Cardiac Valvular Disorders LPN Chapter 23 PDF

Chapter 23 CARDIAC VALVULAR DISORDERS Within the normal heart, blood flows in one direction because of the presence of heart valves. There are four valves in the heart: mitral, tricuspid, pulmonic, and aortic (see Fig. 21.2). The chordae tendineae and papillary muscles are attachment structures fo...

Chapter 23 CARDIAC VALVULAR DISORDERS Within the normal heart, blood flows in one direction because of the presence of heart valves. There are four valves in the heart: mitral, tricuspid, pulmonic, and aortic (see Fig. 21.2). The chordae tendineae and papillary muscles are attachment structures for both the mitral and tricuspid valves. They ensure that these valves close tightly. Damage to the valves or their surrounding structures can result in abnormal valvular functioning (Fig. 23.1). The valves of the left side of the heart are more commonly affected. There are two major types of valvular dysfunction: stenosis and insufficiency. Forward blood flow is reduced if the valve is narrowed (stenosed) and does not open completely. If the valve does not close completely, blood backs up; this is referred to as regurgitation or insufficiency. Either type of valve damage increases the heart's workload and increases pressure in the affected heart chamber due to a backup of blood flow. These conditions may result from congenital defects, infections, or rheumatic fever. Valvular disorders are summarized in Table 23.1 and discussed in more detail in the following sections. WORD BUILDING stenosis: stenos---narrow insufficiency: in---not + sufficiens---sufficient regurgitation: re---again + gurgitare---to flood FIGURE 23.1 Openings of stenosed and insufficient valves compared with a normal valve. Rheumatic Fever Rheumatic fever is an autoimmune reaction about 2 to 4 weeks after tonsillopharyngitis due to group A streptococci. Although rheumatic fever can occur at any age, it typically occurs between ages 5 and 15. Rheumatic fever and subsequent rheumatic heart disease and valvular damage can be prevented by detecting and treating streptococcal infections promptly with penicillin. This rare complication of untreated strep throat or scarlet fever is not commonly seen in the United States. Worldwide it is common in developing countries. A throat culture is used to diagnose a streptococcal infection. Predominant signs and symptoms include polyarthritis, subcutaneous nodules (painless), a painless rash, carditis with valvulitis, Sydenham chorea (brief, rapid, uncontrolled movements that occur 1 to 8 months after the infection) with unusual exhibition of emotions. Minor signs and symptoms include fever; arthralgia (joint pain); and red, hot, swollen joints and pneumonitis, a rare complication. Rheumatic heart disease may not be evident for years after rheumatic fever; however, when manifested, the valves are most affected. Mitral Valve Prolapse Pathophysiology and Etiology During ventricular systole, as pressure in the left ventricle rises, the flaps of the mitral valve normally remain closed and stay within the atrioventricular junction. In mitral valve prolapse (MVP), however, one or both flaps bulge backward into the left atrium (like a parachute) during systole. This can happen when one flap is too large or if a defect occurs in the chordae tendineae that secure the valve to the heart wall. If the bulging flaps do not fit together, blood can leak backward into the left atrium (mitral regurgitation). Increased pressure on the papillary muscles results in ischemia (inadequate blood supply) within the muscle, causing further dysfunction of the mitral valve. MVP results from changes in the valve structure (myxomatous degeneration), connective tissue disorders (Ehler-Danlos syndrome---a group of inherited connective tissue disorders affecting the skin, blood vessels, and joints with cardiac abnormalities being common such as MVP), or a hereditary trait or gene mutation. It is the most common form of valvular heart disease for both genders. Risk rises with age (Shah et al, 2020). Signs and Symptoms Most patients with MVP are asymptomatic and have a good prognosis (see Table 23.1). MVP severity ranges from having a murmur (caused by blood leaking backward) to chordae tendineae rupture with mitral regurgitation. The murmur is best heard at the heart apex. It begins in the middle of systole (midsystolic) and becomes more intense until the end of systole. Symptoms may include anxiety, atypical chest pain not related to exertion, arrhythmias causing palpitations, dizziness or syncope (fainting), fatigue, and dyspnea (shortness of breath), especially when lying flat or during activity. Complications Rare complications include mitral regurgitation, arrhythmias, heart failure (HF), emboli, or infective endocarditis (IE). Table 23.1 Cardiac Valvular Disorders Summary Valve Disorder Signs and Symptoms Diagnostic Tests Complications Therapeutic Measures Priority Nursing Diagnoses Mitral valve prolapse None Murmur Atypical chest pain Palpitations Arrhythmias Dizziness Syncope Fatigue Dyspnea Anxiety Echocardiogram Electrocardiogram (ECG) Cardiac catheterization Emboli Infective endocarditis Mitral regurgitation Arrhythmias Heart failure (HF) None Beta blockers Antiarrhythmics Aspirin or anticoagulants Valvuloplasty Valve replacement Decreased Activity Tolerance Decreased Cardiac Output Mitral stenosis None Murmur Chest pain Palpitations Dizziness Syncope Fatigue Edema Exertional dyspnea Cough Hemoptysis Respiratory infections ECG Chest x-ray Echocardiogram Doppler ultrasound Transesophageal endoscopy (TEE) Cardiac catheterization Magnetic resonance imaging (MRI) Emboli HF None Anticoagulants Antiarrhythmics Valvuloplasty Valve replacement Decreased Activity Tolerance Decreased Cardiac Output Mitral regurgitation None Murmur Chest pain Palpitations Syncope Fatigue Exertional dyspnea Cough Hemoptysis Peripheral edema Acute: Pulmonary edema Shock ECG Chest x-ray Echocardiogram Doppler ultrasound TEE Cardiac MRI Cardiac catheterization Arrhythmias Emboli HF None Angiotensin-converting enzyme (ACE) inhibitors Antiarrhythmics Anticoagulants Valvuloplasty Valve replacement Decreased Activity Tolerance Decreased Cardiac Output Aortic stenosis None Angina Murmur Syncope Orthopnea Exertional dyspnea Fatigue HF ECG Chest x-ray Serial echocardiograms Stress (exercise) test Computed tomography (CT) scan MRI Cardiac catheterization HF Valve replacement: Surgical or transcatheter Decreased Activity Tolerance Decreased Cardiac Output Aortic regurgitation None Forceful pulse Murmur Chest pain Palpitations Fatigue Exertional dyspnea Corrigan pulse Diaphoresis ECG Chest x-ray Echocardiogram Cardiac catheterization HF Life-threatening arrhythmia Symptoms of shock Diuretics Vasodilators Valve replacement Decreased Activity Tolerance Decreased Cardiac Output Diagnostic Tests Auscultation for a murmur or a click caused by the stress on the chordae tendineae or valve leaflets when they prolapse is the first diagnostic step for MVP. A normal electrocardiogram (ECG) is common, although inverted (downward) T waves (indicating ischemia) may be seen (see Fig. 25.6). A two-dimensional echocardiogram with Doppler and a transesophageal echocardiography can show valve abnormalities and identify mitral regurgitation from MVP. For more severe cases, cardiac catheterization can show the bulging flaps of the mitral valve on a coronary angiogram (dye-injected X-ray). Therapeutic Measures MVP is a benign disorder. No treatment is needed unless symptoms become severe. A healthy lifestyle, including a heart-healthy diet, exercise, stress management, and avoidance of stimulants such as caffeine, can help prevent symptoms. Treatment depends on severity of symptoms and may include beta blockers to reduce the heart rate and perhaps relieve chest pain, aspirin or anticoagulants to help prevent formation of blood clots on the valve, and antiarrhythmics (also known as antidysrhythmics) for an arrhythmia. Surgical repair or replacement of the valve can be done for severe cases of MVP. (See surgical interventions discussion later in the chapter.) CRITICAL THINKING & CLINICAL JUDGMENT Mr. Goldfarb, age 51, presents with chest pain, increase in fatigue with exercise, weight gain, and job stress. He reports a history of MVP with surgical repair 3 years ago. Critical Thinking (The Why) How does weight gain and stress affect cardiac health? Clinical Judgment (The Do) What data do you collect for Mr. Goldfarb's medical and surgical history of MVP? What patient-centered resources do you provide to help Mr. Goldfarb manage his MVP? Suggested answers are at the end of the chapter. Mitral Stenosis Pathophysiology and Etiology Mitral stenosis (MS) results from thickening of the mitral valve flaps and shortening of the chordae tendineae, causing narrowing of the mitral valve opening. Older patients with MS usually have calcification and fibrosis of the mitral valve flaps. This obstructs blood flow from the left atrium into the left ventricle. The left atrium enlarges to hold the extra blood volume caused by the obstruction. Due to the increased blood volume, pressure rises in the left atrium; in turn, pressure rises in the pulmonary circulation and the right ventricle. The right ventricle dilates to handle the increased volume. Eventually, the right ventricle fails from excessive workload, reducing blood volume delivered to the left ventricle and decreasing cardiac output. Rheumatic fever is the major cause of MS, which is seen in older adults who had rheumatic fever as children or in those in developing countries. Even though rheumatic fever is rare in developed nations, when it does occur, any resultant rheumatic heart disease may not appear for 5 to 10 years or longer after the rheumatic fever is resolved. This time frame depends on the severity of the rheumatic fever. Less common causes of MS include congenital defects of the mitral valve, systemic lupus erythematosus, and calcium deposits. Signs and Symptoms Patients can be asymptomatic with MS (see Table 23.1). A click or low-pitched murmur might be heard as a rumbling