MS CH 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders PDF

4068_Ch24_462-498 15/11/14 1:35 PM Page 462 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders KEY TERMS MAUREEN MCDONALD acute coronary syndrome (ah-KYOOT KOR-uh-nareee sin-dr-OME) anastomosed (an-AST-tah-most) aneurysm (AN-yur-izm) angina pectoris (an-JYE-nah PEK-tuh-riss) a...

4068_Ch24_462-498 15/11/14 1:35 PM Page 462 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders KEY TERMS MAUREEN MCDONALD acute coronary syndrome (ah-KYOOT KOR-uh-nareee sin-dr-OME) anastomosed (an-AST-tah-most) aneurysm (AN-yur-izm) angina pectoris (an-JYE-nah PEK-tuh-riss) arteriosclerosis (ar-TEER-ee-oh-skleh-ROH-siss) atherosclerosis (ATH-er-oh-skleh-ROH-siss) collateral circulation (kuh-LAH-tur-al SIR-kew-LAY-shun) coronary artery disease (KOR-uh-nare-ee AR-tuh-ree dih-ZEEZ) endarterectomy (en-DART-tur-eck-toe-me) embolism (EM-buh-lizm) high-density lipoprotein (HY DEN-sih-tee LIH-pohPROH-teen) hyperlipidemia (HY-pur-LIH-pih-DEE-mee-ah) intermittent claudication (IN-tur-MIT-tent KLAW-dihKAY-shun) low-density lipoproteins (LOH DEN-sih-tee LIH-pohPROH-teen) lymphangitis (lim-FAN-jee-EYE-tiss) myocardial infarction (MY-oh-KAR-dee-yuhl in-FARKshun) peripheral arterial disease (puh-RIFF-uh-ruhl ar-TEERee-uhl dih-ZEEZ) plaque (PLAK) Raynaud’s disease (rah-NOHZ dih-ZEEZ) thrombosis (throm-BOH-siss) varicose veins (VAR-ih-kohz VAINS) venous stasis ulcers (VEE-nus STAY-siss UL-sers) 462 LEARNING OUTCOMES 1. Explain the etiologies, signs, symptoms, and therapeutic measures of coronary artery disease, angina pectoris, and myocardial infarction. 2. List data to collect for patients with coronary artery disease, angina pectoris, or myocardial infarction. 3. Describe what therapeutic measures are used to treat coronary artery disease, angina pectoris, and myocardial infarction. 4. Explain the etiologies, signs, and symptoms for each of the peripheral vascular disorders. 5. Identify therapeutic measures used to treat peripheral vascular disorders. 6. Plan nursing care for patients with a peripheral vascular disorder. 4068_Ch24_462-498 15/11/14 1:35 PM Page 463 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders Cardiovascular diseases (CVDs) are the leading cause of disability and death in the United States. Diseases of the heart and peripheral vessels can affect quality of life and alter the ability of the individual to perform tasks of everyday living. Many factors leading to cardiovascular diseases can be controlled or modified. Education is important in preventing and treating occlusive CVDs. An estimated 83.6 million American adults have one or more types of CVDs. In 2012, an estimated 785,000 Americans will have had a new myocardial infarction (MI) and 470,000 a recurrent MI. About every 25 seconds, a person in the United States will ha ve a coronary e vent, and e very minute someone will die from one (Roger et al, 2012). More than one in three women have some form of CVD, which occurs on a verage about 6 years later than in men, often after menopause. In 2010, incidence of coronary heart disease (CHD) was greatest in people over age 65. The prevalence among men was 7.8% and in women, 4.6%. The average age for a person having a first heart attack is 64.5 for men and 70.3 for women. Smoking lowers this age for both genders but more so for women. Because women typically have heart attacks at older ages than men, the y are more likely to die from heart attacks within a few weeks. It is interesting to note that the prevalence of CHD decreases with higher education. People with less than a high school education had rates of 9.2%, whereas those with a college degree had rates of 4.6 % (Centers for Disease Control and Prevention, 2011). 463 TABLE 24.1 ATHEROSCLEROSIS SUMMARY Diagnostic Tests Cholesterol Triglycerides Arteriogram Therapeutic Measures Low-fat, low-cholesterol diet Smoking cessation Increased exercise—walk 30 minutes daily Priority Nursing Diagnoses Deficient Knowledge related to selfcare and health promotion Pain related to reduced vascular or coronary artery blood flow ARTERIOSCLEROSIS Arteriosclerosis is a disorder characterized by thick ening, loss of elasticity, and calcification of arterial walls. This condition is part of the aging process in which the intimal lining of the artery wall loses elasticity and weakens. This weakening is due to the high pressure that carries blood within arteries. Normal artery ATHEROSCLEROSIS Atherosclerosis is the formation of plaque within the arterial wall. Arteriosclerosis and atherosclerosis are conditions that may begin in early childhood and progress without symptoms through adult life. It causes coronary artery disease (CAD), leads to CHD (Table 24.1). Pathophysiology Atherosclerosis is a multistep process that af fects the inner lining of the artery (Fig. 24.1). First injury to the endothelial cells that line the walls of the arteries occurs, causing inflammation and immune reactions. Damage to the endothelium stimulates the growth of smooth muscle cells. These cells secrete collagen and f ibrous proteins. Lipids, platelets, and other clotting factors accumulate. Scar tissue replaces some of the arterial wall. • WORD • BUILDING • arteriosclerosis: arterio—artery + sklerosis—hardness Atherosclerotic artery FIGURE 24.1 (Top) Cross-section of normal coronary artery. (Bottom) Coronary artery with atherosclerosis narrowing the lumen. An early indication of injury is a fatty streak on the lining of the artery. This buildup of f atty deposits is kno wn as plaque. It is composed of smooth muscle cells, fibrous proteins, and cholesterol-laden foam cells. Plaque has irregular, jagged edges that allow blood cells and other material to adhere to the wall of the artery. The portion of the plaque that faces the bloodstream develops a fibrous cap, a firm shell that often contains calcium. Over time this buildup becomes calcified and hardened, causing turb ulence that damages cells 4068_Ch24_462-498 15/11/14 1:35 PM Page 464 464 UNIT FIVE Understanding the Cardiovascular System and increases the b uildup within the v essel. Sometimes the plaque’s fibrous cap tears or ruptures, and a blood clot forms. This blood clot can completely block the coronary artery, or it may break loose and lodge within a smaller artery leading to the heart. The vessel may also become stenosed (narrowed) by plaque buildup. This buildup of plaque may cause partial or total occlusion of the artery , resulting in reduced blood flow. The area distal to the occlusion may become ischemic as a result. Etiology Risk factors for atherosclerosis can be divided into two categories: those that can be modif ied and those that cannot (Table 24.2). Diagnostic Tests Total cholesterol levels above 200 mg/dL increase risk of MI (see Table 21.3). Low-density lipoproteins (LDLs) increase CAD risk, but high-density lipoproteins (HDL) are protective against CAD. A risk factor for premature CAD is a high Lp(a) cholesterol (a genetic variation of plasma LDL) level. Apolipoprotein B particles in LDL-type cholesterol are able to infiltrate the arterial wall, rapidly causing damage. People with a higher proportion of apolipoprotein B to apolipoprotein A are at a much higher risk for CVD. C-reactive protein (CRP) can indicate low-grade inflammation in coronary vessels and long-term heart disease risk. Elevated blood glucose levels can increase the risk for