Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders

Transcription

1 Chapter 29 Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders LEARNING OBJECTIVES On completion of this chapter, the learner will be able to: 1. Define valvular disorders of the heart and describe the pathophysiology, clinical manifestations, and management of patients with mitral and aortic disorders. 2. Describe types of cardiac valve repair and replacement procedures used to treat valvular problems and the care needed by patients who undergo these procedures. 3. Describe the pathophysiology, clinical manifestations, and management of patients with cardiomyopathies. 4. Describe the pathophysiology, clinical manifestations, and management of patients with infections of the heart. 5. Describe the rationale for prophylactic antibiotic therapy for patients with mitral valve prolapse, valvular heart disease, rheumatic endocarditis, infective endocarditis, and myocarditis. 763

2 764 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION Structural disorders of the heart present many challenges for the patient, family, and health care team, as do the conduction and vascular disorders discussed in Chapters 27 and 28. Problems with the heart valves, holes in the intracardiac septum, cardiomyopathies, and infectious diseases of the heart muscle alter cardiac output. Treatments for these diagnoses may be noninvasive, such as medication therapy and activity and dietary modification. Invasive treatments, such as valve repair or replacement, septal repair, ventricular assist devices, total artificial hearts, cardiac transplantation, and other procedures may also be used. Nurses have an integral role in the care of patients with structural, infectious, and inflammatory cardiac conditions. Acquired Valvular Disorders The valves of the heart control the flow of blood through the heart into the pulmonary artery and aorta by opening and closing in response to the blood pressure changes as the heart contracts and relaxes through the cardiac cycle. The atrioventricular valves separate the atria from the ventricles and include the tricuspid valve, which separates the right atrium from the right ventricle, and the mitral valve, which separates the left atrium from the left ventricle. The tricuspid valve has three leaflets; the mitral valve has two. Both valves have chordae tendineae that anchor the valve leaflets to the papillary muscles and ventricular wall. The semilunar valves are located between the ventricles and their corresponding arteries. The pulmonic valve lies between the right ventricle and the pulmonary artery; the aortic valve lies between the left ventricle and the aorta. Figure 29-1 shows valves in the closed position. When any of the heart valves do not close or open properly, blood flow is affected. When valves do not close completely, blood flows backward through the valve in a process called regurgitation. When valves do not open completely, a condition called stenosis, the flow of blood through the valve is reduced. Disorders of the mitral valve fall into the following categories: mitral valve prolapse (ie, stretching of the valve leaflet into the atrium during systole), mitral regurgitation, and mitral stenosis. Disorders of the aortic valve are categorized as aortic regurgitation and aortic stenosis. These valvular disorders lead to various symptoms that, depending on their severity, may require surgical repair or replacement of the valve to correct the problem (Fig. 29-2). Tricuspid and pulmonic valve disorders also occur, usually with fewer symptoms and complications. Regurgitation and stenosis may occur at the same time in the same or different valves. MITRAL VALVE PROLAPSE Mitral valve prolapse, formerly known as mitral prolapse syndrome, is a deformity that usually produces no symptoms. Rarely, it progresses and can result in sudden death. Mitral valve prolapse occurs more frequently in women than in men. In recent years, this disorder has been diagnosed more frequently, probably as a result of improved diagnostic methods. Pathophysiology In mitral valve prolapse, a portion of a mitral valve leaflet balloons back into the atrium during systole. Rarely, the ballooning stretches the leaflet to the point that the valve does not remain closed during systole (ie, ventricular contraction). Blood then regurgitates from the left ventricle back into the left atrium (Braunwald et al., 2001). Clinical Manifestations Many people have a ballooned leaflet but no symptoms. Others have symptoms of fatigue, shortness of breath, light-headedness, dizziness, syncope, palpitations, chest pain, and anxiety (Braunwald et al., 2001; Freed et al., 1999; Fuster et al., 2001). Fatigue may occur regardless of the person s activity level and amount of rest or sleep. Shortness of breath is not correlated with activity levels or pulmonary function. Atrial or ventricular dysrhythmias may produce the sensation of palpitations, but palpi- Glossary allograft: heart valve replacement made from a human heart valve (synonym: homograft) annuloplasty: repair of a cardiac valve s outer ring aortic valve: semilunar