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Cardiovascular and Renal Medications

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1 Cardiovascular and Renal Medications
Chapter 15 Cardiovascular and Renal Medications

2 Chapter 15 Lesson 15.1

3 Learning Objectives Identify the approved way to give different forms of antianginal therapy Discuss the uses and general actions of cardiac drugs used to treat dysrhythmias Describe the common treatment for various types of lipoprotein disorders

4 Cardiovascular System: Major Arteries

5 Cardiovascular System: Major Veins

6 Urinary System

7 Antianginals and Peripheral Vasodilators
Nitrates: “Universal Vasodilators” Directly cause vascular smooth muscle to relax in arterial and venous circulation Decrease myocardial oxygen use Increase collateral-vessel circulation to the heart Calcium Channel Blockers Dilate coronary arteries and arterioles Reduce response of electrical conduction system Narrowing or constriction of smooth muscle in the coronary arteries and peripheral vascular system reduces the amount of blood flow to the heart. This lack of blood supply results in diminished oxygen and nutrient flow to the heart, causing chest pain, or “angina,” and peripheral vascular disease. Arterial relaxation reduces the pressure the heart has to pump against. Venous relaxation causes blood pooling and decreases venous return to the heart. Nitrates are readily absorbed under the tongue, through the skin, and orally. Nitroglycerin is a nitrate. The half-life of nitroglycerin is only 1-4 minutes. Calcium is an electrolyte that helps move electrical impulses through cardiac tissue. Calcium channel blockers are drugs that help slow down the flow of calcium ions across the cell membrane, which reduces the amount of calcium available to move electrical impulses. There are many actions of these drugs.

8 Main Components of Microcirculation

9 Antianginals and Peripheral Vasodilators (cont.)
Action and Uses Nitrates Acute and chronic anginal attacks Reduce the workload of the heart Peripheral Vasodilators Relax the smooth muscles of peripheral arterial vessels to increase peripheral circulation Used to treat leg pain caused by vasoconstriction Patients with occlusive arterial disease have blockages in peripheral arteries. This causes swollen, painful feet and ulcers around the ankles. Peripheral vasodilators have been used with limited success. Patients who may benefit from peripheral vasodilators include those with intermittent claudication, arteriosclerosis obliterans, Raynaud disease, nocturnal leg cramps, and vasospasm caused by blood clots.

10 Site of Action of Peripheral Vasodilators

11 Antianginals and Peripheral Vasodilators (cont.)
Adverse Reactions Nitrates: Flushing, postural hypotension, tachycardia, confusion, dizziness, fainting, headache, lightheadedness, vertigo, weakness, drug rash, localized pruritus, skin lesions, eye and mouth edema, local burning in mouth, nausea and vomiting Peripheral Vasodilators: Headache, weakness, tachycardia, flushing, postural hypotension, dysrhythmias, confusion, severe rash, nervousness, tingling, and sweating Some nitrates contain tartrazine, a chemical that may cause an asthmatic type of allergic reaction. Peripheral vasodilating agents have a stronger action when taken with antihypertensives and alcohol. This leads to hypotension. What are the nursing implications for the LPN/LVN regarding these drugs? What patient teaching should be done for nitrates? (Storage? Expiration date?) For peripheral vasodilating agents? How should patients be taught to use nitroglycerin during an acute anginal attack? What are some drug interactions with nitrates or peripheral vasodilators?

12 Antidysrhythmics Four Classes
Class I: disopyramide, procainamide, quinidine Lengthen the refractory period Decrease cardiac excitability Class II: acebutolol, esmolol, propranolol Reduce sympathetic excitation (reduce loading) Class III: amiodarone Lengthen the time it takes for one cell to fire and recover Class IV: verapamil Blocks calcium entry into the myocardium, prolongs resting phase People with heart disease or other problems that affect the heart muscle are at risk of developing irregular heartbeats, or cardiac dysrhythmias. Dysrhythmias may be fast or slow, with an irregular or regular pattern. The most common causes of dysrhythmias are an irritation to the heart tissue after a myocardial infarction, fluid and electrolyte imbalances, diet, hypoxia, and drug reactions. Dysrhythmias vary in patients in regularity and intensity. An electrocardiogram is needed to determine the type of dysrhythmia a patient is experiencing. Halter monitors are portable ECG machines that take an ongoing tracing of the heart’s electrical function. Antidysrhythmics act on each individual cell of the heart.

