all right let's discuss the Raz system or the renin Angiotensin aldosterone system really exciting stuff for you doing here guys so first I want to talk about pressures of the body right and so we have different pressures that we need within the body in order to um understand how blood flow occurs and how much blood flow we need in order for there to be exchanges metabolism right and how how all that works right so remember we talk a lot about the map or that mean arterial pressure and you should be able to Cal calculate this I want you to know that the standard pressure for that is 70 to 110 millimeters of mercury right if it's too high then you have Vaso constriction and not enough pressure to the kidneys right because it can't it's just too much pressure and they can't filter correctly if it's too low then I don't have enough pressure as well to filter so we need that nice beautiful 70 to10 um then inside the kindy we're talking about a 60 to 90 millimeter of mercury amount right so we're moving farther away from the heart it means that the map or the mean arterial pressure in the Glam maruli is going to be lower than it is as it's coming out of the heart rate we consider things like hypertension that's uncontrolled if I keep a map too high for too long and then that becomes too high of a pressure in the glami for too long which is how we end up with renal damage right chronic renal damage we can end up acutely with an acute kidney injury because our map is too low um so those kidneys they want their pressure and they want it just how they like it right so then as the pressure moves away we start to head towards the capillary bed so I want you to think like the fingers the toes right and so we're going to see a pressure around 35 millimeters of mercury by the time we hit the capillary beds then we have to now go we went from arterial now we went the capillaries and now we're coming back Venus to empty into the heart right and that emptying that pressure as you're emptying back into the heart from the superior and inferior vnea it's called the CVP or a central Venus pressure if you haven't taken 210 you haven't really talked about it too much but you will talk about it in 210 and how that can be affected and how we can monitor that so typically 2 to six millimeters of mercury is where we like to see Central Venus pressure um as that pressure is going back in the heart you don't want too much pressure on the right side of the heart right because the right side is supposed to be that low pressure system um and if you take it back to 2011 or what you will learn into a one is that once you go from fetal to newborn circulation the right side of the heart becomes the lower pressure system remember the whole thing comes down to the fact that the kidneys are sensitive they like a lot of pressure but not too much pressure right so we want to have that 60 to 90 millimeters of mercury but less than 60 and we're not profusing the kidneys and when that happens they send out this help signal right and I like to see it is like a bat signal woo woo woo we need help right and so the body says you know what I'm coming in here here I am to save the day and I'm going to activate this renin Angiotensin aldosterone system right so my blood pressure goes down right and what I have is I have angiotensinogen that's released from the liver and it helps convert Angiotensin one into Angiotensin 2 right so I have Angiotensin and renin which becomes Angiotensin one then I use my Angiotensin converting enzyme which comes from my cute little lungs here right Angiotensin converting enzyme to convert Angiotensin one and Angiotensin 2 right then my Angiotensin 2 attaches to the Angiotensin receptor sites all over the body and that's going to cause three things to kind of occur right so in the sympathetic nervous system what you're going to have is you're going to have Vaso construction so systemic Vaso constriction which is going to increase the pressure to the kidneys um and also there's a little bit of asoc constriction that occurs in the kidneys because we're kind of holding on to our volume at this point then you have ADH secretion from the posterior to pituitary gland right and its job antidiuretic hormone is going to be to hold on to sodium and water right they go together that holding on to sodium and water is going to increase that intravascular volume and help increase the blood pressure right then finally you're going to have aldosterone release from those adrenal glands that sit on top of the kidneys and those are going to further hold on to more salt more water and increase that intravascular volume that's how the Raz system works okay you may have to go back and listen to that a second time to make sure you fully understand so cute little graphic here that helps explain exactly how the RAS system works we'll talk about it or show it in in class when you actually get this lecture so but what happens when we have too much Raz right our little cute superhero got way too buff and now I'm going to cause some problems right so I have overactivation of the renin Angiotensin aldosterone system and I have Vaso constriction or excuse me I have hypertension so I can use several different medications here that we're going to talk about that can help stop that hypertension Cascade is what it's called it stops the hypertension and blocks it from from creating it right so we're not going to differentiate which one would be ordered first typically we'll see the ace inhibitor ordered first but they can be ordered for different situations on different patients right our job is to know the safety Parts involved in and understand how the medication works so we're going to talk about it here so the first one we're going to talk about is the renin Inhibitors so these are a little bit newer um they're not as common and the example of that is Alice Kieran and its job is it's going to block that conversion of angiotensinogen into Angiotensin one right so I stop the renin I inhibit the renin the wrists are kind of like the other wrists here in in this category of the Raz there's angioedema hyper calmia so things you want to teach your patient is to avoid grapefruit juice avoid taking you know with a high fat meal because that would prevent absorption proper absorption if you wanted more information on this your ATI Farm 9.0 chapter 18 and 19 is going to talk about this we're going to talk now about our ACE inh inhibitors Angiotensin converting enzyme inhibitor right so I prevent the conversion of angiotensin one to Angiotensin 2 and these are going to end in your pills right so if I stop the conversion of angiotensin one into Angiotensin 2 I don't have any visoc constriction I don't have any aldosterone or ADH release right and so I stop all of that process this is kind of our gold standard when we talk about heart failure patients the concern is as that glami pressure reduces the potassium and creatinin levels can increase the other concerns are chronic dry cough at night which becomes so unbearing that they take these patients off it or sometimes they develop spontaneous angiodema with no warning right the other concern we have just like our Alpha Drugs and some of our medications like calcium channel blockers are first dose could cause that first dose can cause orthostatic hypotension so you really got to watch these patients you really need to teach them safety involved with it um but for more again chapter 19 for this one then you have your R which is Angiotensin receptor blocker I block that receptor site and these are going to end in your sartans right so Val sartin low sartin they're going to be almost the exact same as the ACE inhibitors but kind of less side effects right so unlike the ace inhibitor there's not as much of a concern for that cough or that hyperemia that's going to be involved in it there is still still a chance of the angioedema but we're going to monitor for one of the other medications I want to talk about is spaone or Al Doone is the other way it's called and it's going to be an aldosterone antagonist so this is used a lot of times in our chronic congestive heart failure patients or our therosis patients it is a potassium sparing diuretic it can be um used with feros amide as well it's not really recommended but you will see it in certain situations um the concern is it does increase the potassium because it's not in the loop of Henley where we um exchange out potassium and then therosis patients cannot metabolize that aldosterone so this is great um to prevent them from holding on to fluid in the abdomen right it helps them get rid of that sodium and water so again chapter 19 the final one that I want to kind of talk about on this slide is the neurolysin Inhibitors right we see this a ton in practice especially with our congestive heart failure patients and there's a reason for it and I'm going to talk about it so neurolysin Inhibitors or also known as in tresto is sacubitril and Val sardin and these block the enzyme of neurolysin and Angiotensin 2 okay a study that was done on this this was actually stopped early because it was so effective at reducing cardiovascular death and heart failure complications versus enalopril which is an Ace inhibitor alone the challenge is again like a lot of these other classes you have to be careful right because potassium sparing diuretics can along with this medication can further worse in hyperkalemia some of the adverse effects that we talk about when we talk about this medication are angio EMA again hyper calmia hypotension dizziness renal failure again these are all kind of got to give you the same thing um and also really use caution with nids because they can worsen that renal function for these patients this medication is covered in your chapter 20 of your farm manual if you'd like more information on it all right you survive the Raz lecture short sweet to the point understanding how that whole hypertension Cascade Works um if you have any questions please reach out to your instructors myself always try and make myself available make an appointment let's chitchat on some things all right thanks for your time