Atherosclerosis and Coronary Artery Disease (CAD) - LPN Chapter 24 PDF

ATHEROSCLEROSIS Arteriosclerosis is the thickening, loss of elasticity, and calcification of arterial walls. It occurs with aging. Atherosclerosis is the formation of plaque in the arteries. Arteriosclerosis and atherosclerosis are both conditions that may begin in early childhood and progress with...

ATHEROSCLEROSIS Arteriosclerosis is the thickening, loss of elasticity, and calcification of arterial walls. It occurs with aging. Atherosclerosis is the formation of plaque in the arteries. Arteriosclerosis and atherosclerosis are both conditions that may begin in early childhood and progress without symptoms through adulthood. Atherosclerosis causes coronary heart disease (CHD), also known as coronary artery disease (CAD), discussed shortly. WORD BUILDING arteriosclerosis: arterio---artery + sklerosis---hardness Pathophysiology Atherosclerosis is a multistep process that affects the inner lining of the artery (Fig. 24.1). Injury to the endothelial cells that line the walls of the arteries occurs, causing inflammation and immune response. Damage to the endothelium stimulates the growth of smooth muscle cells. These cells secrete collagen and fibrous proteins. Lipids, platelets, and other clotting factors accumulate. This buildup of fatty deposits that adheres to the wall of the artery is known as plaque. It is composed of smooth muscle cells, fibrous proteins, and cholesterol-laden foam cells. The plaque develops a fibrous cap that calcifies. The plaque's fibrous cap can tear or rupture, and a blood clot forms on the plaque. The clot can completely block the coronary artery, or it may break loose and lodge within a smaller artery leading to the heart. The artery may also become stenosed (narrowed) by the plaque buildup causing partial or total occlusion of the artery, resulting in reduced blood flow. The area distal to the occlusion can become ischemic as a result. FIGURE 24.1 (Top) Cross section of normal coronary artery. (Bottom) Coronary artery with atherosclerosis narrowing the lumen. Etiology Risk factors for atherosclerosis can be divided into two categories: those that can be modified and those that cannot (Table 24.1). Patient education to prevent risk factors is important. Table 24.1 Risk Factors for Atherosclerosis/Coronary Artery Disease Risk Factors That Cannot Be Changed Age Men have increased incidence after age 50. Women have increased incidence after menopause. Ethnicity Black 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 Diabetes mellitus Increases the risk of hypertension, obesity, and elevated blood lipids. Hypertension Vasoconstriction increases myocardial oxygen demand. Elevated serum cholesterol Level above 200 mg/dL increases risk of developing CAD. Elevated low-density lipoprotein (LDL) particle number or apolipoprotein B Infiltrates arterial wall, rapidly causing damage. Elevated serum homocysteine Increases CAD risk. Foods that contain folic acid (e.g., fruits, green leafy vegetables) reduce homocysteine level. Excessive alcohol use Raises blood pressure, increases triglycerides, and causes irregular heartbeats. Obesity Increases heart workload and risk of hypertension, diabetes, glucose intolerance, and hyperlipidemia. Sedentary lifestyle Increases obesity, hypertension, and hyperlipidemia. Emotional stress Increases heart workload and risk for hypertension. Tobacco use, secondhand and thirdhand smoke Causes vasoconstriction and increases myocardial oxygen demand. Decreases high-density lipoproteins (HDLs). Diagnostic Tests Total cholesterol levels above 200 mg/dL increase risk of CAD and myocardial infarction (MI; Table 24.2). Elevated low-density lipoproteins (LDLs) and low levels of high-density lipoproteins (HDLs) are associated with increased risk of CAD. A risk factor for premature CAD is a high level of Lp(a) cholesterol (a genetic variation of plasma LDL). An excellent predictor of MI risk is the LDL particle number. It is measured directly or indirectly as apolipoprotein B, the protein particle in each LDL. A high LDL particle number with a low LDL still creates a high risk for MI. (The amount of cholesterol contained in each LDL particle varies.) Apolipoprotein B particles in LDL-type cholesterol are able to infiltrate the arterial wall, rapidly causing damage. C-reactive protein (CRP) can indicate low-grade inflammation in blood vessels and an increased CAD 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). Table 24.2 Atherosclerosis Summary Diagnostic Tests Cholesterol Low-density lipoprotein (LDL) particle number Triglycerides Arteriogram Therapeutic Measures Low-fat, low-cholesterol diet Smoking cessation Exercise Priority Nursing Diagnoses Acute Pain Deficient Knowledge Therapeutic Measures A healthy lifestyle, preventing risk factors, medications, and regular physical examinations are helpful in controlling atherosclerosis. Diet Because plaque within arteries is primarily caused by fatty deposits, an adherence to a heart-healthy diet (Dietary Approaches to Stop Hypertension \[DASH\] eating plan) is beneficial (see Chapter 22, "Nutrition Notes"). Smoking The risk of developing CAD is greater in cigarette smokers than in nonsmokers. Risk is proportionate to the number of cigarettes smoked. Smoking contributes to a loss of HDL. Smoking also causes vasoconstriction, which leads to angina pectoris and cardiac arrhythmias. The benefits of smoking cessation are dramatic and almost immediate. Education about the risks of smoking and effects of exposure to secondhand and thirdhand smoke should be presented to patients and their families. Thirdhand smoke is residual nicotine and toxic chemicals left on surfaces (e.g., skin, hair, clothing, bedding, carpets, floors, furniture, walls) by tobacco smoke. The American Cancer Society has many programs to help people quit smoking (visit 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 starting an exercise program, patients should consult their health-care provider (HCP). Medications Lowering lipid levels is the primary therapy for atherosclerosis. If dietary control is not effective, medication is also used (Table 24.3). It may take 4 to 6 weeks before lipid levels respond to medication therapy. For those with familial hypercholesterolemia, which is a genetic disorder that prevents the removal of LDL due to a chromosome 19 defect, injectable monoclonal antibodies agents such as alirocumab (Praluent) and evolocumab (Repatha) are used. Table 24.3 Medications Used to Lower Lipid Levels vMedication Class/Action Statins First-line medications to reduce low-density lipoprotein (LDL) by reducing cholesterol synthesis. Examples atorvastatin (Lipitor) fluvastatin (Lescol XL) lovastatin (Mevacor) pravastatin (Pravachol) rosuvastatin (Crestor) simvastatin (Zocor) Nursing Implications Monitor liver function studies. Monitor for rhabdomyolysis (lethal breakdown of skeletal muscle). Teach: Take medication in evening when cholesterol synthesis is highest. Report muscle pain to health-care provider. Fibrates Reduce triglycerides. Examples clofibrate (Atromid-S) fenofibrate (TriCor) gemfibrozil (Lopid) Nursing Implications Teach: Take 30 minutes before morning and evening meal. May increase the effects of anticoagulants and hypoglycemia. Niacin Prevents conversion of fats into very low LDLs. Rarely used because of flushing. Examples niacin (nicotinic acid) extended-release niacin (Niaspan) Nursing Implications Teach: Take aspirin 30 minutes before taking medication to reduce flushing. Cholesterol Absorption Inhibitor Inhibits the absorption of cholesterol. Decreases LDLs and increases high-density lipoproteins (HDLs). Examples ezetimibe (Zetia) Nursing Implications Teach: Take with liquids and meals. Take other medications 1 hour before or 4 hours after. Combination Agent See each agent. Examples Vytorin = ezetimibe (Zetia) + simvastatin (Zocor) Nursing Implications See each agent.  CORONARY ARTERY DISEASE CAD is the obstruction of blood flow through the coronary arteries to the heart muscle cells, typically from atherosclerosis. Prevention Risk factors for CAD are listed in Table 24.1. Risk factors that can be modified should be changed (see therapeutic measures for atherosclerosis above). Low-dose aspirin may be recommended for certain patients by their HCP to prevent the formation of a thrombus. Million Hearts® 2022 is a national initiative to prevent 1 million heart attacks and strokes within 5 years (https://millionhearts.hhs.gov). Evidence-based priorities to improve cardiovascular health for everyone focus on cholesterol management, self-measured blood pressure monitoring, hypertension control, tobacco cessation, and cardiac rehabilitation. CUE RECOGNITION 24.1 A patient who has hypertension and had an episode of angina is tearful and frightened. The patient asks you how to prevent future pain episodes. What action do you take? Suggested answers are at the end of the chapter. Angina Pectoris Angina pectoris is chest pain due to ischemia resulting from a reduction in coronary artery blood flow and oxygen delivery to the myocardium. Angina is a symptom, not a disease. Types of Angina STABLE ANGINA. Stable angina occurs with moderate exertion in a pattern familiar to the patient. The pain is predictable and lasts a few minutes. It can usually be relieved by resting and use of prescribed nitroglycerin. WORD BUILDING angina pectoris: angina---to choke + pectora---chest VASOSPASTIC ANGINA. This type of angina is caused by coronary artery spasms and is serious. The pattern of occurrence is often cyclical, with the pain happening about the same time each day. The pain lasts longer than stable angina, can occur with exercise or at rest, and often occurs at night. MICROVASCULAR ANGINA. Spasms in the walls of the tiniest arteries of the heart reduce coronary blood flow and result in microvascular angina. Compared with other types of anginal pain, this pain is often more severe and lasts longer. Signs and Symptoms Patients (especially men) often describe anginal chest pain as discomfort, burning, fullness, heaviness, pressure, or squeezing (Fig. 24.2). The pain can radiate to adjacent areas such as one or both arms (left arm is common), shoulders, neck, jaw, or back. If pain is present in the shoulders, neck, jaw, arms, or back due to a cardiac problem but there is no chest pain, then it is referred pain. 