chloride alright so that's something to remember with respect to calcium channel blockers
35:53
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