13 Conduction System of the Heart

14 Antidysrhythmics (cont.)
Action and Uses Quinidine and Procainamide Treat rapid and irregular dysrhythmias by decreasing the excitability of myocardial cells Bretylium Slows conduction rate in the ventricles, slows norepinephrine release in the myocardium Disopyramide Slows the depolarization of cardiac cells The exact type of irregular rhythm can only be determined by taking an ECG. It is important to find the cause of the dysrhythmia. Most dysrhythmias are caused by (1) increased sensitivity of the electrical cells in the heart, resulting in irregular or early ectopic beats and (2) electrical activity moving through abnormal conduction pathways, triggering myocardial cells to fire improperly. Depolarization is the movement of electrolytes in and out of the cell as it gets ready to send another electrical impulse.

15 Antidysrhythmics (cont.)
Lidocaine Increases the strength of electrical impulses Adenosine Stops the heart for several seconds to allow it to convert to normal sinus rhythm Beta-adrenergic blockers (propranolol) Decrease the heart beta-receptor response to epinephrine and norepinephrine Many patients refuse to continue taking adenosine after experiencing its effects. Many of the antidysrhythmics are so powerful they should only be used in critical care units. What are some of the medication-specific adverse effects of these drugs? Antidysrhythmics often cause or worsen heart failure or urinary retention. Patients with a past history of heart failure should be watched closely. Drug interactions: the effect of quinidine is increased by potassium and decreased by hypokalemia. The action of verapamil is stronger if the patient is taking digitalis and beta blockers. Beta blockers have many drug-specific interactions. How can the steps of the nursing process be applied here?

16 Antihyperlipidemics Types of Lipoproteins
Chylomicrons (mostly triglycerides) Formed from absorption of dietary fat in intestine Very low-density lipoproteins (VLDLs) Made up of large amounts of triglycerides that were made in the liver (pre-beta lipoproteins) Low-density lipoproteins (LDLs) Breakdown of VLDLs linked with cholesterol and protein High-density lipoproteins (HDLs) Clear out excess cholesterol from tissue Lipoproteins are described by how thick or dense they are. Chylomicrons are usually present for 1 to 8 hours in the plasma after the last meal. Nearly all the triglycerides in plasma that are not in chylomicrons are considered to be VLDLs. About 75% of plasma cholesterol is moved in the form of LDLs. High LDL levels indicate cholesterol levels that are higher than the body needs. Patients are at high risk for developing atherosclerosis. HDLs block the uptake of LDL cholesterol by the vascular smooth muscle cells and may prevent atherosclerotic activity.

17 Path of Lipid Metabolism

18 Antihyperlipidemics (cont.)
HMG-CoA Reductase Inhibitors Highly effective for lowering LDL levels Fibric Acid Derivatives Highly effective for lowering triglyceride and increasing HDL levels Bile Acid Sequestrants Form an insoluble compound with bile salts to reduce serum cholesterol levels Niacin Effective at lowering LDL levels and increasing HDLs Research suggests high LDL levels can lead to coronary artery disease. Evaluation of LDL and HDL levels is of primary importance, because research has shown that lowering serum lipids or cholesterol can reduce the risk of atherosclerotic heart disease. HMG-CoA reductase inhibitors (statins) are extremely costly but highly effective. Liver function tests should be closely monitored when taking these drugs. Fibric acid derivatives are not as effective as HMG-CoA reductase inhibitors in lowering LDL levels. Gemfibrozil and fenofibrate are well tolerated but can cause liver toxicity and gallstones. The liver uses cholesterol to replace the bile excreted by bile acid sequestrants. These drugs increase triglyceride levels. Adverse GI side effects include constipation, nausea, and bloating. Niacin is highly effective. Its use is limited by the side effect of flushing in the face and neck. What are some significant points for the LPN/LVN to include in patient teaching?