atherosclerosis. Radiological studies of the arteries can be performed to show narrowed or occluded vessels (see Chapter 21). Therapeutic Measures A healthy lifestyle, controlling risk factors, medications, and medical exams are helpful in controlling arteriosclerosis and atherosclerosis. Diet Because the formation of plaque within arteries is primarily caused by fatty deposits, an adherence to a healthy diet is recommended by the AHA. Heart-healthy foods include a variety of those colorful fruits and vegetables that have no trans fat; are low in saturated fat, cholesterol, sodium, and added sugars; and those that are high in whole-grain fiber and lean protein (“Nutrition Notes”). The AHA has guidelines and diets for decreasing fat and cholesterol intake at http://mylifecheck.heart.org. Smoking The risk of developing CAD is two to six times higher in cigarette smokers than in nonsmokers. Risk is proportionate to the number of cigarettes smok ed. Smoking contributes to a TABLE 24.2 RISK FACTORS FOR ATHEROSCLEROSIS/CORONARY ARTERY DISEASE Risk Factors That Cannot Be Changed Men have increased incidence after age 50. Women have increased incidence after Age menopause. Ethnicity African Americans have a higher incidence of atherosclerosis. Gender Men have more risk factors and higher incidence of coronary artery disease (CAD). Genetics CAD risk factors such as hyperlipidemia can run in families. Risk Factors That Can Be Changed or Controlled Increases the risk of hypertension, obesity, and elevated blood lipids. Diabetes Hypertension Vasoconstriction increases myocardial oxygen demand. Elevated serum cholesterol Level above 240 mg/dL increases the risk of developing CAD. Elevated apolipoprotein B Infiltrate arterial wall, rapidly causing damage Elevated serum homocysteine Increases CAD risk. Foods that contain folic acid (fruits, green leafy vegetables) reduce homocysteine level. Excessive alcohol use Raises blood pressure, increases triglycerides, causes irregular heartbeats. Obesity Increases heart workload and risk of hypertension, diabetes, glucose intolerance, hyperlipidemia. Sedentary lifestyle Increases obesity, hypertension, hyperlipidemia. Stress Increases heart workload and risk for hypertension. Tobacco use including passive smoking (secondhand) Causes vasoconstriction and increases myocardial oxygen demand. Decreases high-density lipoproteins. 4068_Ch24_462-498 15/11/14 1:35 PM Page 465 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders Nutrition Notes Controlling Blood Cholesterol With Diet Two-thirds of the body’s cholesterol is produced by the liver and intestines. Most people produce less cholesterol or increase its excretion in response to high levels of dietary cholesterol, but others respond weakly. In particular, obese indi viduals respond less to reductions in dietary saturated fat and cholesterol than do lean persons (Flock, Green, Kris-Etherton, 2011). Although only foods of animal origin contain cholesterol, some v egetable oil products contain trans fats, potent risk factors for cardiovascular disease. The basis for the cholesterol-lowering diet is: • Reducing saturated fat to less than 7% of total kilocalorie intake • Reducing dietary cholesterol to less than 200 milligrams per day. In dietary studies of about 1 month duration where all foods were provided, LDL cholesterol is reduced by 22 to 30%, whereas in community-based studies of more than 6 months’ duration, where dietary advice is the basis of the intervention, reduction in LDL cholesterol is about 15%. This amount is possibly suf ficient to reduce the need for pharmaceutical interventions (Harland, 2012). Specific strategies to lower blood cholesterol include the following: • Reducing saturated fat intake by choosing • 2 to 3 servings per day of nonfat or low-fat dairy products • 5 ounces of lean meat per day, trimming fat from meat, rinsing browned ground beef, and skimming fat from meat juices for soup or gravy • 2 egg yolks per week; egg whites, egg substitutes as desired Adding foods for which the U.S. Food and Drug Administration has approved health claims such as: • Foods rich in marine omega-3 fatty acids (herring, mackerel, rainbow trout, salmon, sardines, swordfish, and tuna) • Foods containing soluble fiber (Kellogg’s Bran Buds, barley, oatmeal) • Soy-containing foods • Foods containing plant sterols (butter and margarine spreads, juices, salad dressings, soy milk) that interfere with intestinal absorption of cholesterol. Note, however, that they are contraindicated in a rare autosomal recessive disorder called sitosterolemia. loss of HDL. These proteins are the best cholesterol to have in the body to decrease the risk of CVDs. Smoking also causes vasoconstriction, which leads to angina pectoris and cardiac dysrhythmias. The benefits of smoking cessation are dramatic and almost immediate. Education about the risks of 465 smoking and effects of exposure to secondhand and thirdhand (residual nicotine and other chemicals left on indoor surfaces—from skin, clothing, and hair to bedding, carpets, floors, furniture, and w alls—by tobacco smok e) smoke should be presented to patients. The American Cancer Society has many programs to help patients quit smoking. Visit its website at www.cancer.org. Exercise Increased activity raises HDL levels. Increasing physical activity may also lower insulin resistance and facilitate weight loss. Over time, exercise also leads to the development of collateral circulation, which allows blood to flow around occluded sites. Before beginning an exercise program, consult a health care provider (HCP). Medications Lowering lipid levels is the primary therap y for atherosclerosis. When dietary control is not effective, medication is also used (Table 24.3). It may take 4 to 6 weeks before lipid levels respond to drug therapy. If one drug does not control lipids, another drug can be added. CORONARY ARTERY DISEASE Coronary artery disease is the obstruction of blood flow through the coronary arteries to the heart muscle cells, typically from atherosclerosis. Blood flow reduction resulting from CAD can cause angina, MI, or sudden death if blood flow is not restored. Prevention Risk factors for CAD are listed in Table 24.2. The risk factors that can be changed should be modified following the AHA’s guidelines (see therapeutic measures for atherosclerosis). Low-dose aspirin as recommended by an HCP can be used to prevent the formation of a thrombus. Angina Pectoris Pathophysiology When an increased w orkload is placed on the heart, as in exercise or strenuous activity, there is an increased demand for oxygen. Normally, when the heart muscle needs more oxygen, the coronary arteries dilate to carry more blood and oxygen. However, with CAD, the narrowed vessels are unable to dilate and supply the heart muscle with this e xtra blood and oxygen. This inability to supply more blood and oxygen causes myocardial ischemia and can produce its symptom, angina pectoris (chest pain). Angina may also result from other conditions that cause myocardial ischemia such as vasospasm, valvular heart disease, hypertension, or heart failure (HF). • WORD • BUILDING • angina pectoris: angina—to choke + pectora—chest 4068_Ch24_462-498 15/11/14 1:35 PM Page 466 466 UNIT FIVE Understanding the Cardiovascular System TABLE 24.3 MEDICATIONS USED TO LOWER LIPID LEVELS Medication Class/Action Statins First-line drugs to reduce low-density