So, um, let me share my screen. We’re going to talk about anti-hypertensives. So the big thing here to understand, and I’ve, I’ve kind of already given it away because I gave you the cheat sheet, but there is, um, a mechanism in our body that causes our blood pressure to go up if we need it to go up. And what is that mechanism? Or you kind of give it away? Sure. My chat is on her. So what happens in our body for blood pressure goes down. There’s this system that kicks in. Yeah, the Russ, the Rennet Angiotensin aldosterone system. So its entire job is to increase our blood pressure. Now the Renin Angiotensin aldosterone system is not the source or the cause of hypertension, typically, typically a lot of other things going on. However, because it’s sole purpose in our body is to increase perfusion to the kidneys.
So increase our blood pressure, increase our cardiac output. We can actually target that system to help bring our blood pressure down. Because if we stop any part of that cycle, then we kind of stopped that increase. Does that make sense? So when you’re looking at antihypertensives, understanding this system makes all the difference in the world. There’s one antihypertensive we will talk about that is not on this system. So we’ll make sure that we covered that one. But the other one, two through six are, so that’s the helpful part. So let me share my screen and we are going to talk about,
okay.
Blood pressure meds. So I will, I’m gonna run through this and I will jump back over. Um, I can see the chat. So you guys feel free to drop questions or whatever you need, um, as you have them. And I will happily answered them. So this is our Renin Angiotensin aldosterone system. So this system responds specifically to a drop in perfusion to the kidneys. So if I have a decreased blood pressure, then my kidneys are going to go, oh no, I’m not getting the perfusion that I need. And they’re going to release this hormone called Renon. So that’s the initiation. So perfusion to the kidneys, profusion to the kidneys, so I’m not getting enough blood flow to my kidneys for them to be able to function and do what they need to do. So then they’re going to respond, they’re going to release Renton and Renton is going to come into contact with a hormone called angiotensinogen. Angiotensinogen is just already in our bloodstream. It’s already circulating in our body. Um, we already have it and so it’s going to contact the angiotensinogen and that’s going to convert into angiotensin one. Okay, so we get this initial conversion Renon converts angiotensinogen to Angiotensin one. Um, yes, this is made by the liver. To answer your question, so we get angiotensin one. Angiotensin one starts circulating throughout our body and it gets to the place where ace is. Where is ace? Ace is angiotensin converting enzyme. Where does this hormone hangout?
Yes. Good job. So angiotensin converting enzyme is in our lungs, so we convert to angiotensin one. It circulates throughout our body, gets to our lungs, comes into contact with ace and gets converted right to Angiotensin two and angiotensin two is our powerhouse. This is the hormone that does all the things that we need it to do. So if we don’t get all the way to angiotensin two, we don’t get that power that we would get before. Okay. So angiotensin two is our powerhouse and it does four things. Four things. Always remember these four things. The first is it increases outdoor [inaudible] secretion. What does aldosterone do in our kidneys? What does it cause?
[inaudible]
so I’ll start giving you a hint. Aldosterone causes retention
of,
so increased aldosterone causes retention of fluid. But how, what do we retain first without Asteron? This is how I remembered. He see this end here.
So what do we, what are your team first?
Sodium. There you go. Good job guys. So I’ll toss around. Causes increased retention of Sodium, which causes retention of water. That water follows sodium pay. So we retain sodium, we retain water. The second thing we do is we increase antidiuretic hormone. So antidiuretic means instead of diary saying we’re going to retain what?
This one’s easy. Just water.
Yep. Great. Good job guys. So we increase aldosterone, which increases retention of sodium and therefore water. And we increase our antidiuretic hormone, which causes retention of water. So all of these things are going to cause increase fluid in our system. And so if we look at hemodynamics, which is always important when we’re talking about blood pressure, what we’re seeing is an increase in preload. Preload is the volume, the fluid that comes into my heart, and therefore we end up with an increased blood pressure. Okay? So all of this, the target for all of these is to get an increased blood pressure. The third thing that we see with angiotensin two, which is one of the more powerful things we see is vasoconstriction. How does vasoconstriction help increase my blood pressure? What does that do for me? Think Chemo Dynamics.