sound over the heart apex during diastole. The click or murmur is more pronounced right before systole. The most common symptoms, which are often unnoticed because they develop gradually as disease severity increases, are exertional dyspnea and intolerance to activity. Additional pulmonary symptoms include hemoptysis (bloody sputum), hoarseness, cough, and respiratory infections. Fatigue, dizziness, syncope, and more rarely chest pain result from decreased cardiac output. Palpitations from atrial flutter or atrial fibrillation caused by atrial enlargement may occur. Complications Stasis of blood in the left atrium could form a thrombus. A moving thrombus called an emboli could cause a stroke. If the right ventricle fails, symptoms of right-sided HF can occur (see Chapter 26). Diagnostic Tests Transthoracic two-dimensional color flow Doppler echocardiogram and Doppler ultrasound are the noninvasive gold standard tests for evaluation of valvular disease. They show the narrowed mitral valve opening and decreased motion of the valve. Exercise stress echocardiography can be helpful for severe symptoms. The ECG shows enlargement of the left atrium and right ventricle and changes in the P waveform (see Fig. 25.1). Atrial flutter or fibrillation may be seen (see Chapter 25). An incidental chest x-ray examination shows enlargement of the left atrium. Therapeutic Measures When the patient is asymptomatic, no treatment is needed. Anticoagulants might be given to prevent emboli from stasis of blood in the atrium. Atrial fibrillation, an irregular heart rhythm, or HF may develop and require treatment (see Chapter 26). If invasive treatment is needed, percutaneous balloon valvotomy (a balloon dilates the stenosed heart valve) can be done in the cardiac catheterization lab (Fig. 23.2). Surgical treatment can include valvular repair (valvuloplasty), but mitral valve replacement is typically needed (Fig. 23.3). FIGURE 23.2 Percutaneous balloon valvuloplasty. FIGURE 23.3 Mitral valve replacement with mechanical valve. CUE RECOGNITION 23.1 A patient who has mitral valve stenosis is experiencing shortness of breath, oxygen saturation (SaO2) 90%, hoarseness, palpitations, and dizziness. What action do you take? Suggested answers are at the end of the chapter. Mitral Regurgitation Pathophysiology and Etiology Mitral regurgitation (MR), or insufficiency, is the incomplete closure of the mitral valve leaflets. It allows backflow of blood into the left atrium with each contraction of the left ventricle. This extra blood volume is added to the incoming blood from the lungs. With chronic MR, the increase in blood volume dilates and increases pressure in the left atrium. In response to the extra blood volume delivered by the left atrium, the left ventricle compensates by dilating. If the compensatory mechanism of dilation is inadequate, pressure rises in the pulmonary circulation and then in the right ventricle as blood volume backs up from the left atrium. The left ventricle and eventually the right ventricle may fail from this increased strain. Causes of MR include rheumatic heart disease, endocarditis, rupture or dysfunction of the chordae tendineae or papillary muscle, MVP, hypertension, myocardial infarction (MI), cardiomyopathy, annulus calcification, aging, or congenital defects. Signs and Symptoms Patients with MR are usually asymptomatic initially. A murmur may be heard. It begins with S1 (first heart sound) and continues during systole up to S2 (second heart sound). With severe MR, HF symptoms can develop as the left ventricle fails (see Table 23.1). Exertional dyspnea, fatigue, syncope, cough, hemoptysis, and edema may occur. If acute MR develops, as in papillary muscle rupture following MI, pulmonary edema and shock symptoms will be exhibited. Complications Palpitations due to atrial fibrillation may result as the left atrium enlarges. Pulmonary hypertension or HF may occur (see Chapter 26). Endocarditis is a risk due to the damaged valve. Diagnostic Tests Two-dimensional echocardiogram with Doppler or transesophageal echocardiogram (TEE) confirms MR with left atrial enlargement and regurgitation of blood. For severe symptoms, cardiovascular MRI may be useful. Therapeutic Measures Without the presence of symptoms and depending on the cause, medical treatment is not usually required. If atrial fibrillation with rapid heart rate develops, calcium channel blockers or beta blockers may be ordered. Anticoagulants are used to prevent thromboembolisms. When symptoms develop and surgery is needed, a mitral valve repair or percutaneous mitral valve repair is preferred over mitral valve replacement when possible. Aortic Stenosis Pathophysiology and Etiology In aortic stenosis (AS), blood flow from the left ventricle into the aorta is obstructed through the stenosed aortic valve. The opening of the aortic valve may be narrowed from thickening, scarring, calcification, or fusing of the valve's flaps. To compensate for the difficulty in ejecting blood into the aorta, the left ventricle contracts more forcefully. In chronic AS, the left ventricle hypertrophies to maintain normal cardiac output. As narrowing increases, the compensatory mechanisms are unable to continue. The left ventricle fails to move blood forward, resulting in decreased cardiac output and HF. The major causes of AS are congenital defects or rheumatic heart disease. Calcification of the aortic valve may be age related and occurs after age 60. Signs and Symptoms Many years may pass before signs or symptoms of AS are observed (see Table 23.1). Early symptoms include exertional angina, exertional dyspnea or activity intolerance, and exertional dizziness or syncope. Late end-stage symptoms are angina, syncope, and HF signs and symptoms. A systolic murmur can develop, beginning just after systole (S1) with increasing intensity until midsystole, then decreasing and ending right before the second heart sound (S2). Complications HF, pulmonary hypertension, life-threatening arrhythmias, sudden cardiac death, endocarditis, and emboli can occur. Diagnostic Tests Ultrasound may be used initially and shows thickness of aortic valve leaflets and their reduced motion. Then two-dimensional and Doppler echocardiogram shows thickening of the left ventricular wall, impaired movement of the aortic valve, and the severity of the disease. The ECG commonly shows enlargement of the left ventricle and left atrium. Therapeutic Measures Aortic valve replacement is the only effective treatment for AS. For those considered high risk for traditional open-heart surgery, a transcatheter aortic valve replacement (TAVR) can be done (see the section on heart valve replacement). Valvotomy is used only for those who are unable to have valve replacement. If symptoms of HF are present, they are treated. Medications that reduce the contractility of the heart and, subsequently, cardiac output are avoided to prevent further HF. CLINICAL JUDGMENT Mrs. Pryor, age 48, has aortic stenosis and is admitted to the hospital with angina. She had an episode of syncope two days ago. She reports that she tires easily. Mrs. Pryor asks what aortic stenosis is. What do you tell Mrs. Pryor? How do you document this education? If Mrs. Pryor experiences angina, whom do you collaborate with? What interventions do you perform for the anginal episode? What do you contribute to Mrs. Pryor's plan of care for safety? What discharge education do you reinforce for the patient regarding digoxin on signs and symptoms indicating the medication should be held? Suggested answers are at the end of the chapter. Aortic Regurgitation Pathophysiology and Etiology In chronic aortic regurgitation (AR), the aortic valve cusps may become scarred, thickened, or shortened. Chronic AR may slowly develop over many years or decades. A backflow of blood from the aorta into the left ventricle occurs if the aortic valve cusps do not close completely. The left ventricle's blood volume increases with this backflow of blood; this is in addition to the normal flow of blood from the left atrium. To handle the increased volume, the left ventricle compensates with dilation and hypertrophy to deliver a stronger contraction ejecting more blood volume to maintain cardiac output. Over time, the heart's contraction weakens and the left ventricle fails, causing cardiac output to drop. Congenital defects, aging, rheumatic heart disease, syphilis, severe hypertension, and ankylosing spondylitis can cause AR. Acute causes include endocarditis or aortic dissection. Signs and Symptoms Symptoms may not become apparent for many years with chronic AR (see Table 23.1). Initially, the patient may report feeling a forceful heartbeat that is more pronounced when lying down. Palpitations and pounding in the head may also be experienced. Next, exertional dyspnea, fatigue, and worsening levels of dyspnea (e.g., orthopnea, paroxysmal nocturnal dyspnea) occur after years of progressive valvular dysfunction. A murmur is heard during diastolic after the second heart sound. The palpated pulse is forceful and then quickly collapses (Corrigan pulse). The diastolic blood pressure decreases to widen the pulse pressure. This compensates for an increase in systolic blood pressure. Later in the disease, atypical angina pectoris may occur. This often happens at rest or at night, along with diaphoresis, when a lower pulse rate results in delivery of less oxygen to the myocardium. Eventually, symptoms of HF develop if the left ventricle fails. In acute aortic dysfunction, profound symptoms of pulmonary distress, chest pain, and cardiogenic shock symptoms occur and require immediate treatment. Diagnostic Tests An echocardiogram, Doppler echocardiogram, or transesophageal echocardiogram detect an enlarged left ventricle and severity of the AR. Cardiovascular MRI can provide accurate disease severity assessment and effect on ventricular function. Therapeutic Measures Treatment with vasodilators or diuretics may be useful to reduce systolic blood pressure and, subsequently, cardiac workload or heart failure prior to surgery or for patients who cannot have surgery. Aortic