lipoprotein by reducing cholesterol synthesis. Fibrates Reduce triglycerides. Bile Acid Sequestrants Lower cholesterol by binding bile acids, so stored cholesterol is used to make more bile acids. Niacin Prevents conversion of fats into very low-density lipoproteins. Rarely used because of flushing. Cholesterol Absorption Inhibitor Inhibits the absorption of cholesterol. Decreases LDLs and increases HDLs. Combination Agent See each agent. Examples Nursing Implications atorvastatin (Lipitor) fluvastatin (Lescol XL) lovastatin (Mevacor) pravastatin (Pravachol) simvastatin (Zocor) rosuvastatin (Crestor) Monitor liver function studies. Monitor for rhabdomyolysis (lethal breakdown of skeletal muscle). Teaching: Explain to take in the evening when cholesterol synthesis is highest. Teach patient to report any muscle pain. fenofibrate (TriCor) clofibrate (Atromid-S) gemfibrozil (Lopid) Tell patient to take 30 minutes before morning and evening meal. May increase the effects of anticoagulants and hypoglycemia. colestipol (Colestid) colesevelam HCl (Welchol, Sankyo) cholestyramine (Questran) Fruits and vegetables high in fiber should be added to diet to reduce constipation and other gastrointestinal effects noted with bile acid sequestrants. May interfere with absorption of digoxin, thiazides, and beta blockers. niacin (Nicotinic acid) extended-release niacin (Niaspan) Take aspirin 30 minutes before taking drug to reduce flushing. ezetimibe (Zetia) Tell patient to take with liquids and meals and to take other drugs 1 hour before or 4 hours after. Vytorin (Zetia + Zocor) See each agent. LEARNING TIP Angina pectoris is not a disease. It is the symptom of ischemia that results from a lack of oxygen and blood flow to the heart muscle. Types of Angina Angina can be classified as stable (less serious) or unstable. STABLE ANGINA. Stable angina is chest pain that occurs with moderate exertion in a pattern that is f amiliar to the patient. The pain is predictable and can usually be managed with nitroglycerin (NTG) and rest. The pain of stable angina usually subsides when the activity is stopped. VARIANT OR VASOSPASTIC ANGINA (PRINZMETAL’S ANGINA). This type of angina is caused by coronary artery spasms and is serious. The pattern of occurrence is often c yclical, with the pain presenting about the same time each day . The pain has a longer duration than stable angina, can occur with e xercise or at rest, and often occurs at night. Signs and Symptoms Anginal pain manifests in se veral ways. Patients (especially men) often describe the pain as heaviness, tightness, squeezing, viselike, or crushing in the center of the chest or adjacent to the chest (Fig. 24.2). The pain can radiate down one or both arms, with pain in the left arm being more common, into the shoulder, neck, jaw, or back. Patients may also describe heaviness in their arms or a feeling of impending doom. During the episode of pain, the patient may be pale, diaphoretic, or dyspneic. The pain is usually brought on by e xertion and subsides with rest. It can be relieved with a vasodilator such as NTG. Episodes of chest pain may increase in frequency and severity over time. If patients do not heed the w arning to stop their activity and rest, they may be at risk for MI or sudden death. 4068_Ch24_462-498 15/11/14 1:35 PM Page 467 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders Front 467 Back Neck or jaw Shoulder Intrascapular Chest Left arm pain radiation common Epigastric Wrist Hand FIGURE 24.2 Common locations of anginal pain, which may vary in combination and intensity. Any event that increases oxygen demand can cause an anginal attack. Most often, precipitating e vents include lar ge meals, exercise, cold, stimulant drugs such as cocaine or amphetamines, stress, and emotional tension. Angina commonly occurs in the morning between 0600 and 1200 when the patient arises and the workload of the heart increases. Women often e xperience angina symptoms atypically . They can experience chest pain, ja w pain, or heartb urn but often have atypical symptoms of shortness of breath, fatigue, nausea, or less severe pain. Atypical symptoms should be recognized as possibly being cardiac related so that they are not ignored and treatment is sought. (See the “Women and Heart Health” section.) chemical stress testing, cardiac computed tomography (CT) scan, cardiac magnetic resonance imaging (MRI)/magnetic resonance angiogram (MRA), radioisotope imaging, and coronary angiography (see Table 21.3). Diagnostic Tests VASODILATORS. NTG, a nitrate, is the drug of choice for Common tests for diagnosing CAD or angina causes include electrocardiogram (ECG), exercise stress test, echocardiography, Therapeutic Measures Treatment for CAD and angina is directed at relie ving and preventing anginal episodes that could lead to a MI. The risk factors identified for the patient determine the course of treatment. Weight reduction following a heart healthy diet and stress reduction may help slow disease progression. The three major groups of medication used for reliving angina are vasodilators (nitrates), calcium channel block ers, and beta blockers (Table 24.4). acute anginal attacks. Nitrates dilate coronary arteries to increase oxygen to the myocardium and dilate peripheral TABLE 24.4 MEDICATIONS USED TO TREAT ANGINA PECTORIS Medication Class/Action Antiplatelets Inhibit platelet activation, adhesion, or procoagulant activity. Examples Nursing Implications aspirin Enteric coated may be given for daily dosing. Monitor for bleeding. nitroglycerin (Nitrostat, NitroQuick); nitroglycerin lingual spray (Nitrolingual Pumpspray) isosorbide dinitrate (Isordil) isosorbide mononitrate (Imdur, ISMO) Document onset, type, radiation, location, and duration of chest pain. Take apical pulse and BP pre- and postadministration. Place sublingual (SL) tablet in buccal pouch to lessen burning sensation under tongue. Do not shake aerosol canister before administration of lingual spray. Statins (See Table 24.2.) Nitrates Vasodilate to reduce preload and afterload. Reduce oxygen consumption of myocardium. Continued 4068_Ch24_462-498 15/11/14 1:35 PM Page 468 468 UNIT FIVE Understanding the Cardiovascular System TABLE 24.4 MEDICATIONS USED TO TREAT ANGINA PECTORIS—cont’d Medication Class/Action Angiotensin-Converting Enzyme Inhibitors Block production of angiotensin II, a potent vasoconstrictor. Vasodilate and improve cardiac output and exercise tolerance. Calcium Channel Blockers Dilate peripheral arteries, decrease myocardial contractility, depress conduction system, and decrease workload of the heart. In variant angina, reduce coronary artery spasm. Beta Blockers Decrease pulse, BP, and cardiac output and suppress renin activity. Decrease the risk of sudden death. Anti-Ischemic Agent Antianginal agent used as combination therapy for those not responding to other antianginal. Examples Nursing Implications Teaching: Explain to rise slowly, especially with SL spray. If chest pain is not relieved, call 911. Tablets should be replaced every 3 to 6 months. Keep tablets in original bottle as become inactive when exposed to light, air, heat, and moisture. Burning or tingling sensation may be felt under the tongue with SL nitroglycerin. Use of erectile dysfunction medications is contraindicated because they can cause a drop in blood pressure. Explain to avoid alcohol. nitroglycerin (Transderm Nitro, Nitro-Bid) nitroglycerin