Okay.
If I increase vasoconstriction, especially out in the periphery, what does that do for my blood pressure? How so? If these increase preload, this one,
okay.
Increases afterload. So amber said it shunts blood from less important areas. Absolutely. So we’re going to constrict out in my periphery and we’re going to pull that blood back up to my heart and it’s going to increase my afterload. It’s going to increase that resistance and that’s ultimately gonna help increase my blood pressure. Awesome. Good job. Fourth thing angiotensin two does is it increases sympathetic nervous system activity. What is our sympathetic nervous system response? What’s the other? How do we, how do we talk about that sympathetic nervous system response?
[inaudible]
yeah, so this is our fight or flight k. So what happens in fight or flight? My blood pressure goes up, my heart rate goes up. I get vasoconstriction also see some things in my lungs. I’ll see some bronco, Bronco dilation and I’ll see pupillary dilation. I’ll see a lot of other things. But specifically to cardiac, um, we’re going to see increased blood pressure and increased heart rate because of this vide a fight or flight response. So vasoconstriction. Okay. So these are the four main things. The angiotensin two deaths. This is our past. This is how we increase our blood pressure. So if we’re trying to decrease our blood pressure, we truly can, um, stop this system really at any point. We can block it here, we can block it here, we can block it here, here, here, here, and anywhere we block it, we’re going to cause, um, the opposite to happen, right?
We’re going to stop increasing our blood pressure and allow our blood pressure to come back down. So one thing I want you to realize guys, if you’re having trouble with the screen-share, try logging out and logging back in. Okay? So what I want you to realize is that the higher up we cause a problem or the higher up we block, the more generalized our, our, uh, actions are going to be not necessarily stronger but generalized. Okay? So the higher up we are, the more generalized, the farther down we are, the more specific. So again, not necessarily stronger or weaker, but generalized versus specific. Okay? Does that make sense? So let’s look specifically at the actual drugs. Let me clear some of the, yeah. Ready? Okay. So the first one we’ll look at is are angiotensin receptor blockers or our ar B’s. And we’re going to go through quick drug cards on each of these in a second. So I just want to give you an overview and then we’ll talk more specifics. So arb is angiotensin receptor blockers. So what affects are my angiotensin receptor blockers going to have in my system?
I’m going to block this, this, this, and this, right? Because I’m blocking it so far up the system that I’m actually blocking all of these processes. All of these processes aren’t going to happen cause I’m literally never going to get there. Okay? So I’m going to block these receptors. I can’t convert to angiotensin one. I stopped this process all the way up here and I’m going to get a generalized response where none of this stuff can really happen as effectively as it happened before. Okay? So again, not necessarily stronger, not necessarily stronger, but more generalized. All of the things. Okay. All the things are affected. So it, amber, specifically, this affects the conversion of angiotensinogen to angiotensin one. So this is up here. Okay. So the next drug is ace inhibitors. So if I have an ace inhibitor and I can’t use my converting enzyme, then I’m actually going to block here and I’m never gonna get to angiotensin two.
So again, you’re seeing all of these things being restricted, all of them, because I’m never getting to my powerhouse. This is my powerhouse. But here’s how I want you to remember this. Okay? Remember, like I said, the higher up, the more generalized you are and the farther down the more specific. So even though arb and ace inhibitors both prevent us from getting to Angiotensin two, we have more specific responses from ace inhibitors than we have from arb because they’re farther down the line. And specifically the one thing we see more specifically with ace inhibitors than we do with Erbs is the effect on the vasoconstriction. So if I block phase oh constriction, what do I cause, or what do I allow to happen? What’s the opposite of vasoconstriction?