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. Women might also experience chest pain, jaw pain, or heartburn with angina but often have atypical symptoms. These include shortness of breath, fatigue, nausea, or pain that is described as less severe. Atypical symptoms should not be ignored. Treatment should be sought immediately. (See the "Women and Heart Health" section.) FIGURE 24.2 Common locations of anginal pain, which may vary in combination and intensity. Diagnostic Tests Common tests used to diagnose CAD or anginal causes include electrocardiogram (ECG), exercise stress test, echocardiography, chemical stress testing, cardiac computed tomography (CT) scan, cardiac magnetic resonance imaging (MRI)/magnetic resonance angiogram (MRA), radioisotope imaging, and coronary angiography. Therapeutic Measures Risk factors identified for the patient determine treatment to prevent anginal attacks with activity and MI. Weight reduction, a heart-healthy diet, smoking cessation, and reduction of emotional stress may help slow disease progression. Three major classes of medications---nitrates, beta blockers, and calcium channel blockers---and a newer medication, the antianginal ranolazine (Ranexa), are used alone or in combination for reducing angina (Table 24.4). Nitroglycerine (NTG), a vasodilator, is the medication of choice for acute anginal attacks. For acute use, it is available sublingually (buccal, powder, spray, tablet) or intravenously in the hospital. When administered sublingually, NTG may relieve chest pain within 1 to 2 minutes (Box 24.1). Long-acting nitrates (oral or topical: ointment, transdermal patch) are used to prevent acute chest pain. To prevent development of nitrate tolerance, a common issue with nitrates, the ointment or patch is removed for a 10- to 12-hour nitrate-free period (removed at bedtime/reapplied in the morning for exertional angina; removed in the morning/reapplied at bedtime for nocturnal angina). Oral nitrates (non-extended-release capsules) are also scheduled to give the patient a nitrate-free period. BE SAFE! ACT FAST! Sublingual Nitroglycerin   If after one tablet and 5 minutes have elapsed, pain is unrelieved or worsens, especially with symptoms of an MI, call 911. Take two more doses, 5 minutes apart, if needed while waiting.   For angina, take one NTG tablet. If the symptoms are not worsening but are not completely relieved, repeat a tablet every 5 minutes up to a total of three tablets. If pain is not relieved after three tablets, call 911. BE SAFE! AVOID FAILURE TO COMMUNICATE! Inform patients who take nitrates not to take medications for erectile dysfunction, such as sildenafil (Viagra), tadalafil (Cialis), or vardenafil (Levitra). These types of medications dilate blood vessels and may cause a significant drop in blood pressure if used with nitrates. Table 24.4 Medications Used to Treat Angina Pectoris Medication Class/Action Antiplatelets Inhibit platelet activation, adhesion, or procoagulant activity. Examples aspirin clopidogrel (Plavix) ticagrelor (Brilinta) Nursing Implications Enteric-coated aspirin beneficial for daily use. Monitor for bleeding. Beta Blockers Decrease heart rate, contractility, and BP to reduce cardiac workload and exertional angina. Decrease the risk of sudden death. Examples atenolol (Tenormin) metoprolol (Lopressor, Toprol XL) Nursing Implications If pulse is less than 60 bpm or systolic BP less than 90 mm Hg, consult HCP before administering medication. Teach: Explain need to rise slowly. Abrupt withdrawal may result in diaphoresis, palpitations, headache, and tremors. Calcium Channel Blockers Dilate peripheral arteries, decrease myocardial contractility, depress conduction system, and decrease workload of the heart. In vasospastic angina, reduce coronary artery spasm. Examples amlodipine (Norvasc) diltiazem (Cardizem, Dilacor XR) felodipine (Plendil) verapamil (Calan SR) Nursing Implications If pulse is less than 60 bpm or systolic BP less than 90 mm Hg, notify HCP before administering medication. Nitrates Vasodilate to increase blood flow to coronary arteries and reduce preload and afterload to reduce oxygen consumption of myocardium. Nursing Implications: Do not use any NTG with erectile dysfunction medication as it can cause a significant drop in blood pressure. Document onset, location, type, radiation, and duration of pain. Monitor blood pressure (BP) pre- and postadministration. Examples Fast Acting: nitroglycerin sublingual powder (GONITOR) nitroglycerin sublingual, buccal (Nitrostat, NitroQuick) nitroglycerin sublingual spray (Nitrolingual, Nitromist) Nursing Implications Teach: See Be Safe! Act Fast! and Box 24.1. Long Acting: nitroglycerin (Transderm Nitro, Nitro-Bid) nitroglycerin patch (Nitro-Dur, Nitrek) isosorbide dinitrate (Isordil) isosorbide mononitrate (Imdur, ISMO) nitroglycerin extended release (Nitro-Time) Wear gloves to protect yourself from hypotension from touching the ointment or patch medication. Remove patch before magnetic resonance imaging or defibrillation. Teach: Remove current transdermal ointment or patch before applying a new dose to prevent overdose. Rotate application sites. Apply ointment or patch to clean, dry, hairless area daily. Provide nitrate-free period as prescribed. Teach: Provide nitrate-free period as prescribed. Anti-Ischemic Agent Antianginal agent used as combination therapy for those not responding to other antianginal medication. Examples ranolazine (Ranexa) Nursing Implications May not be as effective in women. Prolongs QT interval on electrocardiogram. Statins See Table 24.3. Box 24.1 Key Points for Using Fast-Acting Nitroglycerin   Carry nitroglycerin (NTG) at all times.   Keep NTG tablets tightly sealed in the dark container to protect from heat, light, and moisture.   Maintain a fresh supply of NTG tablets, replacing it as needed, or every 6 months for maximum effect.   Use NTG before an activity known to cause chest pain.   Tingling should be felt under the tongue when sublingual (SL) NTG tablets are used.   Pour SL packet of powder under the tongue to dissolve without swallowing.   Do not shake NTG aerosol canister before spraying it on or under the tongue, and close mouth immediately.   NTG may cause lightheadedness. Sit or lie down when taking NTG, if possible. Rise slowly to prevent falls, especially with sublingual spray.   NTG may cause a headache initially for 1 to 2 weeks. Aspirin may relieve it. Beta blockers are initial therapy for exertional angina prevention. They decrease heart rate and contractility and lower blood pressure to reduce the workload of the heart. Beta blockers are not effective for coronary artery spasms, so they should not be used for vasospastic angina. LEARNING TIP To help you identify beta blockers, remember that their generic names end with -olol. Calcium channel blockers dilate the coronary arteries and peripheral vessels, which increases the myocardial oxygen supply and reduces cardiac workload. They are ineffective in relieving acute anginal attacks. Antiplatelets are used to prevent cardiovascular events that would occur from blood clots and cause angina. Statins prevent and treat atherosclerosis since cholesterol and inflammation in artery walls are involved in atherosclerosis development (see Table 24.3). Nursing Process for the Patient With Coronary Artery Disease and Angina Data Collection Record height, weight, allergies, over-the-counter and prescription medications, use of herbs, and typical diet. Identify the patient's nonmodifiable and modifiable risks for atherosclerosis and CAD. Obtain vital signs and oxygen saturation. Note dyspnea, labored respirations, diaphoresis, nausea, skin color, and temperature. Note a history of chest pain, fatigue, or activity intolerance. Document the patient's description of anginal pain, factors making the pain worse or better, how long the patient has had angina, triggering activities, and how the pain has been relieved in the past (see Table 21.2). Nursing Diagnoses, Planning, and Implementation Acute Pain related to reduced perfusion of coronary arteries Expected Outcome: The patient will report an absence or acceptable level of pain within 30 minutes of reporting pain.   Ask patient to rate pain with a scale (such as 0 to 10) to provide consistent pain reporting.   Administer oxygen as prescribed to increase oxygen availability to myocardium to ease pain.   Administer fast-acting NTG (sublingual) as prescribed to provide pain relief.   Notify HCP if pain is unrelieved after three doses of NTG or as prescribed, or if vital signs change. Chest pain unrelieved by nitrates (sublingual) may represent MI.   Remain with patient and provide emotional support. A patient who has chest pain should never be left alone. Deficient Knowledge related to ineffective management of regimen for coronary artery disease Expected Outcome: The patient will report understanding of management of atherosclerosis and CAD.   Identify patient's readiness to learn, desired learning needs, baseline knowledge and feelings about incorporating lifestyle changes into daily routine to prioritize teaching topics.   Include significant other as appropriate to support patient during learning.   Explain pathophysiology of atherosclerosis and CAD, control of risk factors, management of CAD symptoms and medications to promote understanding and reduce complications.   Provide information about community resources that can assist in making lifestyle changes.   Encourage questions and allow patient the opportunity to verbalize new information and skills to enhance learning. Evaluation Interventions are successful if the patient is pain-free, demonstrates increased understanding of atherosclerosis and CAD and their management, and states plans to modify risk factors of CAD. CUE RECOGNITION 24.2 You are caring for a patient who reports chest pain. What action do you take? Suggested answers are at the end of the chapter.  ACUTE CORONARY SYNDROME Acute coronary syndrome (ACS) refers to conditions involving myocardial ischemia: unstable angina, non--ST-elevation MI (NSTEMI), and ST-elevation MI (STEMI). With unstable angina, the ischemia does not cause enough cardiac damage to release cardiac biomarkers. NSTEMI is caused by a partial coronary artery blockage. STEMI is usually caused by a complete blockage of a coronary artery. In a small percentage of patients with a STEMI, there is no obstruction (i.e., cocaine, embolism, myocarditis, spasm). (See Chapter 25 for ST-segment definition.) MI due to ischemia is discussed. Silent Ischemia Silent ischemia occurs without pain. It can carry great risk because the ischemia goes undetected. Older adults, women, and those with hypertension or diabetes most often have silent ischemia. Sudden Cardiac Death Sudden cardiac death is cardiac arrest triggered by lethal ventricular arrhythmias or asystole (see Chapter 25) from an abrupt occlusion of a coronary artery. Immediate treatment is required to attempt to prevent death. Myocardial Infarction The ability of the heart to contract, relax, and propel blood throughout the body requires healthy cardiac muscle. An acute MI due to ischemia results in the death of heart muscle cells from a sudden partial or complete blockage of a coronary artery. The extent of the cardiac damage varies depending on the location and amount of blockage in the coronary artery. Cellular death may be avoided with timely and effective reperfusion. Pathophysiology Ischemic injury evolves over several hours before complete necrosis and myocardial infarction 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. Once necrosis takes 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. It is susceptible to becoming necrosed. If treatment is initiated within the first hour of symptoms of the MI and restores the blood supply from the blocked artery, 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 develop collateral circulation. The area affected by an MI depends on the coronary artery (Fig. 24.4). Being familiar with the anatomy of the heart and the area of the MI helps the nurse anticipate arrhythmias, conduction disturbances, and heart failure. All of these are the major complications of MIs (Table 24.5). The left coronary artery supplies the anterior wall of the heart, which also includes most of the left ventricle. 