NCLEX Pharmacology Class

Good morning, everyone. Can you see me? I think I can see my face on Facebook. Because I'm also streaming. I mean, yeah, I'm also sharing my Facebook. All right, we have so far we have 27 viewers right. Can you hear me? Can you hear me there in Facebook? Okay. I wanted to see some comments from you guys. Good morning here in Texas. If you can see I'm wearing a Texas shirt because I'm currently situated here in Beaumont, Texas. Just about two hours from Houston. So Houston is the capital of South East Texas. It's not used on which is the capital about you know, the whole Texas? Absolutely. It's Austin. It's the capital of one of the big cities here. In fact, the big city, the biggest city here in southeast Texas. Okay, so loud and clear. So can you also share IPass process? I guess I post processing, also sharing it to our Facebook page. And yeah, if you have a chance, kindly also share it to your social media platform. Okay. All right. So first things first, my name is Jay. I am one of the educators in IPOs online review and mentoring Academy. I am here in like I said, I'm here in Beaumont, Texas. It's been a while already. So I've been a nurse for quite that long, since 2003. So I've been a nurse for 20 years. I was in Saudi for about four years. I was in the education, not in the school, but primarily in the hospitals.

Doing the competencies, orientation and all those stuff preceptorship and some trainings for the staff, nurses they're in so one of the hospitals, they're in Saudi Arabia. I came here to the US and became a medical surgical telemetry nurse, I'm assigned in a very active floor, medical surgical, you know that very well. And yeah, it's, you know, medical surgical here in the US, is one of the major units, or specialties. And I guess it's not only in the US, I guess, for the entire world. But well, in the context of NCLEX, you will expect more questions related to medical surgical, especially cardio. That's why our topic for today is about congestive heart failure, and more particularly about your cardio pharmacology. So those medications that are usually given for a patient having congestive heart failure, by the way, talking about my background, just to continue. I'm like I said, I'm the Lead educator, of I pass online review and monitoring Academy. If you see my background, it says 11 cycle. So I'm inviting you everyone to join us on our 11th cycle. It's a three month long, or not orientation, but program. So we just had our orientation. So it's going to be three months. But I know it's going to be temporary. Okay, just sacrifice for three months. Absolutely. You can also access it for the whole year. It's sort of like an unlimited program, if you were not able to, to master it in three months, and then you can do it for another three months. If not, and then another three months. So that's, that will run for four cycles in one year. Because it's no, it's every three months. Okay, so I'm inviting you everyone to join our program. And please, we already had the figures of the percentage of passing, coming from NCSBN from April to June. So it was skyrocketing.

From about the increase is about 15 to 20%. So I will tell you guys that this is about time to take your NCLEX okay, this is about time to take your NCLEX because again, the figures are really skyrocketing. And what I'm thinking is that probably in the next two years or three years, they usually revise the exam in you know, the NCSBN for every three years. I'm expecting that they will change the difficulty level because you know what? The this is just my opinion though, because again, the figures are really high. Okay, so it's just about time to take your NCLEX this time. Okay, so for those who are here listening right now, can I see the comment if put your put your place? Where are you situated? If you're from the Philippines put there in the Philippines, okay? Or you can put more specifically your place or your locality there in the Philippines, if you're from the Middle East put it there. By the way, this is a joint project by Connetics USA nurses recruiting agency, we call it Connetics College, we're doing it every Monday, okay, including the English reviews, or lectures, and as well as other reviews or lectures or discussions related to your NGN NCLEX. Okay, so if you notice, I'm not gonna go discuss about case study today. All right, because you've been bombarded with case studies as the highlight of your next generation NCLEX. This time, I'm going to discuss to you about certain concepts, which is also common, a very common topic in your case studies in the actual exam. Okay, so let's dig in a little bit about your CHF specially or your carrier pharmacology, the most common medications. Miss Nema is from Pakistan. And Sheila is also from the Philippines. Please kindly share, if you have your Facebook platform, I guess better if you share it also in your Facebook. So we can share a lot of you know, Again, the purpose of this Connetics college is to bring you know, the information's especially, of course, in the context of your NCLEX every one of us are dreaming to come here in the US.

And this is also applicable to Australia and Canada. But I guess Connetics is primarily deploying nurses here in the US. If you also know this, guys, this is a good start on our discussion, right? So it says trust the weight, my background, trust the weight, embrace the uncertainty and enjoy the beauty of becoming okay, you will become a USRN some times there are uncertainties along the way. But it's just temporary. It's just normal in a certain process. Sometimes you fail. You fail, but it's not necessarily a failure. What do I mean by that? Because failing is a process. All right. But failure is an end. So along the way, you will have low scores in your test. But that is not the final the final is your, your actual sitting of your NCLEX Okay, so what do I What do I mean by that, you know, when you like fail in your, in your test, that means to say that you need to do more and more and more build, build, build, always have to build knowledge, practice, practice, practice. That's the secret of your NCLEX All right, so without further ado, I guess I need to who else from the Philippines Maria, I guess I have to share my screen. So we can start again and not going to use a PowerPoint here guys. Instead, I'm going to just share my drawing up. So I can do the more of your discussions today.

There, I guess you can see my screen now. So if you notice, I think Facebook is kind of live a little bit on my end. Either it's something about the signal or what if you noticed a draw heart? Right. Okay, and I'm gonna share also some PDF files, like just a little bit of video files to explain more about your CHF, the stages and as well as the medications. Okay. And then let me explain each medications that are commonly given in your CHF. Okay, it's a pretty common topic in your NCLEX not only in your, you know, case studies, but as well as other formats of your exams. Okay, so isn't it right? And again, our purpose here is not just to pass the NCLEX is for you to be able to keep up with the complexity of nursing here in the US. Okay, that's why they basically change your, your format of examination in your NCLEX because we wanted to keep up with the complexity of the disease conditions nowadays. And one of them of course, is your CHF, the bulk of your medical surgical concepts in your in your NCLEX is really big. And usually they are ask you about CHF. And mind you guys medical surgical is also the bulk of the whole NCLEX. So it's just right for us to discuss big topics like this. All right, so let's start off with your if you notice I have put in a drawing of your heart. Let's just start with the basics before you understand before you understand, you know the mechanisms why we are giving these medications. Right. So let's start off with your heart right here. This is I'm going to divide it in your area right the guy's skin gonna get a yes from you guys.