Yeah, Basal dilation. So with ace inhibitors, we tend to see more vasodilation effects than we saw with [inaudible] with a RBS. Okay. Now the, what is the number one annoying, awful side effect of Ace inhibitors? Yes. Awesome. Mary, you guys are awesome. So the number one awful side effects of ace inhibitors is the cough. Here’s how I want you to remember this. We have more vasodilation with ace inhibitors. Think about if all the blood vessels in your throat suddenly start to dilate. Everything in your, all of blood vessels in your throat are dilating and now your throat’s all congested because of all this phase of dilation. That’s what causes the cough. Okay? So that’s the biggest difference between the arb and ace inhibitors is you see a little bit more based on dilation. Therefore all of the vessels in the throat start to get congested and you end up with this cough.
So if we have someone on an ace inhibitor, they end up with a cough. What drug do we typically transfer them to boot up to an arb. Okay. Like I said, arb is, are not necessarily stronger. They’re just a little bit more generalized. Amber, we do see that a little bit. That’s part of it. Um, but this vasodilation is thought to be a huge part of it as well. Amber asked if there was a, the increase in Brady kinds in the lungs there is. Um, but this is really thought to be a huge contributor to the specifically to the nagging cough, um, in the back of the throat specifically. All right, so we’ve talked about are two general ones are two ones that are gonna Kinda affect everything. So now we have one that affects each part of the process as well. So over here in Aldosterone, which drug class is going to block out Doster own, uh, increasing.
What do y’all think? There is a drug whose generic name is owl. That tone and that’s how I remember it. And there are potassium sparing diuretics. So amber asked if there’s an ethnic component to the reaction to ace inhibitors. Yes, absolutely. There’s certain ethnicities that tend to lean towards this, uh, angioedema cough more likely than others. And African Americans are, are some of them. So it’s just a, it’s a genetic component to that. So the drug class we have that blocks our aldosterone reaction is our potassium sparing diuretics. Most common of these is spear on a lactone, otherwise known as owl doc. Tone, and that’s how I remember this. That’s how I remember. This is the one that affects our [inaudible]. So if I don’t have aldosterone, then I can actually excrete that sodium and water. Right? So I blocked this. I excrete sodium and water and I can decrease my preload.
So same thing over here at ADH. The drug class that I put on, this is the loop diuretics. Now do loop diuretics actually effect ADHD? No they don’t, but they do cause increased excretion of water. So really what it’s doing is it’s doing the opposite. It’s doing the opposite effect of the ADH. It may not or it’s not directly affecting it, but indirectly it’s counteracting that ADH effect. So we excrete water. So both of these things are causing excretion of fluid, which is going to cause a decrease in preload, which is then of course going to allow my blood pressure to actually come down. Okay, two more debt classes. One is basil dilators. There’s a couple different possible ones. The big ones you’re going to see are things like nitrates, so that’s like your nitroglycerin. And then you also will see hydralazine. Hydralazine is actually a direct vasodilator. So both of these are going to allow for vasodilation, which is the opposite of vasoconstriction. It’s gonna decrease our afterload
and allow the blood pressure to come down. Okay, amber, I see your question. I’m gonna answer you in just a second. Last one really fast is our Beta blockers right here. Why don’t you guys feel to see it? There’s our Beta blockers. So our Beta blockers are going to block that sympathetic nervous system activity and it’s going to allow my blood pressure to come back down. Now what’s the number one thing Beta blockers actually affect? Is it blood pressure or is it something else? What are they a blockers really effect. Yeah. Good job guys. So the Beta blockers are actually going to cause my heart rate to come down, which is gonna cause my overall cardiac cardiac output to decrease, which will cause my blood pressure to be able to come down. So Beta blockers, remember heart rate, that’s our big thing. So real quick, amber asks, our diarrhetics the only class that effect aldosterone. So really it’s anything that affects your kind of adrenal glands. But in terms of blood pressure, when we’re talking blood pressure, what we’re going to see is spear electron, potassium sparing diuretics. Um, there’s other medications that are more hormonal related that our guys act. Your Renal, your adrenal glands that could affect aldosterone but they’re not specifically blood pressure medications. Does that make sense?
