Transcript for:
6c - Cardiovascular Drugs - Antihypertensives

this is Professor Hoffman and we're continuing our discussion on topic six or for cardiovascular drugs in Pharmacology for nursing and topic 6C we're going to look at the class of various classes of drugs that make up the anti-hypertensives so in your reading guide we're looking at learning objectives uh 6 through n so we're going to be looking at ACE inhibitors arbs beta blockers and calcium channel blockers uh and you have your uh links to your reading guides uh to reading uh content uh there so as we move into the antihypertensive the first two classes are going back to that um diagram for the ren Angiotensin aldosterone system so as we talk about what's happening and why we're using these drugs please refer back to that to make sure you're comfortable with what's happening or how they're being affected so first class we want to look at are the pills bonaza p capap Anala theil uh so if you see pill p r i l in the suffix there's a good chance you're looking at an Ace inhibitor so again in this case the acei stands for Angiotensin converting enzyme inhibitor and we want to go back and look at the actions so we're looking at blocking that Angiotensin converting enzyme from making from andot tensin one to becoming angot tensin 2 because what was one of the responses of angot tensin 2 it was to go to the vascular system and cause Vaso constriction to increase our blood pressure so if we use an Ace inhibitor we're blocking that conversion so angot tenson 2 is now not not being produced it cannot go to the vascular spaces to create that Vaso constriction so we end up with vasod dilation we're going to use it for hypertension um when we talk about um evidence-based practice in the last uh video uh for this series we'll see how it falls into place with um with national guidelines for treating hypertension especially essential hypertension uh we're also going to use it in heart failure because by decreasing that um resistance by causing that vasod dilation the heart is not going to have to pump is hard it's not going to be pumping as against as much pressure so ACE inhibitors are going to be extremely important and effective in heart failure so hypertension and heart failure because again they're causing vasod dilation by blocking the formation of angiotensin 2 so we've just blocked on that whole bottom section of the renin Angiotensin aldosterone system so some reactions with ACE inhibitors uh hypotension we're going to get vasod Dil that is going to cause a decrease in blood pressure we need to be aware of that that's our goal but we want to make sure it doesn't go too low and we end up with a hypotensive um experience for the patient uh come back to cough here in a little bit um the neutropenia granular a granular cytosis angioedema are just some changes on blood production angiodema there's going to be some interference uh with um fluid leaving the interstitial space so we're going to get some fluid built up potentially so we just need to be aware of that angio angio edema or unexplained edema that's not tied into a fluid overload is a possible side effect or adverse reaction uh with a hyperemia want you to sort of think through the process we're blocking Angiotensin 2 going to the vascular spaces so we get Vaso dilation we're also blocking it going down to the adrenal gland so we're stopping the production of aldosterone and again remember aldosterone normally we go to the kidneys and tell them to hold on to um uh sodium you hopefully remember from anatomy and physiology and pathopysiology if we hold on to sodium we're going to lose potassium normally so in this case we're blocking that action aldosterone's not going um to the kidneys at the same level as it normally does so we're not losing as much potassium as we normally would so we're running the risk now of hyper calmia again because we've blocked that part of the renan Angiotensin aldosterone system under nursing considerations is a drug that should not be used uh by patients who are pregnant so it's going to have a black box warning to make that very clear to us uh we want to monitor the blood pressure the cough that's mentioned it's a side effect it's a persistent nagging cough it's strictly tied into some individuals response to the drug they need to report that because it becomes an indication for switching from this to the next uh drug class that we're going to look at uh in terms of the angioedema or this buildup of fluid out in um the tissues we're going to watch for facial swelling or any pressure on the Airways again as a potential effect adverse reaction so the next class of drugs are the arbs the arbs or Angiotensin receptor blocker now how this differs from the one we just talked about Angiotensin 2 is still being formed we're not affecting that enzyme andot tensin 2 is in circulation but this drug class will go to the tissues that will normally be responsive to that an Angiotensin to and they block those receptor sites so these are your sens s a r t n's as part of the generic name is a good indication you're talking about an ARB again it's blocking those receptor sites so we still get that blockage of everything Downstream in the renin renin otens aldosterone system diagram we still get vasod dilation we still get Interruption of aldosterone going to the kidneys so we're s getting a lot of the same effects of the ARB of the ACE inhibitors but doing it differently we're not stopping the production of angiotensin 2 we're blocking its ability to work so again just a different approach to get to some of the same side effects however we don't have the reaction of the cough so someone who has a persistent nagging cough um from Ace inhibitor that can be an indication to switch them over to an ARB uh reactions going to be similar hypotension the angioedema the hyperkalemia um very similar to the ACE