Miss Lauren is also where are you from? Where are you situated? Miss Lauren, watching from La Crosse, Sheila. To come on. So I need your participation also here because I'm going going to ask you questions as well. Okay, and I know you can also relate if you're working right now in your certain units like medical surgical or ICU. You can relate to this. Because again, these are common situations or diseases found in ICUs. Right? Yes, watching from Mindanao. We have Gemar, right. Yeah, Miguel is also from Laguna Philippines. Who else? I need one more, so I can start Come on guys. This is absolutely my start. When I do my discussions in iPass online review and mentoring Academy I usually start with a yes. So it can start. So are pleased to get your participation here. Come on. Come on. One more. One more. One more guys. Come on. Okay, so big. It's also from the Philippines. Right? The northern part of the Philippines not done the most North, but somewhere in Bhutan, right. Watching from Philippines is Lorna. So I'm going to divide this your heart right here. I'm going to I'm going to divide it into two. Right, this is your left portion. And make use of this why? Yeah, why pen? Is this your left? And this is your right. Okay. I mean, sorry, this is that's on my left? No, this is your right. And this is your left side of your heart. Let me just draw something like a heart. So right sided and left sided. You know where I'm going here, right? So I'm going to discuss to you some cardio pulmonary circulation. If you don't memorize your cardiopulmonary situation, that's very elementary, you better ask yourself, Okay, that can I make it or not? You know what I mean? Like, it's a pretty straight up advice. Because when you say like, cardio pulmonary circulation, it's very basic. If you don't really memorize that one, that means to say that you have to double time and triple time, but it doesn't mean that you cannot make it. Okay? If you're probably you're telling yourself that I can make it because, you know, I'm very you know.

Forgive me the word but I know I don't want to say the word but well, I, I need to double diamond triple time because I cannot make it because you know, this is very basically I can memorize it. No, it's not. Okay, everything is doable here. Okay, your NCLEX is very doable, though. It's, for me, it's not difficult. Okay, for everybody. For me, it's not really difficult. It's just challenging. Those are two different things, because difficulty is sort of like a subjective thing. It might be difficult for me, but for you, it's not difficult. Alright, or the other way around? Again, in general, this NCLEX is challenging. So what do I mean by that you have to double time or triple time, if you don't know the basics, for example. That's why my target is always knowing and understanding the basics, especially understanding the principles over facts. That's the secret in acing your NCLEX, especially your new generation NCLEX, or next generation and Lex, let's go back to our lecture here. Right Heart. And this is your left heart, query straight up recommendation, right or see some somebody's laughing here. I mean, that recommendation, but a thought that you have, when I memorize this one, I think I need to, I think I need to memorize this, because that's very basic. And that's a concept that you need to understand because if you understand that, everything will follow. Alright, so you need to understand those, those topics. I'm also going to discuss about cardiac output. Okay, so this is your right and talking too much. This is your right and this is your left heart. Okay, let's divide it.

So you will understand what are the etiology of your right sided heart failure at the same time, what are the symptoms of your heart failure? Quote, unquote, it theology and symptoms actually doesn't really matter that much in your CHF. Okay, because it doesn't change the manner of your management, right or left you are still going to give your Aussie might for example that does not make sense. Okay? Again if the ology doesn't really matter, it's not really an absolute matter or factor in your, in your management of your CHF. You're gonna give still your Eros in my at any time especially if your patient is having acute exacerbation or be compensated CHF or heart failure. Okay, so anatomy and physiology. All right, this is your vena cava right coming from your upper extremity and your lower extremity, right. I'm talking about here your cardiovascular system, your cardiovascular system is basically what cardiovascular system is your circulatory system. So the affected organ system here in your CHF is your cardiovascular system or also known as your circulatory system, from the word itself circulatory. The function of that is to circulate your fluids that similar dynamics to circulate your fluids and of course, your blood, your blood contains lots of nutrients and oxygen as well primarily to this to be distributed in the entire system.

For example, in your brain, a major organ that controls everything, right, including your heart, including your liver, including your lower extremities, your muscles, your GI everything, your renal, okay, so one of the most important organs to be given with cardiac output. Let's talk about output later on, let's go back to this one circulatory system or cardiovascular system from the word itself, cardio vascular, so that means to say your heart as your pump, and your vascular, which means to say your blood vessels. This is where your blood and your fluids are being circulated. And it's being just pumped out by your heart. So basically, your heart is a pump, okay? And your blood vessels are the containers. Okay, so I'm going to draw something like this. So it's an additional knowledge, I hope I can extend I don't know, because this is not an not a, an hour, you know, discussion, this is going to be alert. So this is your tag, for example, right here, that's what I'm talking about. That's the container. This is basically your circulatory system or cardiovascular system. This is how I explained to you what is a part of the vascular system. Okay, a very important concept. And right here, this is your pump. This is your attack, which contains water, okay, which contains water, it's represented by your, by your blood, okay, circulating in your blood vessel. So your bank right here, I'm going to draw like this. This is your tank, which is the container which contains blood. And right here, the arrow, just look at my arrow here. And this is your heart.

So in order for you to pump that, I'm going to draw something like a brain in here. So this is your brain, like I said, that's the most important organ or major organ to be perfused with the blood, which contains oxygen, and as well as your carbohydrates as the primary nutrients for you to make ATP, right. So this is again, let me label it again. This is your tank, which contains your fluids and that is basically your blood. Okay, so I'm gonna put an arrow, your blood, and this is your heart right here. And this is your brain, the most important organ to be to be perfused. Okay, your heart is basically your pump, your blood cannot go to your brain without the presence of your pump. Okay, you need to perfuse this brain because that's, again, that's the most important organ in your body to control everything. All right, and you have an enough container, like, you know, the size is just adequate enough to accommodate the blood in order for you to also contribute in perfusion to the major organs like your brain. So it really has to be like consistent to one another. So your heart and as well as your bank, which is your blood vessel, and at the same time, your blood, the most important is your brain. And your heart acts as a pump to effectively distribute your, your fluids, your blood into the most important organs in your body, like your brain. Okay, you have to have a good size of your bank.

When I talk I'm talking about the size I'm talking about. Either you vasodilate and you're constrained. If you base a daily good distribution, alright, but not too much, just enough basal dilation, okay, because remember, your blood vessels are semi permeable. If you also have basal constriction, that's gonna be a problem. All right. It's okay to have a good vascular resistance or constriction. Because that means to say that, you know, your blood can also go like you know, a little bit of pressure so that your blood will be propelled on distributed to the you know, to the organs, right? You need some systemic vascular resistance, you know your SVR as well to distribute your to distribute your blood. Okay, so the blood vessel, that tank can change in size, it's either your basal constrict or you basically dilate the pump can be, you know, can be deceased as well, for example, in the presence of your CHF, it may not pump well, because primarily your CHF is a pump failure, it may not pump well to distribute your or to effectively distribute your blood into major organs. Okay, in the presence of your CHF, for example. Okay, so that's how you understand these are the most important concepts. So you need to understand what is cardio vascular system, circulatory system, which will circulate your blood effectively into the entire, you know,  organ system. Alright, let's start it off. Again. I think I got stuck up here in this drawing. So this is your superior vena cava. Right, let me put it in white again.