valve located between the left ventricle and the aorta autograft: heart valve replacement made from the patient s own heart valve (ie, the pulmonic valve is excised and used as an aortic valve) cardiomyopathy: disease of the heart muscle chordoplasty: repair of the stringy, tendinous fibers that connect the free edges of the atrioventricular valve leaflets to the papillary muscles commissurotomy: splitting or separating fused cardiac valve leaflets heterograft: heart valve replacement made of tissue from an animal heart valve (synonym: xenograft) heterotopic transplantation: procedure in which the recipient s heart remains in place and a donor heart is grafted to the right and anterior of it; the patient has two hearts homograft: heart valve replacement made from a human heart valve (synonym: allograft) leaflet repair: repair of a cardiac valve s movable flaps (leaflets) mitral valve: atrioventricular valve located between the left atrium and left ventricle orthotopic transplantation: the recipient s heart is removed, and a donor heart is grafted into the same site; the patient has one heart prolapse (of a valve): stretching of an atrioventricular heart valve leaflet into the atrium during systole pulmonic valve: semilunar valve located between the right ventricle and the pulmonary artery regurgitation: backward flow of blood through a heart valve stenosis: narrowing or obstruction of a cardiac valve s orifice total artificial heart: mechanical device used to aid a failing heart, assisting the right and left ventricles tricuspid valve: atrioventricular valve located between the right atrium and right ventricle valve replacement: insertion of a device at the site of a malfunctioning heart valve to restore blood flow in one direction through the heart valvuloplasty: repair of a stenosed or regurgitant cardiac valve by commissurotomy, annuloplasty, leaflet repair, or chordoplasty (or a combination of procedures) ventricular assist device: mechanical device used to aid a failing right or left ventricle xenograft: heart valve replacement made of tissue from an animal heart valve (synonym: heterograft)

3 Chapter 29 Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders 765 FIGURE 29-1 The valves of the heart (aortic or semilunar, tricuspid, and mitral) in closed position. Coronary arteries Aortic (semilunar) valve Tricuspid valve Mitral valve tations have been reported while the heart has been beating normally. Another puzzling symptom is chest pain, which is often localized to the chest and may last for days. Anxiety may be a response to the symptoms experienced by the patient; however, some patients report anxiety as the only symptom. Some clinicians speculate that the symptoms may be explained by dysautonomia, a dysfunction of the autonomic nervous system, although no consensus exists about the cause of the symptoms experienced by some patients with mitral valve prolapse. Physiology/Pathophysiology Backward Heart Failure Forward Heart Failure Aortic stenosis limits forward flow of blood from the left ventricle Aortic regurgitation permits blood flow back into the left ventricle Not enough blood flows through the aorta for the body's needs (decreased cardiac output) Increased blood volume and pressure in the left ventricle Left ventricular hypertrophy and dilation; blood from the left atrium cannot get into the left ventricle Mitral stenosis limits the forward flow of blood into the left ventricle Mitral regurgitation permits blood flow back into the left atrium Angina pectoris, postural hypotension, fatigue, dizziness Increased blood volume and pressure in the left atrium Left atrium hypertrophy and dilation Increased blood volume and pressure in the pulmonary veins Pulmonary congestion (shortness of breath and pulmonary edema), increased pulmonary vascular pressure FIGURE 29-2 Pathophysiology: Left heart failure as a result of aortic and mitral valvular heart disease and the development of right ventricular failure. Increased work for the right ventricle, right ventricular strain Right ventricular failure

4 766 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION Assessment and Diagnostic Findings Often, the first and only sign of mitral valve prolapse is identified when a physical examination of the heart discloses an extra heart sound, referred to as a mitral click. The systolic click is an early sign that a valve leaflet is ballooning into the left atrium. In addition to the mitral click, a murmur of mitral regurgitation may be heard if progressive valve leaflet stretching and regurgitation have occurred. A small number of patients experience signs and symptoms of heart failure if mitral regurgitation exists. Medical Management Medical management is directed at controlling symptoms. If dysrhythmias are documented and cause symptoms, the patient is advised to eliminate caffeine and alcohol from the diet and to stop smoking; antiarrhythmic medications may be prescribed. Chest pain that does not respond to nitrates may respond to calcium channel blockers or beta-blockers. Heart failure is treated the same as it would be for any other patient with heart