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. This leads to severe changes in the hemodynamic status of the patient. LEARNING TIP To remember coronary artery occlusion and subsequent myocardial infarction location, personalize the locations with initials of places familiar to you. Location Coronary Artery Resulting MI Location Los Angeles Left anterior descending Anterior Cedar Point Circumflex Posterior Rhode Island Right Inferior The right coronary artery supplies the heart's inferior wall and parts of the atrioventricular node and the sinoatrial node. An occlusion of the right coronary artery leads to an inferior MI and abnormalities in cardiac conduction. Serious arrhythmias can occur early in an inferior MI that may be life-threatening. The left circumflex coronary artery supplies the heart's lateral wall and part of the posterior wall. A blockage in this artery causes a lateral wall infarction of the left ventricle. FIGURE 24.3 Myocardial infarction. Areas of ischemia, injury, and necrosis caused by a blockage in the left anterior coronary artery. FIGURE 24.4 Coronary arteries. (A) Anterior view. (B) Posterior view. Table 24.5 Complications of Myocardial Infarction Complication Types or Symptoms Interventions Arrhythmias Premature ventricular contractions, ventricular tachycardia, ventricular fibrillation, heart block Continuous cardiac monitoring Protocol treatment of arrhythmias (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 arrhythmias Intra-aortic balloon pump Thrombolytic therapy Dopamine, 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 diuretics as ordered Emboli Dependent on location of emboli Anticoagulants to prevent clots Supportive symptom treatment Rupture of muscles or valves of the heart, septal rupture Signs of cardiogenic shock, death Immediate treatment of myocardial infarction to limit extent of damage Pericarditis (inflammation of the pericardium) Chest pain, increased with movement, deep inspiration, or cough; pericardial friction rub (fine grating sound) Position upright, leaning forward Anti-inflammatory medications Signs and Symptoms Chest pain is the classic symptom of an MI. The pain begins suddenly and is not relieved by rest or administration of NTG. Pain occurring in the center of the chest is usually described as crushing, as if an elephant is standing on the chest. Chest pain can radiate to shoulders, one or both arms, hands, neck, throat, lower jaw, teeth, upper abdomen or back. 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). The heart rate may be rapid and the heart's rhythm irregular. An extra heart sound (S3 or S4) may be present, which is a sign the myocardium is failing. Table 24.6 Myocardial Infarction Summary Signs and Symptoms Classic Crushing, vicelike chest pain with radiation to arms, shoulder, hands, neck, throat, lower jaw, teeth, 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 Shortness of breath Fatigue Epigastric or abdominal pain Chest discomfort, pressure, or burning Arm, shoulder, neck, jaw, or back pain Discomfort/pain between shoulder blades Indigestion or gas pain Nausea or vomiting Diagnostic Tests Electrocardiogram (ECG) Serum cardiac troponin I or T Serum myoglobin Serum creatine kinase-MB (CK-MB) Complete blood count (CBC) Serum magnesium and potassium Vital signs, oxygen saturation Therapeutic Measures Antiplatelets (e.g., aspirin) Oxygen Nitrates Percutaneous coronary interventions and stents Thrombolytics Anticoagulants Beta blockers Statins Myocardial revascularization (coronary artery bypass grafting) Daily weight Bedrest with use of bedside commode/bathroom Low-sodium diet advanced to diet as tolerated; no caffeine Cardiac rehabilitation Complications Arrhythmias Heart failure Cardiogenic shock Valvular insufficiency Priority Nursing Diagnoses Acute Pain Decreased Cardiac Output Fear TIMELY SYMPTOM TREATMENT. Individuals, especially women, often deny or fail to recognize that an MI is occurring because they experience symptoms that are atypical or similar to other mild conditions such as indigestion ("Gerontological Issues"). Patients have reported that the symptoms of an MI they experienced were not what they expected. If people expect and do not experience the dramatic heart attack symptoms seen on television shows (which are usually not the same as those in real life), they are likely to delay seeking treatment. Waiting 2 to 24 hours before seeking medical care is common, yet the first hour after symptom onset is crucial for administering reperfusion treatments that restore blood flow, minimize tissue damage, and save lives. Individuals should not drive themselves or let someone drive them to the hospital when having chest pain. Calling for emergency medical services allows lifesaving treatment to begin. Individuals, especially women, need to be educated that "time is muscle." As time passes during an MI, more muscle is lost. Women and Heart Health Heart disease remains the leading cause of death in women in the United States (Office on Women's Health, 2019). Compared with men, women tend to have acute MIs at an older age, with a higher mortality rate and more complications, such as ventricular fibrillation and heart failure. This may be due to women waiting longer than men do before seeking help. Women may have classic chest pain, but they are also likely to have other symptoms as well that men do not typically have. Atypical symptoms reported by women may include extreme fatigue, epigastric pain, lower jaw pain, indigestion, nausea and vomiting, dyspnea, shortness of breath, or cramping in the chest. Many women note prodromal symptoms a month before an acute MI. These symptoms include unusual fatigue, sleep disturbances, and shortness of breath. Gerontological Issues Myocardial Infarction With age, the heart has decreased elasticity, which increases both resistance to its pumping action and the workload of the myocardium. Older adults should be taught never to neglect symptoms of shortness of breath, fatigue, fast or slow heartbeats, or chest discomfort. For older adults, the following is common with MI:   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 adults, especially those older than age 85.   Because the older adult has had more time than younger people to develop collateral circulation, they often do not have as many complications with an MI.   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. Diagnostic Tests Patients with a strong familial history of MI should be considered at risk until an MI is ruled out. Combined indicators of an MI are patient history, ECG changes, and elevated levels of highly sensitive cardiac troponin T (cTnT) or I (cTnI), and myoglobin and creatine kinase (CK)-MB if used (see Chapter 21). The ECG may show the area that is infarcted as well as ischemic areas of the heart. Myocardial damage can be seen as ST-elevation, the presence of a Q wave, or T-wave abnormalities (Fig. 24.5). Serial ECGs monitor changes indicating damage or ischemia. Magnesium and potassium levels are checked. Both are essential for normal cardiac function, especially for those on diuretic therapy. FIGURE 24.5 Electrocardiogram changes during STEMI myocardial infarction. (A) Injury: ST-segment elevation. (B) Ischemia: ST-segment inversion. (C) Necrosis: large Q-wave and ST-segment elevation. Therapeutic Measures Time until intervention is directly related to mortality (Box 24.2). Medical treatment should be sought within 5 minutes for unrelieved chest pain or other symptoms. The goal is to restore blood flow to the heart muscle within 90 minutes of the patient's arrival at the emergency department. Box 24.2 Preventing Delays in Myocardial Infarction Treatment   Understand symptoms, the "time is muscle" principle, and that a delay in calling for help results in untoward effects.   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 department policies that reduce delays, such as having equipment and medication readily available. PERCUTANEOUS CORONARY INTERVENTION WITH STENTING. Coronary artery stenting with drug-eluting stents is the preferred percutaneous coronary intervention (PCI) for cardiac revascularization. A stent is an expandable metal mesh tube that is implanted during angiography at the site of the atherosclerotic blockage in the coronary artery (Fig. 24.6). It provides support to the coronary artery wall at the area of stenosis to keep the artery open and the blood flowing through the artery. Drug-eluting stents, which are coated with immunosuppressant medication, are more effective in preventing the need for revascularization of the artery than is percutaneous transluminal cardiac angioplasty (PTCA). The drug 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. Complications associated with stent placement include thrombosis (formation of a blood clot inside a blood vessel), bleeding from anticoagulation, stent occlusion, or coronary artery dissection. FIGURE 24.6 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. THROMBOLYTIC THERAPY. PCI, when available onsite, has greatly reduced the use of thrombolytics to dissolve a blood clot that is occluding a coronary artery. When used, the thrombolytic medication 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 a thrombolytic within 30 minutes of arrival in the emergency department. OXYGEN. Arterial blood gases (ABGs) guide the patient's oxygen needs. Routine oxygen was not found to be beneficial when oxygen levels were normal (Abuzaid et al, 2018). MEDICATION. Table 24.7 summarizes pharmacological treatment of MI. Antiplatelet medication is given to reduce platelets from forming clots. Chewing one nonenteric aspirin (165--325 mg) is prescribed after diagnosis of acute coronary syndrome. For acute cardiac-related pain, NTG is given sublingually or by IV drip. NTG causes vasodilation, which supplies increased blood flow to the myocardium, thereby relieving ischemia and reducing the pain. Nitrates should not be given if the patient has taken a phosphodiesterase inhibitor for erectile dysfunction, as catastrophic hypotension may result (see "Be Safe!" earlier in the chapter). Morphine sulfate is given carefully for ischemic pain that is unrelieved by other therapy, as it may worsen patient outcomes. Dual antiplatelet therapy may be given long term after an MI. Antiarrhythmics are given if atrial or ventricular arrhythmias occur (see Chapter 25). Table 24.7 Medications Used to Treat Myocardial Infarction Medication Class/Action Anticoagulants Heparin: Inhibits conversion of prothrombin to thrombin to prevent thrombus formation. Examples heparin sodium Nursing Implications Do not give if bleeding risk. Dose regulated by heparin antifactor Xa or activated partial thromboplastin time (aPTT Goal: 1.5 to 2.5 times control). Monitor for bleeding. Low Molecular Weight Heparin (LMWH): Antithrombotic prophylaxis of ischemic complications in non-ST-elevation myocardial infarction with aspirin therapy. Examples dalteparin (Fragmin) enoxaparin (Lovenox) fondaparinux (Arixtra) Nursing Implications Do not remove prefilled syringe air bubble. Rotate sites. Give deep subcutaneously: Hold fold of skin while