So the blood that goes circulatory system, right, so you expect me to draw some arrows. Okay, so from New York is sweet, you know, they're in New York, probably, it's a, I think it's, no, the time is one hour advanced than here in Texas, right. Or two hours, if I'm not mistaken, dates, one hour, right. And this is another arrow from your inferior vena cava. This is SVC or superior vena cava. IVC is inferior vena cava. So the arrow from your superior vena cava, which is the blood coming from upper extremities from the head, for example, from the arms, goes right here, and this arrow from the lower extremities is your, you know, inferior vena cava, and it goes into your right atrium, this is the arrow, that's your right atrium, and it goes into your right ventricle, to pull up to prevent backflow, it has to have a certain you know, a certain portion there, which is your valve, again, to prevent backflow, that is what we call as your tricuspid valve. And it goes into your into your pulmonary artery, this is your pulmonary artery that goes into the lungs, if you notice this is blue colored, because it's, it's less oxygenated, it goes into your lungs to pick up some oxygen, I'm talking about your blood talking about your you know, your RBCs to pick up oxygen and to dump your you know, your carbon dioxide in the lungs is able to like eliminate it through the process of your exploration, right. And then you're going to inhale and then of course, your your RBCs is going to pick up some oxygen as well, and it goes back to the heart.

Okay, so this is going to the lungs can you follow to pick up oxygen and to damp eliminate your carbon dioxide, it's eliminated through the process of exploration, it's going to pick up oxygen again, like I said, from the lungs and going back to your heart, this time we are discussing about the left. Okay, it goes into your left atrium, after your left atrium, it goes to your left ventricle to prevent backflow as well to prevent backflow you also have your bicuspid valve there. Okay, we need that right? To prevent backflow. And that blood coming from your left ventricle goes into your aorta and into the entire system. If you notice, guys, this is called a dread because it's already or it has already picked up some oxygen from your, from your, from your lungs. Okay, it's already read containing oxygen and you need that together with your force your sugar into many other systems in your body. Okay, this is process. This is process guys. So let me clear it out. Let me clear it out. Come on. Let me clear it out. So I can explain more. All right. Okay, so this is your right atrium. Let me just label it and that is your right ventricle. Okay CHF, how many types of CHF Of course you will answer me how many types? We have left and right CHF right. Left CHF. Let's start it off with your right Muna and your left CHF. Right CHF, and your left CHF, those are the two things to remember right sided CHF and your left sided CHF. Okay, what do you mean by that? Remember, this is CHF congestive heart failure your heart is failing okay either failing from the right and failing from the left okay. When you say like failing from the from the right side, this one is failing for some reasons, right for example, like your Bob is not working. If the bug is not working, you know and there is like a form of backflow there. What will happen? Okay, it will absolutely increase the pressure. If the pressure is too much and then it will fail.

All right, what will happen to the arrow here? What will happen to the arrow, the arrow backflows, right? If it backflows to your vena cava as again, if your right side portion of your heart is failing, okay? What the expect pressure will build up. Okay, for example, it's because of the Bob's request, but Bob is not working okay, and back close to your vena cava and as well as your inferior vena cava. So what they expect this is talking about fluids, it will pull in your brain, it will cause too much pressure in your brain, it will cause jugular vein this thing, these are the signs and symptoms, it will also backflows to your to your inferior vena cava. It causes Osiris, okay, it causes splenomegaly, it causes hepatomegaly. It causes edema, peripheral edema, alright, so through your superior vena cava and as well as your inferior vena cava. So that's going to be a problem. So the symptoms related to your right sided heart failure is more on to your systemic related to your systemic venous circulation, because it backflows to the brain, through your superior vena cava at the same time, your inferior vena cava causing what? edema, for instance, that's the usual, you know, symptom of your symptom of your peripheral edema, symptom of your right sided heart failure. Let's go to your left side. Okay, so your left side guys left sided heart failure. In other words, the left side is failing. All right, this side here is failing. What do you expect? What do you expect if the left side portion of your heart is failing? So instead of the arrow going towards this way, it will backflow because it's already failing? Too much pressure? What happens is that it will go back to the lungs, right? It will go back to the lungs, what will happen the fluids This is talking about circulatory system, this is talking about the fluids in the tank, right, and it goes back to your lungs causing what pulling of fluids causing pulmonary edema.

This time it's not peripheral edema. This time it's pulmonary edema. So you expect that the left side portion? I mean, the left sided heart failure causes what respiratory symptoms, right respiratory symptoms, and what are the usual cause of your left side and heart failure. The usual course of your left side and heart failure is your MI. Okay, your myocardial infarction. Myocardial infarction is is a type of acute coronary syndrome. In other words, coronary means to say what coronary is the coronary artery talking about your coronary arteries supply in blood to your myocardium. Okay, and that whenever, you know, you don't take care of your coronaries, it will cause some plaque formation, and eventually it will cause some clot formation. So plaques and bloods are two different things, it could be a fatty break, and then eventually it will lead into clot formation. And what will happen, it will cause significant blockage to your coronary artery. Okay, if you notice also, if you are going to block your coronary arteries, it will bring damage to your work to your left side portion. Because your left side portion is the most demanding portion of your heart. Considering you know, the muscles are very thick. The good thing about it is that it is supplied by coronary artery which is also large, the you know, the LED particularly your left anterior descending artery is one of the largest that's the usually affected artery in your acute coronary syndrome, that may lead into myocardial infarction, where like I said, left side portion is the most demanding because the muscles are thicker. So it needs like it you know, it needs to contract it needs it needs to contract well, right because of the demand of your, of your major organs.

Okay, so it's prone to that it's prone to damage, okay, it's prone to disease conditions. So what will happen then if you have acute coronary syndrome, that's the most common cause of your failing heart. That's the most common cause of your left sided heart failure. Okay, so your MI, MI is the acute manifestation, basically of your acute coronary syndrome. It's like a spectrum. Right? It's like a spectrum. The severe form is your MI, especially of your ST elevation MI, St. elevation MI is the severe form of your myocardial infarction coming from one of the spectrums of your acute coronary syndrome. Okay. So if that is you know, if you have acute coronary syndrome or MI, it's not supplying blood to your left side portion of your heart, again, it will fail. Okay, so it will progressively fail, it will cause left sided heart failure. Now, if it's failing again, if it's failing, you know the flow of your circulation goes back to your lungs, what will happen it will pull fluids later on it will cause pulmonary edema. Okay. So again, right sided portion is more on to the systemic venous circulation. Right and Left side that is more on the same on top of other symptoms. It's more on to your left side that symptoms, right? I'm talking about your respiratory, right respiratory symptoms I told you, I'm not gonna discuss one by one the signs and symptoms and the etiology.