19 Chapter 15 Lesson 15.2

20 Learning Objectives List the general uses and actions of cardiotonic drugs Explain the actions of different categories of drugs used to treat hypertension Identify indications for electrolyte replacement

21 Internal Anatomy of the Heart

22 Coronary Arteries

23 Coronary Arteries

24 Cardiotonics Actions Uses
Increase the contraction strength or force (positive inotropic action) Slow the heart rate Uses Treatment of CHF and rapid or irregular heartbeats (atrial fibrillation, atrial flutter, frequent PVCs or paroxysmal atrial tachycardia) Cardiotonics, often referred to as cardiac glycosides, make the heart beat slower and stronger. The digitalis preparation digoxin is the major cardiac glycoside. It has been used for many decades. All cardiotonic drugs have the same basic drug action. They differ only in the speed and duration of action. Chronotropic drugs affect the rate or rhythm of the heart. Dromotropic drugs influence the speed of the electrical impulse as it passes through the nerve or cardiac muscle fibers. PVCs are premature ventricular contractions.

25 Cardiotonics (cont.) Adverse Reactions Drug Interactions
Digitalis toxicity: serum digoxin levels verify The amount of medication that is helpful (therapeutic) and the amount that is harmful (toxic) are not very different. Don’t confuse the sound-alikes digoxin and digitoxin Drug Interactions Nursing Implications and Patient Teaching Cardiotonics are powerful and can be toxic to the heart. The symptoms of digitalis toxicity may begin slowly and are easy to overlook; however, toxicity can occur quickly, especially in the elderly. Symptoms include bradycardia, dysrhythmia, tachycardia, apathy, confusion, delirium, disorientation, drowsiness, mental depression, headache, visual changes (blurred vision, yellow/green vision, halos around dark objects), anorexia, diarrhea, nausea, vomiting, severe weakness. Nursing implications include taking an apical pulse for a full minute prior to administering the dose of digoxin. If the apical pulse is less than 60, the medication is held (not given) and the physician immediately notified. What patient and family teaching will the LPN/LVN be expected to give?

26 Antihypertensives, Diuretics, and Other Drugs Affecting the Urinary Tract
Indirectly reduce blood pressure by producing sodium and water loss and lowering the tone or rigidity of the arteries Types Thiazide and sulfonamide diuretics Loop diuretics Potassium-sparing diuretics Hypertension is a disorder in which the patient’s blood pressure is elevated above normal limits for age. Blood pressures above 150/90 mm Hg are associated with accelerated vascular damage of the heart, brain, and kidneys, which leads to increased risk of death. Primary hypertension affects 80% to 90% of people with high blood pressure; the cause is unknown. The other 10% to 20% have secondary hypertension, in which elevated blood pressure is the result of another disease process or problem. Loop diuretics block the active transport of chloride, sodium, and potassium in the thick ascending loop of Henle. These drugs work well in patients with impaired renal function. Potassium-sparing diuretics increase the excretion of water and sodium by saving potassium. These drugs are used in patients with kidney disease or who are at risk for potassium imbalance.