giving injection. Do not massage site. Teach: Monitor for bleeding. Antiplatelets Inhibit platelet activation, adhesion, or procoagulant activity. Examples aspirin clopidogrel (Plavix) prasugrel (Effient) ticagrelor (Brilinta) vorapaxar (Zontivity) Nursing Implications Teach: Chew aspirin when myocardial infarction (MI) suspected. Report bleeding or bruising. Glycoprotein IIb/IIIa Inhibitors Inhibit platelet aggregation during percutaneous coronary intervention. Examples abciximab (ReoPro) bivalirudin (Angiomax) eptifibatide (Integrilin) tirofiban (Aggrastat) Nursing Implications Prevent injury due to bleeding risk. Monitor vital signs and ECG. Teach: Report bleeding or bruising. Thrombolytics Dissolve blood clots in blood vessels. Examples alteplase; tissue plasminogen activator \[t-PA\] (Activase) reteplase; rPA (Retavase) tenecteplase; TNK (TNKase) Nursing Implications Most effective when given within 6 hours of acute coronary event. Goal is 30 minutes from arrival in emergency department. Baseline international normalized ratio (INR), activated partial thromboplastin time (aPTT), platelet count, and fibrinogen levels checked. Avoid venipunctures for 24 hours after administration. Beta Blockers See Table 24.4. Nitrates See Table 24.4. Statins See Table 24.3. Additional Medications as Needed Specific for medications given. Examples antiemetics anxiolytics antacids stool softeners Nursing Implications Control nausea, vomiting, anxiety, gastric upset, and straining/constipation. ACTIVITY. Initially, patients are kept on bedrest to decrease myocardial oxygen demand. A bedside commode for bowel movements is usually ordered to reduce straining on a bedpan. Activity is advanced gradually when stable as tolerated. DIET AND WEIGHT LOSS. Initially, a low-sodium, clear liquid diet is ordered as tolerated, which helps reduce the risk of vomiting. Then, small, easily digested, heart-healthy meals are served. Caffeine is restricted because it increases heart rate and causes vasoconstriction. Fluids may be restricted if the patient is in heart failure as well. If the patient is overweight, weight loss can reduce cardiac workload. A dietitian can help the patient and family to devise a weight-loss diet for the patient. Coronary Artery Bypass Graft During coronary artery bypass graft (CABG) surgery, the saphenous vein from the leg and/or an internal mammary artery from the chest wall is used to reroute blood around a segment of a coronary artery that is narrowed by atherosclerosis (Fig. 24.7). One or more vessels can be bypassed (see "Patient Perspective"). The surgery can be done either on cardiopulmonary bypass (arrested heart surgery) or off cardiopulmonary bypass (beating heart surgery). See Chapter 21. FIGURE 24.7 Myocardial reperfusion by coronary artery bypass graft surgery. Patient Perspective Keith When I was 72, a heart catheterization showed significant coronary artery blockage, so I had five coronary artery bypass grafts performed. It was a long surgery. I felt disoriented for several days afterward, mostly while I was in the intensive care unit. I was provided excellent care at home after discharge from the hospital. I had a capable visiting nurse, physical therapist, or occupational therapist almost every day. Physical therapy was difficult at first but shortly became routine and easy. I have had a strange sensation in my legs at the incision sites ever since surgery but no pain. I have not experienced depression, although I hear post-op depression is common. My experience during cardiac rehab of three sessions per week for 12 weeks was outstanding. I enjoyed the association with others in the same situation. We even staged a graduation when we finished. I wore a tuxedo jacket with my gym shorts! Since completing my rehab, I have maintained a minimum 40-minute exercise schedule three times per week. I am trying to be more conscious of my diet. I do this because I want to stay healthy for a long time. CARDIOPULMONARY BYPASS: ON PUMP. Most bypasses are done while the heart is stopped with cardiopulmonary bypass (on pump) in use. While the median sternotomy is made, the vein graft is being removed from the body. The graft is flushed with a heparinized solution to check for leaks and then set aside for use during the surgery. After the patient is placed on cardiopulmonary bypass and the heart is stopped, one end of the graft is anastomosed (joined) to the coronary artery distal to the occlusion, and the proximal end of the graft is anastomosed, often to the ascending aorta. CARDIOPULMONARY BYPASS: OFF PUMP. This surgery is done with the heart beating and does not use the cardiopulmonary bypass (off pump). A device is used to stabilize a vessel while the surgeon works on it. Either traditional median sternotomy or minimally invasive surgery can be used. MINIMALLY INVASIVE SURGERY. Less-invasive approaches include the minimally invasive direct CABG (MIDCAB), which is done off pump, and totally endoscopic CABG (TECAB), which can be done on or off pump. MIDCAB is done through a small fifth intercostal incision. TECAB uses three or four chest holes for insertion of robotic arms and a camera that a surgeon views to control the robotic arms. Nursing Process for the Patient Experiencing Myocardial Infarction DATA COLLECTION. A thorough history is obtained to identify risk factors that may contribute to an MI. All patients admitted with chest pain are treated for a possible MI until it has been ruled out. Continuous cardiac monitoring and serial ECGs and laboratory values determine the degree of cardiac damage and detect life-threatening arrhythmias. Controlling ischemic pain immediately helps diminish anxiety and the negative physiological effects pain has on the body. Screening for depression, common after an MI, is important for appropriate therapy referrals. NURSING CARE TIP Surgical site infection following CABG (i.e., mediastinitis) is a "Never Event." This means that Medicare will not pay the hospital for care for this condition, as it never should have occurred. Use infection-control procedures at all times to prevent this surgical site infection. NURSING DIAGNOSES, PLANNING, IMPLEMENTATION, AND EVALUATION. See "Nursing Care Plan for the Patient With Myocardial Infarction." Also see "Nursing Care Plan for the Patient Undergoing Surgery" in Chapter 12. Patients undergoing cardiac surgery will have a chest tube placed. Chest tube drainage is observed, and more than 200 mL/hr should be reported. Vital signs, peripheral pulses, electrolytes, ABGs, and ECGs are monitored. Acidosis, low calcium and magnesium levels, and abnormal potassium levels decrease cardiac contractility and cardiac output. Acute pain may be experienced due to sternotomy, leg incisions, or internal mammary artery resection. The patient should be taught sternal precautions: no pushing or pulling with arms; hug pillow with all movements; do not use arms to rise out of a chair; do not lift more than 5 to 10 pounds; do not raise elbows above shoulders; and bend elbows and lower head for grooming. Patient Education Education about the therapeutic regimen includes information about the disease, medications, diet, activity, and rehabilitation needs that may require lifestyle changes, such as smoking cessation, exercise, stress management, and weight loss. Heart disease can affect all aspects of a patient's lifestyle, including family and job roles. Patients recovering from cardiac disorders are often anxious about resuming sexual activity but are embarrassed to discuss it. This is an area that is often overlooked when caring for patients. Sexuality counseling should be offered to patients and their partners. Patients often have misconceptions that are unfounded but interfere with resuming sexual activity. If patients have angina, NTG can be taken prophylactically before sexual activity. After an MI, sexual activity can be resumed in 1 to 2 months or when the patient can climb two flights of stairs without symptoms, as approved by the HCP. Patients are given information to make an informed decision on when they are ready to resume this physical activity. Referral to a sexuality counselor for information on ways to cope with sexual issues in relation to the illness can be helpful to the patient. Cardiac Rehabilitation and Exercise Cardiac rehabilitation to improve cardiac function and quality of life begins when the patient's acute symptoms are relieved (see "Evidence-Based Practice"). Phase 1 of rehabilitation occurs in the hospital. Activities for each hospital day, such as types and amounts of self-care and activity, are specified in protocols. Phase 2 occurs 4 to 6 weeks after discharge in an outpatient program. It focuses on returning the patient to previous levels of activity and function. Phase 3 follows, during which patients are encouraged to maintain optimal physical fitness and continue healthy lifestyles that include exercising and losing weight to maintain an ideal body weight. CRITICAL THINKING & CLINICAL JUDGMENT Mr. Jones was transferred to the critical care unit after a quadruple coronary artery bypass graft. Preoperative vital signs were blood pressure 144/84 mm Hg, apical pulse 62 beats per minute (regular), respiratory rate 18 breaths per minute, and temperature 98.4°F (36.9°C). Postoperative data collection findings are blood pressure 100/56 mm Hg, apical pulse 115 beats per minute, respiratory rate 28 bpm (irregular and shallow), temperature 99.8°F (37.7°C), lung sounds diminished with crackles in bilateral bases, chest tube intact with 300 mL of red drainage over 1 hour, pedal pulses weak bilaterally, and chest and leg dressings dry and intact. Critical Thinking (The Why) Why might Mr. Jones's blood pressure be decreased? Why might Mr. Jones's apical pulse be elevated? Which data collection findings require action? Clinical Judgment (The Do) What priority action do you take? With which health-care team members do you collaborate? What patient education topics do you reinforce in sessions with the patient and family? Suggested answers are at the end of the chapter. Evidence-Based Practice: Clinical Question What are the effects of eHealth-based interventions on patient adherence to components of cardiac rehabilitation? Evidence A systematic review including 105 studies was conducted on eHealth and its effect on patient adherence to components of cardiac rehabilitation. Most studies focused on medication adherence, and others looked at adherence to diet, physical activity, vital signs, weight, step counts, smoking, and fluid restriction. It was found that telemonitoring and Web-based applications for self-care behavior were more effective than telephone calls to promote patient adherence. Implications for Nursing Practice Nurses and health-care team members may find it beneficial to include telemonitoring and Web-based applications for self-care to encourage and support patients in reducing modifiable risk factors for cardiovascular disease. References: Kebapci, A., Ozaynak, M., & Lareau, S. (2020). Effects of eHealth-based interventions on adherence to components of cardiac rehabilitation: A systematic review. Journal of Cardiovascular Nursing, 35(4), 74--85. CRITICAL THINKING & CLINICAL JUDGMENT Mrs. Sims, age 43, is admitted to the intensive care unit