valve replacement is typically the surgery that is required. Rarely, an aortic valve repair can be done. Nursing Process for the Patient With a Cardiac Valvular Disorder Data Collection A history is obtained that includes information presented in Table 23.2. Vital signs are measured, heart sounds are auscultated to detect murmurs, and signs and symptoms of HF are noted and reported (see Chapter 26). Table 23.2 Data Collection for Patients With Cardiac Valvular Disorders Data Collection Subjective Data Questions Health History Infections (rheumatic fever, endocarditis, streptococcal or staphylococcal, syphilis)? Congenital defects? Cardiac disease (myocardial infarction, cardiomyopathy)? Respiratory Dyspnea at rest, on exertion, when lying, or that awakens patient? How many pillows are you accustomed to sleeping on? Cough or hemoptysis? Cardiovascular Chest pain, qualities---when does it occur? Loss of consciousness? Edema? Palpitations, dizziness, fatigue, activity intolerance? Medications What medications are you taking? Knowledge of Condition What is the reason that you are here today? Have you ever been diagnosed with any type of heart disease? Coping Skills How do you normally cope with stressors? Support system? What, if anything, seems to help alleviate symptoms? Have there been any adaptations in lifestyle and/or environment? Objective Data Respiratory Crackles, wheezes, tachypnea, use of accessory muscles Cardiovascular Murmurs, extra heart sounds, arrhythmias, edema, jugular venous distention, Corrigan pulse, increased or decreased pulse pressure or blood pressure Integumentary Clubbing; cyanosis; diaphoresis; cold, clammy skin; pallor Diagnostic Test Findings Review test results. Nursing Care Plan for the Patient With a Cardiac Valvular Disorder Nursing Diagnosis: Decreased Cardiac Output related to cardiac valvular stenosis or insufficiency or heart failure Expected Outcome: The patient will have adequate cardiac output as evidenced by vital signs within normal parameters for patient; strong pulses, warm extremities; lack of dyspnea and minimal fatigue. Evaluation of Outcome: Are the patient's vital signs within normal parameters for the patient, pulses strong, extremities warm, without dyspnea or fatigue? Intervention Rationale Evaluation Monitor heart and lung sounds, vital signs, oxygen saturation, chest pain, skin temperature, capillary refill and peripheral edema. Indicators of cardiac output decline are new onset of murmurs, hypotension, tachycardia, reduced SaO2 chest pain, edema or crackles in the lungs. Are vital signs, oxygen saturation, and heart and lung sounds within the patient's normal parameters? Is skin warm, capillary refill less than 3 seconds with no chest pain or peripheral edema? Administer oxygen as ordered. Supplemental oxygen increases oxygen to the heart by increasing the oxygen saturation in the blood. Does oxygen saturation remain within normal patient parameters at rest and with activity? Elevate head of bed 45 degrees. Venous return to heart is reduced and chest expansion improved when head of bed is elevated, which increases the amount of oxygen coming into the lungs. Is there use of accessory muscles of respiration? Does patient report shortness of breath? Intervention Rationale Evaluation Geriatric Review cardiac medications and presence of side effects, and teach patient side effects to report. Toxic side effects are more common, owing to altered metabolism and excretion of medications in the older adult. Are side effects present for medications patient is taking? Does patient understand side effects to report? Nursing Diagnosis: Decreased Activity Tolerance related to decreased oxygen delivery from cardiac valvular stenosis or insufficiency and output Expected Outcome: The patient will exhibit normal changes in vital signs and less fatigue in response to activity. Evaluation of Outcome: Does the patient have normal changes in vital signs with activity? Does the patient report less fatigue with activity? Intervention Rationale Evaluation Assist as needed with activities of daily living (ADLs). Conserve energy with ADL assistance. Are all ADLs completed? Are vital signs within range during activity? Geriatric Slow pace of care and allow patient extra time to perform activities. Patients can often perform activities if allowed time to slowly perform them and rest at intervals. Does blood pressure remain within normal patient parameters when changing position? Ensure safety when mobilizing older patient. Orthostatic hypertension is common in the older adult. Does patient ambulate without feeling faint or unsteady? Nursing Diagnoses, Planning, Implementation, and Evaluation The major nursing diagnoses for all the valvular disorders are the same. They include those for HF as well, if symptoms of HF are present. See "Nursing Care Plan for the Patient With a Cardiac Valvular Disorder." Patient Education Education should include caregivers and focus on the understanding of the nature of the disorder, health maintenance including medications, prevention of complications, and early recognition of symptoms in order to seek medical care. Highest-risk patients are counseled according to the AHA guidelines for prophylactic antibiotics to prevent IE (see "Prevention" under "Infective Endocarditis" later in this chapter). For patients on warfarin (Coumadin), international normalized ratio (INR) should be regularly monitored (see "Learning Tip"), a consult with a dietitian and diet education is essential (see "Nutrition Notes"), and a medical ID should be used (see Patient Teaching Guidelines for this chapter on Davis Edge). LEARNING TIP   Before administering the anticoagulant warfarin, the patient's INR value must be compared with the desired therapeutic INR value to determine whether it is safe to give the warfarin.   An INR range of 2 to 3 is therapeutic for patients on warfarin who have a blood clot, tissue heart valve, or atrial fibrillation. For a mechanical heart valve, the therapeutic INR range is usually 2.5 to 3.5. Hold the warfarin until any value outside of therapeutic range is reported to the HCP for patient safety.   Check for bleeding or ecchymosis (excessive bruising) prior to warfarin administration and, if present, report these findings to the HCP for orders regarding warfarin administration. Nutrition Notes The most important role of vitamin K is its participation in blood clotting. Vitamin K is required for the activation of four (factor II or prothrombin, VII, and X) of the 13 proteins (factors) involved in the blood clotting process. These four proteins contain several glutamic acid residues that must be activated by an enzyme (gamma-glutamyl carboxylase). This enzyme requires vitamin K as a coenzyme. Foods sources of vitamin K include green leafy vegetables (collard greens, turnip greens, kale, broccoli), legumes, and some vegetable oils. Anticoagulants such as warfarin interfere with vitamin K function by preventing the conversion of vitamin K to its active coenzyme form. It is important to inform patients that, to maintain a therapeutic level of warfarin, they should eat a consistent amount of these types of foods on a day-to-day basis rather than increase or decrease the amounts. Inconsistent day-to-day intake can alter the effects of the warfarin and make it difficult to establish and maintain a therapeutic INR. A consultation with a dietitian can be helpful in developing a meal plan (National Institutes of Health, 2020). Cardiac Valve Repairs A commissurotomy repairs a stenosed valve, most commonly the mitral valve. It can be done via percutaneous (preferred), open with bypass, or rarely via closed surgical approach. The valve flaps that have adhered to each other---and thus closed the opening between them, known as the commissure---are separated during one of these approaches to enlarge the valve opening. Annuloplasty is the repair or reconstruction of the valve flaps or annulus. Sutures or a prosthetic ring may be placed in the valve annulus to improve closure of the leaflets. The mitral valve is the most common valve repaired in this way. Similar procedures are used on the tricuspid valve. Heart Valve Replacement Valves used for cardiac valve replacement may be either mechanical or biological (tissue). Research is ongoing to develop tissue engineered heart valves. Tissue valves (bioprosthesis) come from xenograft (porcine \[pig\] and bovine \[cow\]; also known as a heterograft) or allograft (a human cadaveric or living donor; also known as a homograft); see "Cultural Considerations." Allografts are available in limited numbers because they rely on donors. An autograft (self-donor) in the Ross procedure uses the patient's own pulmonary valve to replace the removed aortic valve; an allograft (human donor) pulmonary valve then replaces the patient's pulmonary valve. Visit www.lifenethealth.org for more information on allografts. Cultural Considerations Religious groups such as Jewish, Muslim, Hindu, Buddhist, and Seventh Day Adventists may not consume pork or beef products depending on their beliefs. It is important that patients' and families' views about cardiac valve options such as porcine (pork-derived) and bovine (beef-derived) tissue valves are discussed in case they wish to avoid them (Koshy et al, 2020). For mitral valve replacement, a left atriotomy is made after the patient is on cardiopulmonary bypass (CPB). For an aortic valve replacement, an incision is made above the right coronary artery in the aorta. Then, in either valvular procedure, the diseased valve is excised and the new valve sutured in place. The incision is closed. Surgery then continues as described in Chapter 21. WORD BUILDING commissurotomy: commissura---joining together + tome---incision annuloplasty: annulus---ring + plasty---formed TAVR is a minimally invasive procedure that replaces the valve without removing the defective valve. A balloon catheter is introduced via the femoral artery. It is inserted through the diseased valve and inflated to open the stenosed valve leaflets. For mitral valve valvoplasty, after the balloon