patch (Nitro-Dur, Nitrek) Remove patch before MRI or defibrillation. Teaching: Remove old transdermal patch before applying new patch. Rotate application sites. Apply patch to clean, dry, hairless area. Remove at bedtime so tolerance does not develop. captopril (Capoten) lisinopril (Prinivil, Zestril) ramipril (Altace) enalapril (Vasotec) If pulse is less than 60 beats per minute or systolic blood pressure (BP) less than 90 mm Hg, notify HCP. Give 1 hour before meals. Give captopril on empty stomach. Teaching: Take first doses at night to adjust to lower BP. Rise slowly. Check BP weekly. Report development of dry cough or other side effects. diltiazem (Cardizem, Dilacor XR) amlodipine (Norvasc) nicardipine (Cardene) felodipine (Plendil) If pulse less than 60 beats per minute or systolic BP less than 90 mm Hg, notify HCP. Administer before meals and at bedtime. metoprolol (Lopressor, Toprol XL) atenolol (Tenormin) Beta blockers are contraindicated in asthma, heart block, bronchoconstriction. If pulse less than 60 beats per minute or systolic BP less than 90 mm Hg, notify HCP. Teaching: Explain to rise slowly. Abrupt withdrawal may result in diaphoresis, palpitations, headache, and tremors. ranolazine (Ranexa) May not be as effective in women. Prolongs QT interval on ECG. 4068_Ch24_462-498 15/11/14 1:35 PM Page 469 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders vessels so the heart does not ha ve to work so hard to pump blood into them. NTG can be administered sublingually , orally, transdermally, intravenously (IV), or as a lingual spray. When administered sublingually, NTG may relieve chest pain within 1 to 2 minutes (Box 24-1). BE SAFE! Sublingual NTG: AHA guidelines instruct people to immediately call 911 after one tablet and 5 minutes if pain remains unrelieved and symptoms of a MI are occurring. Transdermal NTG: Wear gloves to protect yourself from hypotension from touching the ointment or patch medication. Always remove the previous ointment or patch before applying a new one to prevent overdose. 469 12-hour nitrate-free period. Headaches may be e xperienced when nitrates are first begun. This side effect usually subsides after a week or two and can be relieved with aspirin. CALCIUM CHANNEL BLOCKERS. Calcium is required for electrical excitability of cardiac cells and contraction of the myocardium and v ascular smooth muscle. Calcium channel blockers relax vascular smooth muscle, which leads to decreased peripheral v ascular resistance (afterload) and decreased myocardial oxygen demand. These drugs dilate main coronary arteries, increasing the myocardial oxygen supply. Calcium channel blockers are also used to decrease systolic and diastolic blood pressures and to slow the heart rate. Because these drugs are slow acting, they are ineffective in relieving acute anginal attacks. Side effects of calcium channel blockers are usually mild and include constipation, fluid retention, headache, and dizziness. BE SAFE! Long-acting nitrates are used to prevent chest pain rather than to treat acute pain. They can be given orally, in ointment, or by transdermal patches. A problem with long-acting nitrates is the development of a tolerance to the drug. To prevent tolerance, the patch or ointment is usually remo ved at bedtime and reapplied in the morning, giving the patient an 8- to Box 24-1 Key Points for Using Sublingual Nitroglycerin • Carry nitroglycerin (NTG) tablets at all times. • Keep NTG tablets tightly sealed in the original container and protected from heat, light, and moisture. • Replace NTG prescription at least every 6 months for maximum effect or every 3 to 4 months if carried in a pocket next to body heat. • Take NTG tablet before an activity known to cause chest pain. • Sit or lie down when taking NTG tablets, if possible. • Take one NTG tablet. If the symptoms are not worsening but not completely relieved, your HCP may tell you to repeat a tablet every 5 minutes up to a total of three tablets. If pain is not relieved after three tablets, call 911. • If pain is unrelieved after one NTG tablet and other symptoms of myocardial infarction are present, call 911 for emergency medical care. • Tingling should be felt under the tongue when NTG tablets are used. • NTG may cause a headache initially. Aspirin may relieve it. • NTG may cause lightheadedness. Rise slowly to prevent falls. Those who take nitrates should not use drugs such as sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra) for erectile dysfunction because these types of drugs dilate blood vessels and may cause a significant drop in blood pressure if used together. BETA BLOCKERS. Beta blockers decrease heart rate, lo wer blood pressure, and prevent release of renin. This results in decreased workload on the heart to help pre vent anginal attacks. Because of these decreased ef fects, beta block ers should be used with caution in patients with an y degree of HF because it may mak e HF worse. There are nonselective and selective types of beta-adrenergic blockers. People with asthma or chronic obstructive pulmonary disease (COPD, including emphysema, bronchitis, and bronchiectasis) should avoid nonselective beta-adrenergic blockers because the y cause bronchoconstriction. Metoprolol (Lopressor) and atenolol (Tenormin) are cardioselective and can be used in patients with asthma and COPD. Beta blockers are not effective for coronary artery spasms and should not be used for variant (Prinzmetal’s) angina. LEARNING TIP To help you identify beta blockers, remember that their generic names end with -olol. ANGIOTENSIN-CONVERTING ENZYME INHIBITORS. Angiotensin- converting enzyme (ACE) inhibitors block production of angiotensin II, which is a potent v asoconstrictor. This action reduces peripheral arterial resistance (v asodilation), which 4068_Ch24_462-498 15/11/14 1:35 PM Page 470 470 UNIT FIVE Understanding the Cardiovascular System STATINS. Cholesterol and inflammation in artery walls are in- • Notify HCP of ECG changes. ST-segment elevation may indicate a MI (see Chapter 25). • Offer the patient assurance and emotional support to decrease anxiety. Emotional support is important because patients and their families are often afraid that the patient may die. • Promote rest and decrease anxiety for the patient with chest pain to help relieve stress and chest pain. • Document patient data in the medical record to communicate patient’s problem and outcome. ANTIPLATELETS. Aspirin and clopidogrel (Pla vix) are com- Deficient Knowledge related to ineffective management of regimen for atherosclerosis or coronary artery disease lowers blood pressure. ACE inhibitors may cause retention of potassium in some patients. If a patient taking an ACE inhibitor develops a dry cough, inform the HCP so the medication can be changed. volved in atherosclerosis development. Statins lower cholesterol levels by reducing cholesterol production in the li ver (see Table 24.3). They also reduce inflammation and CRP le vels, which improves patient outcomes in CAD. Statins are used to prevent and treat atherosclerosis and the disorders caused by it. monly used antiplatelets that help prevent cardiovascular events. Nursing Process for the Patient With Atherosclerosis, Coronary Artery Disease, and Angina Data Collection A health history is obtained regarding the patient’s nonmodifiable and modifiable risk for atherosclerosis and CAD. A history of chest pain, fatigue, or