inhibitors still a blackbox warning on pregnancy still watching for the signs of the angioedema now calcium channel blockers are going to work um in both arteries and in the cardiac muscles and they block the move of calcium calcium is electrolyte that as it is shifted from extracellular to intracellular spaces um in response to stimuli is responsible for muscle contraction and also in the heart to the conduction system of the heart those specific cells so if we block that those channels so calcium cannot make that shift uh in the same way or as quickly as it would normally we're going to end up slowing conduction in the heart so that's going to slow heart rate it's also going to decrease the contractility or the strength of contractions while out in the arteries it's going to cause them to relax and dilate so what we end up doing is we decrease the workload of the Heart by saying you don't have to beat as fast or as strong and at the same time we also decrease the afterload or the resistance so the calcium channel blockers are going to be helpful at two fronts it's going to work on the heart to decrease rate and contractility so it's not working as hard but it's also going to dilate the arterials so there's less resistance so it doesn't have to push um push against so much resistance so again it's going to help heart uh the pump action it's also going to help with the pipes going to be seeing it used in hypertension with angena which is chest pain uh related cardiovascular coronary artery disease uh because of the work on conduction it's also going to be helpful with some tach cardia um disease process it's just going to slow that that conduction conduction and responsiveness down of the conduction tissue in the heart so it's going to end up slowing the heart rate down as well uh some things we need to be aware of we have someone with severe heart failure if we decrease that workload that heart rate and that Contra contractility even more we're going to increase the heart failure because we're going to make the heart even less effective so have to be very aware of that if we're dealing with a heart failure patient again we're going to see hypotension because the heart not pumping as hard we don't have as much cardiac output plus we have less resistance in the arteries conduction process is going to cause some braic cardia um may have some chance from edema just from uh fluid pooling and getting some vascular um or hydrostatic pressure um if we have conduction issues in the heart where there are some blockages this may slow it down and increase those um hepatic we're looking at um how the liver handles this excess use calcium channel blockers may cause some liver damage as well so we just want to monitor those levels so we're going to monitor blood pressure and heart rate teaching is going to involve dosing compliance make sure we're following instructions closely not overdoing it not underdoing it teach the patients how to monitor their own pulse to make sure that they're not getting too slow of a heart rate second item there is we need to have them avoid grapefruit juice in an earlier uh video we talked about an enzyme that's produced by the in the liver that is responsible for metabolizing a lot of different um things in circulation including a lot of drugs calcium channel blockers are one of those class of drugs that should normally be um metabolized and broken down so we don't go into toxicity by that enzyme grapefuit grapefruit juice blocks that enzyme so we want to avoid grapefruit juice um or have our patients avoid grapefruit juice with calcium channel blockers so we can avoid calcium channel blocker toxicity uh the next drug class is looking at the sympathetic nervous system and using adrenergic responses so we're looking at this case on the heart beta 1 receptors we want to block those these are your OLS o o in the uh generic names the Atenolol hopal La Propranolol natalo um so what they're going to do is we're going to decrease that sympathetic response so we're going to increase or decrease heart rate and decrease contractility so very similar to calcium channel blocker working from a different approach not having that same effect though on the um on the arteries and the vascular system so this is really focused on that beta 1 receptor site we're going to use this again for hypertension it's going to help slow the heart rate down in that conduction system so it's going to help with some Tachi arhythmia we're going to use it in case of of chest pain by decreasing the workloads of heart so our workload doesn't exceed our supply of oxygen so our side effects uh we're looking again hypotension braic cardia worsening heart failure because we're slowing the heart rate down and decreasing contractility which can be a danger for uh patient with heart failure with heart is already not pumping effectively uh we want to watch out for any beta 2 um potential effects particularly if we have a non-selective beta blocker so with our COPD patients we're going to see some Bronco constriction uh some CNS uh some things we've talked about earlier when we're looking at the adrenergic drugs considerations again it's slowing the heart rate so we need to teach the patients to assess uh their own heart rate we want to monitor heart rate before giving the drug to make sure it's in an acceptable range going watch blood pressure again the beta 1 site receptors also exist uh in the liver which impacts um stored glucose release so with our diabetic patients we want to monitor their glucose levels closely uh patient teaching again compliance compliance compliance I going to teach them to check their own pulse and their blood press at home and remind them do not discontinue this abruptly there's a reason to discontinue it needs to be tapered over time uh so that those are the anti-hypertensive drug classes to focus on uh for this course