catheter is inserted into the right atrium, it is threaded through a small hole pierced into the right atrial septum that emerges into the left atrium. The catheter is passed through the mitral valve. Inflating the balloon within the mitral valve opens the stenosed valve flaps. Complications may include arrhythmias, emboli, hemorrhage, and cardiac tamponade. A balloon valvuloplasty results in fewer complications than traditional open-heart surgery. Complications of Valve Replacement Tissue valves have a low incidence of thrombus formation. They do not require lifelong anticoagulant therapy. However, they do not last as long as mechanical valves because of degenerative changes and calcification. Mechanical valves are durable (lasting 20 to 30 years). However, they create turbulent blood flow, requiring lifelong anticoagulant therapy to prevent blood clots. Anemia from hemolysis of red blood cells as they come in contact with mechanical valve structures can occur. Also, IE can occur due to microorganisms growing on the valve leaflets or the sewing ring of mechanical valves. These growths can make valves incompetent or can break off to become emboli. Nursing Process for the Preoperative Cardiac Surgery Patient DATA COLLECTION. Baseline data collection is important for postoperative comparison and to begin discharge planning. Pain management, circulatory status, and results of diagnostic tests are all significant. Typing and crossmatching for units of blood as ordered is done. NURSING DIAGNOSES, PLANNING, IMPLEMENTATION, AND EVALUATION. See the "Nursing Process for Preoperative Patients" in Chapter 12. Nursing Process for the Postoperative Cardiac Surgery Patient After cardiac surgery, the patient goes to a cardiac universal bed (CUB) unit or an intensive care unit (ICU) to be monitored for 1 to 2 days. In a CUB unit, the patient recovers in the same room until discharge, which avoids transfers to other units and increases continuity of care. In an ICU, as recovery progresses, the patient is transferred to a step-down or general surgical unit for continued cardiac monitoring. DATA COLLECTION. The patient is accompanied to ICU/CUB by the anesthesiologist. The anesthesiologist gives the nurse a report of the procedure, complications, and hemodynamic and ventilatory management of the patient. The patient remains on a cardiac monitor and mechanical ventilator for up to 24 hours. A head-to-toe assessment of the patient is performed. It includes dressings, tubes (chest tube, nasogastric tube, urinary catheter), and IV lines. Of importance are signs of awakening, pain, lung and heart sounds, and palpation of the entire chest and neck to detect crepitus (air in the subcutaneous tissue from opening the chest). Trends in cardiac output are monitored. Body temperature is continuously monitored if warming measures such as a warming blanket are used. Warming is discontinued when the core body temperature nears 98.6°F (37°C). Warming should occur slowly to avoid peripheral vasodilation, which can result in shock. While being rewarmed, patients are monitored for shivering. Shivering may be felt as a fine vibration at the mandibular angle of the jaw. Shivering greatly increases cardiac oxygen needs. As ordered, paralyzing agents given with narcotics eliminate shivering. Complete blood count (CBC), electrolytes, coagulation studies, and arterial blood gases (ABGs) are monitored. After the initial transfer assessment, vital signs, oxygen saturation, and cardiac pressures are monitored. They are recorded every 15 to 30 minutes, with decreasing frequency as the patient stabilizes. Intake and output are measured. A 12-lead ECG is done to detect perioperative MI. A chest x-ray is done to check central line and endotracheal tube placement and to detect a pneumothorax or hemothorax, diaphragm elevation, or mediastinal widening from bleeding. Awakening with many questions, strange auditory and tactile sensations, and the inability to speak is frightening and frustrating to the patient. Give explanations regarding procedures in simple terms. Keeping eye contact with the patient and using touch appropriately can be soothing to the patient. Communicating with the intubated patient is done with simple closed-ended questions for yes and no answering, nonverbal gestures, communication boards, or magic slates. The family will need a great deal of support during this time. After cardiac surgery, pain is monitored in relation to the patient's preoperative anginal or MI-associated pain. Chest pain after surgery can be frightening. Knowing that chest pain can occur from the surgical incision rather than from anginal or MI pain is comforting to the patient. NURSING DIAGNOSES, PLANNING, IMPLEMENTATION, AND EVALUATION. Nursing diagnoses for postoperative care after cardiac surgery are discussed in the "Nursing Care Plan for the Postoperative Patient" in Chapter 12. After cardiac surgery, the patient will have a chest tube in place. Monitor the amount of drainage in the chest tube. Report amounts above 200 mL per hour to help prevent complications.  INFLAMMATORY AND INFECTIOUS CARDIAC DISORDERS The layers of the heart are the endocardium, pericardium, and myocardium (Fig. 23.4). They can become inflamed or infected, leading to endocarditis, pericarditis, and myocarditis, respectively. Infective Endocarditis Infective endocarditis, or IE, is an infection of the endocardium that occurs primarily in hearts with artificial or damaged valves and in those who inject drugs. Men develop IE more often than women, as do older adults compared with younger adults. FIGURE 23.4 Layers of the heart. Pathophysiology and Etiology Cardiac defects result in turbulent blood flow that erodes the normally infection-resistant endocardium. IE begins when the invading organism (most commonly bacteria but possibly a fungi or other organism) attaches to eroded endocardium where platelets and fibrin deposits have formed a vegetative lesion. Then, more platelets and fibrin cover the multiplying organism. This covering protects the microbes, reducing the ability to destroy them. Damage to valve leaflets occurs as the vegetation grows. As blood flows through the heart, the vegetation may break off and become emboli. Damaged valves from conditions such as MVP with regurgitation, rheumatic heart disease, congenital defects, and valve replacements are especially prone to bacterial invasion. The mitral valve is the valve most commonly infected, with the aortic valve second. HF may result from valve damage, especially of the aortic valve. Risk factors include compromised immune system, intravenous catheter, artificial heart valve, congenital or valvular heart disease, history of IE, IV drug use, and gingival gum disease. Prevention Dental disease may be a contributing factor to IE. Therefore, daily tooth brushing and flossing along with regular dental care is important. The AHA (2021) recommends antibiotic prophylaxis before certain dental procedures that manipulate oral tissue for the highest risk individuals who have a history of IE, a prosthetic heart valve or valve repair, a heart transplant with abnormal valve function, or certain congenital heart defects. It is not routinely recommended for any other medical procedures. Signs and Symptoms The onset of symptoms can be rapid or slow. Fever (99°F to 103°F \[37.2°C to 39.4°C\]) is a common sign (Table 23.3). Chills, anorexia, weight loss, aching muscles and joints, fatigue, dyspnea, cough, night sweats, and hematuria may occur. A new or different murmur is heard with valvular damage. Splinter hemorrhages may be seen in the distal nailbed (black or red-brown longitudinal short lines). Petechiae (tiny red or purple flat spots) resulting from microembolization of the vegetation may occur on mucous membranes, conjunctivae, or skin and may be seen in less than half of patients with IE (Fig. 23.5). Janeway lesions (small, painless red-blue lesions on palms and soles) are an acute finding. Osler nodes (small, painful nodes on fingers and toes) from cardiac emboli are a late finding (Fig. 23.6). Roth spots, which are hemorrhages in the retina that have a white center, can occur. Complications Vegetative emboli can be a major complication of IE. If organ embolization occurs, signs and symptoms vary based on the affected organ. For example, brain emboli may produce changes in level of consciousness or stroke. Kidney emboli cause pain in the flank area, hematuria, or renal failure. Pulmonary emboli result in sudden dyspnea, cough, and chest pain. Spleen emboli cause abdominal pain. Emboli in the small blood vessels can impair circulation in the extremities. Heart structures can be damaged or destroyed by IE, leading to MI or arrhythmias. Stenosis (narrowing) or regurgitation (leakage) of a heart valve may also result. As the infection progresses and causes more damage to heart structures, HF may occur. Abscesses may also develop in the heart or other parts of the body. Diagnostic Tests Table 23.3 lists diagnostic tests for IE. Positive blood cultures identify the causative organism. Echocardiogram shows cardiac vegetation and effects. Cardiac CT scan or MRI may be used to identify other areas of infection. Therapeutic Measures Prompt diagnosis is followed with hospitalization and IV antibiotics. The specific pathogen will be identified by blood cultures. The length of therapy is dependent on the type of pathogen, often up to 6 weeks. A combination of two antibiotics may be used. Rest and supportive symptom care are also used. When afebrile without complications, the patient is discharged to continue IV antibiotic therapy at home. Monitoring is continued by the home health-care nurse and laboratory testing. After therapy ends, a transthoracic echocardiogram should be done to visualize the valves. WORD BUILDING petechiae: petecchia---skin spot Surgical replacement or repair of valves is needed for severely damaged heart valves, prosthetic valve infection, multiple emboli from damaged valves, or HF. Surgery may be needed for infections that do not resolve. Table 23.3 Infective Endocarditis Summary Signs and Symptoms