Okay,
so you have a hormone medications that are anti adrenals, um, that affect the adrenal glands that affect like, like steroids that affect our output from our adrenal glands. Cause that’s where aldosterone comes from. That will affect your aldosterone. However, when we’re talking about antihypertensive medications, then we’re only talking about potassium sparing, diuretics being the ones that effect this aspect of blood pressure. Okay? All right, so let’s just run through a really quick job card for each one. And again, I’m going really quickly because I want you guys to remember to focus on the most important things. So first one, we’ll look at a RBS. Sometimes when I do these drug cards, I like to just write my suffix. So our suffix for our arb, these are our tents, so losartan, Valsartan and things like that. And so these are our angiotensin receptor blockers. Their anti-hypertensives.
Okay.
Again, we’re just going to go super quick through these. Okay. So we said the action of are angiotensin receptor blockers is to block conversion of angiotensinogen angiotensin. No, Gen two angiotensin one. Okay. So things we use it for hypertension, also heart failure. We’ll use it for heart failure as well. Okay, so every single antihypertensive medication, what do you assess before and after you get every single one? Yes, exactly. So pre administration and post administration, we’re looking at blood pressure. Okay. Now we know the, one of the big effects here is we’re gonna decrease sodium and water retention, which means we’re actually going to excrete sodium and water. So what other things might we need to look at on this patient? If we’re excrete ing more sodium and excrete more water, what other things do we need to assess on this patient?
Yeah, sodium levels, right? Is it a huge effect? Not really, but we should totally evaluate sodium levels. What about the water aspect? What are we looking at with this patient? Because we know we’re excluding more water, possibly potassium. We might have some effects on potassium cause we know we’re affecting the ADH and the Alda aldosterone part. What else? Hydration. How do we assess fluid status guys? How do we assess fluid status? We could do a weight potentially. What if we just look at their urine output, right? We’re causing them to excrete more water, right? Or if we just look at their urine output, look at their intake and output, whether they’re signs of dehydration, things like that. Okay, so a lot of what you assess before, you’re also going to assess after you’re also going to continue watching, study, studying. So side effects. What is the number one side effect of every antihypertensive medication?
These are the easy ones you’re giving. Yeah, there you go. Decreased blood pressure. So watch for hypotension. Okay, now, so what I’ll explain to you guys is any time we’re effecting fluid, okay? Anytime we’re affecting preload, we’re also going to put them at huge risk for Ortho static, hypotension, orthostatics anytime we affect water, we’re also going to put them at risk for this orthostatic hypotension. So we’re looking at things like dizziness, right? Especially when they stand up. So what I want you guys to always focus on is the most common and the highest priority things you’re going to see specifically with these drugs. Remember, we’re going to cause the, uh, the, um, preload effects. We’re also going to have some vasodilation. So anytime we have vasodilation, we’re going to have orthostatic hypertension. So when you think about, uh, a RBS, think about blood pressure, think about intake and output cause we know we’re affecting that sodium and water and then think about, um, orthostatics because you’ve got phase dilation and water excretion. Okay. So next one we’ll look at is our ace inhibitors and what is the, um, suffix for ace inhibitors?
Yeah, pro. So this is like your captive Pril, your listen approval, things like that. So antihypertensive, same as all the rest action is block conversion of Angiotensin one to angiotensin two. So we’re going to block that. We’re going to prevent getting our angiotensin two. Same thing. We give this for hypertension and possibly heart failure. Biggest nursing consideration is looking for that cost, right? If they have that cough or if they have that, um, uh, angio edema, we need to convert them to an arb. We need to basically, we’re going to call it an allergy and we’re going to get them off this medication onto a different one. So same thing, every medication or every antihypertensive, we’re going to assess blood pressure before and after and ace inhibitors similarly to arb. These are going to affect our preload and they’re going to affect our afterload cause we’re also gonna see that effect on our, um, basal dilation, the basic construction aspect.
