Understanding Cardiovascular Drug Treatments

Female 1: Drugs Affecting the Cardiovascular and Hematological System. Cardiac Cycle. The timeframe is from the beginning of one heartbeat to the beginning of another. In systole, the ventricles contract. We have increased pressure that occurs from the ventricular contraction and this causes the mitral and the tricuspid valves to shut. The aortic and the pulmonic valves open and this allows ejection of the blood into the aorta and the pulmonary artery. During diastole, the ventricles relax. This allows the mitral and the tricuspid valves to open and allows blood to flow into the atria. Atrial contraction occurs at the end of diastole and pushes the blood from the atria into the ventricles. Unoxygenated blood is returned via the superior and inferior vena cava to the right atrium, or it is moved then through the cycle to the right ventricle. Blood leaves the right ventricle via the pulmonary artery to be re-oxygenated in the lungs. The oxygenated blood returns to the left atrium via the pulmonary veins and then moves into the left ventricle. Blood is ejected from the left ventricle to the body via the aorta. The stroke volume is the amount of blood that leaves the left ventricle with each contraction. This is normally about 75 milliliters. Now, it is dependent upon several factors. First of all is the preload. And this is the passive stretching force on the ventricular muscle that is created by the amount of blood that has filled the heart. And so, it's the amount of blood that is there at the end of diastole. The preload is affected also by several things. And so, we look at the venous return. And this is the amount of blood that is returned from the periphery to the heart. If there's not enough blood returning, then you're going to have a lower preload. If the atrial contractility also will affect your preload. And so, the ability of the atria to contract forcefully enough to move the blood from the atria into the ventricles will also affect this preload because otherwise, you're going to have stasis. And then, the amount of blood left in the ventricle also affects our preload. Think about somebody that has actual failure and they don't have the ability to move the blood out into the central circulation. If that blood is actually staying in the ventricles and the atria have good contractility and move that blood into the ventricles, you're going to have that buildup and increased stretching of the ventricular muscle. Some other things that actually will affect our stroke volume, the contractility. This is the force that the ventricular squeezing so that the ventricle is able to achieve and eject the blood into the systemic circulation. If you have a very weak muscle or a damaged muscle that say somebody had a myocardial infarction. And instead of replacing that with that elastic muscular strength, they replace it with scar tissue. They are going to have decreased stability and decreased contractility. Some of the other things that can also affect our stroke volume. This is the concentration of catecholamines in the heart. The more catecholamines, the greater the contractility. And so, somebody that has a lot of that force, you will see more force of contraction. The last thing we want to discuss is the afterload. The afterload is the resistance against which the left ventricle must eject its blood. And so, it's the resistance that it has to overcome. When we look at this I always have compared it to the straw and a garden hose. If you had a straw, a drinking straw next to a garden hose and you looked at the diameter, there's an obvious difference there. Think if you were trying to force fluid into either of those structures, it would be a lot easier to do it in the hose because it's more open, more dilated. And so, when we look at afterload, if we have somebody that has a constricted or smaller diameter of a vessel, it is going to require a lot more force and workload, and therefore, the heart may not be able to eject that blood. And so, when we look at the peripheral resistance, this is a key factor. So the cardiac output is the volume of blood that leaves the left ventricle in 1 minute. The stroke volume, which remember we said is around 75 milliliters per stroke times the heart rate. And so, when we're looking at the cardiac output, the body likes a set amount, let's just say around 2.5 to 3 liters. So if you have somebody that has a poor stroke volume due to damage to the heart or decreased volume, then the way that the body will compensate is by increasing the heart rate. So if you have a low stroke volume, then the heart rate is going to increase. If they've got a lower heart rate, then usually we're going to see a heart that is able to have a larger stroke volume. And so, what we look at is these factors are going to be going up and down so that the body ends up with a good cardiac output that is sufficient to meet its oxygen needs. It's just of heart failure. Several compensatory mechanisms attempt to maintain cardiac output and meet the body's systemic demands. This causes a chronic activation of the sympathetic nervous system. So with all of the changes involved with the sympathetic nervous system and that we can start to see changes in myocardial hypertrophy and myocardial hypercontractility. The increased sympathetic drive also results in the activation of the renin-angiotensin-aldosterone system, the RAAS system, everybody's favorite. This results in systemic vasoconstriction and sodium retention. So let's break this down a little bit more. So when we have decreased cardiac output and systemic pressure, renin is released as again the kidneys are not getting adequately perfused. Now, renin is the enzyme produced in the kidneys in response to impaired blood flow and tissue perfusion. The release of the renin acts on angiotensinogen and this is from the liver and it forms angiotensin I. Now, this next part I really want you to listen to because when we talk about drugs, this is where we're interacting. The vascular endothelium, particularly in the lungs, has the enzyme that is produced, the angiotensin-converting enzyme. So this is where ACEs actually work. And this production of this enzyme stimulates the production of the angiotensin II. Now, angiotensin II is a powerful vasoconstrictor. And it actually will trigger a cascade of effects that are aimed at restoring blood flow to the vital organs and enhancing tissue perfusion. So number one, it acts on the adrenal cortex to release aldosterone. Now, this release of aldosterone acts on the kidneys to increase sodium retention, and with the sodium comes the fluid. So now we have increased fluid being retained in the vascular system. And our sick heart wasn't doing well as it was. Number two, it stimulates the release of vasopressin, and this is the antidiuretic hormone. And this causes increased retention of fluid by the kidneys. It also stimulates cardiac hypertrophy and this is that adding of extra muscle. And then, the last thing is it causes arterial vasoconstriction. The problem is that this increases the resistance referred to as the afterload that that left ventricle is having to pump again, making it even more ineffective. So it increases the filling pressures inside the heart and it increases the stress on the heart because now we've got increased stretch of the muscle. When we have this increased stretch in the cardiac tissue, this stimulates the release of the natriuretic peptides. The response that the body follows is to increase sodium excretion -- -- by the kidneys, increased diuresis, direct vasodilation, and it increases glomerular filtration rate. It also reduces the renin production from the kidneys. So all of these things are aimed at correcting or at least to assist in correcting this fluid overload caused by this sympathetic innervation that took place. Previous slide. Heart failure is a condition that results in low cardiac output because the heart is unable to pump sufficient blood to meet the metabolic demands of the body. The normal compensatory mechanisms of the body that cause fluid retention result in increased preload. While the vasoconstrictive actions of angiotensin do increase the afterload. The overall interaction can cause decreased cardiac output from the left ventricle. This results in an increased heart rate to ensure perfusion. Common risk factors are coronary artery disease and hypertension, and these are major causes. We also see people developing heart failure following myocardial insults. Drug therapy for congestive heart failure aims to alter one or more of the factors affecting the heart to improve overall cardiac function. It's a common list of medications that can be utilized in the care of individuals with heart failure. Please do not think that the way they are listed is the order in which they would necessarily be utilized. It is just an easy way for you to remember. So let's go through these. ACE inhibitors and I've also added the ARBs there. Again, will interrupt the RAAS system and stop that production of the ACE enzyme and going from angiotensin I to angiotensin II. So it interrupts that. It also decreases the secretion or the production of the aldosterone, which lessens the fluid and sodium retention. Beta-blockers. Beta-blockers can be utilized though very cautiously as they decrease the overall requirements for oxygen. They also decrease the overall workload of the heart. Calcium channel blockers again can be utilized to slow and decrease the force of contraction. Digoxin is a cardiac glycoside. Now, I am going to tell you upfront that this is an older medication. We are still learning it as you will still frequently see it utilized and frequently see it on your NCLEX. This medication, while it does have some very inherent risk associated with it does increase the overall force of the myocardial contraction. And so, it can help people with a very poor ejection fraction have a better outflow of blood. And then diuretics. These can be utilized by care providers to decrease the amount of fluid retention. When we talk about treating somebody that has congestive heart failure or heart failure, our goal is going to be to decrease that workload of the heart while increasing circulation. So we want to unload some of that excess fluid. We want to sit the patient upright because that improves their ability to have that respiratory function. And then, there's a lot of the medications which we are going to be discussing. Nitrates you've previously discussed. But think about the effect they would have on the body and the heart as they vasodilate. They allow the heart to pump and circulate that blood with decreased effort. Diuretics. We're going to be talking about Lasix here shortly. ACE inhibitors and digoxin. Now, if we're trying to unload fluid using medications such as furosemide or Lasix, we need to decrease their intake as well. The whole goal is we're going to try and decrease the afterload or that peripheral resistance that the heart is having to pump against. And so, some of the other things that can decrease that are things like sodium restriction because it will decrease the amount of fluid that the body is holding onto. And then, we want to go ahead and test things like digoxin levels and potassium levels. So the way to remember it is the pneumonic unload fast. ACE inhibitors or angiotensin-converting enzyme inhibitors are used in treatment of hypertension as well as in heart failure. Now, we are going to actually use captopril or Capoten as our prototype though I do want to make you aware that enalapril or Vasotec may be more commonly seen if it is only being used for heart failure and not hypertension as well. The pharmacodynamics of captopril is that it inhibits the angiotensin-converting enzyme. This angiotensin-converting enzyme changes the inactive angiotensin I to active angiotensin II. So angiotensin II is a very potent vasoconstrictor. With decreased angiotensin II, we lose this vasoconstriction. And so, we actually have relaxation of the peripheral vasculature. Decreases in angiotensin II also result in decreased aldosterone. Now, aldosterone actually is responsible for increasing retention of sodium and water and this increases the circulating volume. If the aldosterone is decreased or blocked, it's going to prevent that sodium and water retention. And so, we will have decreased peripheral resistance and decreased circulating volume. Now, when you think of somebody that has heart failure, all of these things are going to assist. The cardiac output is actually going to be increased without increasing the heart rate and the peripheral resistance is going to be lowered without affecting this. It also will increase renal blood flow, but it doesn't have any effect of a glomerular filtration rate. Now, one thing to be aware of is that the potassium may be slightly increased. And this is actually a result of the decreased aldosterone. Remember I said that aldosterone will have you retaining sodium. Well, if there is no aldosterone, the sodium is actually excreted by the kidneys. But because the kidneys like to keep a balance of the electrolytes, they will hold on to another positive