Okay it doesn't change the manner it doesn't really change the manner of your management. Okay or for your congestive heart failure, you're still gonna get the basic medications that are given. Okay, so CHF right sided CHF in terms of symptoms and left sided CHF, another classification is what we have systolic CHF and as well as dystonic CHF and your diastolic CHF peristaltic. CHF. Systolic CHF is basically what when you say systolic, this is something to do with pump failure. systole is contraction, so pumping. So pump failure, the installing failure is more on to your feeling failure. Feeling failure, in a sense, diastole is what relaxation because during relaxation, your heart is spilling blood to your ventricles, particularly in your left ventricles. And remember, in your left ventricles, it's already oxygenated, okay, so it has to be oxygenated. This is before you inject that to the entire circulation. So when your heart is failing, with regards to feeling, okay, what will happen? It's a feeling failure. In other words, you are not able to feel you are not able to fill in blood into your ventricles. So that will compromise your cardiac output. So let's talk about your cardiac output guys. This is what we need from your heart. So basically, this is what we need from your heart, your cardiac output, your cardiac output is, let's write it here. Records of output is equal to MIP, or your mean arterial pressure, okay, you get your mean arterial pressure from your work to diastolic blood pressure, plus one systolic blood pressure by three narrow words, this is talking about blood pressure.

Okay, your MIP your mean arterial pressure is equal to cardiac output, your cardiac output also is equal to what your heart rate, okay? It runs in one minute, of course, times your stroke volume. Okay, your stroke volume is actually a product of your end diastolic volume, which is about 120 ml. Okay? If you don't understand this much, and then you have to repeat it. Okay, repetition is the key here. And this Dalek volume is the amount of blood every end of your diastole other words, every end of your relaxation. Okay, that's about 120 ml. So whenever your heart relaxes, it will fill in the yesterday. Remember, the yesterday is about filling, it will fill in blood into your heart, into the chambers of your heart, particularly your you know your ventricles, more specifically your left ventricle, because that's the most important part. That's about 120 ML, again, and the sonic volume is the amount of blood filled in your ventricles whenever they will relax. Okay, it's very important, you know, it's something about a volume, something about your volume. Okay, so and that's Dalek volume, minus one minus or subtracted with your, your end systolic volume. So and systolic volume from the word itself systolic, which means to say what contraction. So this is the amount of blood whenever day contract or after day will contract. So this is about 50 ml. Again, this is all going to be after contraction, it means to say it's a lot lesser than your MS Dalek volume. And storage volume is the amount of blood filled in in your ventricles when they relax. And end systolic volume is the amount of blood after they contract. So that's about 50 ml. So when you total this one stroke volume is about 70 ML, okay, in a normal individual heart rate is about 70. Right? It's about 70. You know, a normal individual would have like six to 100, let's just put like 70 ml. So when you multiply your heart rate and your stroke volume, that's about 4900. Let's just say five liters of blood.

That's the total amount of blood in your body. Okay? In a normal human individual, that's about four to five. In other words, in single minute, all right, in a single minute, all your blood practically speaking all your blood, the volumes of beer that the total volume of your blood circulates into your heart and into your lungs to pick up oxygen and goes back to the heart and distributed as a perfusion to profuse your brain and all the other major organs in your body. Okay, that's your cardiac output, by the way. Okay, I would like you to tell you something about this the stroke volume, your stroke volume is affected by what? The contractility of your heart. Okay? So these are the parameters. So we just specified it using your ma SONIC VOLUME and your end systolic volume, right? So, your anesthetic volume and your end systolic volume, your stroke volume is influenced by your contractility of your heart, your heart contractility, the muscles of your heart, the myocardium. It's also influenced by what it's also influenced by your preload. Preload is basically stretching, right? Preload is basically stretching. Preload is basically start stretching, and this is talking about the volume, why it's talking about the volume, okay, because the more you stretch your heart, the more you stretch your heart, the more ventricular filling, it will go to the chambers of your heart.

Okay. And we have this what we call as your Starling slow. The longer you stretch your heart, the stronger your myocardial contraction is, okay, again, Sterling slow. So this is influenced also by Sterling slow. Well, this is getting deeper now. Sterling slow. So what do you think about your, you know, your, your knowledge now in your cardiology, so you have to assess, you have to assess your knowledge, if you really know this, because NGN next generation, and Greg's answering case studies is not just answering simple things, it's actually coming from your knowledge, connecting the dots, what is starting slow, what is preload? Something about the volume, contractility, it may seem too much, but if you know this principles, everything will follow. Okay? Everything will follow. So be you might ask me like, this is deep? No, it's not. That's why ng n. You know, I told you and the I mean, patients are getting more complex and complex, we need to keep up with the knowledge of the doctor. So we will be able to carry out what is best for our patients with complex disorders. You know what I mean? That's why you have to build up your knowledge like this. It's very important actually, this is very basic, if you think about it, okay. So contractility, we have the preload stretch, the stretching of your heart, and this is talking about Sterling slow, Sterling slow is, the longer it will relax and talking about your muscles. The harder the, or the forceful the contraction is. So when you fill in, because it relaxes, well, it fills in volume. So more volume is filled in in your ventricles. So the more volume in your when because the more blood oxygen, I mean, the more blood containing your ventricles, which is oxygenated. And when it contracts really forceful, it will bring about good or output. That makes sense. That's your preload. It's influenced by your words, startling, slow. Preload is basically stretch, the more you stretch it, the more volume of blood containing that's ventricular feeling, basically. And also, we also have your after load.

Okay, the after load. So after load is after load, this is the amount of pressure that needs to be overcome. Okay, for example, let me go back to your heart here. So this is your aorta, if you're a Yorta is disease because you have a systemic hypertension. So this will cause you to have arterial hypertension, this will cause you to have a very tense Yalta, causing lots of pressure. So you need to inject the blood into your aorta. But the aorta is disease. Okay, you have long standing hypertension, for example. So what do you what do you think will happen? It will just simply backflow, right, it will simply backflow to your to your left ventricle. So you need to overcome that. So after load is that after load is the amount of brush pressure that you need to overcome? I think I'm really running out of time and talking too much. I think I'm only allowed for one hour. Is that okay? To extend more? Because I told you earlier that I'm going to discuss, you know, more specifically about medication, I don't know, if you're learning and just say yes, and then I'll continue. Guys, are you okay? Are you okay with these kinds of concepts? All right. So, your, your stroke volume is influenced by contractility, your preload, which is the stretching of your heart, and as well as your afterload after load is the amount of pressure that your heart needs to overcome. So that amount of pressure is coming from your data. So one specific problem that increases your after alone is your arterial hypertension, because it will reflect in your aorta. It will also reflect in your heart. If you notice, it's something about circulation, everything is connected. Everything is connected. Alright, so let's continue. So these are the things. You're contractility, your preload and afterload. I'll go back to this concept later on once I discuss about your heart when you have a heart failure question is absolutely this is not any more a question? Is your heart stress? Definitely it stressed out. Okay, definitely, it's stressed out, okay. So you don't want to stress out your heart some more.

That's the principle of your medications. That's why you give medications because you don't want to stress out your heart some more. Remember, this is a chronic disorder. This is a long standing disorder. If it's a long standing disorder, it means to say that progressively, every now and then it's scaling, it's giving stress to your heart. So you don't want that you want this patient to live a little longer. So you give medications that will not stress out their heart. Okay, because if you are going to stress out your heart, this is where the complications comes in. What's the what's the complication of your CHF? The severe form of your CHF we're in your heart is not we cannot effectively distribute blood to the point that your blood pressure is too low. That is already your cardiogenic shock. cardiogenic shock is a circulatory shock, right, it's a circulatory shock, which means that your heart is not any more effectively or cannot effectively distribute blood, you know, to the entire system. And it's manifested by your work, low blood pressure, all circulatory shock, like or cardiogenic. Shock is basically low blood pressure. Okay, so it's something about your circulation circulatory system again. So again, you relate that to the functions of your heart as the pump.