So not only will we see low blood pressure, but we’re also going to see what kind of hypotension, anytime we effect fluid and afterload. Yep. Orthostatic hypotension. So watch for dizziness, watch for things like that. Same thing. We’re going to affect our sodium and water excretion. So we need to be looking at our sodium. We need to be looking at our intake and output. We need to be looking at our urine output, all of the same things we were looking at for, um, [inaudible]. We’re also gonna look at for prills except with that one exception of keeping an eye out for the cost. So amber is asking about bun and creatinine. They should not be affected unless you’re actually having kidney damage. Um, severe dehydration could cause your bun to go up, but if you’re looking at these things, you’re hopefully gonna catch that before we actually affect your lab values. Does that make sense? So you should be watching your intake and output and your signs of dehydration first. Okay. Awesome. Next one. Let’s talk about, oops, I’m gonna, I’m gonna skip. Let’s talk about diuretics. So let’s talk about your, uh, potassium sparing.
Okay.
And again, the big common one here is going to be your spironolactone.
Yeah,
I’m so therapeutic. Antihypertensive or you could even say it’s a diuretic, one of the two. So action is decrease.
Okay.
Um, your aldosterone secretion, which means I’m actually going to excrete sodium and therefore water. Does this one have a huge effect on potassium?
Okay.
No, right? Cause it’s potassium-sparing. Now some people will say that you can get increased potassium, right? With these drugs, we’re going to watch our sodium. We’re going to watch our intake output and then the question mark about potassium. So here’s what I want you guys to know. If this patient has a normal diet, they will not have any issues with potassium. Okay? The only time you might see a problem with potassium is if they have a high potassium diet. Okay? That’s the only time. And I can tell you that from personal experience, I was personally on this medication for 10 years and my potassium never went about 4.2 so potassium sparing diuretics are only a risk for high potassium if they also have a high potassium diet. Amber brings up a good point. Salt substitutes are made with potassium chloride, so always keep an eye out for that. If your patient’s on assault restriction but they’re also on this medication, then you have a potential for problems. Okay, so again, it’s an antihypertensive. So we’re looking at blood pressure before and after, but it’s also a diuretic. So what’s the big, big, big thing we need to look at for any patient? Getting any kind of diuretic,
eyes, nose, and urine output you’re not put before and after. Okay. So always watch your eyes, nose and your fluid status. Always Watch your urine output before and after. Now we specifically, we’re looking out for low blood pressure cause we deal with every antihypertensive. Okay, we’re going to look out for a dehydration because we’re specifically focusing on getting rid of fluids, right? So we’ve got to watch that. And then what’s the other type of, of hypotension we can get anytime we dropped somebody. Fluids.
Okay.
Ortho static. Exactly. So this is where you start to really look at things that are specific to this drug. Okay. So let’s shift and let’s talk about loop diuretics. What is the most common loop diuretic that we give in anywhere?
Yep.
Yeah. Lasix. What’s the generic name for lasix?
[inaudible]
got it. Know generic names guys. That’s what’s going to be on the [inaudible]. Okay. So first of mine, generic names, furosemide or lasix. There’s also things, uh, w you Mennonite or BW. Max is another one. So that idea at the end is gonna be your, your hint there. Okay. So for OSA, mine is our generic name. Lasix is our tithing. So action is it’s going to cause a excretion.
Okay.
Of Water in the loop of Henley. So like I said, does this one actually, uh, directly affect antidiuretic hormone? No, it doesn’t. Antidiuretic hormone works in the tubules. The convoluted tubules loop. Diuretics work in the loop of Henley, but it does the opposite. So we’re going to excrete, we’re just going to start dumping water when we start dumping water. What are we also dumping with the water?
Okay,
what happens with [inaudible]? We start dumping all that water out of the loop of Henry. Yes. Potassium. So we start dumping all this water and we’re also going to start losing all of our potassium. Okay. So what is the number one thing you must check before you give lasix? Blood pressure of course. But what’s the other thing? Potassium always, always, always check your potassium before and after you give lasix. The effect on sodium is relatively small. With lasix, you will see some retention, but you typically won’t see, um,
[inaudible]
an increase in sodium. Typically our bodies will balance that out pretty well with the other mechanisms. But your body will struggle to handle the loss of potassium. So we’re going to give this lasix and lose a ton of potassium. So chances are we may have to replace that potassium with some potassium chloride. Okay. The other thing besides the same things we’ve already said, wash their blood pressure. Watch for orthostatic. What’s the other thing you need to be thinking about? You’re giving someone a diuretic, right?