with a diagnosis of atypical chest pain that radiates to her left shoulder and down her left arm. She has a history of midsternal chest cramping. Her pain increases with activity and decreases with rest. She smokes 1.5 packs of cigarettes per day and is 50 pounds overweight. The cardiac monitor shows normal sinus rhythm without arrhythmias. She has nitroglycerin sublingual ordered as needed for chest pain. One hour after admission, Mrs. Sims reports acute midsternal chest pain radiating to her left neck and lower jaw. The cardiac monitor shows sinus tachycardia of 108 bpm with occasional premature ventricular contractions. Her blood pressure is 100/70 mm Hg, respirations are 20 breaths per minute and unlabored, and skin is warm and dry. Critical Thinking (The Why) What is likely occurring with Mrs. Sims? How is angina differentiated from an MI? What are the indicators of an MI that will be checked for Mrs. Sims? What medical interventions could be used for Mrs. Sims? Clinical Judgment (The Do) What priority actions do you take? What do you remain vigilant about? What psychosocial actions do you provide Mrs. Sims? With which health-care team members do you collaborate? What patient-centered education topics do you reinforce in educational sessions with Mrs. Sims and her family? Suggested answers are at the end of the chapter. Nursing Care Plan for the Patient With Myocardial Infarction Nursing Diagnosis: Acute Pain related to decreased coronary blood flow causing myocardial ischemia Expected Outcomes: The patient will report an absence or acceptable level of pain within 30 minutes of reporting pain. Evaluation of Outcomes: Does the patient state that pain is reduced? Intervention Rationale Evaluation Monitor pain level with a pain rating scale and its characteristics. Identifies severity and type of pain. What is pain level, location, duration, intensity, and radiation? Administer nitrates and analgesics as needed and prescribed. Relieves pain. Is pain relieved? Assist with alternative pain relief measures (e.g., positioning, rest, relaxation techniques). These measures help decrease oxygen demand. Does patient express pain relief and decreased emotional stress? Geriatric Monitor and ensure that older patient's pain is relieved. Pain is not an expected part of the aging process as may be believed. Does patient report pain is relieved? Nursing Diagnosis: Decreased Cardiac Output related to ischemia or infarction, changes in heart rate and rhythm, and decreased contractility Expected Outcomes: The patient will maintain adequate cardiac output and tissue perfusion. Evaluation of Outcomes: Does the patient have vital signs and urine output within normal limits (WNL)? Intervention Rationale Evaluation Monitor blood pressure, heart rate, electrocardiogram and urine output, and report abnormalities. These are indirect indicators of cardiac output. Are indicators WNL? Monitor peripheral pulses, capillary refill, color, and temperature. These are indicators of adequate tissue perfusion. Does patient have strong peripheral pulses, capillary refill less than 3 seconds, pink nailbeds, and warm skin? Administer cardiac medications as ordered by health-care provider. Helps improve cardiac output and tissue perfusion. Does patient show signs of improved contractility, increased cardiac output, and tissue perfusion? Promote quiet environment and rest in semi-Fowler position. Decreases cardiac workload. Is patient relaxed? Geriatric Observe for atypical pain or no pain with dyspnea or fatigue. In acute myocardial infarction (MI), older adults may not have typical chest pain or may have a silent MI. Does patient have atypical symptoms of MI? Monitor for medication side effects. Older patients may have more medication toxicity due to reduced renal and hepatic function. Does patient exhibit side effects of medications? Nursing Diagnosis: Decreased Activity Tolerance related to imbalance between oxygen supply and demand, weakness, and fatigue Expected Outcome: The patient will tolerate progressive activity as evidenced by heart rate, blood pressure, pulse oximetry, and respiratory rate WNL. Evaluation of Outcome: Is the patient's heart rate, blood pressure, pulse oximetry, and respiratory rate WNL with progressive activity? Intervention Rationale Evaluation Obtain baseline vital signs and observe and stop activity and report abnormal responses, if heart rate over 120 beats per minute or 20 beats over resting rate, systolic blood pressure increases more than 20 mm Hg, chest pain, dizziness, skin color changes, diaphoresis, dyspnea, arrhythmias, excessive fatigue, and ST-segment changes on ECG occur. Observation allows detection of abnormal responses to stop activity. Are vital signs WNL and activity tolerated without symptoms? Maintain progression of ordered activities as tolerated. Initial activities: Activities of daily living, dangling feet at bedside for 15 minutes, using commode with assistance. Progressive activities: Out of bed to chair for 30 to 60 minutes, partial bath, range-of-motion exercises. Patient should have increasing activity to condition the myocardium. Is patient able to progress activity? Geriatric Slow the pace of care but allow independence. Allow patient extra time to complete activity to reduce cardiac demand and fatigue. Is patient able to complete care without symptoms or fatigue? Request referral for cardiac rehabilitation. Older adults benefit comparably to younger persons from exercise programs. Does patient participate in cardiac rehabilitation?  PERIPHERAL VASCULAR SYSTEM Peripheral vascular disease (PVD) may be either arterial or venous in origin. Understanding whether the origin of the problem is arterial or venous can prevent serious complications. Arterial Thrombosis and Embolism Pathophysiology Acute arterial occlusions are often sudden and dramatic. They are most common in the lower extremity. A thrombus (blood clot) adheres to the artery wall. Acute arterial thrombi occur with injury to an arterial wall, sluggish flow, or plaque formation secondary to atherosclerotic changes. Other causes of arterial thrombosis are polycythemia, dehydration, and repeated arterial needlesticks. If a thrombus breaks off and travels, it becomes an embolism that occludes an arterial vessel that is too small to allow it to pass. Causes of an arterial embolism are arrhythmias, prosthetic heart valves, MI, and rheumatic heart disease. Signs and Symptoms Usually there is an abrupt onset of symptoms with acute arterial occlusion, unless collateral circulation has developed that is able to supply blood flow to the occluded area. Symptoms depend on the artery occluded, the tissue supplied by that artery, and whether collateral circulation is present. The clinical signs of acute arterial occlusion are known as the six Ps: pain, pallor, pulselessness, paresthesia (numbness), paralysis, and poikilothermia (assumes the environmental temperature). There is decreased movement in the affected extremity. The extremity is pale, mottled, and without pulses distal to the occlusion. The extremity will feel cold because blood provides warmth. Therapeutic Measures Immediate treatment is necessary to save the affected limb. IV fluids and anticoagulant therapy, usually with IV unfractionated heparin (UFH), is started immediately to prevent further clotting. UFH has no effect on the existing clot. The patient remains on UFH therapy for several days. UFH levels are monitored with activated partial thromboplastin time (aPTT) or antifactor Xa. After 3 to 7 days, a low molecular weight heparin (LMWH) such as enoxaparin (Lovenox), dalteparin (Fragmin), or tinzaparin (Innohep) or an oral anticoagulant such as warfarin (Coumadin) is started. LMWH medications often require no laboratory monitoring. Warfarin takes 3 to 5 days to reach therapeutic levels. UFH is continued until a therapeutic warfarin level is reached, unless LMWH injections are used for bridging therapy. Warfarin levels are monitored by international normalized ratios (INRs). Daily adjustments in warfarin doses are made to reach therapeutic levels. Other types of anticoagulants may also be used. For patients with severe occlusions, especially if the risk of limb loss is imminent, surgery is usually performed to save the extremity. During an emergency embolectomy or thrombectomy, the artery is cut open, the emboli or thrombus is removed, and the vessel is sutured closed. In milder cases, thrombolytic agents may be used to dissolve the clot. Peripheral Arterial Disease Peripheral arterial disease (PAD) is a disorder of the arterial circulation usually caused by chronic, progressive narrowing of arterial vessels that leads to obstruction or occlusion. PAD usually affects the lower extremities. Atherosclerosis is the leading cause of occlusive disease. PAD can be described as organic or functional. Organic disease is caused by structural changes from plaque or inflammation in the blood vessels. Functional disease is a short-term localized spasm in the blood vessel, as occurs in Raynaud disease. Pathophysiology The purpose of the arterial system is to deliver oxygen-rich blood to the vascular beds. Anything that impedes this flow causes an imbalance in supply and demand for oxygen. Decreased nutrition, cellular waste accumulation, and development of ischemia occur distal to the obstruction. With increased debris and sluggish flow, thrombosis and embolism can become major problems. The body has several mechanisms that attempt to compensate for reduced blood flow, including peripheral vasodilation, anaerobic metabolism, and development of collateral circulation. However, these mechanisms are not intended to meet the ongoing blood supply needs of the body. It takes time for collateral circulation to develop. Blood vessels eventually reach their limit of dilation, and anaerobic metabolism is only a very short-term compensatory mechanism. Eventually, a lack of blood supply produces signs of ischemia. If not corrected, this results in ulceration, gangrene, and necrosis of the extremity; amputation of the limb may become necessary. CRITICAL THINKING & CLINICAL JUDGMENT Mrs. Mehta is a resident with severe rheumatoid arthritis that has limited her mobility for 7 months. She is returning to her room following physical therapy in a wheelchair when she suddenly reports severe pain in her left groin. Critical Thinking (The Why) What might be possible causes of this sudden symptom? Clinical Judgment (The Do) What priority action do you take? What action do you take for abnormal findings? How do you document Mrs. Mehta's signs and symptom? Suggested answers are at the end of the chapter. Signs and Symptoms Many people with PAD, especially women, may have no early symptoms. It is not until late in the course of PAD when diminished blood flow begins to produce changes within the extremities that symptoms occur. Pain in the calves associated with activity or exercise, a common symptom, is called intermittent claudication. When blood supply to the muscles is decreased, the muscles are unable to receive adequate oxygen. As ischemia increases, the muscle develops a cramping-type pain that usually subsides when activity is stopped. As PAD worsens, the pain is present even at rest, indicating severe arterial occlusion. Skin