activity intolerance is noted. Allergies and current medications, including over-the-counter and prescription drugs are documented. Height, weight, and diet history are recorded. Assess anginal pain by patient’s description of pain: type, location, and pain radiation to other areas of the body . Note skin color and temperature. Note any factors that may make the pain worse or better. This will provide information to determine improvement or lack of impro vement in pain. Ask how long the patient has had angina, triggering activities, and how the pain has been relieved in the past. Note the presence of dyspnea, labored respirations, diaphoresis, or nausea. Obtain vital signs, blood pressure, apical pulse, respiration, and oxygen saturation to provide a baseline of the patient status. Nursing Diagnoses, Planning, and Implementation Acute Pain related to reduced coronary artery blood flow and increased myocardial oxygen needs causing an imbalance between oxygen supply and demand EXPECTED OUTCOME: The patient will report an absence of pain. • Ensure vascular access is established. IV access may be necessary to use to administer drugs for pain relief. • Administer oxygen as ordered via nasal cannula to increase oxygen availability to myocardium. • Obtain a 12-lead ECG as ordered to determine ischemia or injury of the myocardium with evaluation of the ST segment. • Administer aspirin as prescribed to decrease platelet aggregation. • Administer morphine as prescribed to provide pain relief. • Administer nitroglycerin (sublingual, spray) as ordered. Notify HCP if pain is unrelieved after three doses of NTG or as prescribed, or if vital signs change. Chest pain unrelieved by nitrates may represent unstable angina or MI. • Remain with patient and reassess pain in 5 minutes after administration of medication. A patient who has chest pain should never be left alone. EXPECTED OUTCOME: The patient will report understanding and management of atherosclerosis and CAD. • Identify cognitive or physical impairments that would interfere with the patient’s ability to learn desired information. • Include significant other as appropriate to support patient during learning. • Collect data on patient’s present understanding of atherosclerosis and CAD to determine baseline knowledge. • Collect data on patient’s readiness to learn and desired learning needs and feelings about incorporating lifestyle changes into daily routine to prioritize teaching topics. • Determine cultural beliefs because they may influence learning. • Provide for patient’s physical comfort during teaching to increase learning. • Use appropriate teaching tools to meet individual learning needs, such as pamphlets, diagrams, or other written materials in simple language. • Use an interpreter as needed and provide written materials in patient’s native language to facilitate understanding. • Explain pathophysiology of atherosclerosis and CAD, control of risk factors, and management of CAD symptoms to promote understanding. • Explain action, side effects, and importance of taking medications as prescribed to relieve pain and prevent complications. • Provide information about community resources that can assist in making lifestyle changes, such as weight loss, smoking cessation, stress management, and exercise. • Teach patient to monitor blood pressure and heart rate as appropriate and to report chest pain or dyspnea, which may point to the presence of complications from CAD. • Help patient plan how to incorporate information into daily life to increase likelihood that change will occur. • Encourage questions and allow patient opportunity to verbalize new information and skills to enhance learning. • Document teaching and evaluation of patient knowledge to validate understanding. Evaluation Interventions are successful if the patient is pain free and has an increased understanding of atherosclerosis and CAD and their management and states that he or she will modify risk factors of CAD. 4068_Ch24_462-498 15/11/14 1:35 PM Page 471 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders ACUTE CORONARY SYNDROME The term acute coronary syndrome (ACS) is used to encompass the continuum of CAD such as unstable angina pectoris and MI. Acute coronary syndrome is caused by a sequence of inflammatory processes mediated by activated macrophages, plaque rupture, tissue factor expressions and platelet activation leading to thrombus formation and coronary vessel occlusion. Unstable Angina Unstable angina occurs in patients with worsening CAD and is noted by its changing or unpredictable pattern. Rest does not decrease the chest pain of unstable angina.This pain may even occur when the patient is at rest. The episodes of chest pain with unstable angina increase in frequency and severity, placing the patient at risk for myocardial damage or sudden death. Symptoms of angina usually occur when an artery is narrowed by at least 60% to 70%. Myocardial Infarction An MI (heart attack), results in the death of heart muscle.The affected myocardial cells in the heart are permanently destroyed. An MI occurs from a partial or complete blockage of a coronary artery, which decreases the blood supply to the cells of the heart supplied by the blocked coronary artery. The extent of the cardiac damage varies depending on the location and amount of blockage in the coronary artery. This is a potentially devastating condition. The ability of the heart to contract, relax, and propel blood throughout the body requires healthy cardiac muscle. Results depends on the speed and effectiveness of treatment. MI is identified by type. Non–ST -segment elevation MI (NSTEMI) is also known as a non–Q-wave MI. An ST-segment elevation MI (STEMI) is also known as a Q-wave MI and is the deadliest type because it is usually caused by a complete blockage of the artery. (See Chapter 25 for ST-segment definition.) With timely reperfusion, cell death may not occur , which reduces the amount of permanent damage. Those experiencing an MI are typically men o ver age 40 with atherosclerosis. Although MIs can occur at an y age in men or women, women who smoke and use oral contraceptives have a higher risk. 471 take place. The ischemic process affects the subendocardial layer, which is most sensitive to hypoxia. This process leads to depressed myocardial contractility. The body’s attempt to compensate for decreased cardiac function triggers the sympathetic nervous system to increase the heart rate. The change in heart rate increases myocardial oxygen demand, further depressing the myocardium. Prolonged ischemia can produce se vere cellular damage and necrosis of cardiac muscle. Once necrosis tak es place, the contractile function of the muscle is permanently lost.The heart has a zone of ischemia and injury around the necrotic area (Fig. 24.3). The zone of injury is next to the necrotic area and is susceptible to becoming necrosed. If treatment is initiated within the first hour of symptoms of the MI, the area of damage can be minimized. Around the injury zone is an area of ischemia and viable tissue. If the heart responds to treatment, this area can rebuild and maintain collateral circulation. If prolonged ischemia tak es place, the size of the infarction can be quite large. The size of the infarction depends on how quickly the blood supply from the blocked artery can be restored. The area affected by an MI depends on the coronary artery involved and the e xtent of occlusi ve coronary disease (Fig. 24.4). Being familiar with the anatomy of the heart and the area of the MI helps the nurse anticipate dysrhythmias, conduction disturbances, and HF, which are the major complications of MIs (Table 24.5). Silent Ischemia Silent ischemia occurs without pain and can carry great risk. The older adult and those with hypertension or diabetes most often have silent ischemia. Area of ischemia Sudden Cardiac Death Sudden cardiac death is cardiac arrest triggered by lethal ventricular dysrhythmias or asystole from an abrupt occlusion of a coronary artery (see Chapter 25). Prompt treatment is required in an attempt to prevent death. Pathophysiology MI does not happen immediately . Ischemic injury evolves over several hours before complete necrosis and inf arction Area of injury Area of necrosis FIGURE 24.3 Myocardial infarction. Areas of ischemia, injury, and necrosis caused by a blockage in the left anterior coronary artery. 