Okay.
So heart rate, you can always watch with any antihypertensive, but there’s no direct effect on heart rate with with any of the ones we’ve talked about so far. There’s no direct effect on heart rate and so it’s not, that’s why the only reason I’m not putting it on the list is because it’s not directly affected. Um, fluid status. So urine output. If you have a patient, let’s say you have a patient who can’t get out of bed,
okay,
can’t get out of bed by themselves. What do you need to make sure they have before you give them a loop diuretic?
Okay,
here’s patient. You’re about to give them a diuretic. They can’t get out of bed yet. Bed pain or urinal, are they going to be able to put themselves on a bed pan?
Okay.
Maybe not. So what do we need to make sure I have a in all, if they’re a male with her female
[inaudible] okay.
Right. Make sure they have their call light guys. Make sure they can get in touch with you. Have a potty plan, whatever it is. We do not put foleys in patients just because they’re getting a diuretic. Okay. We don’t do it. Don’t do it. You can give it, you can put a foley in them for other reasons, but you don’t do it just for your convenience. Okay. I as much as we would love to. So make sure they have their call light. Make sure you have a plan. Make sure you know what the plan is. If you have a female, um, urinals, if you have the urinal section things, honestly, those just started in the last year or so. The little sponge that you put between the Lady of for a female, um, and Hook up deception. I hate them. Um, personally, but I’m a little old school and that might be why.
Um, but either way, whatever your plan is, just make sure you have a plan. So if your patient does have a fully fabulous, empty it out so you can actually check your urine if your patient doesn’t make sure they have a urinal. If your patient is going to need your help, make sure they have a call light. If your patient’s gonna need to go to the bathroom, make sure that their bed is in the lowest position and the brakes are on so that they can get up safely. So whatever it is, just make sure you know what the plan is cause I promise you they’re going to have to pee very, very soon. Okay. All right. So, um, let’s talk about really quickly Beta blockers. So what did we say the number one thing the Beta blockers do? Is it blood pressure or something else?
Yes, they’re going to cause heart rate problems. So yes, you can see some low blood pressure, but what’s the number one possible side effects of Beta blockers that’s different from your other antihypertensives Brady cardiac. Exactly. And I’m zooming through these guys because I want to just hit the highlights for each of these drugs. Brady Cardia is your number one side effect of Beta blockers as well as heart blocks. It’s a Beta blocker, right? So you can have heart blocks, okay? So make sure you’re always watching heart rate. Um, we typically don’t give Beta blockers for a heart rate less than 60, because we know we’re just going to drop it even lower, right? So Brady cardiac number one, possible side effects of Beta blockers besides that hypotension. Okay. So we’re decreasing our sympathetic nervous system activity and we’re allowing that heart rate to come down, allowing that blood pressure to come down.
Okay, so heartflow a heart block is when the, uh, so here’s my heart and I have the essay note up here and the Ab node down here, and then it goes down the bundle of his per Kinsey fibers. A heart block is any time that you lose communication somewhere along this line and it either slows things down or keeps things from moving. So we need to go essay, node, AB, node down to uh, the rest of the ventricles. If we block somewhere in there, we’re not going to get efficient pump. So anytime you give a Beta blocker, if you give it too fast, you can actually cause this electrical conduction to get blocks. And so that’s why I say a heart block is also a possibility with a Beta blocker.
Okay.
So, um, there’s one that, oh, so these are dilators. Um, biggest thing with visa dilators. So nice row, um, are nitrates of any kind and hydralazine and are the two big ones is aware, massively decreasing our afterload and we’re dilating our vessels. Two big things. Anytime we decrease our afterload and visa dilate, we get orthostatic. But the other big thing I want you to know with Vizio dilators, what happens if I [inaudible] all the blood vessels in my brain?