color changes are associated with decreased blood supply. The extremity is pale when the leg is elevated. In a dependent position, it becomes reddish-purple or cyanotic. The extremity is cool to touch even in warm environments. There may be hair loss on the lower calf, ankle, and foot. Other findings include dry, flaky, scaly, pale, or mottled skin. Toenails may be thickened. As occlusion of the arteries progresses, arterial pulses become diminished or absent. Diagnostic Tests The ankle-brachial index (ABI) is used to compare blood pressures in the upper and lower extremities. Normally, blood pressure readings in the thigh and calf are higher than those in the upper extremities. With the presence of arterial disease, thigh and calf blood pressures are lower than the brachial blood pressure. Ankle blood pressure is normally equal to or greater than the brachial blood pressure. When an occlusion occurs in the lower extremities, the blood pressures between the upper and lower extremities become unequal. With arterial insufficiency, the ABI decreases following diagnostic treadmill exercise. A duplex ultrasound measures the velocity of the blood flow. MRI and CT scan can give definitive images of blood vessels and degrees of arterial closure. Plethysmography and angiography can also be used to evaluate arterial flow in lower extremities (see Chapter 21). Therapeutic Measures Conservative treatment is initiated with mild to moderate occlusive disease. Lifestyle modifications to promote vascular health include smoking cessation, exercise therapy, and statins. Cilostazol (Pletal), an antiplatelet medication, treats claudication to improve walking ability. Invasive intervention is considered for the patient who experiences pain at rest or who has leg ulcers that do not heal. This includes balloon angioplasty to dilate a narrowed peripheral vessel, stents to maintain patency of the artery, atherectomy to remove atherosclerotic lesions, or grafting to bypass the occluded area. (See the discussion of vascular surgery later in this chapter.) Statins and antiplatelets are prescribed post-procedure to prevent complications. Raynaud Disease Raynaud disease (also called syndrome or phenomenon) is a local overreaction by the blood vessels that results in vasospasm, primarily in the digits, when exposed to cold or emotional stress. The abnormal vasoconstriction in the small arteries in the digits reduces arterial blood flow. It also can affect the ears, lips, or nose. Primary Raynaud disease does not occur as a result of another disorder. Secondary Raynaud disease may be seen with collagen diseases such as rheumatoid arthritis, scleroderma, systemic lupus erythematosus, or endocrine disorders. Women who live in cold climates are more often affected. With exposure to cold (e.g., opening the refrigerator/freezer, touching cold water) or emotional stress, the affected skin area exhibits obvious skin color changes that can vary. The affected area of skin may turn white and then blue, with reports of coldness and numbness. With warming, pain, tingling, and redness (hyperemia) occur. Normal blood flow returns in about 15 minutes. Initial therapy goals are to improve quality of life and prevent tissue injury from ischemia. Education on avoiding cold, keeping warm, and managing emotional stress is essential for patients with Raynaud disease. To protect hands from cold, gloves should be worn when going outside, cleaning a refrigerator, or preparing cold foods. Patients are instructed in the importance of protecting the hands from injury and avoiding vasoconstrictors such as smoking, alcohol, caffeine, and emotional stress. Immersing the hands in warm water may decrease vasospasm. A calcium channel blocker may be prescribed if preventive measures do not effectively prevent vasoconstriction. Other medications such as nitrates may be used if initial therapy is not effective. Thromboangiitis Obliterans (Buerger Disease) Thromboangiitis obliterans, or Buerger disease, is a rare recurring inflammation and thrombosis of small and medium arteries and veins in the limbs. The cause is unknown but may be autoimmune. It is only known to be associated with tobacco (cigarettes, cigars, smokeless) or cannabis use. To stop its progression and risk for amputation, all use of tobacco and cannabis must be avoided. Periodontal disease may be a factor in the development of the disease. Symptoms include intermittent pain or claudication (pain with activity) in the legs and feet or arms and hands, tingling, numbness in the feet or hands, reddish or blue tinged feet or hands, pale fingers or toes with cold exposure, and vein inflammation under the skin if a blood clot occurs. Distal extremity ischemia can lead to ulceration, gangrene, and even amputation. There is no cure, so there is urgency in helping the patient cease smoking. Treatments such as intermittent pneumatic compression to increase blood flow for pain relief and vasodilators may be tried. The goal of nursing care for patients with Buerger disease is to reduce the complications of ulceration, gangrene, and amputation. Nursing Process for the Patient With a Peripheral Arterial Disorder DATA COLLECTION. Careful assessment of intermittent claudication (leg pain), extremity pulses, capillary refill, temperature, color, presence of edema, and activity intolerance helps identify patients at risk for complications. Absent pulses are reported immediately to prevent limb loss. Skin that is shiny and hairless points to chronic diminished blood flow to the extremity. A serum glucose and lipid panel identifies diabetes and hyperlipidemia, which are significant risk factors for PAD. Skin lesions and ulcerations are photographed for documentation. NURSING DIAGNOSES, PLANNING, IMPLEMENTATION, AND EVALUATION. See "Nursing Care Plan for the Patient With a Peripheral Arterial Occlusive Disorder." Readiness for Enhanced Health Literacy related to complications, medications, or postoperative care Expected Outcome: The patient and family will verbalize self-care measures to be implemented to control disease and prevent complications.   Determine patient's and family's health literacy for the physiology of the disease and treatment and preventive techniques; then provide missing knowledge to determine their ability to learn.   Reinforce teaching of healthy lifestyle and risk factor control for PAD (e.g., smoking cessation, healthy diet, walking programs, hyperlipidemia, and diabetes and hypertension control) to promote circulation and decrease functional impairment and pain.   Explain daily foot care: Inspect feet for ingrown toenails, redness, sores, or blisters; wash feet with warm soap and water; dry with gentle patting; lubricate skin to prevent cracking; wear clean socks; do not walk barefoot; and inspect inside of footwear for foreign objects before inserting foot to promptly identify and report problems. WORD BUILDING hyperlipidemia: hyper---above + lipos---fat + emia---blood Nursing Care Plan for the Patient With a Peripheral Arterial Occlusive Disorder Nursing Diagnosis: Ineffective Peripheral Tissue Perfusion related to interruption of arterial flow in arms and legs Expected Outcome: The patient will show signs of increased arterial blood flow and tissue perfusion. Evaluation of Outcome: Does the patient have strong peripheral pulses, capillary refill less than 3 seconds, warm skin, pink nailbeds, and absence of edema? Intervention Rationale Evaluation Check extremity peripheral pulses, capillary refill, color, temperature, and presence of edema, and skin status every 4 hours, and report abnormal findings. These are indications of adequate tissue perfusion. Are peripheral pulses strong, nailbeds pink, and capillary refill of 3 seconds or less with no edema noted? Maintain extremities lower than heart, feet on floor in sitting position, or head of bed elevated on blocks. Dependent position increases blood flow to the legs and feet. Does patient have adequate tissue perfusion signs? Avoid bending knees, pillows under knees, prolonged sitting, or crossing legs. These activities impede blood flow to extremities. Does patient exhibit understanding of ways to improve peripheral blood flow? EVALUATION. Interventions are successful if the patient and family demonstrate health literacy of the disease and implement interventions to control disease and prevent complications. Aneurysms An aneurysm is a bulging, ballooning, or dilation at a weakened point of an arterial wall. The artery diameter is often increased by 50%. Atherosclerosis, hypertension, smoking, trauma, and congenital abnormalities are risk factors for an aneurysm. Heredity may also play a role. Aneurysms can occur in any artery in the body but are common in the abdominal aorta, which is the focus of the rest of this discussion. An abdominal aortic aneurysm (AAA) is often silent if it is less than 4 cm. The incidence of AAA increases with age. Medicare covers a one-time screening ultrasound for those with a family history of AAA or men ages 65 to 75 with a smoking history of 100 or more cigarettes. Men older than age 50 are at the highest risk of death from rupture and bleeding of an AAA. The mortality rate is high with a ruptured aneurysm. Survival improves with elective repair. Types of Aneurysms The various types of aneurysms are shown in Figure 24.8. A fusiform aneurysm is the dilation of the entire circumference of the artery. A saccular aneurysm is one that bulges on only one side of the artery wall. A dissecting aneurysm occurs when a cavity is formed from a tear in the artery wall, usually the intimal (inner) layer. The layers of the artery wall separate as blood is pumped into the tear with each heartbeat, expanding the cavity, which then becomes prone to rupturing. FIGURE 24.8 Types of aneurysms. (A) Fusiform: The entire circumference of the artery is dilated. (B) Saccular: One side of the artery is dilated. (C) Dissecting: A tear in the inner layer causes a cavity to form between the layers of the artery and fill with blood. The cavity expands with each heartbeat. Signs and Symptoms An AAA usually exhibits few if any symptoms until it enlarges (Table 24.8). Back or flank pain is the classic symptom; the pain is caused by the aneurysm pressing against nerves of the vertebrae. Depending on the location and size of the aneurysm, there may be reports of abdominal pain, a feeling of fullness, or nausea caused by pressure on the intestines. Changing positions may temporarily relieve the symptoms. Because the symptoms are vague, they are often not associated with an AAA. There may be a pulsating mass in the abdomen caused by an AAA that is discovered during routine physical or x-ray examination. Severe, sudden back, flank, or abdominal pain and a pulsating abdominal mass can indicate that the aneurysm may be about to rupture. With rupture and bleeding, signs of shock may develop. Emergency surgery is required for a ruptured AAA to prevent death. Table 24.8 Aneurysm Summary Signs and Symptoms Back pain Flank pain Abdominal fullness Nausea Pulsating mass in abdomen Severe sudden back pain with rupture Diagnostic Tests Ultrasound Computed tomography (CT) scan Aortography Therapeutic Measures Monitor growth of aneurysm Maintain normal blood pressure Surgical repair and