electrolyte with a similar charge, and this is usually potassium. And so, you really do have to monitor for patients especially renal patients or patients that are on other potassium substances as they are more at risk for hyperkalemia. So captopril is actually fairly readily absorbed when taken orally, though it is a problem because food can decrease absorption. And so, it's very important that we teach patients that this is taken an hour before meals or 2 hours after meals so that they can time it appropriately. Because we don't want them to have decreased effectiveness of the medication due to lack of education. It does cross the placenta and it can enter breast milk. And as I mentioned previously, it is a Category D. It does have some risk of teratogenicity, and so, it's very important that we make sure that patients that are of childbearing age females are on birth control and are aware of the risk factors. It is metabolized in the liver and excreted from the kidneys. And so, it's very important also that we monitor how functional somebody's liver and kidneys are because it can affect a risk of toxicity and adverse effects with this medication. ACE inhibitors may be utilized in the treatment for hypertension. They're very useful as part of the treatment in heart failure. They also are considered to be first-line therapy in diabetics in treatment with diabetic nephropathy, not neuropathy, nephropathy. Some of the adverse effects that patients should be educated about. One of the more common ones can be a chronic cough, and this is due to the fact that the enzyme is actually in the endothelium of the lungs. Because we do not have that ACE enzyme, we can have decreased breakdown of the bradykinin and the cytokines, which is thought to be the rationale for the cough. Therefore, they can have more reactive airways. They may develop a chronic cough. While it isn't necessarily harmful, it is the reason most of the patients choose to voluntarily stop the medication, not always contacting their provider. And so, it's very important that if the patient develops a cough, they are told to call their provider. Because we would much rather switch them to another medication, and so you don't want them to just stop the treatment. Patients may also develop hyperkalemia and this is due to the inhibition of the aldosterone, and therefore they do not hold onto sodium at the level of the renal tubules and they will hold on therefore to potassium. Some of the signs and symptoms that you should teach patients to monitor for is an irregular pulse if they start noticing that their pulse is irregular. If they have muscle cramping followed by extreme muscle weakness, nausea, and vomiting. Serious adverse effects is angioedema and neutropenia and this is the decreased neutrophil. So angioedema, it's an acute, very rapid onset, painless. They get swelling of usually short duration involving the face, the neck, the lips, the hands, and the feet. They can have swelling in the throat. So it is important that they notify the provider. Patients also need to be aware of again neutropenia and agranulocytosis. And this agranulocytosis is a lack of all of the cells that are produced in the bone marrow. So you need to teach patients how to monitor for these things. If they start experiencing more infections such as strep throat. If they have bruising that is unexplained. Increased fatigue, which would be the lack of red blood cells. They may need to have occasional CBCs monitored. There is an FDA black box warning for both angiotensin-converting enzyme drugs and your angiotensin receptor-blocking drugs, your ACEs, and your ARBs. There has been an increased risk of neonatal harm after in-utero exposure to the ACEs or ARBs during the second and third trimester. The mechanism is thought to probably be the inhibition of the fetal RAAS system and so this causes decreased kidney function which results in something called oligohydramnios which is that increased fluid surrounding the fetus. It also impairs lung development. So they are considered to be a Category D during the second and third trimester. Now, both drugs are also considered to be teratogenic in the first trimester. In other words, if there is an individual contemplating pregnancy, they should not be prescribed either ACEs or ARBs. If they're currently taking them, the care provider should be approached about an alternative. If a person finds they are pregnant while taking these medications, they should be instructed to immediately notify the care provider so that they can be switched. To maximize the therapeutic effects, patients should be taught to take the medication 1 hour before meals or 2 hours after meals. And this is because we do see decreased absorption with food. To minimize some of the adverse effects is clients need to be taught to continue to monitor their blood pressure. Now, one of the things that we have noticed with ACE inhibitors is that the first couple of doses we can see quite a severe drop in blood pressure and hypotension. For this reason, many care providers actually choose to administer the first couple of doses at night. But it's important for the patient to understand that we do need to monitor their blood pressure and to kind of make sure that it's staying within stable ranges. They should be taught to continue lifestyle changes. So changing diet, exercising, all of the things that they had been previously taught to treat the hypertension. They should be taught signs and symptoms of hypotension; lightheadedness, dizziness, if they are seeing spots before their eyes. They should change position slowly. They also need to be very aware of the signs and symptoms of hyperkalemia; irregular heart rate, muscle weakness, nausea, vomiting. And to notify the care provider if they are experiencing any of these things on a regular basis. We're progressing to the next medications. We want to cover some terminology and you do want to be familiar with this terminology as it will be included in test questions. Inotropic. This is the term that refers to modifying the force or speed of the contraction of the muscles. So when we are talking about the heart, a positive inotropic drug increases the force of the cardiovascular muscle contraction. While a negative inotropic drug weakens the force of contraction. Chronotropic describes the agent that can change the heart rate. So when we talk about the pacemaker of the heart, we're talking about the SA node. So when we talk about a chronotropic drug, chrono is time. A positive chronotropic drug will increase the rate that the SA node sends out the signal so you'll have an increased heart rate. While a negative chronotropic drug will decrease the rate from the SA node, and so you will have a slower heart rate. The last term is dromotropic. And a dromotropic agent is one which affects the conduction speed primarily in the AV node. So what we're referring to is how fast the signals are passed through the AV node. Think of it as a tollgate. So if it is negative, a negative dromotropic drug slows the conduction and so you will have slower conduction through the AV node. Therefore, you will have slower response by the ventricles and response from the muscle. A positive dromotropic would increase the speed of conduction through the AV node, and you would have a faster response. Beta-adrenergic blockers. We'll be studying two medications in this class. The first is the non-selective, propranolol and the second is the selective, metoprolol. I will explain more about non-selective and selective drugs. We refer to as being selective or non-selective, we are talking about their preference or their overall effect on different receptors. Now, when we are referring to betas, both beta-1 and beta-2 receptors can be acted upon. Beta-1 and beta-2 receptors are two types of adrenergic receptors. The beta-1 receptors are located in the heart, the kidneys, and fat cells. Their action is to increase the heart rate and the strength of contraction. Beta-2 receptors are located in the bronchioles of the lungs and the arteries of the skeletal muscle. They relax the smooth muscles, they dilate the blood vessels, and they open the bronchioles. So when we refer to beta-adrenergic drugs being non-selective, it's referring that they will have a similar action or similar effect on both beta-1 and beta-2s. So we will see both responses. On the other hand, if we are giving a selective drug, like metoprolol, it is aimed more at beta-1s. So we are going to have more effect only on the cardiac and not on the lungs. Now, one of the ways to really remember that makes it easy is you have one heart beta-1 and two lungs beta-2s and that kind of lets you know where the receptors are primarily affecting. So a couple of things to think about is when we're talking about the beta blockers. These are going to be blocking if they are non-selective both beta-1 and beta-2 receptors. Because they are blocking, we are blocking the normal response. So for example, let's take a look at the chart. Normally with beta-1 receptors, you have an increased heart rate and an increased force of contraction. With a beta blocker that is non-selective such as propranolol, we will see a slowed heart rate. So think about the term that this applies to. This is a negative chronotrope, and we will have a weaker, less forceful contraction, which term refer to the force of contraction, inotrope. So it is a negative chronotrope and a negative inotrope. If it is non-selective, it will also affect the beta-2 receptors. So when we block the beta-2 receptors, we will see vasoconstriction in the skeletal muscle or peripheral vasoconstriction. We will also see bronchial constriction. Now, think what patients this might cause a problem with. What if somebody has a preexisting asthmatic condition or respiratory condition? Giving a medication such as a non-selective beta blocker could lead to them having an asthma attack. So we have to be very, very careful with these. When we use cardioselective drugs such as metoprolol, they offer the potential advantage of not interfering with the beta-2 receptors or at least having less likelihood of it. So let's say we gave a patient metoprolol. We would see decreased heart rate, decreased force of contraction, and we wouldn't see any beta-2 receptor activity. So we shouldn't see any change in peripheral vasoconstriction, nor should we see any difference in bronchial dilation. Now, having settled this, there is always a risk as we increase doses in our selective beta-1 blockers, we can see some beta-2 effect. So it's important to monitor and to teach a patient to monitor after any medication changes. So the pharmacodynamics of propranolol are that the blockage of beta-1 will actually affect the heart and this will result in a decreased rate and decreased contractility. Now, this is a negative chronotropic and a negative inotropic action. These will result in a decreased cardiac output and therefore decreased blood pressure. It will also slow the atrial ventricular conduction and suppress the automaticity. This is a negative dromotropic. So just to be clear, you have a negative inotropic, a negative chronotropic, and a negative dromotropic when you are using a beta-blocking drug. All of this decreased workload of the heart will result in decreased oxygen demands. This is one of the reasons that we do see better morbidity rates when somebody has suffered a myocardial infarction and they are then given a beta blocker is because it actually decreases the stress on the tissue and we're able to save a lot of that tissue. The effect on the kidneys is it will decrease the release of renin and this will ultimately result in decreased blood pressure. Now, this is where the main difference between metoprolol, which is a selective, and propranolol, which is non-selective is, and it's the beta-2 blockage. Because propranolol is non-selective, it affects both beta-1 and beta-2. So it will have some beta-2 blocking effects. Most of these are going to be seen as adverse effects because they are going to be affecting primarily the pulmonary system. So we see bronchospasms. We can actually see people having a more difficult time breathing. This is especially true and this medication class can be problematic in asthmatics. We have to watch peripheral vasoconstriction. And so, if you have somebody that has Raynaud's, this medication again is extremely harmful. Hypoglycemia. So again, watching people that are diabetics or that suffer from hypoglycemia. So uses for propranolol can be hypertension. We also can use it for angina. Remember how we said it decreases the oxygen needs and the oxygen consumption in the heart. We can use it for cardiac arrhythmias. People with migraines. It is very, very effective. One of the off-label uses, action can be for intention tremors. We can see the beta blockers used. Heart failure. So there's a lot of different effects that can be used from this. Significant contraindications. People that have bradycardic rhythms, complete heart block because again, it is going to affect the conduction and the rate of the heart. And so, this would actually further compromise their rhythm and their ability to meet their