failure (see Chap. 30). In advanced stages of disease, mitral valve repair or replacement may be necessary. Nursing Management The nurse educates patients about the diagnosis and the possibility that the condition is hereditary. Because most patients with mitral valve prolapse are asymptomatic, the nurse explains the need to inform the health care provider about any symptoms that may develop. The nurse also instructs patients about the need for prophylactic antibiotic therapy before undergoing invasive procedures (eg, dental work, genitourinary or gastrointestinal procedures) that may introduce infectious agents systemically. This therapy is prescribed for symptomatic patients and for asymptomatic patients who have both a systolic click and murmur or mitral regurgitation. If in doubt about risk factors and the need for antibiotics, patients should consult their physicians. To minimize symptoms, the nurse teaches patients to avoid caffeine and alcohol. The nurse encourages patients to read product labels, particularly in over-the-counter products such as cough medicine, because these products may contain alcohol, caffeine, ephedrine, and epinephrine, which may produce dysrhythmias and other symptoms. Dysrhythmias, chest pain, heart failure, or other complications of mitral valve prolapse are treated as described in Chapter 30. The nurse also explores with patients possible diet, activity, sleep, and other lifestyle factors that may correlate with symptoms experienced. MITRAL REGURGITATION Mitral regurgitation involves blood flowing back from the left ventricle into the left atrium during systole. Often, the margins of the mitral valve cannot close during systole. Pathophysiology Mitral regurgitation may be caused by problems with one or more of the leaflets, the chordae tendineae, the annulus, or the papillary muscles. A mitral valve leaflet may shorten or tear. The chordae tendineae may elongate, shorten, or tear. The annulus may be stretched by heart enlargement or deformed by calcification. The papillary muscle may rupture, stretch, or be pulled out of position by changes in the ventricular wall (eg, scar from a NURSING RESEARCH PROFILE 29-1 Mitral Valve Prolapse Support Group Scordo, K. A. B. (2001). Factors associated with participating in a mitral valve prolapse support group. Heart Lung, 30(2), Purpose The purpose of this study was to identify factors that influence a patient s attendance at mitral valve prolapse support groups. Study Sample and Design Questionnaires were used for this descriptive study of mitral valve support group leaders, current and former support group participants, and nonparticipants, all of whom had a diagnosis of mitral valve prolapse. A total of 376 questionnaires were analyzed. Findings People with mitral valve prolapse were more likely to participate in support groups if they were older than 50 years of age and participated in other self-help groups. The reason for attending was to obtain more information about mitral valve prolapse, information not usually available from family, friends, and physicians. No relationship was found between participation in a support group and patient gender, education level, marital status, age when first diagnosed, age when symptoms were first experienced, perceived social support, any symptoms experienced, or travel time or distance required to participate in the support group. Nursing Implications Nurses need to be aware that patients with mitral valve prolapse desire information about the condition, and not just at the time of diagnosis or development of symptoms. Nurses can provide education and facilitate support groups. Patients older than 50 years of age and those who participate in other self-help groups may be particularly interested in mitral valve prolapse support groups. myocardial infarction or ventricular dilation). The papillary muscle may be unable to contract because of ischemia. Regardless of the cause, blood regurgitates back into the atrium during systole. With each beat of the left ventricle, some of the blood is forced back into the left atrium. Because this blood is added to the blood that is beginning to flow in from the lungs, the left atrium must stretch. It eventually hypertrophies and dilates. The backward flow of blood from the ventricle diminishes the volume of blood flowing into the atrium from the lungs. As a result, the lungs become congested, eventually adding extra strain on the right ventricle. Mitral regurgitation ultimately involves the lungs and the right ventricle. Clinical Manifestations Chronic mitral regurgitation is often asymptomatic, but acute mitral regurgitation (eg, that resulting from a myocardial infarction) usually manifests as severe congestive heart failure. Dyspnea, fatigue, and weakness are the most common symptoms. Palpitations, shortness of breath on exertion, and cough from pulmonary congestion also occur. Assessment and Diagnostic Findings A systolic murmur is heard as a high-pitched, blowing sound at the apex. The pulse may be regular and of good volume, or it may be irregular as a result of extrasystolic beats or atrial fibrillation.