4068_Ch24_462-498 15/11/14 1:35 PM Page 472 UNIT FIVE 472 Understanding the Cardiovascular System Aorta Aorta Left main coronary artery Circumflex branch of left coronary artery Anterior interventricular branch of left coronary artery A Right coronary artery An occlusion of the RCA leads to an inferior MI and abnormalities in impulse formation and conduction. Serious dysrhythmias can occur early in an inferior MI that may be life threatening. The left circumflex coronary artery feeds the lateral w all of the heart and part of the posterior wall of the heart. A lesion in the circumflex leads to a lateral wall infarction of the left ventricle. LEARNING TIP B Right coronary artery FIGURE 24.4 Coronary arteries. (A) Anterior view. (B) Posterior view. The left coronary artery feeds the anterior w all of the heart, which also includes most of the left v entricle. An occlusion in this area causes an anterior wall MI. When the left ventricle is affected, there can be severe loss of left ventricular function, leading to severe changes in the hemodynamic status of the patient. The right coronary artery (RCA) feeds the inferior w all and parts of the atrioventricular node and the sinoatrial node. To remember which coronary artery occlusion results in a specific MI location, use coast-tocoast U.S. location initials such as those given below. You can personalize the locations with initials of landmarks familiar to you: LOCATION CORONARY ARTERY RESULTING MI LOCATION Los Angeles Left anterior descending Anterior Cedar Point Circumflex Posterior Rhode Island Right Inferior TABLE 24.5 COMPLICATIONS OF MYOCARDIAL INFARCTION Complication Dysrhythmias Types or Symptoms Premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, heart block Interventions Continuous cardiac monitoring Protocols for treatment of dysrhythmias (see Chapter 25) Cardiogenic shock Decreased blood pressure; increased heart rate; diaphoresis; cold, clammy, gray skin Immediate initiation of treatment to decrease infarct size, control pain and dysrhythmias Intra-aortic balloon pump Thrombolytic therapy Dopamine and dobutamine Heart failure/ pulmonary edema Dizziness, orthopnea, weight gain, edema, enlarged liver, jugular venous distention, crackles Correct underlying cause Relieve symptoms Increase cardiac contractility Administer furosemide (Lasix) and digoxin (Lanoxin) Emboli Dependent on location of emboli Anticoagulants to prevent Supportive symptom treatment Rupture of muscles or valves of the heart, septal rupture Signs of cardiogenic shock, death Mortality rate high Immediate treatment of MI to limit extent of damage Pericarditis (inflammation of the heart muscle) Chest pain, increased with movement, deep inspiration, or cough; pericardial friction rub (fine grating sound) Relieved when sits up and leans forward Anti-inflammatory drugs (aspirin, indomethacin [Indocin]) 4068_Ch24_462-498 15/11/14 1:35 PM Page 473 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders 473 Signs and Symptoms Chest pain is a classic symptom of an MI. The pain begins suddenly and continues without relief with rest or administration of NTG. The pain in the center of the chest is usually described as crushing, viselike, or as if an elephant is standing on the chest. The pain may radiate to the back, one or both arms and shoulders, neck, or jaw. The pain can imitate indigestion or a gallbladder attack with abdominal pain and vomiting. Other classic MI symptoms include shortness of breath, dizziness, nausea, and sweating (Table 24.6). When listening to lung sounds, crackles or wheezing may be heard. The pulse may be rapid or irregular, and an extra heart sound (referred to as S 3 or S4) may be present. The presence of an extra heart sound can mean ventricular failure is imminent. TIMELY SYMPTOM TREATMENT. Individuals often deny or fail to recognize that an MI is occurring because the y experience atypical MI symptoms or their symptoms are similar to other mild conditions such as indigestion (“Gerontological Issues”). Patients have reported that the symptoms of an MI that the y experienced were not what they expected. If people expect to have the dramatic heart attack symptoms seen on tele vision (which are usually not the same as those in real life) and the y do not, they are likely to wait to seek treatment. Waiting 2 to 24 hours before seeking medical care is common, yet the first hour after symptom onset is crucial for administering the newer reperfusion treatments that restore blood flow, minimize tissue damage, and save lives. Individuals should not dri ve themselves or let someone else drive them to the hospital if they are having chest pain. Call emergency medical care (911 or local emergency services number) so lifesaving treatment can begin. Because so fe w people arri ve at the emer gency room quickly enough to benefit from reperfusion treatment, several agencies have educational programs to address this issue. Individuals need to be educated that “time is muscle.” As time passes during an MI, more muscle is lost.The National Heart, Lung, and Blood Institute and the AHA promote a campaign called “Act in Time to Heart Attack Signs.” The purpose of the campaign is to educate people on the importance of recognizing heart attack symptoms, working with a HCP to create a heart attack survival plan, and calling 911 as soon as symptoms begin. For more information, visit: www.nhlbi.nih.gov/health/health-topics/topics /heartattack www.womenshealth.gov/heart-health-stroke/heart -disease-stroke-prevention/index.html www.heart.org/HEARTORG. Women and Heart Health Heart disease remains the leading cause of death in w omen in the United States. American women are six times more likely to die of heart disease than breast cancer. Heart disease kills more women than all cancers combined in the over-age65 group. Ethnicity is also a f actor among women. African American women are more likely than Caucasian women to develop heart disease. Women tend to have an acute MI at an older age than men. Women also have a higher mortality rate Gerontological Issues With age, the heart has decreased elasticity and decreased ability to respond to changes in pressure. This increases resistance to its pumping action and increases the workload of the myocardium. Symptoms: • Older patients should be taught never to neglect symptoms of shortness of breath, fatigue, fast or slow heartbeats, or chest discomfort. • MIs that can