oxygen needs. Cardiogenic shock. I do want to clarify. This is an uncompensated cardiac failure. You can see this medication used in heart failure but not in people that are unable to meet any of the body's needs. So again, that would be a clarification that you would really have to monitor for. Raynaud's disease and reactive airway disease. So some of these we've already previously mentioned. Some of the adverse effects that you would need to monitor for is postural hypertension, bronchospasms, and then very seriously would be myocardial infarction or compromised ability to meet the needs of the body with circulation. This medication is well absorbed when given orally. It can also be given parenterally. It is well distributed. One thing to be aware of is that the stability as far as the hyposensitivity may actually not occur for two to three weeks. And so, patients during this time need to be very, very careful with movements and changing position. It is metabolized in the liver and excreted through the kidneys. So the nursing interventions that are going to help us maximize the therapeutic effects. So many of these interventions are going to be stressing and emphasizing to the patients and educating the patients. So first of all, we want them to understand that this is not a medication that they should double the dose. If they have forgotten the dose, they need to leave it and go on to the next one when it comes around. This is not one you want to double up because of the effects that it does have on the blood pressure and on the heart. They should be taking it with food and this will actually increase the bioavailability and decrease GI upset. To minimize the adverse effects, first of all, minimize stressors. This makes it so the medication is actually going to be more effective. They should be checking a peripheral pulse prior to giving the medication and holding it if it is below 60 or if the rate is irregular. They should notify their provider. They should be keeping appointments with their provider so that we can monitor EKGs and blood pressure. If you have this patient coming into the physician's office, into the hospital, this is somebody that we need to be assessing of respiratory assessment as well due to the risk of bronchial constriction. So listening to the airflow, asking if they're having any difficulty breathing. Make sure that if you ever have a patient that has a history of COPD, asthma, respiratory complaints, you should always question if this medication is ordered. There are others that are selective that are not going to put this patient at the same risk. So it's very important that we want to prevent that beta-2 blockage. Know why your patient is receiving the medication. Are they receiving it to decrease angina pain? So we want to know what their pain level is. Has it decreased? Watch for their -- you should have increased tolerance with activity. So again, teach the patient and watch them. Do they know how to take their own pulse, their heart rate? Can they detect if it's regular or irregular? Are they able to verbalize to you how to move safely? Do they know to sit at the edge of the bed? Do they know to sit in a chair and make sure they're not having any dizziness when they first stand up, to stand for a second before they take off walking? Any of those changing positions or safety related to postural hypotension. It's very important they understand never abruptly stop taking the medication. They need to understand that, again, if we remove that blockage, not only is their blood pressure going to go high, but their heart rate. So I had students in the hospital and there was this wonderful little lady, she was 83. She had an abdominal surgery and then had some complications. And they were walking her, they were getting her up and walking her. And she was getting ready to go to a rehab facility and she was funny, funny. She kept saying that she wanted to go to one facility over another because they had better-looking young men aides. And I thought if you're at 84 concerned about that, you go for it girl. But I left the floor, the students were walking. And then I got a call, "We need you to come really quickly. The patient doesn't look well." And I said, "Okay, go back to your basics. Take your vital signs." Well, her heart rate had doubled. I said, "Go back to her history," was this lady I was walking at the time to the floor. What was she on before surgery? Because they said, "No, no, no, she's not on any beta blockers." And I said, "Go look at the prehistory." Well, she had been on a beta blocker before surgery. Because of the complications, she was not restarted on it. It wasn't an issue until she got that stimulation. Her heart rate was 135. Blood pressure was actually low because the heart didn't have time to fill. And of course, she felt very weak. Physician got called. They put her on a cardiac monitor, gave her an IV beta blocker, slowed her down, and then they were going to start her on a maintenance dose. So it's very important that patients understand not to abruptly stop these medications because we can see the blood pressure go way high and the heart rate as well because we're going to lose that blockage effects. Metoprolol is a selective beta-adrenergic blocker. And selective beta blockers have an advantage over non-selective in some cases because they do not usually block the beta-2 receptors. And because of this, they do not block the sympathetic bronchodilation that is so important for patients with lung disease who have asthma, allergic rhinitis. And so, these patients actually need that response. So the beta-1 effect of metoprolol is identical almost to that of propranolol. We see the beta-1 blockage. So the heart is going to decrease the rate and the contractility. Results in decreased cardiac output and decreased blood pressure. It does also slow again the atrioventricular conduction, decreased automaticity, and all of this decreases the oxygen demands. So remember again, these are negative inotropic, chronotropic, dromotropic. It's going to decrease the blood pressure and the oxygen demands, which will help with anginal pain. It decreases the release of renin so we do not have that vasoconstriction and decreases the blood pressure. I do want to point out. Though we do not routinely see beta-2 effects if somebody is at very, very high doses. Sometimes that selectivity is less dependable and they can have some minor to severe respiratory effects. So they use this for metoprolol. Again, very similar hypertension, angina, cardiac arrhythmias, heart failure. We do also see it used for people with open-angle glaucoma who have increased pressure. They can use it for this too, make it so that the fluid can flow out. Contraindications. Bradycardia, complete heart block, shock, people whose heart failure is not compensated, this is not a time to give this medication. Now, while we do see metoprolol being less restrictive and causing that vasoconstriction in the periphery that somebody with Raynaud's cannot tolerate, they still say that it should be used in extreme caution. Adverse effects. Again, people still have to watch for postural hypertension. And serious if they go off it abruptly, they could risk a myocardial infarction. It is absorbed orally very well. Bioavailability is increased when taken with food. And if somebody needs immediate results, we can give it intravenously. It is excreted through the kidneys and metabolized in the liver. For the nursing interventions, I'm just going to have you review those of propranolol. Because other than the risk of respiratory involvement, they are identical. Again, I do want to emphasize if a patient is taking extremely high doses, you do still want to do a very thorough respiratory assessment and ask them if they are having any complications. Because patients on higher doses do run the risk of allergic rhinitis up to bronchospasms. Cardiac glycosides exert positive inotropic effects on the contractility of the heart muscle. Inotropic means related to or influencing the force of myocardial contractility. And so, what we're going to end up with when we talk about a positive inotropic effect is an increased force of contraction. Digoxin or Lanoxin, which is derived from the foxglove plant -- -- is the prototype of this class. And this is just a picture of the foxglove. And so, when we talk about heart failure and that needing for increased force of contractility, this is one of the medications that you will see. Now, this is an older medication and you will generally not see it utilized except for somebody that has left-sided heart failure. The pharmacodynamics of digoxin are several different ones and we're going to talk about the direct and the indirect effects that it has on the cardiac muscle. The overall effect that we see is that it does increase the cardiac output. The first effect is the direct one and it acts on the cardiac muscle itself. It strengthens the force of contraction and this is the positive inotropic effect which was previously mentioned. It does this through increasing the movement of calcium across the myocardial cell membrane during the depolarization. And as calcium is needed for contractions, then we actually get a stronger contraction because we have more calcium that is actually available. It also will affect the electrical conduction system, and so it increases the refractory period at the AV node. This allows the pausing or that period of time that the heart muscles cannot actually be stimulated into contracting again. And so, this actually allows for a little bit of delay. This refractory time is actually very helpful when you have somebody that has rapidly conducted atrial fibrillation. Some of the indirect effects that we can see resulting from digoxin is actually the stimulation of the ANS or the sympathetic nervous system. So it has a vagomimetic effect. It mimics the action of the vagus nerve and so it slows conduction and this is actually a negative dromotropic effect. And it depresses the sinoatrial node and prolongs conduction to the AV node. So it slows the heart rate and this is a negative chronotropic effect. And you want to be familiar with these. So it has a negative chronotropic and the way to remember that is chrono is time. So it slows the timekeeper of the heart. It slows conduction and this is a negative dromotropic and it increases the force of contraction. And so, it's a positive inotropic. Because of the prolonged conduction time, the cardiac output is increased as a result of all of these factors we've just talked about. Absorption can vary some with the type of preparation. How much is absorbed and the time it takes to be absorbed can be affected. One of the things to be aware of is that food, while it can slow down the rate of absorption, it doesn't usually affect the overall preparation. And as digoxin can be irritating to the lining of the stomach, we do usually encourage people to take it with food because again, as they do that on a regular basis, the overall percentage and level of absorption will be balanced out. It can still be administered IV. So a couple of things to be aware of is that it is highly concentrated in the myocardium. We also see increased levels in skeletal muscle, the liver, the brain, and the kidneys. It does cross the blood-brain barrier and the placenta. Therefore, if you have an expectant mother it will get to the fetus. It has a very long half-life. Now, because of that, it takes longer sometimes to get up to that therapeutic level where we've got that therapeutic index. And so because of that, we may sometimes do what we refer to as digitalization. And this is a loading dose. We usually will give three divided loading doses, two to three depending on the patient over a 24-hour period. They are usually given IV and then they are started on a therapeutic maintenance dose. What this does is it gets the blood level up high enough that we can get and achieve that steady state quicker. This is usually done more in somebody that has a rapid atrial fibrillation. It is not as common of a practice in heart failure. So it is metabolized in the liver and excreted in the kidneys. One of the things to be aware of is that because it is excreted in the kidneys, people that have poor renal function a lot of times in our elderly, we see this, then we do need to use lower doses because it is not excreted fully and it does make them more at risk for having digoxin toxicity. This medication again is used in heart failure, atrial fibrillation, and atrial flutter. Do understand that this medication is an older medication. It is not used as a first-line drug in most patients. You will see it used in left-sided heart failure and for fibrillation and flutter. But we have found that the mortality rate is decreased in patients that we use first RAAS inhibitors, beta-blockers, and some of the other classes of medications. One of the things that we do notice is that it can cause some of the same arrhythmias that is actually used to treat, and so it is a difficult medication to use. It does have a higher incidence of problems with it. Some of the contraindications are things like heart block, ventricular fibrillation, sick