5 Chapter 29 Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders 767 Echocardiography is used to diagnose and monitor the progression of mitral regurgitation. Medical Management Management of mitral regurgitation is the same as that for congestive heart failure. Surgical intervention consists of mitral valve replacement or valvuloplasty (ie, surgical repair of the heart valve). MITRAL STENOSIS Mitral stenosis is an obstruction of blood flowing from the left atrium into the left ventricle. It is most often caused by rheumatic endocarditis, which progressively thickens the mitral valve leaflets and chordae tendineae. The leaflets often fuse together. Eventually, the mitral valve orifice narrows and progressively obstructs blood flow into the ventricle. Pathophysiology Normally, the mitral valve opening is as wide as the diameter of three fingers. In cases of marked stenosis, the opening narrows to the width of a pencil. The left atrium has great difficulty moving blood into the ventricle because of the increased resistance of the narrowed orifice; it dilates (stretches) and hypertrophies (thickens) because of the increased blood volume it holds. Because there is no valve to protect the pulmonary veins from the backward flow of blood from the atrium, the pulmonary circulation becomes congested. As a result, the right ventricle must contract against an abnormally high pulmonary arterial pressure and is subjected to excessive strain. Eventually, the right ventricle fails. Clinical Manifestations The first symptom of mitral stenosis is often breathing difficulty (ie, dyspnea) on exertion as a result of pulmonary venous hypertension. Patients with mitral stenosis are likely to show progressive fatigue as a result of low cardiac output. They may expectorate blood (ie, hemoptysis), cough, and experience repeated respiratory infections. Assessment and Diagnostic Findings The pulse is weak and often irregular because of atrial fibrillation (caused by the strain on the atrium). A low-pitched, rumbling, diastolic murmur is heard at the apex. As a result of the increased blood volume and pressure, the atrium dilates, hypertrophies, and becomes electrically unstable, and the patient experiences atrial dysrhythmias. Echocardiography is used to diagnose mitral stenosis. Electrocardiography (ECG) and cardiac catheterization with angiography are used to determine the severity of the mitral stenosis. Medical Management Antibiotic prophylaxis therapy is instituted to prevent recurrence of infections. Congestive heart failure is treated as described in Chapter 30. Patients with mitral stenosis may benefit from anticoagulants to decrease the risk for developing atrial thrombus. They may also require treatment for anemia. Surgical intervention consists of valvuloplasty, usually a commissurotomy to open or rupture the fused commissures of the mitral valve. Percutaneous transluminal valvuloplasty or mitral valve replacement may be performed. AORTIC REGURGITATION Aortic regurgitation is the flow of blood back into the left ventricle from the aorta during diastole. It may be caused by inflammatory lesions that deform the leaflets of the aortic valve, preventing them from completely closing the aortic valve orifice. This valvular defect also may result from endocarditis, congenital abnormalities, diseases such as syphilis, a dissecting aneurysm that causes dilation or tearing of the ascending aorta, or deterioration of an aortic valve replacement. Pathophysiology In aortic regurgitation, blood from the aorta returns to the left ventricle during diastole in addition to the blood normally delivered by the left atrium. The left ventricle dilates, trying to accommodate the increased volume of blood. It also hypertrophies, trying to increase muscle strength to expel more blood with abovenormal force raising systolic blood pressure. The arteries attempt to compensate for the higher pressures by reflex vasodilation; the peripheral arterioles relax, reducing peripheral resistance and diastolic blood pressure. Clinical Manifestations Aortic insufficiency develops without symptoms in most patients. Some patients are aware of a forceful heartbeat, especially in the head or neck. There may be marked arterial pulsations that are visible or palpable at the carotid or temporal arteries. This is a result of the increased force and volume of the blood ejected from the hypertrophied left ventricle. Exertional dyspnea and fatigue follow. Progressive signs and symptoms of left ventricular failure include breathing difficulties (eg, orthopnea, paroxysmal nocturnal dyspnea), especially at night. Assessment and Diagnostic Findings A diastolic murmur is heard as a high-pitched, blowing sound at the third or fourth intercostal space at the left sternal border. The pulse pressure (ie, difference between systolic and diastolic pressures) is considerably widened in patients with aortic regurgitation. One characteristic sign of the disease is the water-hammer pulse, in which the pulse strikes the palpating finger with a quick, sharp