occur without the presence of pain, a silent MI, most often occur in the older adult or those with diabetes regardless of age. • When pain is not present, the only symptom may be a sudden onset of shortness of breath or fainting, restlessness, or a fall. • Atypical presentation of MI symptoms is normal in older people, especially those older than age 85. Because the older adult has had more time to develop collateral circulation than younger people, they often do not have as many complications with an MI. Therapies: • In the older adult, reperfusion therapies such as angioplasty and bypass surgery seem to be superior in improving quality of life without increasing mortality risk. Statin therapy has also been shown to reduce mortality in those over age 80. TABLE 24.6 MYOCARDIAL INFARCTION SUMMARY Signs and Symptoms Classic Crushing, viselike chest pain with radiation to arm, shoulder, neck, jaw, or back Shortness of breath Dizziness Nausea Sweating Atypical Absence of chest pain Fatigue Cramping in chest Anxiety Feeling of impending doom Falling More Common in Women Epigastric or abdominal pain Chest discomfort, pressure, burning Continued 4068_Ch24_462-498 15/11/14 1:35 PM Page 474 474 UNIT FIVE Understanding the Cardiovascular System TABLE 24.6 MYOCARDIAL INFARCTION SUMMARY—cont’d Arm, shoulder, neck, jaw, or back pain Discomfort/pain between shoulder blades Shortness of breath Fatigue Indigestion or gas pain Nausea or vomiting Diagnostic Tests ECG Serum cardiac troponin I or T Serum myoglobin Serum CK-MB CBC Serum magnesium and potassium Vital signs, oxygen saturation, intake and output Therapeutic Measures Medications Oxygen Morphine sulfate Nitrates Fab Four cardiac medications: aspirin, statin, ACEI, beta blocker Platelet aggregation inhibitors Thrombolytics Anticoagulants Antidysrhythmics Vasodilators Percutaneous coronary interventions and stents Myocardial revascularization–CABG Fluid restriction Daily weights Bedrest with bedside commode/ bathroom privileges Low-sodium diet advanced to diet as tolerated; no caffeine Cardiac rehabilitation Complications Priority Nursing Diagnoses Dysrhythmias Heart failure Cardiogenic shock Valvular insufficiency and are more likely to have complications such as ventricular fibrillation and HF than men. Women may have classic chest pain, but they are also likely to have other symptoms as well that men do not typically have. Research is focusing on understanding women and cardiac disease. Atypical symptoms reported by women may include extreme fatigue, epigastric pain, jaw pain, indigestion, nausea and vomiting, dyspnea, shortness of breath, or cramping in the chest. A high percentage of women (more than 50%) noted prodromal symptoms a month before an acute MI. These symptoms included unusual f atigue, sleep distur bances, and shortness of breath. Fe wer than 30% reported chest discomfort. Delay in seeking care has also been identified in women. Women also often do not associate their symptoms with a heart attack because the y believe it is a male condition. Women with atypical symptoms usually delay treatment, and when treated have less aggressive management, which leads to increased mortality. Diagnostic Tests Patients with a strong familial history of MI should be considered at risk until an MI is ruled out. Indicators of an MI are patient history, ECG, and serum cardiac troponin I orT, myoglobin, and CK-MB levels (see Chapter 21). C-reacti ve protein levels are elevated in the presence of inflammation. Magnesium levels are also checked, especially for those on diuretic therapy. Before thrombolytic or heparin therapy, international normalized ratio (INR) and partial thromboplastin time (PTT) are determined. The ECG usually shows the area that has inf arcted, as well as the ischemic areas of the heart. Myocardial damage can be seen as ST-segment elevation, the presence of a Q-w ave, or T-wave abnormalities (Fig. 24.5). Serial ECGs are done to monitor changes indicating damage or ischemia. A B Acute Pain Anxiety Decreased Cardiac Output Deficient Knowledge ST segment C Q wave FIGURE 24.5 Electrocardiogram changes during myocardial infarction. (A) Injury: ST-segment elevation. (B) Ischemia: ST-segment inversion. (C) Necrosis: large Q-wave and ST-segment elevation. 4068_Ch24_462-498 15/11/14 1:35 PM Page 475 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders Therapeutic Measures Treatment should be sought within 5 minutes for an y unrelieved chest pain. The AHA recommends chewing one uncoated adult aspirin at the onset of chest pain as directed by an HCP. Delays in seeking care can limit treatment options and result in more cardiac damage (Box 24-2). Time until intervention is directly related to mortality. Guidelines now consider first medical contact to interv ention rather than “door-to-needle” time. The goal is to restore blood flow to the heart muscle within 90 minutes or less of the patient’s arrival at the emergency department door. Percutaneous coronary intervention should be initiated within 90 minutes. A reperfusion drug, when used, should be gi ven within 30 minutes of the patient arriving at the emergency department (Barto, 2013). The presence of chest pain indicates a lack of oxygen to the myocardium. Patients reporting chest pain are treated as if they have an MI until proven otherwise through testing. OXYGEN. Oxygen is administered immediately, usually at 2 L/min via nasal cannula. Oxygen therapy may be limited to the first 6 hours in stable patients. Too much oxygen can lead to systemic vasoconstriction, which may increase myocardial workload. Arterial blood gases (ABGs) are drawn to determine the patient’s oxygen needs. Oxygen saturation should be monitored and kept above 94%. Oxygen can be administered via mask if higher concentrations are needed. Mechanical ventilation can be provided when indicated by ABGs. PERCUTANEOUS CORONARY INTERVENTION. Percutaneous coronary intervention (PCI) is a mechanical procedure to increase blood flow and oxygen to the myocardium. Emer gency PCI is being used frequently in the management of acute MI, with improved outcomes for patients. 1 2 3 475 4 FIGURE 24.6 Percutaneous coronary intervention: Balloon angioplasty opens narrowed coronary arteries. plaque is compressed. The dilated vessel is able to deliver more oxygen-rich blood to the myocardium. Angioplasty can be done with or without the placement of stents. Coronary Artery Stent. A coronary artery stent, placed during angioplasty, is used to prevent closure of a coronary artery from an atherosclerotic lesion. A stent is an expandable metal mesh tube that is implanted at the site of blockage in the coronary artery (Fig. 24.7). A stent provides support to a coronary artery wall at the area of stenosis to keep blood flowing through the artery. Complications associated with stent placement include thrombosis (formation of a blood clot inside a blood vessel), BALLOON ANGIOPLASTY. In a cardiac catheterization laboratory, a catheter with a balloon tip is inserted, usually via the femoral artery, and advanced into the heart to open the blocked coronary artery (Fig. 24.6). Once the blocked artery is entered, the balloon on the catheter is inflated and the atherosclerotic A Box 24-2 Preventing Delays in Myocardial Infarction Treatment • Understand symptoms and the “time is muscle” principle. • Develop an action plan and rehearse it. • Understand normal emotional responses of anxiety, denial, or embarrassment. • Educate family to follow action plan. • Establish protocols in workplaces for employees experiencing myocardial infarction. • Establish emergency room policies that reduce delays, such as having equipment and medication readily available. B C FIGURE 24.7 Insertion of a coronary artery stent: (A) A balloon catheter with a collapsed stent is advanced to the location of a coronary artery lesion. (B) The balloon is inflated, which expands the stent and compresses the lesion to increase the artery opening. (C) The balloon is then deflated and removed, leaving the expanded stent in place to prevent the artery from closing. 