graft Complications Rupture Hemorrhage Shock Priority Nursing Diagnoses Acute Pain Risk for Deficient Fluid Volume Risk for Ineffective Peripheral Tissue Perfusion Diagnostic Tests Abdominal ultrasound, CT scan, MRI, or aortography diagnose an AAA. Small aneurysms, less than 4 cm, are monitored for enlargement with ultrasound about every 6 to 12 months. Therapeutic Measures Medical treatment includes smoking cessation, gentle exercise such as walking and bike riding, avoiding lifting of heavy objects, blood pressure control to prevent arterial wall rupture, and beta blockers to slow AAA enlargement. Elective surgical repair (a bypass graft) is performed for pain, signs of circulatory compromise, or an aneurysm larger than 5.5 cm or rapidly enlarging. An open surgical repair or an endovascular stent graft may be done to repair an AAA. Open repair is done under anesthesia. The dilated aorta section is removed and replaced with a synthetic graft that is sutured in place. Endovascular grafting involves the placement (through the femoral artery) of a stent graft at the site of the AAA. Dye is used to guide a balloon catheter that positions and opens the graft against the aorta wall. Blood flows through the stent graft to reduce pressure on the aneurysm, which will shrink over time. A fenestrated (perforated) endograft is used when the AAA is near other arteries, such as the renal arteries, to maintain their blood flow. Endovascular surgery requires less hospitalization time (2 to 3 days) and has a quicker recovery. Lifelong monitoring of the endograft is necessary. Nursing Process for the Patient With an Abdominal Aortic Aneurysm DATA COLLECTION. Careful monitoring of a patient with an AAA is necessary. Emotional stress may be a risk factor that should be addressed. Patient understanding must be determined so patients understand their medication regimen and the importance of taking antihypertensives as prescribed. The patient is cared for in the intensive care unit after surgery. NURSING DIAGNOSES, PLANNING, IMPLEMENTATION, AND EVALUATION. See Chapter 12, "Nursing Care Plan for the Postoperative Patient." Ineffective Peripheral Tissue Perfusion related to aneurysm Expected Outcome: The patient will have palpable peripheral pulses; adequate capillary refill; and normal color, temperature, motor, and sensory function of extremities.   Monitor circulation, movement, and sensation in extremities every 1 to 4 hours to detect reduced blood flow to minimize risk of ischemia and necrosis.   Measure abdominal girth every shift to detect increasing girth indicating bleeding into abdomen.   Monitor complete blood count (CBC) as ordered to detect insidious bleeding into abdomen or significant hematoma formation. EVALUATION. Interventions are successful if the patient does not develop postoperative complications and maintains normal neurovascular checks. Varicose Veins Varicose veins are elongated, tortuous, dilated veins. Primary varicosities are likely caused by a structural defect in the vessel wall. Along with the defect, the dilation of the vessel can lead to incompetent venous valves. Valves normally help prevent blood from refluxing. If reflux occurs, it can cause further dilation of the vessel and blood pooling in the lower extremities. Superficial veins are most often involved in primary varicosities. Secondary varicosities are caused by an acquired or congenital pathological condition of the deep venous system. Etiology Wall defects have been identified as a familial tendency. Any factor that contributes to increasing hydrostatic pressure within the leg, such as obesity, prolonged standing, or pregnancy, can promote venous dilation. Signs and Symptoms The appearance of telangiectasias (spider veins) indicates minor chronic venous disease. More advanced disease can cause dull pain, cramping, edema, and feelings of heaviness in the lower extremities, especially after prolonged standing. This can usually be relieved by walking or elevating the extremity. With secondary varicosities, pain and disfigurement can be more severe. Edema or ulceration can develop if venous return is severely compromised. Therapeutic Measures To help prevent varicose veins from prolonged standing during your nursing career, consider wearing compression stockings. The primary goals for varicose vein therapy are to improve circulation, relieve pain, and avoid complications. Conservative treatment is exercise, leg elevation, and compression therapy (e.g., compression stockings, intermittent pneumatic compression pump, or compression bandages) as prescribed. Injection sclerotherapy to collapse the vein and laser or light therapy can treat superficial varicosities. Minimally invasive ablation to seal the vein includes radiofrequency or laser ablation. These procedures can be done in the HCP's office with local anesthesia. Traditional vein stripping that is done in surgery is rare. Venous Insufficiency Venous insufficiency is a chronic condition. Damaged or aging valves within the veins interfere with blood return to the heart, causing pooling of blood in the lower extremities. Chronic venous insufficiency can lead to venous stasis ulcers. Venous Stasis Ulcers Venous stasis ulcers are the end result of chronic venous insufficiency. Dysfunctional valves in the venous system prevent or reduce venous blood return. As venous pressure increases, venous stasis occurs. Over time, the congestion and decreased venous circulation lead to changes in the lower extremities. There may be edema and a brownish discoloration of the leg and foot, with the surrounding skin hardened and leathery in appearance. The brown color occurs when veins rupture, releasing red blood cells into the tissues; the red blood cells then break down and stain the tissue brown. Stasis ulcers develop from the increased pressure and rupture of small veins. Signs of skin breakdown are most commonly seen at the medial malleolus of the ankle. Stasis ulcers are a serious complication of venous insufficiency that are difficult to cure and can affect the patient's quality of life. THERAPEUTIC MEASURES. The focus of treatment is to decrease edema and heal skin ulcerations. Compression with stockings or bandage wraps is necessary to decrease edema. Elevation of the legs and feet above the heart is important to assist with venous drainage of lower extremities. Patients are advised not to keep legs dependent and to avoid long periods of standing or sitting to prevent increased pressure and pain. The foot of the bed should be elevated 5 to 6 inches. In addition, patients should be encouraged to exercise and walk often during nonacute episodes. They should be informed not to cross their legs or wear constrictive clothing that decreases venous blood return to the heart. Skin ulcers are cultured and treated with topical antibiotics if needed. Wound care can be chronic and challenging (see Chapter 54). An Unna boot is a gauze dressing coated with zinc oxide, calamine, and glycerine. It may be used to promote healing in severe ulcers. Zinc promotes wound healing and can be soothing. The Unna boot is applied snugly and provides compression therapy as well. It is changed every 2 to 7 days. Skin grafting may be necessary if ulcerations are severe or do not heal. Nursing Process for the Patient With a Venous Disorder DATA COLLECTION. Risk factors and knowledge of contributing factors for venous disorders are identified for teaching plans. Symptoms and concerns about body image are noted. Leg appearance, presence of edema, and ulcerations are observed. Patient-coping skills are identified to cope with the chronic ulcers that may impact quality of life. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. Acute Pain related to edema in extremities Expected Outcome: The patient will report an absence or acceptable level of pain within 30 minutes of reporting pain.   Elevate legs above heart level and avoid long periods of sitting or standing to reduce impaired venous return or pooling of fluid.   Utilize compression therapy as ordered to reduce edema. Impaired Skin Integrity related to chronic venous congestion Expected Outcome: The patient will have intact skin.   Note and document size, shape, and depth of wound to evaluate healing of wound over time.   Provide a comprehensive plan for wound care including pressure relief, treatments, and nutrition as ordered to ensure that quality wound care is provided.   Provide wound care as ordered to aid in wound healing. Ineffective Health Self-Management related to deficient knowledge of venous disorder Expected Outcome: The patient will report understanding of how to manage venous disorder.   Identify patient's understanding of the venous disorder to determine baseline knowledge.   Explain venous disorder pathophysiology, signs and symptoms, prevention, and therapeutic regimen to empower patient to manage disorder.   Explain that tight-fitting clothes at tops of legs or waist should not be worn to prevent venous occlusion.   Explain how to control risk factors and prevent varicose veins (e.g., weight reduction, elevation of the extremities, walking, exercise, and compression therapy) to assist blood flow return to the heart.   Document reinforcement of teaching and evaluation of patient knowledge to communicate patient progress toward goal attainment. Also, see Chapter 12 for the "Nursing Care Plan for the Postoperative Patient." EVALUATION. Interventions are successful if the patient reports pain is at an acceptable level and verbalizes an understanding of venous disease and prevention. Vascular Surgery Vascular impairments requiring surgery may be acute or chronic. They may involve arteries, veins, or lymphatic vessels. When intermittent claudication becomes severe or disabling or when the limb is at risk for amputation, then surgical vascular grafting may be done. Nursing Process for the Patient Undergoing Preoperative Vascular Surgery DATA COLLECTION. Circulatory status and pain control needs are monitored. Laboratory test results, including CBC, INR, partial thromboplastin time (PTT), and bleeding time, are reviewed. NURSING DIAGNOSES. The nursing diagnoses for preoperative vascular surgery may include the following:   Acute or Chronic Pain related to ischemia of tissue distal to occlusion or aneurysm   Anxiety related to unknown outcome, pain, powerlessness, or threat of death   Deficient Knowledge, preoperative and postoperative procedures, related to unfamiliar process See Chapter 12 for preoperative nursing process information. Embolectomy and Thrombectomy When an artery becomes completely occluded by an embolus or thrombus, it is considered a surgical emergency. Surgical removal to restore blood flow and oxygenation to the tissue distal to the occlusion is imperative to decrease ischemia and necrosis. Vascular Bypasses and Grafts Vascular bypass surgery involves the use of either autografts, such as the patient's own saphenous vein, or a synthetic graft material. The graft is anastomosed to the artery proximal to the occlusion and tunneled past the occlusion. The distal end of the graft is anastomosed to the artery (Fig. 24.9). The graft is assessed for hemostasis and function. The wound is then sutured closed. FIGURE 24.9 Aortofemoral bypass. Endarterectomy Arteriosclerotic