Dyspnea, cough Fatigue, weakness Fever, chills, aching muscles Heart murmur Janeway lesions, Osler nodes, Roth spots Nailbed splinter hemorrhages Petechiae Weight loss Diagnostic Tests Blood cultures Complete blood count Echocardiogram or transesophageal echocardiogram Chest x-ray Electrocardiogram Therapeutic Measures Antibiotic prophylaxis per criteria Acute therapy: Prolonged IV antimicrobial medications such as penicillin, vancomycin, amphotericin B Antipyretics Rest Valve replacement or repair Complications Emboli Heart failure Abscesses Priority Nursing Diagnoses Decreased Cardiac Output Decreased Activity Tolerance FIGURE 23.5 Petechiae. FIGURE 23.6 Osler nodes. Nursing Process for the Patient With Infectious Endocarditis DATA COLLECTION. A patient history is obtained that includes risk factors for IE and recent infections or invasive procedures (Table 23.4). Vital signs are recorded, and heart sounds are auscultated for murmurs. Signs of HF and emboli are noted. The HCP should be notified immediately if circulatory impairment (e.g., cool or cold skin, increased capillary refill time, cyanosis, or absent peripheral pulses in an extremity) or symptoms of organ-related emboli are detected. NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. See the nursing diagnosis Decreased Cardiac Output under "Nursing Care Plan for the Patient With a Cardiac Valvular Disorder." Decreased Diversional Activity Engagement related to restricted mobility from prolonged intravenous (IV) therapy Expected Outcome: The patient will state diversional activities are satisfying.   Plan relaxing and fun activities for patient to do during IV therapy, using the patient's input to increase patient self-esteem through increased patient control. EVALUATION. Interventions are successful if the patient's vital signs are within normal parameters for the patient, pulses are strong, extremities are warm, no dyspnea or fatigue are present, and the patient participates in diversional activities. Table 23.4 Data Collection for Patients With Infective Endocarditis Data Collection Subjective Data Questions Health History Infections (rheumatic fever, scarlet fever, previous endocarditis, streptococcal or staphylococcal, syphilis)? Cardiac disease (valvular surgery, congenital)? Childbirth? Invasive procedures (surgery, dental, catheterization, IV therapy, cystoscopy, gynecological)? Injectable drug use? Gastrointestinal Malaise? Anorexia? Weight loss? Respiratory Dyspnea on exertion or orthopnea (when lying down)? Cough? Cardiovascular Palpitations, chest pain, fatigue, activity intolerance? Musculoskeletal Weakness, arthralgia, myalgia? Medications Steroids, immunosuppressants, prolonged antibiotic therapy? IV drug use? Knowledge of Condition What is your understanding of this condition? Objective Data Body Temperature Fever, diaphoresis Respiratory Crackles, tachypnea Cardiovascular Murmurs, tachycardia, arrhythmias, edema Integumentary Nailbed splinter hemorrhages; petechiae on lips, mouth, conjunctivae, feet, or antecubital area; paleness Renal Hematuria Diagnostic Test Findings Positive blood cultures, anemia, elevated white blood cell count, elevated erythrocyte sedimentation rate, electrocardiogram showing conduction problems, echocardiogram showing valvular dysfunction and vegetation, chest x-ray examination showing heart enlargement (cardiomegaly) and lung congestion PATIENT EDUCATION. Education provides patients and families with the ability to provide IV antibiotics at home and maintain health to prevent future IE. Good hygiene, including brushing with a soft-bristle toothbrush (to prevent gum trauma) twice a day, flossing daily, and having biannual dental cleaning, is important. Good skin care includes bathing, proper hand-washing technique, avoiding nail biting, not popping pimples or lancing boils, and cleansing and applying antibiotic ointment to cuts. Recognition of symptoms (e.g., fever, chills, sweats), seeking prompt medical care, and a statement of patient's understanding along with printed material for home reference promote health maintenance. CRITICAL THINKING & CLINICAL JUDGMENT Mrs. Jones, age 28, is admitted to the hospital with a fever of 100°F (37°C), chills, fatigue, anorexia, and pain in her joints. A physical examination reveals splinter hemorrhages in the left index finger nailbed and petechiae on her chest. She is diagnosed with a heart murmur and infective endocarditis. Critical Thinking (The Why) Why is a heart murmur heard with endocarditis? What do splinter hemorrhages look like? What do petechiae indicate? What type of medication would the nurse expect to be ordered to treat the infection? Why does Mrs. Jones have chills if her temperature is elevated? What signs and symptoms might occur if the complications of heart failure develop? Clinical Judgment (The Do) How would Mrs. Jones's data collection findings be documented? What health-care team members will you collaborate with to care for this individual? Acetaminophen (Tylenol) 650 mg every 6 hours for pain is ordered. It comes as 325 mg tablets. How many tablets would be given for each dose? Suggested answers are at the end of the chapter. Pericarditis Pathophysiology and Etiology Pericarditis is an acute or chronic (greater than 3 months) inflammation of the pericardium (the sac surrounding the heart for protection and to reduce friction). The inflammation creates a problem for the heart as it tries to expand and fill. As a result, ventricular filling is reduced, which then decreases cardiac output and blood pressure. Acute pericarditis usually resolves in less than 4 to 6 weeks but can persist up to 3 months or reoccur at any time. The cause may be unknown or due to infections (e.g., viruses, bacteria, fungi, or Lyme disease), Dressler syndrome (autoimmune response), medications, neoplastic disease, post--cardiac injury (e.g., after myocardial infraction, cardiac surgery, trauma), renal disease or uremia, or rheumatic disorders (e.g., systemic lupus erythematosus, rheumatoid arthritis). There are several forms of chronic pericarditis. It is the result of fibrous scarring of the pericardium. The heart becomes surrounded by a thickened, stiff sac that limits the stretching ability of the heart's chambers for filling and may result in HF. Chronic constrictive pericarditis results from neoplastic disease and metastasis, radiation, or tuberculosis. Signs and Symptoms Chest pain is the most common symptom of acute pericarditis (Table 23.5). The pain is located substernally and over the heart. It may radiate to the clavicle, neck, and left scapula. Typically, the chest pain is an intense, sharp, creaky, grating pain that increases with deep inspiration, coughing, moving of the trunk, or lying flat. For some, the pain is not as intense and is instead a dull ache. The pain is often relieved by sitting up and leaning forward. Other symptoms depend on the cause of the pericarditis. They may include orthopnea, low-grade fever, fatigue, cough, and edema. A pericardial friction rub is a grating, scratchy, high-pitched sound that is the result of friction from the inflamed pericardial and epicardial layers rubbing together as the heart fills and contracts. Depending on the severity of the pericarditis, the rub may be faint when auscultated or loud enough to be audible without auscultation. It may be heard intermittently or continuously. It is usually heard over the lower left sternal border of the chest during each heartbeat. Chronic constrictive pericarditis produces dyspnea and signs and symptoms of right-sided HF. It may also cause atrial fibrillation. Table 23.5 Pericarditis Summary Signs and Symptoms Chest pain Cough Dyspnea, orthopnea Edema Low-grade fever Palpitations Pericardial friction rub Weakness Diagnostic Tests Complete blood count Blood chemistry Chest x-ray Electrocardiogram Echocardiogram Magnetic resonance imaging Computed tomography scan Therapeutic Measures Treat underlying cause Anti-inflammatory medication Corticosteroids Pericardiocentesis Pericardial window Pericardiectomy Complications Pericardial effusion Cardiac tamponade Priority Nursing Diagnoses Acute Pain Anxiety Decreased Cardiac Output LEARNING TIP To simulate the sound of a pericardial friction rub, hold the diaphragm of a stethoscope against the palm of one hand; listen through the stethoscope as you rub the index finger of the opposite hand over the knuckles of the hand holding the diaphragm. This sound is similar to a pericardial friction rub. Diagnostic Tests Table 23.5 lists diagnostic tests for pericarditis. Initially, the ECG reveals new widespread ST segment elevation which resolves over time (see Fig. 25.8). Echocardiogram results will show a pericardial effusion (buildup of fluid in pericardial space) when present. Erythrocyte sedimentation rate and C-reactive protein (CRP) are elevated from inflammation and can be monitored to show therapy effects. A CT scan or MRI may show a thickened pericardium. Therapeutic Measures Mild acute cases may resolve without treatment. The cause is determined for appropriate treatment such as antibiotics for bacterial infections. NSAIDs or aspirin are given along with colchicine (Colsalide) to resolve inflammation and reduce pain. Corticosteroids are used if initial treatment is not effective. Hemodialysis is used to treat uremic pericarditis. If the patient is unstable, prompt intervention is required, such as an emergency pericardiocentesis. Chronic effusive pericarditis can be treated with a pericardial window, which is a surgical opening to remove a portion of the outer pericardial layer, allowing continuous drainage of pericardial fluid into the pleural space. Chronic constrictive pericarditis is treated with pericardiectomy, which is the surgical removal of the entire tough, calcified pericardium, relieving constriction of the heart and allowing normal filling of the ventricles. Complications A pericardial effusion is the most common complication of pericarditis. A rapidly developing effusion, such as one occurring from trauma, can produce symptoms with smaller amounts of fluid than slowly