sinus syndrome. The reason is think about the effect that we talked about that digoxin has. It delays the conduction; it delays the heart rate. And so, if you have somebody that already has problematic or spotty conduction of the electrical system or has a poor pacemaker, you don't want to use digoxin because it's going to thoroughly compromise your heart muscle. We have to really watch because it can cause severe bradycardia and block. And this is again seen primarily with digoxin toxicity. Some of the adverse effects to be aware of, common ones that we watch for are cardiac toxicity. And again, this is primarily seen with somebody that's going to have that lower heart rate. Some of the causes can be electrolyte imbalances, primarily hypokalemia. So you have somebody with lower potassium or low magnesium, they are going to get a larger effect in the cardiac tissue with the digoxin. Hypercalcemia, it potentiates the effect of the digoxin. Now, there are in your textbook a table that talks about some of the antidotes that we will use. One of the ones that is expensive and not used really frequently, but I do want to mention it is digoxin immune fab, Digibind. And this actually, when we have high levels of digoxin that we do need to remove, we can give this IV, it does bind with certain percentages of the digoxin and makes it unable to bind with the receptors of the tissue. And therefore the medication is ineffective and we lose some of that overall effect. This is just a reminder, educate your patients. So there are several things that we can do to actually maximize the therapeutic effects. First of all, digitalization. As I mentioned previously, this will be given usually for atrial fibrillation. And so, they will receive two or three evenly spaced larger-than-normal doses. These are loading doses. What we are doing is raising the level of the medication and so, that the patient is at a steady state much quicker. And so, then we can go ahead and put them on a maintenance dose. It is very, very important that when we do this that we make sure that the patient is on cardiac monitoring, that we are making sure that they have adequate fluid intake, and that they have good excretion because remember this is excreted through the kidneys and we do have to monitor that. So it does help us to achieve that rapid onset of therapeutic effects. And we do then just need to monitor for the adverse effects. Digoxin has a very narrow therapeutic window. And so, the therapeutic range is 0.5 to 2.0 nanograms per milliliter. We do actually see some patients that can start exhibiting signs of toxicity even when they are within that normal range. The patients we usually see this occurring with are renal patients because they seem to build up and to start showing signs of toxicity much quicker than other patients. And so, we do want to monitor patients to make sure that they are within that normal range as well as assessing them for any signs of toxicity. It's important that when patients are on digoxin and they come into a facility that we look when their last therapeutic range was when it was drawn. That we check with the physician, do you want it checked? We make sure that patients know how frequently they should be getting blood work done. We also want to assess patients for bradycardia. Now, this is something that we assess prior to administration. In an adult we want their heart rate to be greater than 60. And so, we're going to listen to the apical pulse for a full minute. This has to be a full minute because especially if somebody has atrial fibrillation, you do not want to get it during a period of rapid heart rate or slow heart rate and get a number that is actually inaccurate. And so, it's very important that we take it for a full minute. In an adult we want the rate to be greater than 60. In a teen or younger child, we want it to be greater than 70. And in a young infant, we want it to be greater than 110. So what we're looking at is that we want it to be greater than a bradycardic rate for that age group. So it's important that we assess for any bradycardia. We want to monitor for any electrolyte imbalances. We've already mentioned that low potassium and magnesium can actually place the patient at risk for digoxin toxicity. Now, guys, I don't know about you but I do not sit at home and suddenly have a little light come over my head and I say, "Oh, I think I'm experiencing hyperkalemia." It would be really nice if that happened, but it doesn't. Or, "Oh, I've got hypokalemia, hypomagnesemia." You need to teach patients what that feels like. And so, one of the easiest ways to be able to have a patient identify both the low potassium and the magnesium because they have very similar signs and symptoms. They actually you will get a lot of cramping in the legs. They have increased electrical conduction with the magnesium and so they get a lot of irritability. So if you say, you know, you've got a lot of cramping maybe the paresthesia, that's probably the easiest one for them to identify. High calcium actually will also place a patient at risk for digoxin toxicity. So with high calcium or hypercalcemia, everything gets very slow. Unfortunately, mentation, muscle movements, bowels, everything slows down. And so, it's important that if the patient says, "You know, I just feel so tired and sluggish and I'm falling," that we look for other things that could indicate that they may have high calcium. And then, know who's at risk for it. So it's very important that you as the nurse be aware if they are taking other medications that do put them at risk for this. For example, if you have a patient that is taking hydrochlorothiazide. Hydrochlorothiazide is a diuretic. It can cause them to lower their potassium magnesium, but it also causes them to hold on to the calcium. So it puts them at increased risk of having some of these electrolyte imbalances. So this is why it is so important that as a nurse, that you are putting that picture together and educating your patients. So you have to monitor, make sure that the imbalances are corrected before we are doing administration. You also want to assess for non-cardiac signs of digoxin toxicity. These if you will remember GI, a lot of anorexia, nausea, vomiting, diarrhea. Patients will complain of headache and blurred vision. You will also hear them complaining or saying they've got yellow vision. A lot of patients will complain of yellow halos around objects and lights. I have heard some that are a little bit blue but yellow, and so you'll hear it referred to as yellow vision. It's a very common thing. Unfortunately, confusion. And so we do need to monitor for this. We need to teach patients how to monitor for these things as well. And so, when we're teaching them to look for bradycardia, they're not going to listen to an apical pulse. Teach them how to do a radial pulse. And then, if it's below 60, rest for a little bit and take it again. If it's still below 60, to call their physician and not take their medication until they talk with the physician. It's important that they know the signs and symptoms of digoxin toxicity. If they start having a lot of GI upset. If they notice that they've got a lot of diarrhea. Are they having trouble remembering things or are family members picking up on that along with a slower heart rate? They may need to go in and get their digoxin level checked. This is medication comes in little white and little yellow tablets. It does not really have a nasty taste. A lot of elderly people so they don't forget to take their medication will put them out on tables. This is not a medication you want a grandchild getting into or anybody getting into. So make sure they understand to keep this out of the reach of children and that if they -- to decrease their GI upset, it can be taken with food to decrease that. This is just a fun little mnemonic to kind of help you remember some of the signs and symptoms of digoxin toxicity. So bradycardia or heart block. Remember, we're going to usually go with the number 60. Anything below 60, the patient shouldn't be taking it and we shouldn't be giving it. Blurred vision or yellow vision. Remember those yellow halos. Occasionally, we can see a rash, abdominal pain, nausea, vomiting, diarrhea, a lot of GI symptoms. And then, delirium and confusion. Nesiritide is the prototype drug in the human B and B class of drugs. This is a newer class of drugs and I just want to mention it because I think we're going to see more of them as time progresses. So nesiritide is actually a vasodilator and it acts just like the B natriuretic peptide. Now, the B natriuretic peptide is secreted primarily by the ventricles in response to fluid and pressure overload. So when we get that increased stretch happening on the tissues, then we see an increase in the B natriuretic peptide being actually excreted. So it is administered primarily by a bolus and then an IV administration. So you will most likely not see this medication unless you are working in a monitored critical care bed. It is usually fairly immediate and they actually start seeing effects within 15 minutes. So if somebody comes in in extreme fluid overload, this is a good way to help them relax those vessels and get that fluid down a little bit more in the periphery so that we can get some other interventions in place. And then, the nesiritide acts to compensate for the decreased cardiac function because it decreases or reduces the cardiac preload and the afterload. And because it does all this, it actually will produce something similar to a diuretic effect because it increases the sodium secretion and it suppresses the RAAS system. And so, all of these things help a heart that is actually not functioning well. So another class of drugs I would like you to at least be familiar with because I do think we are going to see more use from this are the angiotensin receptor neprilysin inhibitors. And I'm going to use the trade name because I really could not find a good pronunciation for the other. So this is Entresto. Entresto actually is going to assist in modulation of the natriuretic system and it inhibits the enzyme neprilysin. Now, neprilysin actually degrades the vasoactive peptides. And so, because of this, what it does is when it's added to an ARB, it helps decrease and block the activity in the RAAS. And so, we don't have the aldosterone, and the sodium, and the fluid retention. It also is going to decrease the conversion of angiotensin I to angiotensin II. And then, we get some of that vassal relaxation going on in the periphery. And so, we have that decreased preload and decreased afterload. So because of this, it's got a really good effect in people with chronic heart failure that does not react well to other medications. Now, I do want you to be aware that the drug is a pro-drug, which means that it's given in its less active form, and it is more active following metabolism. It takes about 30 minutes after it's administered to start seeing it in the system. It takes about 3 days to reach steady state and this is when it's given twice daily. So nursing interventions. This medication can actually be given without regard for food. Again, you do want to give it usually twice daily. And so, we want that to be evenly spaced. We do need to make sure that if people are switching from an ARB or an ACE, that they usually have about 36 hours, what they call a washout period to get the other drug out of the system before we start this one. So we do not have that duplication of efforts. Assessing for therapeutic effects. Why would we be giving that? Monitor for if we have increased stabilization of the signs and symptoms in their chronic heart failure. Do they have increased activity tolerance, decreased shortness of breath, decreased nocturia? What are their labs showing us? What are the BUN, and the creatinine, and the potassium? It's important that we make sure that these remain within acceptable limits. When we're looking for adverse effects, it's very important that we monitor for vital signs, monitor for hypotension, and that they monitor themselves at home. We want to look for any abnormal lab values, especially for the creatinine, and the potassium, kidneys, and then our electrolytes. And then, for anything that indicates a worsening of their heart failure, a cough, persistent coughing, or dizziness. Teach the patient that frequent blood pressure and monitoring is necessary. And again, go over the options and where they can get it checked. They need to be reminded to change position slowly. And then, to tell their provider if they are put on a potassium supplement or currently taking a potassium supplement or a potassium-sparing diuretic. Now remember, this is important because with an ARB, they do not have that aldosterone secretion, they don't have the sodium retention and therefore they do have a little bit more potassium retention. So this does put them more at risk for hyperkalemia. They need to notify the provider of any swelling. Again, we are still at some risk for angioedema and to let the provider know immediately. And then, they are encouraged to drink adequate fluids so that they do not have hypotensive episodes.