Again, your cardiogenic shock is the severe form of your CHF. In fact, that's, you know, that's the really the, the culprit of your cardiogenic shock, pump failure. If you see the books, you see cardiogenic, shock, password, pump failure, what are we talking here, it's pump failure, for example, you know, pump failure, one, one type of your congestive heart failure, but it doesn't stop there, because there's also one, you know, type of heart failure. Anyway, cardiogenic shock, we don't want that. Because again, it will really give your patient and the principle of your management, the medication is to lessen the stress in your heart. If you lessen the stress in your heart, and everything will follow, you will also lessen the burden to your brain, like a burden to your symptoms or burden to your renal system on all the rest of the major organs in your body. Okay, so let's talk about where am I now? Let's talk about the medications. There you go. Let's talk about the medications. Give me the let me put it in whites. Give me the pacification of your Metoprolol and Carvedilol. Come on guys, give me the classification of your metoprolol or Kirbyville. Remember, this is all I wanted to see it from you guys from your screen. Again, now why am I discussing this in the first place? Because most of the time you will get CHF case studies. So it's just about time to go back again to our concepts. All right.

It's easier now because there's lots of lectures in your program if you have your program that talks about how to answer these studies, but the question is, how can you dig in some information to answer your case studies. That's why we're going back to our concepts Metoprolol and your car visa. These are laws. These are beta blockers day. What about your Lisinopril? What about your Lisinopril, guys, Lisinopril, Lisinopril, our ACE inhibitor? Okay. Lisinopril, our ACE inhibitor. ACE inhibitor is what you know, with the prills ACE inhibitors or angiotensin converting enzyme inhibitor. angiotensin converting enzyme messes up everything you need to prevent that from happening. I'm talking about this mechanism, that enzyme is produced by your lungs and I'll discuss that later on. So to start on, is also something to do with angiotensin, this is angiotensin receptor blocker, Angiotensin Receptor Blocker, if you notice angiotensin right. So these are the substances that are role players big role players in stressing out your heart. So we are preventing that from happening by giving inhibitors like this. Okay, so if you're awesome is what if you're awesome mind is a look diuretics. Right? It's a look diuretic. So this two here, and this one is your entire side diuretic. Okay, so look diuretics. Both of them are diuretics. I'm just going to abbreviate it. Alright, so look diuretics. Is your

Last in mind, you know that very well, especially given in the acute exacerbation of your CHF. I told you CHF is a chronic disorder that it's only waiting for an exacerbation are also known as your acute Bay compensated heart failure. When you say in medicine they compensated when you say in medicine day compensated it means to say that your heart is fully maxed out. It's losing physiologic balance, it's okay to compensate, right, it's okay to compensate. But the compensating is not good because compensating is still still you have you know, your official logic balance to keep your balance but they compensating is not good, because you are already losing your physiologic balance. In other words, if you translate it to your heart failure, your heart is already maxed out in the presence of your acute exacerbation, and as well as your acute decompensated heart failure or acute decompensated heart failure. That's why you give your awesome mind as a diuretics, you know, because you want them to eliminate excessive fluids. You want them to believe the shortness of breathing of your patient coming from what pulmonary edema, okay, so other than that, we also have some diuretics here, this is also a diuretic, Right. but more particularly, this is a an aldosterone, aldosterone blocker. Right? This is an aldosterone blocker. digoxin is a cardiac glycoside. This is a cardiac glycoside. I'm just going to write it through this way. It's a cardiac glycoside. But we don't want to give the jocks in. Because the jocks in is what the jocks in is a very toxic kind of, it's a last resort. It's a very toxic kind of medication, which will kill your kidneys later on. And if you are going cold ENCODE data and take it down to your notes, guys. And if you're going to get the jocks in as well together with your furosemide combine it together, it will bring about more toxicity to your digoxin.

Okay, more toxicity to your digoxin, it will actually, you know, three points or two folds will bring toxicity to your, to your kidneys primarily. So he's a cardiac glycosides. Okay, so who made and dopamine these are dobutamine these are to increase your blood pressure, especially given for a patient having cardiogenic shock already. Again, go genic shock is course low blood pressure we're in you want this patient to have increased blood pressure. So give the glutamine or dopamine, especially in the last stages of your heart failure. cardiogenic shock is usually in the last stages of your heart failure, especially if you don't take care of it. Using these medications and many other you know, interventions. Okay, hydrazine is an antihypertensive, I'm just going to put here in your dobutamine and dopamine, as you know, to increase your blood pressure I'm going to include here because they always going to ask you about this your meal renewal. Okay, these are absolutely different, you know, different medications, right. But all for the purpose of what different medications in terms of its mode of action, but its specific mode of action, but definitely it will bring about increasing your blood pressure in the presence of your cardiogenic shock hydrolyzing isosorbide. And, yeah, hydrogen isosorbide these are to decrease your blood pressure. These are anti hypertensive medication. So it will bring about low blood pressure.

Because you know, Hypertension is we don't want hypertension, we don't want our afterload Okay, so it will somehow decrease the amount will definitely or primarily decrease your afterload. Okay, so you want stress your heart, so decrease after load and then you will not stress your heart? Let's start it off with your okay. Are you ready with my with mine? Some you know, physiology here? Let's go back to our official ology. Why are you giving your beta blockers first? Why are you giving your beta blockers first? Now, in your heart failure, decrease cardiac output or increase cardiac output Come on? Is it increased cardiac output or decreased cardiac output? Come on, guys, I want to see it from your chat room. In your heart failure. Remember, what you want from your heart is a cardiac output in a normal individual, but if you have heart failure, what they expect decrease cardiac output. Am I right? Come on. I want to see your answers. Come on. I want to see your answers. I want to see your answers decreased cardiac output. Alright, so decrease cardiac output. Now, if you have decreased cardiac output in your kidneys, let's start off with your kidneys.

If you have decreased cardiac output in your kidneys, let me throw a little bit about kidney and the kidney. There you go. That's your kidneys guys. And then it's your bladder and then you urinate. Right? So these are your kidneys. If there is decreased cardiac output In your kidneys, it's a normal response for your kidneys to produce what training, right? ran in coming from your work your juxtaglomerular apparatus is composed of three different cells, your granular cells, Lacy cells, and as well as your macula densa, I'm not going to dwell about that your juxtaglomerular apparatus this is actually you know, an apparatus, ourselves in your, in your, in your kidneys that is very sensitive to low perfusion or low cardiac output. All right. So in other words, this is stimulated, so random is produced, this is a substance that will circulate, it will go to your liver, here comes the liver. There we go, that's the liver, it will go to your liver and we will tell your liver Hey, liver, can you make a substance right? Can you make a substance that will bring about increase in your cardiac output or increase in your blood pressure? So basically, if you have decreased cardiac output as well, you also have decreased blood pressure. Right? So, you know, collectively, you know, decreased cardiac output renin will tell your liver, can you make certain substance, alright, to bring about increase in your cardiac output or increase, you know, blood pressure specifically. Alright, so this is your angiotensinogen. Okay, so the labor this time we'll produce.