developing effusions, such as pericarditis from tuberculosis, with larger amounts of fluid. The increasing fluid presses on nearby tissue, such as lung tissue producing dyspnea, cough, and tachypnea. The heartbeat sounds distant. As the fluid accumulation grows, cardiac tamponade, another complication of pericarditis, can occur. Cardiac tamponade is a life-threatening compression of the heart by fluid accumulated in the pericardial sac. Cardiac output decreases. To compensate, the heart rate increases. Then, blood pressure falls as compensatory mechanisms fail. Symptoms of decreased cardiac output, such as restlessness, confusion, tachycardia, and tachypnea, occur. Jugular venous distention is present from increased venous pressure, and heart sounds are distant. Cardiac tamponade requires emergency treatment with pericardiocentesis. The pericardium is punctured with a needle, and excess fluid in the pericardial sac is removed (Fig. 23.7). Fluid obtained during pericardiocentesis can be examined to diagnose the cause. Complications include bleeding, infection, pneumothorax, or heart damage from laceration of a coronary artery or the myocardium. Nursing Care Nursing care focuses on relieving the patient's pain and anxiety and maintaining normal cardiac function. Pain is rated and treated as ordered. Allowing the patient to assume a position of comfort by sitting up and leaning forward also relieves pain. Reinforcing teaching about pericarditis and its treatment relieves anxiety, giving a feeling of control by allowing the patient to make knowledgeable health-care decisions. FIGURE 23.7 Pericardiocentesis. Myocarditis Pathophysiology and Etiology Myocarditis is inflammation of the myocardium. The amount of muscle destroyed with myocarditis determines the extent of damage to the heart and resultant heart failure. The heart may enlarge in response to the damaged muscle fibers. However, most cases of myocarditis are benign, with few signs or symptoms. WORD BUILDING cardiac tamponade: kardia---heart + tamponade---plug pericardiocentesis: peri---around + kardia---heart + centesis---puncture myocarditis: myo---muscle + kardia---heart + itis---inflammation Myocarditis is a rare condition that most commonly develops after a viral infection, including COVID-19 in some cases. Other causes are bacteria, parasites, fungi, rickettsiae, or protozoa. Noninfectious causes may include autoimmune, cocaine abuse, cardiac transplant rejection, or (rarely) COVID-19 vaccination for young men. Acute myocarditis occurs for 3 months or less; chronic myocarditis lasts 3 months or more. Signs and Symptoms Signs and symptoms of myocarditis vary from none to severe cardiac manifestations. Fatigue, fever, pharyngitis, malaise, muscle aches, gastrointestinal discomfort, and enlarged lymph nodes may occur early from a viral infection. Cardiac manifestations such as chest pain, tachycardia, palpitations, dyspnea, and symptoms of heart failure may occur about 2 weeks after a viral infection. Occasionally, sudden death may occur. Diagnostic Tests Chest x-ray, echocardiogram, MRI or radionuclide ventriculography are helpful to show heart structure and function. An ECG shows arrhythmias, commonly sinus tachycardia. Blood tests include CBC with differential, cardiac troponin levels to look for heart damage, and brain natriuretic peptide (BNP) or N-terminal pro-BNP (NT-proBNP) for suspected heart failure. An endomyocardial biopsy during cardiac catheterization may be used to diagnose myocarditis. Therapeutic Measures Treatment is aimed at the cause, if known. Limiting physical activity to reduce cardiac workload during recovery is essential. Exercise increases myocardial inflammation and mortality. The use of alcohol, tobacco, and NSAIDs should be avoided. Symptoms of HF may be treated with medications such as angiotensin-converting enzyme (ACE) inhibitors, angiotensin II receptor blockers (ARBs), beta blockers, or diuretics to reduce the heart's workload. Severe myocarditis may require inotropic medications to vasodilate and strengthen contraction, ventricular assist device, or heart transplantation. Nursing Care Nursing care is aimed at maintaining normal cardiac function by monitoring vital signs and symptoms, and administering medications as ordered. Interventions to reduce fatigue include providing assistance as needed, allowing for frequent rest periods, and teaching energy conservation methods. Determining diversional activities with the patient when activity is restricted further reduces patient anxiety. Cardiac Trauma Two types of cardiac trauma can occur: nonpenetrating and penetrating. Nonpenetrating injuries, or contusions, occur from blunt trauma such as motor vehicle accidents or contact sports in which direct compression or force is applied to the upper torso. Contusions may vary from small bruises to hemorrhage. There may be no external trauma indicating cardiac injury. The patient may be asymptomatic or exhibit signs and symptoms identical to an MI. In severe contusions, laboratory results may show elevated creatine kinase MB (CK-MB, an enzyme) or troponin I (a protein). If bleeding into the pericardial sac occurs, cardiac tamponade can occur. If signs of shock are present, a pericardiocentesis must be performed. With its own pressure, the tamponade may seal the area of bleeding, so no cardiac decompensation occurs. In this case, only bedrest and observation are required. There are no long-term effects with most contusions. With severe contusions, however, scarring and necrosis of the myocardium may decrease cardiac output and increase the risk for cardiac rupture. Penetrating traumas include an external injury to the chest, such as a stab or gunshot wound, or an internal injury, such as invasive lines that penetrate the cardiac muscle. Complications vary depending on the size, location, and cause of injury. Tamponade occurs from bleeding into the pericardial sac if the pericardium is sealed off by clot formation. A hemothorax develops if blood drains into the pleural space in the chest. A pneumothorax occurs if air collects in the pleural space. Signs and symptoms of hemorrhage and myocardial ischemia can be noted. Surgical repair may be indicated. Cardiomyopathy Cardiomyopathy is abnormality and enlargement of the heart muscle that leads to ineffective pumping of the blood. It is often a genetic condition. There are three types of cardiac structure and function abnormalities in cardiomyopathy: dilated, hypertrophic, and restrictive (Fig. 23.8). A consequence of each type of cardiomyopathy can be HF, myocardial ischemia, or MI due to reduced cardiac output. There is no cure. Dilated Cardiomyopathy In dilated cardiomyopathy, the size of the heart chambers increases and the walls of the heart become thin. Because the heart is weakened, cardiac output is reduced. Blood moves more slowly from the left ventricle, often resulting in blood clot formation. Dilated cardiomyopathy is the most frequent type of cardiomyopathy and one of the most frequent causes of HF. The left ventricle is most often affected. Dilated cardiomyopathy may be genetic (family testing may be recommended) or caused by infectious myocarditis, hypertension, heart valve disorders, MI, chronic alcohol or cocaine use, metals such as lead, elevated iron levels, HIV, thiamine or zinc deficiencies, cardiac infections, chemotherapy, or neuromuscular disorders. WORD BUILDING cardiomyopathy: kardia---heart + myo---muscle + pathy---disease Hypertrophic Cardiomyopathy Hypertrophic cardiomyopathy is a hereditary disorder that is transmitted as an autosomal dominant trait (family testing with ECG and echocardiogram is recommended). Prognosis and life span are very good, as symptoms often do not develop to restrict lifestyle. Thickening (hypertrophy) of the cardiac muscle wall, often of the upper ventricular septum and left ventricle during adolescence, occurs. The hypertrophy may occur asymmetrically. Hypertrophic cardiomyopathy causes the ventricular wall to be rigid. Therefore, it does not relax to allow normal ventricular filling. If the mitral valve is affected and, along with the enlarged septum, obstructs the outflow of blood through the aortic valve, it is known as obstructive hypertrophic cardiomyopathy. Occasionally, sudden death can occur, primarily in those who are young. FIGURE 23.8 Comparison of the normal heart structure with each type of cardiomyopic heart structure. Restrictive Cardiomyopathy Restrictive cardiomyopathy impairs ventricular stretch, limiting ventricular filling. Cardiac muscle stiffness is present with no ventricular dilation, although systolic emptying of the ventricle is normal. Restrictive cardiomyopathy is the rarest form of cardiomyopathy. It may be caused by infiltrative diseases such as amyloidosis that deposit the protein amyloid within the myocardial cells. This makes the muscle stiff and resistant to stretching for easy ventricular filling. Treating the underlying cause may help reduce heart damage. Signs and Symptoms Manifestations of cardiomyopathy depend on the type of abnormality, with varying degrees of HF (Table 23.6). Often there are no early symptoms, and it can occur abruptly. With dilated cardiomyopathy, left ventricular and then right-sided HF with a poor prognosis are seen. Dyspnea on exertion, orthopnea, extreme fatigue, and sometimes atrial fibrillation occur. With hypertrophic cardiomyopathy, if symptoms develop, middle to older age is the most common time. These symptoms can include exertional dyspnea, fatigue, chest pain, syncope, dizziness, and palpitations related to obstruction of cardiac output through the aortic valve. With restrictive cardiomyopathy, HF symptoms result from the ventricles' inability to fill during diastole. Syncope, arrhythmias, and thrombi may occur. Table 23.6 Cardiomyopathy Summary Signs and Symptoms Angina Arrhythmias Dyspnea Edema Fatigue Syncope Diagnostic Tests Brain natriuretic peptide (BNP) Electrocardiogram Chest x-ray Cardiac catheterization Cardiac magnetic resonance imaging Echocardiogram Therapeutic Measures Anticoagulants Antihypertensives Diuretics