Female 1: Drugs Affecting the
Cardiovascular and Hematological System. Cardiac Cycle. The timeframe is from the beginning of one
heartbeat to the beginning of another. In systole, the
ventricles contract. We have increased pressure that occurs
from the ventricular contraction and this causes the mitral and
the tricuspid valves to shut. The aortic and the pulmonic valves open
and this allows ejection of the blood into the aorta and
the pulmonary artery. During diastole, the
ventricles relax. This allows the mitral and the tricuspid valves
to open and allows blood to flow into the atria. Atrial contraction occurs at the end
of diastole and pushes the blood from the atria into
the ventricles. Unoxygenated blood is returned via the superior
and inferior vena cava to the right atrium, or it is moved then through the
cycle to the right ventricle. Blood leaves the right ventricle
via the pulmonary artery to be re-oxygenated
in the lungs. The oxygenated blood returns to the
left atrium via the pulmonary veins and then moves into
the left ventricle. Blood is ejected from the left
ventricle to the body via the aorta. The stroke volume is the amount of blood that
leaves the left ventricle with each contraction. This is normally
about 75 milliliters. Now, it is dependent
upon several factors. First of all is the preload. And this is the passive stretching force on the
ventricular muscle that is created by the amount of blood that has
filled the heart. And so, it's the amount of blood that
is there at the end of diastole. The preload is affected
also by several things. And so, we look at
the venous return. And this is the amount of blood that is
returned from the periphery to the heart. If there's not enough blood returning,
then you're going to have a lower preload. If the atrial contractility
also will affect your preload. And so, the ability of the atria to contract
forcefully enough to move the blood from the atria into the ventricles
will also affect this preload because otherwise, you're
going to have stasis. And then, the amount of blood left in
the ventricle also affects our preload. Think about somebody that has actual failure and
they don't have the ability to move the blood out into the central
circulation. If that blood is actually staying in the
ventricles and the atria have good contractility and move that blood into the ventricles,
you're going to have that buildup and increased stretching
of the ventricular muscle. Some other things that actually will affect
our stroke volume, the contractility. This is the force that the ventricular squeezing
so that the ventricle is able to achieve and eject the blood into
the systemic circulation. If you have a very weak
muscle or a damaged muscle that say somebody had a
myocardial infarction. And instead of replacing that with
that elastic muscular strength, they replace it
with scar tissue. They are going to have decreased
stability and decreased contractility. Some of the other things that can
also affect our stroke volume. This is the concentration of
catecholamines in the heart. The more catecholamines, the
greater the contractility. And so, somebody that has a lot of that force,
you will see more force of contraction. The last thing we want to
discuss is the afterload. The afterload is the resistance against which
the left ventricle must eject its blood. And so, it's the resistance
that it has to overcome. When we look at this I always have compared
it to the straw and a garden hose. If you had a straw, a drinking straw next to
a garden hose and you looked at the diameter, there's an obvious
difference there. Think if you were trying to force
fluid into either of those structures, it would be a lot easier to do it in the
hose because it's more open, more dilated. And so, when we look at afterload, if
we have somebody that has a constricted or smaller diameter of a vessel, it is going
to require a lot more force and workload, and therefore, the heart may not
be able to eject that blood. And so, when we look at the peripheral
resistance, this is a key factor. So the cardiac output is the volume of blood
that leaves the left ventricle in 1 minute. The stroke volume, which
remember we said is around 75 milliliters per
stroke times the heart rate. And so, when we're looking at the cardiac
output, the body likes a set amount, let's just say around
2.5 to 3 liters. So if you have somebody that has a poor
stroke volume due to damage to the heart or decreased volume, then the way that the body
will compensate is by increasing the heart rate. So if you have a low stroke volume, then
the heart rate is going to increase. If they've got a lower heart rate, then
usually we're going to see a heart that is able to have a
larger stroke volume. And so, what we look at is these factors
are going to be going up and down so that the body ends up
with a good cardiac output that is sufficient to
meet its oxygen needs. It's just of heart failure. Several compensatory mechanisms
attempt to maintain cardiac output and meet the body's
systemic demands. This causes a chronic activation
of the sympathetic nervous system. So with all of the changes involved with the
sympathetic nervous system and that we can start to see changes in myocardial hypertrophy
and myocardial hypercontractility. The increased sympathetic drive
also results in the activation of the renin-angiotensin-aldosterone system,
the RAAS system, everybody's favorite. This results in systemic
vasoconstriction and sodium retention. So let's break this
down a little bit more. So when we have decreased cardiac
output and systemic pressure, renin is released as again the kidneys
are not getting adequately perfused. Now, renin is the enzyme produced
in the kidneys in response to impaired blood flow
and tissue perfusion. The release of the renin acts
on angiotensinogen and this is from the liver and it
forms angiotensin I. Now, this next part I really want you
to listen to because when we talk about drugs, this is
where we're interacting. The vascular endothelium, particularly in
the lungs, has the enzyme that is produced, the angiotensin-converting
enzyme. So this is where
ACEs actually work. And this production of this enzyme stimulates
the production of the angiotensin II. Now, angiotensin II is a
powerful vasoconstrictor. And it actually will trigger a cascade of
effects that are aimed at restoring blood flow to the vital organs and
enhancing tissue perfusion. So number one, it acts on the adrenal
cortex to release aldosterone. Now, this release of aldosterone acts on
the kidneys to increase sodium retention, and with the sodium
comes the fluid. So now we have increased fluid being
retained in the vascular system. And our sick heart wasn't
doing well as it was. Number two, it stimulates
the release of vasopressin, and this is the
antidiuretic hormone. And this causes increased
retention of fluid by the kidneys. It also stimulates cardiac hypertrophy
and this is that adding of extra muscle. And then, the last thing is it
causes arterial vasoconstriction. The problem is that this increases the
resistance referred to as the afterload that that left ventricle is having to pump
again, making it even more ineffective. So it increases the filling pressures inside the
heart and it increases the stress on the heart because now we've got increased
stretch of the muscle. When we have this increased
stretch in the cardiac tissue, this stimulates the release
of the natriuretic peptides. The response that the body follows
is to increase sodium excretion -- -- by the kidneys, increased
diuresis, direct vasodilation, and it increases glomerular
filtration rate. It also reduces the renin
production from the kidneys. So all of these things are aimed at
correcting or at least to assist in correcting this fluid overload caused by
this sympathetic innervation that took place. Previous slide. Heart failure is a condition that results in
low cardiac output because the heart is unable to pump sufficient blood to meet
the metabolic demands of the body. The normal compensatory
mechanisms of the body that cause fluid retention
result in increased preload. While the vasoconstrictive actions of
angiotensin do increase the afterload. The overall interaction can cause decreased
cardiac output from the left ventricle. This results in an increased
heart rate to ensure perfusion. Common risk factors are coronary artery disease
and hypertension, and these are major causes. We also see people developing heart
failure following myocardial insults. Drug therapy for congestive
heart failure aims to alter one or more of the factors affecting the heart
to improve overall cardiac function. It's a common list of medications
that can be utilized in the care of individuals with
heart failure. Please do not think that the way
they are listed is the order in which they would
necessarily be utilized. It is just an easy way
for you to remember. So let's go through these. ACE inhibitors and I've
also added the ARBs there. Again, will interrupt the RAAS system and stop
that production of the ACE enzyme and going from angiotensin I
to angiotensin II. So it interrupts that. It also decreases the secretion or
the production of the aldosterone, which lessens the fluid
and sodium retention. Beta-blockers. Beta-blockers can be utilized
though very cautiously as they decrease the overall
requirements for oxygen. They also decrease the overall
workload of the heart. Calcium channel blockers again can be utilized
to slow and decrease the force of contraction. Digoxin is a cardiac glycoside. Now, I am going to tell you upfront
that this is an older medication. We are still learning it as you will
still frequently see it utilized and frequently see
it on your NCLEX. This medication, while it does have
some very inherent risk associated with it does increase the overall
force of the myocardial contraction. And so, it can help people with a very poor
ejection fraction have a better outflow of blood. And then diuretics. These can be utilized by care providers to
decrease the amount of fluid retention. When we talk about treating somebody that has
congestive heart failure or heart failure, our goal is going to be
to decrease that workload of the heart while
increasing circulation. So we want to unload some
of that excess fluid. We want to sit the patient upright
because that improves their ability to have that
respiratory function. And then, there's a lot of the medications
which we are going to be discussing. Nitrates you've
previously discussed. But think about the effect they would have on
the body and the heart as they vasodilate. They allow the heart to pump and circulate
that blood with decreased effort. Diuretics. We're going to be talking
about Lasix here shortly. ACE inhibitors and digoxin. Now, if we're trying to unload fluid using
medications such as furosemide or Lasix, we need to decrease
their intake as well. The whole goal is we're going to
try and decrease the afterload or that peripheral resistance that
the heart is having to pump against. And so, some of the other things that can
decrease that are things like sodium restriction because it will decrease the amount of
fluid that the body is holding onto. And then, we want to go ahead and test things
like digoxin levels and potassium levels. So the way to remember it is
the pneumonic unload fast. ACE inhibitors or angiotensin-converting
enzyme inhibitors are used in treatment of hypertension as well
as in heart failure. Now, we are going to actually use captopril
or Capoten as our prototype though I do want to make you aware that enalapril or Vasotec may
be more commonly seen if it is only being used for heart failure and not
hypertension as well. The pharmacodynamics of captopril is that it
inhibits the angiotensin-converting enzyme. This angiotensin-converting enzyme changes the
inactive angiotensin I to active angiotensin II. So angiotensin II is a very
potent vasoconstrictor. With decreased angiotensin II,
we lose this vasoconstriction. And so, we actually have relaxation
of the peripheral vasculature. Decreases in angiotensin II also
result in decreased aldosterone. Now, aldosterone actually is responsible for
increasing retention of sodium and water and this increases the
circulating volume. If the aldosterone is
decreased or blocked, it's going to prevent that
sodium and water retention. And so, we will have decreased peripheral
resistance and decreased circulating volume. Now, when you think of somebody
that has heart failure, all of these things
are going to assist. The cardiac output is actually going to be
increased without increasing the heart rate and the peripheral resistance is going
to be lowered without affecting this. It also will increase
renal blood flow, but it doesn't have any effect
of a glomerular filtration rate. Now, one thing to be aware of is that
the potassium may be slightly increased. And this is actually a result
of the decreased aldosterone. Remember I said that aldosterone
will have you retaining sodium. Well, if there is no aldosterone, the
sodium is actually excreted by the kidneys. But because the kidneys like to
keep a balance of the electrolytes, they will hold on to another
positive electrolyte with a similar charge, and