27 Antihypertensives, Diuretics, and Other Drugs Affecting the Urinary Tract (cont.)
Adrenergic Inhibitors Beta-adrenergic blockers Nonselective; block beta1 and beta2 sites Selective; block beta1 sites Central adrenergic inhibitors Cause vascular relaxation and lower blood pressure Peripheral adrenergic antagonists Limit norepinephrine release, prevent vasoconstriction The elderly population are more susceptible to developing adverse reactions (hypotension, impaired mental activity, hypokalemia, increased serum glucose levels) when using diuretics. Lower doses are advised in this population, and the drug is gradually discontinued to avoid a rebound effect. The various adrenergic inhibitors block the transmission of epinephrine and norepinephrine at the alpha and/or beta sites. Nonselective beta blockers reduce the heart rate and force of contraction, prevent renin release, and slow the outflow of sympathetic nervous system messages from the brainstem to the vasomotor center, which tells the body to constrict the blood vessels and increase heart rate. Central adrenergic inhibitors stimulate peripheral alpha-adrenergic receptors, causing brief vasoconstriction, and then stimulate alpha2-adrenergic receptors in the brainstem that coordinate cardiac function. Peripheral adrenergic antagonists decrease total peripheral resistance to blood flow by relaxing smooth muscle. Most of these medications are no longer available in the United States.

28 Antihypertensives, Diuretics, and Other Drugs Affecting the Urinary Tract (cont.)
Alpha1-adrenergic inhibitors Lower peripheral resistance and blood pressure Combined alpha- and beta-adrenergic blockers Angiotensin-Related Agents Angiotensin-converting enzyme inhibitors Angiotensin II receptor antagonists Vasodilators Calcium Channel Blocking Agents The renin-angiotensin mechanism directly increases blood pressure. ACE inhibitors (angiotensin-converting enzyme inhibitors) inhibit the conversion of angiotensin I to angiotensin II in the liver and lungs. Angiotensin II receptor antagonists interfere with angiotensin II acting on the adrenal cortex to increase aldosterone secretion. Vasodilators reduce systolic and diastolic blood pressure by direct relaxation of smooth muscle, which lowers vascular resistance. Calcium channel blocking agents limit the passage of extracellular calcium ions through specific ion channels of the cell membrane in cardiac, vascular, and smooth-muscle cells. This lowers peripheral resistance and decreases blood pressure.

29 High Blood Pressure Stage I: Lifestyle Changes Stage II: Drug Therapy
Adverse Reactions Drug specific Drug Interactions What lifestyle changes may help a patient reduce hypertension risk factors? (Losing weight, increased physical activity, reduction of fat, salt, and calories in the diet, smoking cessation, and reducing alcohol intake) The initial drug of choice is an oral thiazide or adrenergic beta blocker. The drug is started in low dosage and increased as needed until maximum dosage is reached. Loop diuretics are used when hypertension is severe, and blood pressure must be brought down quickly. Antiadrenergic agents may be added if the maximum diuretic or beta-blocker dose is not effective. Vasodilators are most effective when used with a beta-adrenergic blocking agent. Adrenergic-inhibiting agents are powerful and are used only when necessary because of their high risk of side effects. Refer to Table for adverse reactions of these drugs. What are some of the nursing implications and patient-teaching issues for these medications?

30 Drugs Useful in Treating Urinary Problems
Urinary incontinence Treatment: anticholinergics/antispasmodics, alpha-adrenergic agonists, estrogens, cholinergic agonists, and alpha-adrenergic antagonists Benign prostatic hyperplasia Treatment: alpha1-adrenergic receptor blockers Analgesia Treatment: phenazopyridine There are a variety of drugs to treat urinary symptoms related to incontinence, benign prostatic hyperplasia (BPH), and urinary tract pain secondary to infections. Anticholinergic agents used for urinary incontinence stop bladder contraction and decrease the response of some bladder muscles. Antispasmodic drugs directly cause smooth-muscle relaxation. Estrogens may help restore urethral mucosa and increase vascularity, tone, and the ability of the urethral muscle to respond. Benign prostatic hyperplasia (BPH) is a noncancerous growth of the prostate gland that can cause voiding problems. Tamsulosin (Flomax) and finasteride are two drugs specifically used for this problem. What are some of the nursing implications and patient teaching issues for these medications?

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