Okay, and Joe means what blood vessel? Oh, Jen is a complex form, so it needs to break down into a form of angiotensin one. Okay, that's your angiotensin one, you go angiotensin one. Angiotensin one. All right. I like talking about beta blocker here. This time around. And this time, I'm not gonna talk about beta blocker. Later on. I'm not about beta blocker. I'm talking about the ace. So this is basically your rough system. Okay, this is your system, you're running and you're tensing your renin angiotensin aldosterone system. So we're done with your Rehman, which being produced by your, your kidneys, it will circulate in your blood, it goes into the liver, to break down your angiotensinogen and you can see nogen is a complex form, it needs to be broken down into angiotensin one in the presence of your work in the presence of your what enzyme is that in the presence of your ace, angiotensin converting enzyme right where it's it will convert your angiotensin me, not yet. So angiotensin is broken down first to your angiotensin one, angiotensin one is to increase your blood pressure. However, this is not portent, alright, it will increase your blood pressure however, it is not for them, so it needs to be broken down. There you go, it needs to be broken down into angiotensin two. Angiotensin two as a potent, this is a menace.

This is a bad boy here, okay, it will increase your blood pressure too much, in other words is a very potent vasoconstrictor is a very potent substance that will cause bring about you know, increase in your blood pressure. This is converted your angiotensin one is converted from you know from angiotensin one into angiotensin two in order to become a very potent substance or hormone. So through your ace, your ACE is produced in your lungs, I'm going to do something like alarm here mean lungs, right? So let me let me review first renin is produced by your kidneys, it will circulate, it will go through your liver, hey liver, can you break down your angiotensinogen so the liver will break down your angiotensinogen into you know into a simple form, which is angiotensin one. Angiotensin one increases your blood pressure, increased cardiac output. However, it's not really potent, you need to have a certain chemical or substance that really brings out increasing your blood pressure, but we need to have a substance or an enzyme and that is your ace. Okay, your ace. So angiotensin converting enzyme from one to two to now A is a very potent substance that will increase your blood pressure. Okay, there are three things that will happen here. Your angiotensin two will stimulate your what is what's going to happen here in relation to what I'm discussing. Okay, earlier. So this is your blood vessel. You go this is your blood vessel right here. It will stimulate your blood vessel. Okay, remember these are substances, this is going to bind to a specific receptor. Okay specific receptor, which is what we call as your angiotensin two receptors. Okay, in order to produce an effect. So what's the effect on this one based on selection increase in your vascular resistance, increase in your vascular resistance that means to say that it causes, you know, constriction, it causes constriction.

So what will happen? If your blood vessels are constricted? Let's go back to your heart here. If let's go back to your afterload there. So if it constricts, does that increase your afterload? Yes, it will definitely increase your afterload. So does that stress out your heart? Yes, it will stress out your heart. Okay, it will stress out your heart again. And your turns into when it binds to specific receptors in your blood vessels, it will cause what it will cause vasoconstriction increase in your vascular resistance. This is you know, this is basically the purpose of your angiotensin mechanism to increase your blood pressure vasoconstriction. Does that increase your afterload? Yes. Does that stretch your heart? Yes. Is that what you're wanting to have what you want to happen to a CHF patient? You don't want that stress. That's why you need to give a medication to block this. Okay, other than that angiotensin two will cause what it will stimulate. It will also stimulate your adrenal glands. Okay, to work to increase the levels of your work, increase the levels of your aldosterone, aldosterone, okay. Increase the levels of your aldosterone. So increase the levels of aldosterone, what's the effect of your aldosterone? increase retention of your sodium at the same time your water increased sodium retention and water as well. So what do we mean by that? What's the implication increase in your blood pressure?

Okay, increasing the blood pressure. Does that stress out your heart or afterload? The same thing? Yeah. Does that stress out your heart when you know, when you retain your sodium? Of course, that's increased volume. Does that affect your preload? Yes, it will affect your preload. Does that stress out your heart? Yes, it will stress out your heart. Okay. So that's, yeah, that's the adrenal C, we have angiotensin, I mean, renin, we have angiotensin and lastly, your aldosterone. Does that also affect your brain? Yeah, it also affects your brain, by what? By stimulating to increase the levels of your antidiuretic hormone when you like, you know, release your antidiuretic hormone as well, it will also retain fluids in your kidneys. So that's another, you know, effect of your angiotensin. Okay. So in relation to your medications, guys, in relation to your medication, you'll give what you give your angiotensin blocker right here. Okay, we have angiotensin blocker your angiotensin enzyme inhibitors, sorry. So we have your ace inhibitor, and as well as your what you blocked this ace from converting your angiotensin one to angiotensin two. At the same time, you're also blocking your what your angiotensin two using your arm. So does that help? Yes, you're blocked this mechanism in order for you to de stress your heart. You don't want to stress your heart some more because again, you have a heart failure. Okay, so let me talk about your beta blockers this time. Does that make sense? Okay, so I told you, this mechanism here, the RAS mechanism is really like has a role in stressing out your heart some more, that's why you gave your angiotensin converting enzyme inhibitor and as well as your Angiotensin Receptor Blocker, okay, because you want them to block this mechanism in order for you to de stress your heart. Let's talk about your beta blockers. Okay, this is your kidneys, right. So this time, I'm going to draw something like a brain. Okay? This is your brain right here. Okay.

That's your brain. Sorry for my drawing, guys. So your brain innervates your heart. This is your heart right here. When you say innervates your heart it will stimulate your heart to do something, right. Okay, this is your heart. And so this is your brain innervating your heart and it causes increase in your heart rate and talking about the sympathetic nervous system. And it also you know, innervates your heart muscles to increase your contractility. This is what the sympathetic nervous system is doing. Okay. So, here in decreased cardiac output guys in decreased cardiac output because of CHF, it will also stimulate your heart Hey, I'm so tired. Can you do something for me to like, you know, really? Max out what I'm what I usually do. So it will simulate your heart I mean your brain to innervate your heart Some more again to effectively function normally. Alright, but the thing is you cannot correct the problem right because you already have an existing CHF. It's like a vicious cycle. It's like a vicious cycle really. Okay, so increase heart rate this is your heart I'm going to make it in red increase heart rate increase conductivity, increase heart rate is basically what? Coronado tropic effect Okay. Increase contractility is basically I know tropic effect.