this is usually potassium. And so, you really do have to monitor for
patients especially renal patients or patients that are on other potassium substances as
they are more at risk for hyperkalemia. So captopril is actually fairly readily absorbed
when taken orally, though it is a problem because food can
decrease absorption. And so, it's very important that we teach
patients that this is taken an hour before meals or 2 hours after meals so that
they can time it appropriately. Because we don't want them to
have decreased effectiveness of the medication due
to lack of education. It does cross the placenta
and it can enter breast milk. And as I mentioned previously, it is a Category
D. It does have some risk of teratogenicity, and so, it's very important that we
make sure that patients that are of childbearing age females are on birth
control and are aware of the risk factors. It is metabolized in the liver
and excreted from the kidneys. And so, it's very important also that we monitor
how functional somebody's liver and kidneys are because it can affect a risk of toxicity
and adverse effects with this medication. ACE inhibitors may be utilized in
the treatment for hypertension. They're very useful as part of
the treatment in heart failure. They also are considered to be first-line
therapy in diabetics in treatment with diabetic nephropathy,
not neuropathy, nephropathy. Some of the adverse effects that
patients should be educated about. One of the more common ones can be a
chronic cough, and this is due to the fact that the enzyme is actually in
the endothelium of the lungs. Because we do not have that ACE enzyme, we can
have decreased breakdown of the bradykinin and the cytokines, which is thought
to be the rationale for the cough. Therefore, they can have
more reactive airways. They may develop
a chronic cough. While it isn't necessarily harmful, it is
the reason most of the patients choose to voluntarily stop the medication,
not always contacting their provider. And so, it's very important that
if the patient develops a cough, they are told to
call their provider. Because we would much rather
switch them to another medication, and so you don't want them
to just stop the treatment. Patients may also develop hyperkalemia and this
is due to the inhibition of the aldosterone, and therefore they do not hold onto
sodium at the level of the renal tubules and they will hold on
therefore to potassium. Some of the signs and symptoms that
you should teach patients to monitor for is an irregular pulse if they start
noticing that their pulse is irregular. If they have muscle cramping followed by
extreme muscle weakness, nausea, and vomiting. Serious adverse effects is
angioedema and neutropenia and this is the
decreased neutrophil. So angioedema, it's an acute,
very rapid onset, painless. They get swelling of usually short
duration involving the face, the neck, the lips, the hands,
and the feet. They can have swelling
in the throat. So it is important that
they notify the provider. Patients also need to be aware of
again neutropenia and agranulocytosis. And this agranulocytosis is a lack of all of
the cells that are produced in the bone marrow. So you need to teach patients
how to monitor for these things. If they start experiencing more
infections such as strep throat. If they have bruising
that is unexplained. Increased fatigue, which would
be the lack of red blood cells. They may need to have
occasional CBCs monitored. There is an FDA black box warning for
both angiotensin-converting enzyme drugs and your angiotensin receptor-blocking
drugs, your ACEs, and your ARBs. There has been an increased risk of neonatal
harm after in-utero exposure to the ACEs or ARBs during the second
and third trimester. The mechanism is thought to probably be
the inhibition of the fetal RAAS system and so this causes decreased
kidney function which results in something called oligohydramnios which is
that increased fluid surrounding the fetus. It also impairs
lung development. So they are considered to be a Category
D during the second and third trimester. Now, both drugs are also considered to
be teratogenic in the first trimester. In other words, if there is an
individual contemplating pregnancy, they should not be prescribed
either ACEs or ARBs. If they're currently
taking them, the care provider should be
approached about an alternative. If a person finds they are pregnant while taking
these medications, they should be instructed to immediately notify the care
provider so that they can be switched. To maximize the therapeutic
effects, patients should be taught to take the medication 1 hour before
meals or 2 hours after meals. And this is because we do see
decreased absorption with food. To minimize some of the adverse
effects is clients need to be taught to continue to monitor
their blood pressure. Now, one of the things that we have noticed
with ACE inhibitors is that the first couple of doses we can see quite a severe drop
in blood pressure and hypotension. For this reason, many care
providers actually choose to administer the first
couple of doses at night. But it's important for the patient to understand
that we do need to monitor their blood pressure and to kind of make sure that it's
staying within stable ranges. They should be taught to
continue lifestyle changes. So changing diet, exercising,
all of the things that they had been previously
taught to treat the hypertension. They should be taught signs and symptoms of
hypotension; lightheadedness, dizziness, if they are seeing spots
before their eyes. They should change
position slowly. They also need to be very aware of the signs and
symptoms of hyperkalemia; irregular heart rate, muscle weakness,
nausea, vomiting. And to notify the care provider
if they are experiencing any of these things on
a regular basis. We're progressing to
the next medications. We want to cover some terminology and you do
want to be familiar with this terminology as it will be included
in test questions. Inotropic. This is the term that refers to
modifying the force or speed of the contraction
of the muscles. So when we are talking about the heart, a
positive inotropic drug increases the force of the cardiovascular
muscle contraction. While a negative inotropic drug
weakens the force of contraction. Chronotropic describes the agent
that can change the heart rate. So when we talk about the pacemaker of the
heart, we're talking about the SA node. So when we talk about a
chronotropic drug, chrono is time. A positive chronotropic drug will increase the
rate that the SA node sends out the signal so you'll have an
increased heart rate. While a negative chronotropic drug will
decrease the rate from the SA node, and so you will have
a slower heart rate. The last term is dromotropic. And a dromotropic agent is one which affects
the conduction speed primarily in the AV node. So what we're referring to is how fast the
signals are passed through the AV node. Think of it as a tollgate. So if it is negative, a negative
dromotropic drug slows the conduction and so you will have slower
conduction through the AV node. Therefore, you will have slower response by
the ventricles and response from the muscle. A positive dromotropic would increase the
speed of conduction through the AV node, and you would have
a faster response. Beta-adrenergic blockers. We'll be studying two
medications in this class. The first is the non-selective, propranolol
and the second is the selective, metoprolol. I will explain more about
non-selective and selective drugs. We refer to as being selective or non-selective,
we are talking about their preference or their overall effect
on different receptors. Now, when we are referring to betas, both
beta-1 and beta-2 receptors can be acted upon. Beta-1 and beta-2 receptors are
two types of adrenergic receptors. The beta-1 receptors are located in
the heart, the kidneys, and fat cells. Their action is to increase the heart
rate and the strength of contraction. Beta-2 receptors are located in
the bronchioles of the lungs and the arteries of
the skeletal muscle. They relax the smooth muscles, they dilate the
blood vessels, and they open the bronchioles. So when we refer to beta-adrenergic
drugs being non-selective, it's referring that they
will have a similar action or similar effect on
both beta-1 and beta-2s. So we will see both responses. On the other hand, if we are
giving a selective drug, like metoprolol, it is
aimed more at beta-1s. So we are going to have more effect only
on the cardiac and not on the lungs. Now, one of the ways to really remember that
makes it easy is you have one heart beta-1 and two lungs beta-2s and
that kind of lets you know where the receptors are
primarily affecting. So a couple of things to think about is
when we're talking about the beta blockers. These are going to be blocking if they are
non-selective both beta-1 and beta-2 receptors. Because they are blocking, we are
blocking the normal response. So for example, let's
take a look at the chart. Normally with beta-1 receptors,
you have an increased heart rate and an increased
force of contraction. With a beta blocker that is non-selective such
as propranolol, we will see a slowed heart rate. So think about the term
that this applies to. This is a negative chronotrope, and we will
have a weaker, less forceful contraction, which term refer to the force
of contraction, inotrope. So it is a negative chronotrope
and a negative inotrope. If it is non-selective, it will
also affect the beta-2 receptors. So when we block the beta-2 receptors,
we will see vasoconstriction in the skeletal muscle or
peripheral vasoconstriction. We will also see
bronchial constriction. Now, think what patients this
might cause a problem with. What if somebody has a preexisting asthmatic
condition or respiratory condition? Giving a medication such as a
non-selective beta blocker could lead to them having an asthma attack. So we have to be very,
very careful with these. When we use cardioselective drugs such as
metoprolol, they offer the potential advantage of not interfering with the beta-2 receptors
or at least having less likelihood of it. So let's say we gave
a patient metoprolol. We would see decreased heart rate,
decreased force of contraction, and we wouldn't see any
beta-2 receptor activity. So we shouldn't see any change
in peripheral vasoconstriction, nor should we see any difference
in bronchial dilation. Now, having settled this, there is
always a risk as we increase doses in our selective beta-1 blockers,
we can see some beta-2 effect. So it's important to monitor and to teach a
patient to monitor after any medication changes. So the pharmacodynamics of
propranolol are that the blockage of beta-1 will actually affect
the heart and this will result in a decreased rate and
decreased contractility. Now, this is a negative chronotropic
and a negative inotropic action. These will result in a decreased cardiac
output and therefore decreased blood pressure. It will also slow the atrial ventricular
conduction and suppress the automaticity. This is a negative dromotropic. So just to be clear, you have a negative
inotropic, a negative chronotropic, and a negative dromotropic when you
are using a beta-blocking drug. All of this decreased workload of the heart
will result in decreased oxygen demands. This is one of the reasons that
we do see better morbidity rates when somebody has suffered
a myocardial infarction and they are then given a beta blocker is
because it actually decreases the stress on the tissue and we're able
to save a lot of that tissue. The effect on the kidneys is it
will decrease the release of renin and this will ultimately result
in decreased blood pressure. Now, this is where the main difference
between metoprolol, which is a selective, and propranolol, which is non-selective
is, and it's the beta-2 blockage. Because propranolol is non-selective,
it affects both beta-1 and beta-2. So it will have some
beta-2 blocking effects. Most of these are going to be seen as
adverse effects because they are going to be affecting primarily
the pulmonary system. So we see bronchospasms. We can actually see people having
a more difficult time breathing. This is especially true and this medication
class can be problematic in asthmatics. We have to watch peripheral
vasoconstriction. And so, if you have somebody that has Raynaud's,
this medication again is extremely harmful. Hypoglycemia. So again, watching people that are
diabetics or that suffer from hypoglycemia. So uses for propranolol
can be hypertension. We also can use it for angina. Remember how we said it decreases the oxygen
needs and the oxygen consumption in the heart. We can use it for
cardiac arrhythmias. People with migraines. It is very, very effective. One of the off-label uses, action
can be for intention tremors. We can see the beta
blockers used. Heart failure. So there's a lot of different
effects that can be used from this. Significant contraindications. People that have bradycardic rhythms,
complete heart block because again, it is going to affect the conduction
and the rate of the heart. And so, this would actually
further compromise their rhythm and their ability to
meet their oxygen needs. Cardiogenic shock. I do want to clarify. This is an uncompensated