Okay,
what am I gonna get? What am I going to feel? If all of a sudden all of the vessels in my brain start increasing headache? Exactly. So the big side effect with Beta dilators is going to be that headache. I’ve had a patient on a nitro drip that had the worst headache ever and literally within two minutes of turning that drink off, suddenly her headache was completely gone. So just remember that anytime you give it as a dilator, you have a potential for having a patient with a headache. Okay? Same issues. Always check your blood pressure before and after. I’m always think about orthostatic if you’re messing with vasodilation. But the big thing to know is that heart headache. Okay, so there’s one more anti-hypertensive med we haven’t talked about that has nothing to do with the run an Angiotensin aldosterone system. Who knows what it is? We can think of it. Yes. Calcium channel blockers. So calcium channel blockers. What’s are a suffix for calcium channel blockers? He is now [inaudible]. So my car to pin the Pheta piece, those are your calcium channel blockers. So what affects do calcium channel blockers have? That affects my blood pressure
[inaudible]
so calcium, the calcium channels are involved in all of our neuro muscular activity. So it’s actually going to slow conduction in the heart and it’s also going to decrease some contractility. So everything that has to do, oops, contractility, sorry guys. So anything that has to do with that muscular contraction in the heart is going to be affected. So not only is it going to be slower, but it’s also going to be weaker, which sounds like a bad thing, but when you’re pumping really, really hard cause your blood pressure’s too high, decreasing that contractility, all of that is going to help to slow my heart rate and lower my blood pressure. But I will tell you just like Beta blockers, the number one thing we use calcium channel blockers for is the effect on heart rate. It’s this slow conduction. So we can give this for hypertension and we do give this for hypertension, but the number one thing we give this for is for increased heart rate for significant tachycardia. Usually things like SVT atrial fibrillation with rvr, which stands for rapid ventricular response. So if we have our heart responding super, super, super fast to that eighth fit, or if we’re in super ventricular Tachycardia and we have that really, really fast heart rate, typically we’re going to give a calcium channel blocker. Okay. So check before and after art rate always. Okay. Yes. Even irregular heart rates. We’re going to get calcium channel blockers to try to bring them down. Okay. So let me,
okay,
come back to you guys. So you guys should see me now. Hopefully if you don’t see me now. Yeah, you see me? Good. So I’m going to give you guys those links one more time. For those of you who came in a little bit later, one is for the drug card. Oh amber, you saw me the whole time. I’m sorry. Did you try logging out and back in? So one’s for the drug card
and the other one is for the rent an Angiotensin aldosterone system. And the other thing I’m going to give you is there’s actually a lesson in the pharmacology course about this system and how it works in our bodies and how it affects you. Um, so the Beta blockers slide, I’m not going to share my screen again, but uh, specifically the big thing to know is it decreases the sympathetic nervous system activity and causes Brady party as well as hypotension. Okay. Just cause sharing the screen again. So what questions can I answer for you guys? Um, about any of these drugs? I know we went over y’all feel free to jump out if you need to, but what other questions can I answer for you guys about antihypertensives.
Okay,
amber. Oh, okay, got you. That’s why you had a question. What other questions can I answer? So the big thing here guys is understand this system, understand the system, what affects what your more general effects start up here and your more specific effects as you come down. That’s why we get the more specific Mesa dilation issues with the ace inhibitors because they’re farther down the list. Okay. For Beta, Beta one is hard data to is lost. So that’s important when you’re looking at Beta blockers is these things you actually have some that are general and some that are specific. So you may have some that are, um, oh my gosh, there’s a word for it. Like Beta one specifics. You’re really only gonna affect heart rate. You might have some that are generalized that affect heart and lungs. So if we affect lungs, we’re going to actually cause bronco construction. If we bought block Beta two. So we need to be careful and asthmatic. But if you have a Beta specific drug, it’s not necessarily a big deal and an asthmatic because it’s not affecting Beta to one heart, two lungs. Good question. Any other questions? I want to let you guys go because I know Marty over, but that’s what I do cause I like talking about this stuff. All right guys. Hammers off to the dentists. Have a great time. Have a great time. All right guys. Well I hope that was helpful. Check out those links. Check out those, um, that lesson in farm. Hope that helps. Have a great day. Be Your best selves and as always, happy nursing.