Okay. So how do they how was what's the mechanism here, they will release you know, certain substances neurotransmitters, which we call us your norepinephrine to bind into your beta one receptors, okay to bind into your beta one receptors. Okay. So if it binds to your beta receptors, it increases the heart rate. Okay, chronotropic effect, and it will also increase your contractility. Again, in your CHF, it decreases your cardiac output, okay, it decreases your cardiac output to the point that it will stimulate your brain to do something about it. And it will innovate it will stimulate your heart to increase heart rate and to increase contractility. Right? By or through your work through your norepinephrine binding through your beta one receptors, that's chronotropic effect at the same time in your muscles, contractility. That's your inotropic effect, norepinephrine will bind to your beta one receptors to cause a nootropic effect. Right? Because, again, you want your heart to function normally. Okay, so what's the role of your beta blockers here? I'm going to make it in yellow. Okay, what's the role of your beta blockers here? Your beta blockers like are all right, your Metoprolol will block this thing. Okay, I'm gonna block you. So your Metoprolol decreases your heart rate, it relaxes your heart, it de stresses your heart. That's why it's given in your CHF. Did you get the principal here, and it decreased decreases the contractility as well. All right, it decreases your conductivity. In other words, it decreases your nootropic effect.

Okay, it decreases your inotropic effects, again, beta blockers, it will block the binding of your norepinephrine and your beta one receptors to decrease your heart rate and to decrease your inotropic effect your contract Pvt. So it basically relaxes your heart. Okay, it basically relaxes your heart. And one thing is your Metoprolol your Metoprolol that's why you see your patient. That's why you see your patient being given with maypop prologue. Okay, your patient is being given with Metoprolol, your beta blocker. Okay, let's talk about your Carvedilol as well. Carvedilol, what's the difference versus your Metoprolol The good thing about your carburetor is that it will also increase your heart rate, I mean, decrease your heart rate by causing negative chronotropic effect just like your Metoprolol and decreases conductivity as well. The good thing about your Metoprolol as well is that if your brain is, you know, going back to this mechanism, it will also work it will also stimulate your blood vessels. All right, to increase its vascular resistance, systemic vascular resistance, okay, in the presence of your local output into your blood vessels, not only in your heart, by binding to your alpha receptors, Alpha One receptors, okay, Alpha One receptors this time again, this is norepinephrine, and it binds your alpha one receptors to increase your vascular resistance. The good thing about our Carvedilol is that it doesn't only block your beta one, it also blocks your alpha one. So it's like an alpha one receptor blocker at the same time, primarily, your beta one blocker. Okay. And it's not only that it actually also blocks your beta two in your lungs, you know your video, that's why it can trigger asthma as well, in the context of NCLEX, they might ask you about that, because karbi the Lord Metoprolol is good, in a sense, be the one because it's just selected to your beta one.

But Carvedilol will block your beta one will block your alpha one and will also block your alpha I mean your beta two. That's why it can trigger asthma as well. In other words, it's non selective. It's an unselected kind of beta blocker, because we have to write your cardio selective and your non cardio selective cardio selective is you know only to your heart and non cardio selective is not only your heart, but at the same time your lungs. Okay? So that's the difference between your Carvedilol and your Metoprolol. Alright, so again, all for the purpose of distressing your heart because it's already stressed out in the presence of your of your heart failure. Okay, I guess I'm gonna discuss some more because this is a lot to discuss. To give you more information or a more detailed explanation. I'm just gonna finish it with your furosemide because this is the usual thing that we are giving right? Especially in your acute exacerbation. Okay, so CHF, right CHF, I'm going to begin it here again, in your CHF. I told you earlier, if you have CHF, it's a chronic disorder. It's just waiting for acute exacerbation or you know, acute decompensated heart failure. Okay, acute decompensated heart failure. So in other words from chronic to become acute to becoming acute, we don't want acute exacerbation. acute exacerbation is manifested by what shortness of breathing, right manifested by shortness of breathing. They are always going to ask you about complications. Because this is where you exercise your clinical reasoning, your critical thinking your clinical judgment overall. Okay, so NCLEX is always going to ask you about medications like furosemide because again, you're also my is the gold standard of CHF, especially if they have acute exacerbation. Okay. So let's hear it from your furosemide Well, it's very easy if you're also might as a kind of medication that will you know, that will eliminate course, you know, this very well that will eliminate excessive fluids that causes you to have pulmonary edema, so you're eliminating excess fluid so that your patient will be will be eased from shortness of breathing from acute exacerbation, okay? In acute exacerbation, let me write it here guys.

In acute exacerbation of your CHF or acute decompensated heart failure. So what you will do is this mnemonics, so this will help you, okay, this is what you do if you have acute exacerbation of your CHF, what's letter L? What's letter L? This is basically your lasix is the brand name of your furosemide. What is letter M? Morphine. Okay, what is morphine, it's a narcotics, right? It's a narcotics that will bring about relaxation of your patient because you don't want to do this. I mean, you don't want to stress out your heart somewhere, that you're morphine. Alright. So it will bring about some form of a relaxation kind of medication as a narcotic and will bring about comfort to your patient that our n is what nitrates are okay. Nitrates is basically your word nitrates is basically this one here. If you notice I put some isosorbide nitrates or die nitrates, that's your letter N, which is your nitrates. Nitrates is a base of the liter if your base will dilate your blood vessel that will bring about less after load. If it's less after load that means to say what your heart is not, it's not stressed that much. So that's your nitrates. It's a base of the liter is specifically a vino dilator. Right It can also cause like arterial division, but primarily it can cause vasodilation. Okay, it works more on to the venous end of your blood vessel. letter O stands for oxygen. Remember, this is a respiratory problem. If you have an acute exacerbation, in other words, it's really a priority. So you give oxygen and lastly positioning.

Your position your position your patient in an upright position. Okay? you position your patient in an upright position to ease their breathing difficulty during acute exacerbation because again, this is a priority in your the management of your acute exacerbation of your CHF upright position. Okay, if your patient for example, after how many days responding to many medications, admitted in hospital responding to medications, and if they are able to lie down flat, that's a good sign. It means to say you don't need to, you know, instruct them to upright position. All right to eat their briefing. In other words, they are ready to go because they're just lying flat. So that's one side even if you don't really like you know, dig into the interview a patient as long as you see them lying flat from coming from an acute exacerbation, I guess this patient can go home. That's the deciding factor there. Of course, it's hard, it has to be evaluated using your X rays using your chest X rays to see that there is no pooling of fluids or pulmonary edema in their lungs. Right? So that's one way to validate it. Again, this is your mnemonics in your in your acute exacerbation of your CHF. Okay. So, questions so far questions so far? So let me see. What do I need to discuss here? You're also mine is already there. I've already discussed about Ross in mind your amygdala zone and as well as your hydrocortisone, these are diuretics. These are diuretics that are opposite to your philosophy, but both of them eliminates excessive fluids. What's the good thing about your philosophy is that furosemide is or it can act really quick.