cardiac failure. You can see this medication used
in heart failure but not in people that are unable to meet
any of the body's needs. So again, that would be a clarification
that you would really have to monitor for. Raynaud's disease and
reactive airway disease. So some of these we've
already previously mentioned. Some of the adverse effects that you would
need to monitor for is postural hypertension, bronchospasms, and then very seriously would be
myocardial infarction or compromised ability to meet the needs of the
body with circulation. This medication is well
absorbed when given orally. It can also be
given parenterally. It is well distributed. One thing to be aware of is
that the stability as far as the hyposensitivity may actually
not occur for two to three weeks. And so, patients during
this time need to be very, very careful with movements
and changing position. It is metabolized in the liver
and excreted through the kidneys. So the nursing interventions that are going
to help us maximize the therapeutic effects. So many of these interventions are
going to be stressing and emphasizing to the patients and
educating the patients. So first of all, we want them to
understand that this is not a medication that they should
double the dose. If they have forgotten the
dose, they need to leave it and go on to the next one
when it comes around. This is not one you want to double up
because of the effects that it does have on the blood pressure
and on the heart. They should be taking it with food and this
will actually increase the bioavailability and decrease GI upset. To minimize the adverse effects,
first of all, minimize stressors. This makes it so the medication is
actually going to be more effective. They should be checking a peripheral pulse
prior to giving the medication and holding it if it is below 60 or if
the rate is irregular. They should notify
their provider. They should be keeping
appointments with their provider so that we can monitor
EKGs and blood pressure. If you have this patient coming into the
physician's office, into the hospital, this is somebody that we need to be assessing
of respiratory assessment as well due to the risk of
bronchial constriction. So listening to the airflow, asking if
they're having any difficulty breathing. Make sure that if you ever have a patient
that has a history of COPD, asthma, respiratory complaints, you should always
question if this medication is ordered. There are others that are selective that are
not going to put this patient at the same risk. So it's very important that we want
to prevent that beta-2 blockage. Know why your patient is
receiving the medication. Are they receiving it to
decrease angina pain? So we want to know what
their pain level is. Has it decreased? Watch for their -- you should have
increased tolerance with activity. So again, teach the
patient and watch them. Do they know how to take their
own pulse, their heart rate? Can they detect if it's
regular or irregular? Are they able to verbalize
to you how to move safely? Do they know to sit at
the edge of the bed? Do they know to sit in a chair and make
sure they're not having any dizziness when they first stand up, to stand for
a second before they take off walking? Any of those changing positions or
safety related to postural hypotension. It's very important they understand never
abruptly stop taking the medication. They need to understand that,
again, if we remove that blockage, not only is their blood pressure going
to go high, but their heart rate. So I had students in the hospital and there
was this wonderful little lady, she was 83. She had an abdominal surgery and
then had some complications. And they were walking her, they were
getting her up and walking her. And she was getting ready to go to a
rehab facility and she was funny, funny. She kept saying that she wanted to
go to one facility over another because they had better-looking
young men aides. And I thought if you're at 84 concerned
about that, you go for it girl. But I left the floor, the
students were walking. And then I got a call, "We need
you to come really quickly. The patient doesn't look well." And I said, "Okay, go
back to your basics. Take your vital signs." Well, her heart
rate had doubled. I said, "Go back to her history," was this
lady I was walking at the time to the floor. What was she on before surgery? Because they said, "No, no, no,
she's not on any beta blockers." And I said, "Go look
at the prehistory." Well, she had been on a beta
blocker before surgery. Because of the complications,
she was not restarted on it. It wasn't an issue until
she got that stimulation. Her heart rate was 135. Blood pressure was actually low because
the heart didn't have time to fill. And of course, she
felt very weak. Physician got called. They put her on a cardiac monitor, gave
her an IV beta blocker, slowed her down, and then they were going to
start her on a maintenance dose. So it's very important that patients understand
not to abruptly stop these medications because we can see the blood pressure
go way high and the heart rate as well because we're going to lose
that blockage effects. Metoprolol is a selective
beta-adrenergic blocker. And selective beta blockers have an
advantage over non-selective in some cases because they do not usually
block the beta-2 receptors. And because of this, they do not block the
sympathetic bronchodilation that is so important for patients with lung disease who
have asthma, allergic rhinitis. And so, these patients
actually need that response. So the beta-1 effect of metoprolol is
identical almost to that of propranolol. We see the beta-1 blockage. So the heart is going to decrease
the rate and the contractility. Results in decreased cardiac output
and decreased blood pressure. It does also slow again the atrioventricular
conduction, decreased automaticity, and all of this decreases
the oxygen demands. So remember again, these are negative
inotropic, chronotropic, dromotropic. It's going to decrease the blood
pressure and the oxygen demands, which will help
with anginal pain. It decreases the release of renin so
we do not have that vasoconstriction and decreases the
blood pressure. I do want to point out. Though we do not routinely see beta-2 effects
if somebody is at very, very high doses. Sometimes that selectivity
is less dependable and they can have some minor
to severe respiratory effects. So they use this for metoprolol. Again, very similar hypertension, angina,
cardiac arrhythmias, heart failure. We do also see it used for people with
open-angle glaucoma who have increased pressure. They can use it for this too, make
it so that the fluid can flow out. Contraindications. Bradycardia, complete heart block, shock,
people whose heart failure is not compensated, this is not a time to
give this medication. Now, while we do see metoprolol being less
restrictive and causing that vasoconstriction in the periphery that somebody
with Raynaud's cannot tolerate, they still say that it should
be used in extreme caution. Adverse effects. Again, people still have to
watch for postural hypertension. And serious if they go off it abruptly,
they could risk a myocardial infarction. It is absorbed orally very well. Bioavailability is increased
when taken with food. And if somebody needs immediate
results, we can give it intravenously. It is excreted through the kidneys
and metabolized in the liver. For the nursing interventions, I'm just going
to have you review those of propranolol. Because other than the risk of respiratory
involvement, they are identical. Again, I do want to emphasize if a
patient is taking extremely high doses, you do still want to do a very thorough
respiratory assessment and ask them if they are having
any complications. Because patients on higher doses do run the
risk of allergic rhinitis up to bronchospasms. Cardiac glycosides exert
positive inotropic effects on the contractility
of the heart muscle. Inotropic means related to or influencing
the force of myocardial contractility. And so, what we're going to
end up with when we talk about a positive inotropic effect is
an increased force of contraction. Digoxin or Lanoxin, which is
derived from the foxglove plant -- -- is the prototype
of this class. And this is just a
picture of the foxglove. And so, when we talk about heart failure
and that needing for increased force of contractility, this is one of
the medications that you will see. Now, this is an older medication and you
will generally not see it utilized except for somebody that has
left-sided heart failure. The pharmacodynamics of digoxin are several
different ones and we're going to talk about the direct and the indirect effects
that it has on the cardiac muscle. The overall effect that we see is that
it does increase the cardiac output. The first effect is the direct one and
it acts on the cardiac muscle itself. It strengthens the
force of contraction and this is the positive inotropic
effect which was previously mentioned. It does this through increasing
the movement of calcium across the myocardial cell membrane
during the depolarization. And as calcium is needed for contractions,
then we actually get a stronger contraction because we have more calcium
that is actually available. It also will affect the
electrical conduction system, and so it increases the
refractory period at the AV node. This allows the pausing
or that period of time that the heart muscles cannot actually
be stimulated into contracting again. And so, this actually allows
for a little bit of delay. This refractory time is actually
very helpful when you have somebody that has rapidly conducted
atrial fibrillation. Some of the indirect effects
that we can see resulting from digoxin is actually the stimulation of
the ANS or the sympathetic nervous system. So it has a vagomimetic effect. It mimics the action of the vagus
nerve and so it slows conduction and this is actually a
negative dromotropic effect. And it depresses the sinoatrial node
and prolongs conduction to the AV node. So it slows the heart rate and this
is a negative chronotropic effect. And you want to be
familiar with these. So it has a negative chronotropic and the
way to remember that is chrono is time. So it slows the
timekeeper of the heart. It slows conduction and this
is a negative dromotropic and it increases the
force of contraction. And so, it's a
positive inotropic. Because of the prolonged conduction time, the
cardiac output is increased as a result of all of these factors we've
just talked about. Absorption can vary some with
the type of preparation. How much is absorbed and the time it
takes to be absorbed can be affected. One of the things to be aware of is that food,
while it can slow down the rate of absorption, it doesn't usually affect
the overall preparation. And as digoxin can be irritating to the lining
of the stomach, we do usually encourage people to take it with food because again, as they do
that on a regular basis, the overall percentage and level of absorption
will be balanced out. It can still be administered IV. So a couple of things to be aware of is that
it is highly concentrated in the myocardium. We also see increased levels in skeletal
muscle, the liver, the brain, and the kidneys. It does cross the blood-brain
barrier and the placenta. Therefore, if you have an expectant
mother it will get to the fetus. It has a very long half-life. Now, because of that, it takes longer
sometimes to get up to that therapeutic level where we've got that
therapeutic index. And so because of that, we may sometimes
do what we refer to as digitalization. And this is a loading dose. We usually will give three divided
loading doses, two to three depending on the patient over
a 24-hour period. They are usually given IV and then they are
started on a therapeutic maintenance dose. What this does is it gets the blood
level up high enough that we can get and achieve that
steady state quicker. This is usually done more in somebody
that has a rapid atrial fibrillation. It is not as common of a
practice in heart failure. So it is metabolized in the liver
and excreted in the kidneys. One of the things to be aware of is that
because it is excreted in the kidneys, people that have poor renal function a
lot of times in our elderly, we see this, then we do need to use lower doses because it is
not excreted fully and it does make them more at risk for having
digoxin toxicity. This medication again is used in heart failure,
atrial fibrillation, and atrial flutter. Do understand that this medication
is an older medication. It is not used as a first-line
drug in most patients. You will see it used in left-sided heart
failure and for fibrillation and flutter. But we have found that the mortality
rate is decreased in patients that we use first RAAS
inhibitors, beta-blockers, and some of the other
classes of medications. One of the things that we do notice is that
it can cause some of the same arrhythmias that is actually used to treat, and so
it is a difficult medication to use. It does have a higher
incidence of problems with it. Some of the contraindications
are things like heart block, ventricular fibrillation,
sick sinus syndrome. The reason is think about the effect
that we talked about that digoxin has. It delays the conduction;