Corticosteroids Antiarrhythmics Dilated cardiomyopathy: Vasodilators, cardiac glycosides, cardiac resynchronization, implantable cardioverter device, heart transplant Hypertrophic cardiomyopathy: Beta blockers, calcium channel blockers, myectomy, septal ablation Restrictive cardiomyopathy: Vasodilators, heart transplant Complications Heart failure Priority Nursing Diagnoses Decreased Activity Tolerance Anxiety Decreased Cardiac Output Diagnostic Tests Cardiomegaly is visible on a chest x-ray. Echocardiogram shows muscle thickness and chamber size to differentiate between the types of cardiomyopathy. Changes related to enlarged chamber size, tachycardia, and arrhythmias can be seen on the ECG. Cardiac catheterization and biopsy as well as cardiovascular MRI may be useful. An endomyocardial biopsy may be done for restrictive cardiomyopathy. Blood tests may be done to identify HF (BNP), infections, or elevated metal or iron levels. For those with hypertrophic cardiomyopathy, a stress (exercise) test may identify exertional problems due to obstruction. Therapeutic Measures Treatment for both dilated and restrictive cardiomyopathies is palliative, focusing on the underlying cause, if known, and managing HF (see Chapter 26). For dilated cardiomyopathy, treatment focuses on the symptoms of HF. ACE inhibitors, ARBs, beta blockers, diuretics, aldosterone antagonists, and digoxin (Lanoxin) may be given. Biventricular pacing and implantable defibrillators may be used. For severe HF, primarily in those with dilated cardiomyopathy, a heart transplant may be done. A ventricular assist device and extracorporeal membrane oxygenation (ECMO) may be used until a donor heart is found (see Chapter 26). Therapy is not very useful for restrictive cardiomyopathy. Diuretics or nitrates may be used to relieve venous congestion that occurs because of HF. However, a fine balance is needed when using these drugs so that preload is not reduced too greatly, which would worsen symptoms. With atrial fibrillation, anticoagulants are given to prevent emboli formation. Antiarrhythmics or cardioversion is used for arrhythmias. Treatment is not required for most people with hypertrophic cardiomyopathy, as symptoms do not usually develop. For obstructive hypertrophic cardiomyopathy, beta blockers and calcium channel blockers are given to slow the heart rate to allow more filling time and lessen the strength of the heart's contraction. An antiarrhythmic agent might be used. Adequate hydration is vital, helping to maintain cardiac output. Digoxin and vasodilators are avoided because they can increase the obstruction. Strenuous exercise and athletic sports are restricted to prevent sudden death. Lower levels of exercise may be allowed. For patients in whom medical therapy is not effective, dual chamber pacemakers, implantable automatic defibrillators, or invasive procedures are considered. For those without obstruction, fewer treatment options exist. Diuretics are used to reduce elevated pressures along with beta blockers and calcium channel blockers. When medical therapy is not successful, surgery can be done for the hypertrophied muscle to remove part of the ventricular septum (myectomy). This allows greater outflow of blood. For those that are not candidates for surgery, a septal ablation delivers alcohol via a catheter to necrose and reduce septal heart wall thickness over time. Nursing Care Nursing care focuses on maintaining normal cardiac function, increasing activity tolerance, and relieving anxiety. Careful monitoring is done to detect complications, such as HF, emboli, or arrhythmias. The HCP is immediately notified of problems. Maintenance of normal cardiac function includes increasing activity tolerance, planning rest periods, scheduling activities in small amounts, avoiding tiring activities, and providing small meals that require less energy to digest than large meals. Patient and caregiver education is vital due to the chronic nature of the disease and emotional needs. Education increases the sense of control, decreases anxiety, and aids informed decision making (Box 23.1). Home health care may assist in maintaining functional ability and reduce hospitalizations. Box 23.1 Patient Education Cardiomyopathy Patients and families should know the importance of the following:   Adherence to medication regimen to prevent heart failure   Having emergency contact numbers readily available   Cardiopulmonary resuscitation (CPR) training for family members   Availability of hospice care and emotional support for families during the grieving process  VENOUS DISORDERS Venous Thromboembolism Disease Venous thromboembolism (VTE) disease includes DVT and pulmonary emboli. Thrombophlebitis is the formation of a clot, followed by inflammation within a vein. It is the most common disorder of veins. It can occur in any superficial or deep vein but most often affects the legs, thighs, or pelvis. Deep vein thrombosis (DVT) is the most serious form because pulmonary emboli, which can be fatal, can result if the thrombus detaches (see Chapter 31). DVT occurs most often in patients who are immobile because of recent surgery or hospitalization. Pathophysiology and Etiology A venous thrombus is made up of platelets, red blood cells, white blood cells, and fibrin. Platelets attach to a vein wall. Then, a tail forms as more blood cells and fibrin collect. As the tail grows, it drifts in the blood flowing past it. The turbulence of blood flow can cause parts of the drifting thrombus to break off, becoming emboli that travel to the lungs. WORD BUILDING cardiomegaly: kardia---heart + mega---large myectomy: myo---muscle + ectomy---cutting out thrombophlebitis: thromb---lump (clot) + phleb---vein + itis---inflammation Three factors are involved in the formation of a thrombus: stasis of blood flow, damage to the lining of the vein wall, and increased blood coagulation (Table 23.7). They are referred to collectively as Virchow's triad. Prevention Identification of risk factors for thrombosis (see Table 23.7) and patient education promote the use of interventions (discussed later) to prevent thrombosis ("Evidence-Based Practice"). See the Stop the Clot campaign at www.stoptheclot.org. Dehydration should be avoided to reduce thrombus risk. Managing the risk of thrombosis in transgender adults undergoing hormone therapy is important. Hormone therapy can improve overall mental health and gender identity for transgender adults. However, it has been suggested that hormone treatment regimens should avoid ethinyl estradiol or progestin in order to reduce thrombosis risk in this population (Goldstein et al, 2019). Table 23.7 Predisposing Conditions for Thrombophlebitis (Virchow's Triad) Condition Example Venous stasis   Reduction of blood flow Shock, heart failure, myocardial infarction, atrial fibrillation   Dilated veins Vasodilators   Decreased muscle contractions Sitting for long periods (e.g., traveling) Immobility due to fractured hip, paralysis, anesthesia, surgery, obesity, advanced age   Faulty valves Varicose veins, venous insufficiency Venous wall injury Venipuncture, venous cannulation at same site for more than 48 hours, venous catheterization, surgery, trauma, burns, fractures, dislocation, IV medications (potassium, chemotherapy drugs, antibiotics, IV hypertonic solutions), IV contrast agents, diabetes, cerebrovascular disease Increased coagulation of blood Anemia, malignancy, antithrombin III deficiency, oral contraceptives, estrogen therapy, smoking, discontinuance of anticoagulant therapy, dehydration, malnutrition, polycythemia, leukocytosis, thrombocytosis, sepsis, pregnancy BE SAFE! TAKE ACTION! For prevention of thrombophlebitis:   Explain and encourage leg exercises for immobilized patients.   Ambulate as early as possible.   Maintain balanced hydration. Evidence-Based Practice Clinical Question What interventions support vulnerable patient populations taking oral anticoagulants? Evidence A systematic review of 41 studies included 37 studies focused on older adults, with 20 focused on INR monitoring, 17 on education interventions, 2 on health literacy, and 2 on cultural and linguistical diversity (Yiu & Bajorek, 2019). Findings of the review showed that INR monitoring with point-of-care testing, pharmacist-led INR monitoring especially during transition periods, and telephone monitoring were effective for older adults. The review also revealed that there is a need for long-term follow-up, with regular reinforcement of information using multiple modes of conveying the information (written, verbal, and video), that is tailored to a patient's health literacy and culture. Patient understanding helps reduce adverse events and improve INR control. Implications for Nursing Practice Collect data on patient's understanding of his or her prescribed anticoagulant and reinforce teaching using written, verbal, and video information at regular intervals and at each encounter. Reference: Yiu, A., & Bajorek, B. (2019). Patient-focused interventions to support vulnerable people using oral anticoagulants: A narrative review. Therapeutic Advances in Drug Safety, 10. https://doi.org/10.1177/2042098619847423 IMMOBILITY. People traveling long distances (e.g., in cars, airplanes) or with sedentary jobs that require extended periods of sitting or standing should change positions, perform knee and ankle flexion exercises, or walk at regular intervals to prevent stasis of blood. Patients on bedrest should have legs elevated above the level of the heart, if possible, and turn every 2 hours to prevent pooling of blood. Postoperatively or during bedrest, active or passive range-of-motion exercises should be done to increase blood flow. Ambulation should begin as soon as the patient's condition allows. Pain should be controlled to facilitate movement. Deep-breathing aids improve blood flow in large thoracic veins. Smoking should be avoided, as nicotine causes vasoconstriction. PROPHYLACTIC ANTIEMBOLISM DEVICES. Patients with peripheral venous disease, those on bedrest, and those who have had surgery or trauma may use antiembolism devices to improve blood