plaques are dissected from the lining of the arterial wall and removed in a procedure called an endarterectomy. To control blood flow, the artery is clamped on both sides of the occlusion. An incision is made into the artery. The plaque within the artery is removed with forceps. The artery is irrigated to remove further debris and then closed with sutures. Clamps are removed and the skin incision is closed. A drain may be placed to prevent hematoma formation. Angioplasty Minimally invasive techniques can also be used to open plaque-blocked arteries. These techniques include balloon or laser angioplasty. A flexible laser-tipped catheter is inserted into an artery and advanced to the site of the blockage. The laser sends out pulsating beams of light that vaporize the plaque. This procedure is used for patients with smaller occlusions in the distal superficial femoral, proximal popliteal, and common iliac arteries. Stents Stents are placed inside an artery to provide support to the artery walls to keep them open. See the PCI discussion earlier. Complications of Vascular Surgery Bleeding and hemorrhage can occur with any vascular surgery. If hemorrhage occurs, manual pressure is applied to the site of bleeding and the HCP is notified immediately. Drainage may cause swelling and hematoma formation. Drains can be placed to help prevent this. Extensive surgeries may result in significant blood loss, leading to fluid volume deficit or shock. Reocclusion is possible with any vascular surgery. If thrombi or emboli develop and block blood flow, a surgical emergency results. Loss of a pedal pulse may signify reocclusion and must be immediately reported to the HCP. Blood flow needs to be reestablished within 4 to 6 hours to prevent risk of amputation of the extremity. WORD BUILDING endarterectomy: end---inside + arter---artery + ectomy---excision Nursing Process for the Patient After Vascular Surgery DATA COLLECTION. Upon transfer postoperatively to either the intensive care or surgical unit, the patient is positioned comfortably. Head-to-toe data collection is obtained and documented. A patent airway is ensured, and vital signs monitored. The patient's pain level is rated with a pain scale. All IVs and drains are traced to their source, labeled to prevent misidentification, and monitored. Measurement of intake and output is done hourly, then every 4 to 8 hours. CBC, INR, PTT, and electrolytes are monitored. Increasing abdominal girth measurements (for AAA repair) can indicate hemorrhage. Abnormal findings are reported immediately to the HCP. Initially, neurovascular checks are ordered every 15 minutes for the first 2 hours, then every 30 minutes for 1 to 3 hours, and then hourly for aortic or extremity vascular surgery. Neurovascular checks include extremity movement and sensation, presence of numbness or tingling, pulses, temperature, color, and capillary refill (less than 3 seconds normally). Peripheral pulses are palpated or checked with Doppler ultrasound if not palpable. Then, they are compared with the unaffected extremity to detect deficits. If a pulse is absent or weak or the extremity is cool or dusky, the HCP is notified immediately. NURSING DIAGNOSES, PLANNING, IMPLEMENTATION, AND EVALUATION. See Chapter 12, "Nursing Care Plan for the Postoperative Patient." Ineffective Peripheral Tissue Perfusion related to emboli, vascular spasm, or reocclusion Expected Outcome: The patient will have palpable peripheral pulses; adequate capillary refill; and normal color, temperature, motor, and sensory function of extremities.   Monitor circulation, movement, and sensation in extremities every 1 to 4 hours to detect reduced blood flow to minimize risk of ischemia and necrosis.   Avoid constricting measures on affected extremity (e.g., knee gatch of bed, adhesive tape, tight dressings) to prevent further decrease in blood flow to compromised extremity.   Assist the patient with early ambulation as prescribed to reduce complications of immobility and increase blood flow to the extremities. EVALUATION. Interventions are successful if the patient does not develop postoperative complications and maintains normal neurovascular checks. NURSING CARE TIP Neurovascular checks refer to data collection of an extremity. (Note: Neurologic checks refer to data collection of the central nervous system.) The following are areas to examine on an extremity when doing neurovascular checks: NEURO NEUROVASCULAR Movement Pulses Sensation Capillary refill Numbness Color (nailbed or skin) Tingling Temperature CLINICAL JUDGMENT Mr. Janway, age 63, has just returned from surgery after an embolectomy of the right lower leg. He has a history of type 2 diabetes mellitus, hypertension, renal insufficiency, and an MI 3 months ago. He is 6 feet tall and weighs 316 pounds. His gait is impaired, and he uses a cane, although he has not been very active since his MI. What priority data do you collection for Mr. Janway? What additional data do you collect about Mr. Janway's medical history? What priority nursing diagnoses and outcomes do you contribute to the plan of care for Mr. Janway? What priority nursing interventions do you implement for each nursing diagnosis identified? What priority equipment do you obtain to safely care for Mr. Janway? Which health-care team members do you collaborate with for Mr. Janway's care? Suggested answers are at the end of the chapter.  LYMPHATIC SYSTEM The lymphatic system returns fluid from other tissues in the body to the bloodstream. It is a pumpless system with one-way valves that return the fluid to the heart. Any interruption in the flow of lymph results in edema. Lymphangitis Lymphangitis is inflammation of the lymphatic channels due to an infection. The infection can occur in the arms or legs. It is most commonly caused by Streptococcus bacteria but can also result from Staphylococcus bacteria and other organisms. It is a serious infection that can cause sepsis and death. Symptoms include painful red streaks in the extremity. Fever and chills may be present. Lymph nodes in the area of infection can be enlarged and painful. Therapy is initiated with an appropriate antimicrobial agent. Moist heat and elevation help reduce pain and swelling. Nursing Process for the Patient With Lymphangitis DATA COLLECTION. The affected area is monitored for size changes, edema, and skin breakdown to prevent complications. Pain level and fever occurrence are monitored. Abnormal changes are reported to the HCP. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. Acute Pain related to tissue damage and edema from infection Expected Outcome: The patient will report an absence or acceptable level of pain within 30 minutes of reporting pain.   Monitor pain level with a pain rating scale to identify severity of pain.   Administer analgesics as prescribed and recheck pain level in 30 minutes to provide pain relief.   Position extremity for comfort, and elevate to reduce edema, which can cause pressure and pain. Excess Fluid Volume related to congested lymph nodes from infection Expected Outcome: The patient will exhibit no evidence of edema.   Apply moist heat on the extremity as ordered to increase circulation and reduce edema.   Elevate extremity to help improve circulation and prevent edema. EVALUATION. Interventions are successful if the patient reports pain is at an acceptable level and no edema is present. Home Health Hints Cardiac   After open-heart surgery, many patients suffer from depression. Utilize a depression screening tool and follow up with the HCP as needed.   Chest pain from esophageal reflux can mimic cardiovascular symptoms. Ask if the pain is related to consuming large meals, lying down, or bending over, or if it is relieved with antacids or food. Inform the HCP of these findings.   Check the expiration date on the patient's nitroglycerine bottle and facilitate getting a new bottle if needed.   Reinforce teaching for stress management techniques for the caregiver to use: deep-breathing exercises, reading a book, meditation, massage therapy, guided imagery, exercise, socializing with friends, and/or working on a favorite hobby.   Refer to a social worker if caregiver is overwhelmed for services such as respite care or housekeeping services. Vascular   Monitor peripheral pulses and capillary refill. Report absent pulses or slow capillary refill to the HCP.   Reinforce teaching for the patient to monitor extremities. Patients with peripheral vascular disorders are at a high risk for developing lower extremity wounds that are slow to heal.   Reinforce teaching for the patient to stop and rest if pain develops in the lower extremities during exercise. Key Points   Arteriosclerosis (thickening, loss of elasticity, and calcification of arterial walls) and atherosclerosis (formation of plaque in the arteries) both begin in early childhood and progress without symptoms through adulthood. Atherosclerosis causes CAD.   CAD is the obstruction of blood flow through the coronary arteries to the heart muscle cells, typically from atherosclerosis. This blood flow reduction can cause angina, MI, or sudden death if blood flow is not restored.   Angina pectoris is chest pain due to ischemia resulting from a reduction in coronary artery blood flow and oxygen delivery to the heart muscle. Angina is a symptom, not a disease.   Weight reduction, a heart-healthy diet, and emotional stress reduction may help slow CAD progression. Medications used for reducing angina include nitrates, beta blockers, calcium channel blockers, and ranolazine.   Acute coronary syndrome involves ischemia of the myocardium. It includes unstable angina, NSTEMI, and STEMI.   An MI results in the death of heart muscle cells from a sudden partial or complete blockage of a coronary artery, although a few MIs have non-occlusion causes. The extent of the cardiac damage varies depending on the location and amount of blockage in the coronary artery.   PVD may be either arterial or venous in origin. It is important to understand whether the origin of the problem is arterial or venous to prevent serious complications from occurring.   Arterial disorders include arterial thrombosis and embolism, peripheral artery disease, Raynaud disease, and thromboangiitis obliterans (Buerger disease).   Monitoring of extremity pulses, capillary refill, temperature, color, and presence of edema helps identify patients at risk for complications from vascular disorders. Absent pulses are reported immediately to prevent limb loss.   An aneurysm is a bulging, ballooning, or dilation at a weakened point of an arterial wall. Atherosclerosis, hypertension, smoking, trauma, congenital abnormalities or heredity are risk factors for an aneurysm.   Varicose veins are elongated, tortuous, dilated veins that can lead to incompetent venous valves.   In venous insufficiency, damaged or aging valves within the veins interfere with blood return to the heart, causing pooling of blood in the lower extremities. Chronic venous insufficiency can lead to venous stasis ulcers.   Stasis ulcers are a serious complication of venous insufficiency that are difficult to cure and can affect the patient's quality of life. Stasis ulcers develop from the increased pressure and rupture of small veins often at the medial malleolus of the ankle.