it delays the heart rate. And so, if you have somebody that already
has problematic or spotty conduction of the electrical system or has a poor
pacemaker, you don't want to use digoxin because it's going to thoroughly
compromise your heart muscle. We have to really watch because it can
cause severe bradycardia and block. And this is again seen primarily
with digoxin toxicity. Some of the adverse
effects to be aware of, common ones that we watch
for are cardiac toxicity. And again, this is primarily seen with somebody
that's going to have that lower heart rate. Some of the causes can be electrolyte
imbalances, primarily hypokalemia. So you have somebody with lower potassium or low
magnesium, they are going to get a larger effect in the cardiac tissue
with the digoxin. Hypercalcemia, it potentiates
the effect of the digoxin. Now, there are in your textbook
a table that talks about some of the antidotes
that we will use. One of the ones that is expensive
and not used really frequently, but I do want to mention it is
digoxin immune fab, Digibind. And this actually, when we have high levels
of digoxin that we do need to remove, we can give this IV, it does bind with certain
percentages of the digoxin and makes it unable to bind with the
receptors of the tissue. And therefore the medication is ineffective
and we lose some of that overall effect. This is just a reminder,
educate your patients. So there are several things that we can do to
actually maximize the therapeutic effects. First of all, digitalization. As I mentioned previously, this will be
given usually for atrial fibrillation. And so, they will receive two or three
evenly spaced larger-than-normal doses. These are loading doses. What we are doing is raising the
level of the medication and so, that the patient is at a
steady state much quicker. And so, then we can go ahead and
put them on a maintenance dose. It is very, very important that when we do
this that we make sure that the patient is on cardiac monitoring, that we are making
sure that they have adequate fluid intake, and that they have good excretion
because remember this is excreted through the kidneys and we
do have to monitor that. So it does help us to achieve that
rapid onset of therapeutic effects. And we do then just need to
monitor for the adverse effects. Digoxin has a very narrow
therapeutic window. And so, the therapeutic range is 0.5
to 2.0 nanograms per milliliter. We do actually see some patients that can
start exhibiting signs of toxicity even when they are within
that normal range. The patients we usually see this occurring with
are renal patients because they seem to build up and to start showing signs of toxicity
much quicker than other patients. And so, we do want to monitor patients to make
sure that they are within that normal range as well as assessing them
for any signs of toxicity. It's important that when patients are on digoxin
and they come into a facility that we look when their last therapeutic
range was when it was drawn. That we check with the physician,
do you want it checked? We make sure that patients know how frequently
they should be getting blood work done. We also want to assess
patients for bradycardia. Now, this is something that we
assess prior to administration. In an adult we want their heart
rate to be greater than 60. And so, we're going to listen to
the apical pulse for a full minute. This has to be a full minute because especially
if somebody has atrial fibrillation, you do not want to get it during a period
of rapid heart rate or slow heart rate and get a number that
is actually inaccurate. And so, it's very important that
we take it for a full minute. In an adult we want the
rate to be greater than 60. In a teen or younger child, we
want it to be greater than 70. And in a young infant, we want
it to be greater than 110. So what we're looking at is
that we want it to be greater than a bradycardic rate
for that age group. So it's important that we
assess for any bradycardia. We want to monitor for any
electrolyte imbalances. We've already mentioned
that low potassium and magnesium can actually place the
patient at risk for digoxin toxicity. Now, guys, I don't know about
you but I do not sit at home and suddenly have a little light
come over my head and I say, "Oh, I think I'm experiencing
hyperkalemia." It would be really nice if
that happened, but it doesn't. Or, "Oh, I've got
hypokalemia, hypomagnesemia." You need to teach patients
what that feels like. And so, one of the easiest ways to be able to
have a patient identify both the low potassium and the magnesium because they have
very similar signs and symptoms. They actually you will get a
lot of cramping in the legs. They have increased electrical
conduction with the magnesium and so they get a
lot of irritability. So if you say, you know, you've got a
lot of cramping maybe the paresthesia, that's probably the easiest
one for them to identify. High calcium actually will also place a
patient at risk for digoxin toxicity. So with high calcium or hypercalcemia,
everything gets very slow. Unfortunately, mentation, muscle
movements, bowels, everything slows down. And so, it's important that if the patient says,
"You know, I just feel so tired and sluggish and I'm falling," that
we look for other things that could indicate that
they may have high calcium. And then, know who's
at risk for it. So it's very important that you as the nurse
be aware if they are taking other medications that do put them
at risk for this. For example, if you have a patient
that is taking hydrochlorothiazide. Hydrochlorothiazide
is a diuretic. It can cause them to lower
their potassium magnesium, but it also causes them to
hold on to the calcium. So it puts them at increased risk of having
some of these electrolyte imbalances. So this is why it is so important
that as a nurse, that you are putting that picture together and
educating your patients. So you have to
monitor, make sure that the imbalances are corrected
before we are doing administration. You also want to assess for
non-cardiac signs of digoxin toxicity. These if you will remember GI, a lot of
anorexia, nausea, vomiting, diarrhea. Patients will complain of
headache and blurred vision. You will also hear them complaining
or saying they've got yellow vision. A lot of patients will complain of
yellow halos around objects and lights. I have heard some that are a
little bit blue but yellow, and so you'll hear it
referred to as yellow vision. It's a very common thing. Unfortunately, confusion. And so we do need to
monitor for this. We need to teach patients how to
monitor for these things as well. And so, when we're teaching
them to look for bradycardia, they're not going to
listen to an apical pulse. Teach them how to
do a radial pulse. And then, if it's below 60, rest
for a little bit and take it again. If it's still below 60, to call their
physician and not take their medication until they talk
with the physician. It's important that they know the signs
and symptoms of digoxin toxicity. If they start having
a lot of GI upset. If they notice that they've
got a lot of diarrhea. Are they having trouble remembering things
or are family members picking up on that along with a
slower heart rate? They may need to go in and get
their digoxin level checked. This is medication comes in little
white and little yellow tablets. It does not really
have a nasty taste. A lot of elderly people
so they don't forget to take their medication
will put them out on tables. This is not a medication you want a grandchild
getting into or anybody getting into. So make sure they understand to keep this out
of the reach of children and that if they -- to decrease their GI upset, it can
be taken with food to decrease that. This is just a fun little mnemonic to kind
of help you remember some of the signs and symptoms of
digoxin toxicity. So bradycardia or heart block. Remember, we're going to
usually go with the number 60. Anything below 60, the patient shouldn't be
taking it and we shouldn't be giving it. Blurred vision or yellow vision. Remember those yellow halos. Occasionally, we can see a
rash, abdominal pain, nausea, vomiting, diarrhea, a
lot of GI symptoms. And then, delirium
and confusion. Nesiritide is the prototype drug in
the human B and B class of drugs. This is a newer class of drugs and I just want
to mention it because I think we're going to see more of them
as time progresses. So nesiritide is actually a vasodilator and
it acts just like the B natriuretic peptide. Now, the B natriuretic peptide is
secreted primarily by the ventricles in response to fluid
and pressure overload. So when we get that increased stretch happening
on the tissues, then we see an increase in the B natriuretic peptide
being actually excreted. So it is administered primarily by a
bolus and then an IV administration. So you will most likely not see this
medication unless you are working in a monitored
critical care bed. It is usually fairly immediate and they actually
start seeing effects within 15 minutes. So if somebody comes in in extreme
fluid overload, this is a good way to help them relax those vessels and get that
fluid down a little bit more in the periphery so that we can get some other
interventions in place. And then, the nesiritide acts to compensate
for the decreased cardiac function because it decreases or reduces the
cardiac preload and the afterload. And because it does all this, it actually will
produce something similar to a diuretic effect because it increases the sodium secretion
and it suppresses the RAAS system. And so, all of these things help a heart
that is actually not functioning well. So another class of drugs I would
like you to at least be familiar with because I do think we
are going to see more use from this are the angiotensin
receptor neprilysin inhibitors. And I'm going to
use the trade name because I really could not find a
good pronunciation for the other. So this is Entresto. Entresto actually is going to assist in
modulation of the natriuretic system and it inhibits the
enzyme neprilysin. Now, neprilysin actually degrades
the vasoactive peptides. And so, because of this, what it does is
when it's added to an ARB, it helps decrease and block the
activity in the RAAS. And so, we don't have the aldosterone,
and the sodium, and the fluid retention. It also is going to decrease the conversion
of angiotensin I to angiotensin II. And then, we get some of that vassal
relaxation going on in the periphery. And so, we have that decreased
preload and decreased afterload. So because of this, it's got a really good
effect in people with chronic heart failure that does not react well
to other medications. Now, I do want you to be aware that the drug
is a pro-drug, which means that it's given in its less active form, and it is
more active following metabolism. It takes about 30 minutes after it's
administered to start seeing it in the system. It takes about 3 days to reach steady state
and this is when it's given twice daily. So nursing interventions. This medication can actually be
given without regard for food. Again, you do want to give
it usually twice daily. And so, we want that
to be evenly spaced. We do need to make sure that if people
are switching from an ARB or an ACE, that they usually have about 36 hours, what they
call a washout period to get the other drug out of the system before
we start this one. So we do not have that
duplication of efforts. Assessing for
therapeutic effects. Why would we be giving that? Monitor for if we have increased
stabilization of the signs and symptoms in their
chronic heart failure. Do they have increased
activity tolerance, decreased shortness of
breath, decreased nocturia? What are their labs showing us? What are the BUN, and the
creatinine, and the potassium? It's important that we make sure that
these remain within acceptable limits. When we're looking for adverse effects, it's
very important that we monitor for vital signs, monitor for hypotension, and that
they monitor themselves at home. We want to look for any abnormal lab
values, especially for the creatinine, and the potassium, kidneys,
and then our electrolytes. And then, for anything that indicates a
worsening of their heart failure, a cough, persistent coughing,
or dizziness. Teach the patient that frequent blood
pressure and monitoring is necessary. And again, go over the options and
where they can get it checked. They need to be reminded
to change position slowly. And then, to tell their provider if
they are put on a potassium supplement or currently taking a potassium supplement
or a potassium-sparing diuretic. Now remember, this is
important because with an ARB, they do not have that aldosterone secretion,
they don't have the sodium retention and therefore they do have a little
bit more potassium retention. So this does put them more
at risk for hyperkalemia. They need to notify the
provider of any swelling. Again, we are still at some risk for angioedema
and to let the provider know immediately. And then, they are encouraged
to drink adequate fluids so that they do not have
hypotensive episodes.

Transcript for:Understanding Cardiovascular Drug Treatments

Transcript for:
Understanding Cardiovascular Drug Treatments