flow. Knee- or thigh-length compression stockings apply pressure to the leg. They must be applied correctly to avoid a tourniquet effect. Older patients with decreased manual dexterity may need assistance. Stockings should be removed for skin inspection, cleansing, and moisturizing daily. Intermittent pneumatic compression (IPC) devices fill intermittently with air to move venous blood in the legs by simulating contraction of the leg muscles. They may be used in combination with compression stockings for greater effectiveness. PROPHYLACTIC MEDICATION. Low molecular weight heparin (LMWH) can be given postoperatively to prevent thrombosis (Table 23.8). Anticoagulation monitoring is not required with LMWH because of the predictability of its dose-related response. Subcutaneous heparin may also be used postoperatively to prevent thrombosis. Platelet counts must be monitored with either LMWH or heparin to detect heparin-induced thrombocytopenia. Oral anticoagulants such as warfarin (Coumadin) can be used in the high-risk patient to prevent thrombosis. IV THERAPY. Monitoring of IV sites is performed according to institutional policy to detect signs of thrombophlebitis. Venous cannula sites should be changed regularly per institutional guidelines to prevent thrombus formation. Table 23.8 Anticoagulant Medications Medication Class/Action Coumarin Inhibits liver synthesis of vitamin K dependent clotting factors: II, XII, IX, X. Examples warfarin (Coumadin) Nursing Implications Monitor international normalized ratio (INR) regularly and signs of bleeding. Teach patient to report bleeding. Acetaminophen (Tylenol) is given for analgesia instead of aspirin while on warfarin (can continue aspirin for heart disease). Antidote: Vitamin K. Teach: Maintain regular monitoring of INR, report signs of bleeding, and eat amounts that are consistent for foods that are high in vitamin K to maintain INR level (see "Nutrition Notes"). Direct Thrombin Inhibitors Examples dabigatran (Pradaxa) Nursing Implications Monitor for bleeding. Heparin Binds to antithrombin III, which then inhibits fibrin formation. Examples heparin sodium Nursing Implications Monitor heparin antifactor Xa or partial thromboplastin time: 1.5 to 2 times control. Do not give intramuscularly, as can cause pain and hematoma. Monitor for bleeding and decreased platelet count. Antidote: Protamine sulfate. Teach: Report bleeding. Factor Xa Inhibitors Bind with antithrombin III, inhibiting making of factor Xa and the formation of thrombin. Examples apixaban (Eliquis) dalteparin sodium (Fragmin) enoxaparin (Lovenox) fondaparinux (Arixtra) rivaroxaban (Xarelto) edoxaban (Savaysa) Nursing Implications Bleeding rare. Contraindicated with kidney disease due to increased bleeding risk. Compliance is key for efficacy. Teach: Give injection subcutaneously (with a prefilled syringe the air bubble is not to be removed). Thrombolytics Promote fibrinolysis to break down fibrin in blood clot. Examples reteplase; rPA (Retavase) tenecteplase; TNK (TNKase) tissue plasminogen activator; tPA (Alteplase) Nursing Implications Minimize blood draws for 24 hours. Monitor for bleeding. Avoid acetylsalicylic acid, NSAIDs. Signs and Symptoms Symptoms vary according to the size and location of a thrombus. In some cases, the thrombus becomes an embolus (Table 23.9). Table 23.9 Thrombophlebitis Summary Signs and Symptoms Superficial veins: Redness, warmth, swelling, tenderness, induration Deep veins: Swelling, pain, warmth, venous distention, edema and tenderness Diagnostic Tests D-dimer (small protein fragment in blood as a blood clot dissolves) Compression ultrasonography Contrast venography Magnetic resonance imaging or computed tomography Therapeutic Measures Superficial veins: Warm, moist heat; analgesics; NSAIDs; compression stockings Deep veins: Anticoagulants; warm, moist heat; leg extremity elevation above heart level; compression stockings; thrombolytic therapy; thrombectomy; early ambulation Complications Pulmonary embolism Chronic venous insufficiency Recurrent deep vein thrombosis Priority Nursing Diagnoses Acute Pain Impaired Skin Integrity Anxiety SUPERFICIAL VEINS. Thrombophlebitis in a superficial vein may produce redness, warmth, swelling, and tenderness in the area. The vein feels like a firm cord. This effect is called induration. The saphenous vein is the most commonly affected vein in the leg. Varicosity of the vein is usually the cause. In the arm, IV therapy is the most common cause. DEEP VEINS. Patients may have no symptoms with thrombophlebitis in the leg. With a DVT in a femoral vein, swelling, pain, warmth, venous distention, edema, and tenderness of the calf may be present in the affected leg. Obstruction of blood flow from the leg back to the heart causes the edema. An elevated temperature can be present. Cyanosis and edema may occur if the large veins (vena cava) are involved. Complications The most serious complication is pulmonary embolism (PE), a life-threatening emergency (see Chapter 31). Chronic venous insufficiency results from damage to the valves in the vein and can cause venous stasis. Signs and symptoms that may appear years after a thrombus include edema, pain, brownish discoloration and ulceration of the medial ankle, venous distention, and dependent cyanosis of the leg. Post-thrombotic syndrome (PTS) is a symptomatic chronic venous insufficiency after a DVT that occurs in about 50% of DVT patients within 2 years. It occurs from damage to the vein valves that normally prevent backflow of blood within the leg veins. PTS results in pain, swelling, and sometimes leg ulcers, which can reduce quality of life. Routine compression stockings use for those with acute DVTs is not recommended for preventing PTS. Compression use for those with extensive lower leg edema is suggested (Kavali & Vedantham, 2018). Diagnostic Tests Diagnostic tests guide treatment needs (see Table 23.9). Compression ultrasonography is a reliable, rapid bedside test to diagnosis a suspected DVT, allowing quick initiation of treatment. Therapeutic Measures The goals of treatment are to relieve pain and to prevent pulmonary emboli, thrombus enlargement, or development of another thrombus. Superficial thrombophlebitis is treated at home with warm, moist heat; analgesics; NSAIDs; and, for the leg, compression stockings and leg elevation for symptom relief. Determining if the patient will be able and willing to use compression therapy is important. Anticoagulants are not typically needed because the risk of PE is low. A proximal DVT may be treated at home if there is no PE. Mobilization has not shown an increase in risk for PE and DVT progression. Early mobilization in smaller studies has shown a decrease in pain and swelling when a DVT is present (Chatsis & Visintini, 2018). Traditional medical care for DVTs involves a hospital stay. Interventions may include warm, moist heat; elevation of the leg above heart level for swelling; compression stockings; and anticoagulants. Additional classes of anticoagulants that do not require ongoing laboratory monitoring have provided options to the traditional anticoagulant therapy of heparin and warfarin (see Table 23.8). Usually, anticoagulants are prescribed for 3 months. Then, the patient is evaluated for further need for them. Other approaches are venous thrombectomy to remove the clot to prevent pulmonary emboli or chronic venous insufficiency when the risk of pulmonary emboli is great or anticoagulant therapy cannot be used. Occasionally, a permanent or retrievable vena cava filter is placed into the vena cava through the femoral or right internal jugular vein. Once in place, it is opened and attached to the vein wall to trap clots traveling toward lungs without hindering blood flow. Nursing Process for the Patient With Thrombophlebitis DATA COLLECTION. A patient history is obtained that includes questions regarding recent IV therapy or use of contrast media, surgery, extremity trauma, childbirth, bedrest, recent long trips, cardiac disease, recent infections, and current medications that can put the patient at high risk of thrombus. Data are gathered for pain, fever, peripheral pulses, sensation, tenderness, redness, warmth, edema, and a firm, cordlike vein in the affected extremity. Daily extremity circumference measurements are taken and documented (bilateral thighs and calves for leg DVT) and recorded to monitor edema. Coagulation tests are monitored. Signs and symptoms of a pulmonary embolism must be immediately reported to the HCP (see Chapter 31). NURSING DIAGNOSES, PLANNING, AND IMPLEMENTATION. For the patient identified as being at risk for blood clots, the nursing diagnosis Risk for Thrombosis applies. Interventions would include the preventive measures previously discussed. Educating the patient about the disease and its treatment is important to reduce anxiety about complications and to enhance adherence to treatment to prevent complications (see Patient Teaching Guidelines for this chapter on Davis Edge). Acute Pain related to inflammation of vein Expected Outcome: The patient will report satisfactory pain relief within 30 minutes of pain report.   Ask patient to rate pain with a pain rating scale (such as 0 to 10) to provide consistency in pain reporting.   Provide analgesics and NSAIDs, as ordered, to reduce pain.   Apply warm, moist compresses, as ordered, as moist heat penetrates deeply to relieve pain. Impaired Skin Integrity related to venous stasis Expected Outcome: The patient's skin will remain intact.   Observe skin for edema, skin color changes, and ulcers and measure both extremities' circumference at the same site in each extremity daily to detect skin integrity impairment as edematous skin breaks down more easily.   Elevate feet above heart level when at rest to decrease swelling.   Apply compression stockings after acute edema decreases, as ordered, to maintain reduced swelling.   Reinforce teaching for patient to avoid crossing legs or wearing constricting clothes to avoid impairing venous return. EVALUATION. Interventions are successful if the patient is pain-free and skin remains intact.