So it will bring about ease in your difficult everything related to your pulmonary edema, left sided heart failure, hydro prioritize side and your Matala zone or retire side diuretics. Okay, which apps a little slower than your Velocci mine needs a very effective medication as well. The difference between the two of them is that you're awesome I will waste your potassium so be careful using your few Nasima because it will cause you know hypokalemia because it's a potassium wasting diuretics and as you know hydrochloric acid in your medulla and also has Yeah, they are also potassium wasting diuretics. The difference between furosemide hepatitis I'm taller zone between your spinal cord and a parent known is that Spironolactone and your parent on our potassium sparing diuretic so be careful in giving to a patient having hyperkalemia again, pure or semi hydrochloride Matala zone are potassium wasting diuretics. Okay, so be careful about this because it will bring about hypokalemia and spironolactone is a potassium sparing diuretics just like your eplerenone. So be careful if you have hyperkalemia. Remember, high pour hyperkalemia. As long as it's potassium imbalance, it will cause you to have cardiac arrhythmias. Okay, digoxin. What did they tell you? Tell you about the Jackson digoxin is not usually given as a primary defense to your you know, to your heart failure. It's usually given as a last resort, because it's very toxic to your kidneys.

Check for your heart rate, of course, because it has a negative chronotropic effect. Let's just go by the specifics here, especially in your nursing intervention, negative growth tropic effect, in other words, it decreases your heart rate. Okay, the good thing about the digoxin is that it increases your inotropic effect, even if it decreases your chronotropic effect. So negative chronotropic effect and positive inotropic effect. Other words, it increases the contractility of your heart. Okay. So, digoxin, again, you also check for your heart rate, because it will bring down your heart rate, do not give it if it's less than 60. And you also check for hypokalemia because hypokalemia can also trigger toxicity of your digoxin. Okay, so again, hypokalemia can trigger toxicity of your digoxin. Okay. And the Jackson is also not, you also check for your renal, you know, panel, your bun and creatinine. So, check also for your bun, and creatinine. Okay, check for bun and creatinine as well. Apart from checking your heart rate, check also your potassium level, because hypokalemia is or can exacerbate your digoxin toxicity, check for the urine creatinine because it's very toxic to your kidneys. So it's a last resort. And as well as check for your heart rate, because it has a negative chronotropic effect, though it has a negative ground up effect, but it has a positive inotropic effect that will forcefully you know, increase the construct contraction of your heart. And I told you earlier digoxin is not usually given with grace in mind. So you also check for the impact of your acima because it can increase the toxicity of your digoxin as well into two folds or three folds, according to many studies. Okay, your dobutamine and your dopamine and milrinone is given in the last stages of your CHF. I haven't talked about that earlier. But well, the beauty main dopamine and melatonin is given to increase your blood pressure in the presence of your cardiogenic shock. In other words, your VPS you know, your heart is not really producing, you know, its normal function. It's really Mark supermax out, it's dying already. So when you increase your blood pressure in your cardiogenic shock by giving dobutamine dopamine or milrinone these are the drug of choices that we are giving.

Okay, so hydrolyzing And what else what else are the other medications I need to discuss your analysis and you I just want to be dynamic. i The other scene is a is blood pressure lowering medication. Okay, so it causes vasodilation, especially on the arterial end, because you don't want to stress out your heart again, by increasing your afterload the same thing as your isosorbide dinitrate. These are blood pressure medications that decreases your afterload thereby distressing your heart. If you notice I'm always talking about the stress in your heart in the presence of heart failure. This all medications or medications given to the stress your heart, okay, and I dwell more on to your RAS mechanism, your renin angiotensin aldosterone mechanism because that's a major role player in stressing your heart. So we wanted to block your angiotensin converting enzyme at the same time, your, your, your angiotensin two from, you know, from, from dominantly causing an effects. Alright, so what's that, like? Fire alarm or something? Anyway, so this is your, this is your topic for today. So I guess you know, I can expand it some more by discussing this mechanism. This is quite important because this is where you build your knowledge. I told you earlier, it's a pretty straight up kind of advice that if you see yourself that you don't know what a beta blocker is, kind of think. Okay, I mean, yeah, please kindly think that okay, I need to double time. Okay, I need to double time because I need to understand what is a beta blocker? This is very much pharmacology. Okay. Why do I need to give beta blockers because I don't want to stress my heart in the presence of heart failure.

Okay, why do I give Lisinopril is an example of your ace inhibitor dose with pills? Because I don't want this wrasse mechanism to jump my you know, to jack up my CHF. It's messing around. So I wanted to block this ace kind of enzyme in order for me to block you know, the this mechanism, the same thing as with your, your arms, your Angiotensin Receptor Blocker. Well, what's the difference between the two? Well, if your patient cannot tolerate your ACE inhibitors, and then you know, kindly give your Angiotensin Receptor Blocker. In sometimes they're going to ask you in your NCLEX that, you know, what's the precaution when you give your ACE inhibitors and your ARVs both of the medications can cause hyperkalemia. So don't give it to a patient with hyperkalemia because it will increase more of your you know your potassium. Okay, again, your ACE inhibitors and your ARBs will increase your potassium. In other words, be cautious. Check your potassium before giving your ACE inhibitors. It's a very powerful medication, including your arms, because both of them will increase your potassium. So again, hypokalemia hyperkalemia, you know, imbalances can cause cardiac arrhythmias automatic, if you see that your patient must be hooked or attached to a cardiac monitor whatever mitigations that are given, for example, the jocks in, you know, in relation in association with your potassium, you always have to hook your patient on a cardiac monitor, hyper hyperkalemia Okay, so anything else? So I guess I will see you next month for another topic.

So I can probably like bring you some, you know, some more case studies. I mean, some more of this. Discussions like pharmacology, I guess. And, yeah. So I know you're already good in answering case studies. Okay. That's why I brought to this one this topic, because this is what we need in answering any questions, case studies or not, this is what we need in answering, especially case studies, because case studies are all about connecting the dots. And those dots are knowledge. Why are you giving this for a patient IV CHF? And what's the mechanism? Why you are giving this? You know, this medication? And of course, what are the nursing responsibilities? Those are, those are a part of that. That's alright, so I know you feel tired while you're preparing. Give me last one minute. I know you're tired while you are preparing in your index, because it's going to be a challenging one. It's gonna be a challenging one. But with hard work. I know you can make it sometimes you cry, but your cry is absolutely not only for yourself, because if it's only for yourself, that's too selfish. You know, that's, that's a sign of weakness. But if you cry for your family, that's a sign of strength. Okay? And if you feel like you're really tired, guys, so you know, that means to say that you're doing something that means to say that you are doing something, okay? And you're doing it for your family as well. Don't stop until you get, you know, proud to yourself. Don't stop until you get this NCLEX sacrifice is just a temporary thing. Right? When you have your license, it's a permanent thing. No one's gonna take that away from you. God bless everyone. That's the way embrace the uncertainty. Enjoy the beauty of becoming a USRN. See you next month. Okay. Thank you. Thank you. Thank you guys.