4068_Ch24_462-498 15/11/14 1:35 PM Page 476 476 UNIT FIVE Understanding the Cardiovascular System bleeding from anticoagulation, stent occlusion, or coronary artery dissection. Drug-eluting stents are coated with immunosuppressant medication that can be released at the implantation site to reduce the risk of restenosis.The medication is released over months to inhibit smooth muscle cell proliferation to reduce risk of restenosis. Antiplatelet medications are recommended after stent placement to help prevent clot formation. MEDICATION. For those with unstable angina, taking an- tiplatelets, statins, ACE inhibitors, and beta blockers is beneficial. A drug from each of these drug classes should be considered. When taken together, these drugs have a synergistic effect in fighting plaque, which means the y have a greater positive result for the patient. Research has shown that not all eligible patients are prescribed each of these medications. Patient teaching can include the need to ask the HCP about these drug classes to ensure the y receive the ones for which they are eligible. Table 24.7 summarizes pharmacological treatment of MI. MONA is a mnemonic in the Advance Cardiac Life Support guidelines for remembering the medications to give in treating a suspected MI: morphine, oxygen, nitroglycerin, and aspirin. TABLE 24.7 MEDICATIONS USED TO TREAT MYOCARDIAL INFARCTION Medication Class/Action Analgesics Opioid relieves pain. Reduces preload and afterload. Decreases anxiety. Examples Nursing Implications morphine sulfate Monitor vital signs before and after administration. Heparin sodium Do not give if bleeding risk. Dose regulated by heparin anti-factor Xa or activated partial thromboplastin time (aPTT). PTT Goal: 1.5–2.5 times control. Monitor for bleeding. dalteparin (Fragmin) enoxaparin (Lovenox) Do not remove prefilled syringe air bubble. Give deep subcutaneously: hold fold of skin while giving injection. Rotate sites. Teaching: Monitor for bleeding. amiodarone (Cordarone, Pacerone) Contraindicated in AV block or pregnancy. Obtain baseline vital signs and ECG. Monitor for lung toxicity. Teaching: Avoid grapefruit juice with oral form. Aspirin Clopidogrel (Plavix) Chewable aspirin as ordered should be taken as soon as ACS or MI is suspected. Enteric coated may be given daily. Teaching: Take with food. Report bleeding or bruising. bivalirudin (Angiomax) eptifibatide (Integrilin) tirofiban (Aggrastat) abciximab (ReoPro) Prevent injury for bleeding risk. Monitor vital signs and ECG. Angiotensin-Converting Enzyme Inhibitors (See Table 24.4.) Anticoagulants Heparin Inhibits conversion of prothrombin to thrombin to prevent thrombus formation. Low Molecular Weight Heparin Antithrombotic. Prophylaxis of ischemic complications in unstable angina or NSTEMI with aspirin therapy. Antidysrhythmics Inhibit ventricular arrhythmias. Antiplatelets Inhibit platelet activation, adhesion, or procoagulant activity. Glycoprotein 11b/111a inhibitors. Inhibit platelet aggregation. Given IV only during PCI. 4068_Ch24_462-498 15/11/14 1:35 PM Page 477 Chapter 24 Nursing Care of Patients With Occlusive Cardiovascular Disorders 477 TABLE 24.7 MEDICATIONS USED TO TREAT MYOCARDIAL INFARCTION—cont’d Medication Class/Action Examples Nursing Implications Nitroglycerin Document onset, type, radiation, location, and duration of chest pain. Monitor apical pulse and BP. Teaching: Headache may occur but will resolve over time. Change position slowly to avoid orthostatic hypotension and fall risk. alteplase (Activase, tissue plasminogen activator [t-PA]) reteplase (Retavase) tenecteplase (TNKase) Most effective when given within 6 hours of coronary event. Goal is 90 minutes from arrival. Baseline INR, aPTT, platelet count, and fibrinogen levels checked. Avoid venipunctures for 24 hours after administration. Specific for drugs given. Control nausea, vomiting, anxiety, gastric upset, or constipation. Beta Blockers (See Table 24.4.) Nitrates Vasodilate to reduce preload and afterload. Reduce myocardial oxygen consumption. (See Table 24.3 for other forms.) Statins (See Table 24.2.) Thrombolytics Dissolve blood clots in blood vessels or catheters, such as dialysis catheters. Additional Medications as Needed Antiemetics Anxiolytics Antacids Stool softeners ANALGESICS. Analgesics are given for relief of chest pain. Thrombolytic therapy must be started within a specified time range from the onset of symptoms, usually within 1 to 6 hours, before necrosis results. The goal is to give thrombolytics within 30 minutes of arrival at the emergency department door. Glycoprotein 11b/111a inhibitors (Eptifibatide [Integrilin], abciximab [ReoPro], tirofiban [Aggrastat]) are examples of IV medication that can be used as an adjunct to thrombolysis or PCI in patients with unstable angina or non–ST-segmentelevation MI. These drugs work by inhibiting platelet aggregation and are used along with aspirin or Plavix, and heparin. VASODILATORS. NTG sublingually, topically, or by IV drip can be administered for vasodilation to supply more blood to the myocardium to reduce pain and the workload of the heart. In the acute phase, the IV route is usually used. Nitrates should not be given if the patient has a systolic blood pressure of less than 90 mm Hg or 30 mm Hg or more below baseline, severe bradycardia less than 50 beats per minute, or if the patient has taken a phosphodiesterase inhibitor for erectile dysfunction. Catastrophic hypotension may result. ACTIVITY. Initially, patients are kept on bed rest to decrease myocardial oxygen demand. A bedside commode for bowel movements is usually ordered to reduce straining. Then activity is advanced gradually as tolerated. Morphine sulfate is the most commonly used narcotic. It is usually given in increments of 2 to 8 mg IV e very 5 to 15 minutes until pain is relieved. The patients should be monitored for hypotension, respiratory depression, oversedation, and morphine sensitivity. In addition to pain relief, morphine helps decrease anxiety, opens bronchioles, and increases peripheral blood pooling to decrease preload (blood returning to heart) and afterload (pressure within the aorta), which can help increase blood supply and oxygen to the myocardium. THROMBOLYTICS. Thrombolytic therapy is used to dissolv e a blood clot that is occluding a coronary artery . (Note, however, that PCI has greatly reduced the use of thrombolytics.) INTRA-AORTIC BALLOON PUMP. To support the ischemic heart, an intra-aortic balloon pump (IABP) may be used to increase circulation to the coronary arteries and reduce the work of the heart (see Chapter 26). While the heart is relax ed (diastole), the balloon is inflated, sending more blood into the coronary arteries. Just before the heart contracts (systo