stroke and then suddenly collapses. Diagnosis may be confirmed by echocardiogram, radionuclide imaging, ECG, magnetic resonance imaging, and cardiac catheterization. Medical Management Before the patient undergoes invasive or dental procedures, antibiotic prophylaxis is needed to prevent endocarditis. Heart failure and dysrhythmias are treated as described in Chapters 27 and 30. Aortic valvuloplasty or valve replacement is the treatment of choice, preferably performed before left ventricular failure. Surgery is recommended for any patient with left ventricular hypertrophy, regardless of the presence or absence of symptoms. AORTIC STENOSIS Aortic valve stenosis is narrowing of the orifice between the left ventricle and the aorta. In adults, the stenosis may involve congenital leaflet malformations or an abnormal number of leaflets (ie, one or two rather than three), or it may result from rheumatic

6 768 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION endocarditis or cusp calcification of unknown cause. The leaflets of the aortic valve may fuse. Pathophysiology There is progressive narrowing of the valve orifice, usually over a period of several years to several decades. The left ventricle overcomes the obstruction to circulation by contracting more slowly but with greater energy than normal, forcibly squeezing the blood through the very small orifice. The obstruction to left ventricular outflow increases pressure on the left ventricle, which results in thickening of the muscle wall. The heart muscle hypertrophies. When these compensatory mechanisms of the heart begin to fail, clinical signs and symptoms develop. Clinical Manifestations Many patients with aortic stenosis are asymptomatic. After symptoms develop, patients usually first have exertional dyspnea, caused by left ventricular failure. Other signs are dizziness and syncope because of reduced blood flow to the brain. Angina pectoris is a frequent symptom that results from the increased oxygen demands of the hypertrophied left ventricle, the decreased time in diastole for myocardial perfusion, and the decreased blood flow into the coronary arteries. Blood pressure can be low but is usually normal; there may be a low pulse pressure (30 mm Hg or less) because of diminished blood flow. Assessment and Diagnostic Findings On physical examination, a loud, rough systolic murmur may be heard over the aortic area. The sound to listen for is a systolic crescendo-decrescendo murmur, which may radiate into the carotid arteries and to the apex of the left ventricle. The murmur is low-pitched, rough, rasping, and vibrating. If the examiner rests a hand over the base of the heart, a vibration may be felt. The vibration is caused by turbulent blood flow across the narrowed valve orifice. Evidence of left ventricular hypertrophy may be seen on a 12-lead ECG and echocardiogram. Echocardiography is used to diagnose and monitor the progression of aortic stenosis. After the stenosis progresses to the point that surgical intervention is considered, left-sided heart catheterization is necessary to measure the severity of the valvular abnormality and evaluate the coronary arteries. Pressure tracings are taken from the left ventricle and the base of the aorta. The systolic pressure in the left ventricle is considerably higher than that in the aorta during systole. Medical Management Antibiotic prophylaxis to prevent endocarditis is essential for anyone with aortic stenosis. After left ventricular failure or dysrhythmias occur, medications are prescribed. Definitive treatment for aortic stenosis is surgical replacement of the aortic valve. Patients who are symptomatic and are not surgical candidates may benefit from one- or two-balloon percutaneous valvuloplasty procedures. VALVULAR HEART DISORDERS: NURSING MANAGEMENT The nurse teaches all patients with valvular heart disease about the diagnosis, the progressive nature of valvular heart disease, and the treatment plan. The patient is taught to report any new symp- toms or changes in symptoms to the health care provider. The nurse emphasizes the need for prophylactic antibiotic therapy before any invasive procedure (eg, dental work, genitourinary or gastrointestinal procedure) that may introduce infectious agents to the patient s bloodstream. The patient is taught that the infectious agent, usually a bacterium, is able to adhere to the diseased heart valve more readily than to a normal valve. Once attached to the valve, the infectious agent multiplies, resulting in endocarditis and further damage to the valve. The patient s heart rate, blood pressure, and respiratory rate are measured and compared with previous data for any changes. Heart and lung sounds are auscultated and peripheral pulses palpated. The nurse assesses patients with valvular heart disease for signs and symptoms of heart failure: fatigue, dyspnea with exertion, an increase in coughing, hemoptysis, multiple respiratory infections, orthopnea, or paroxysmal nocturnal dyspnea (see Chap. 30). The nurse assesses for dysrhythmias by palpating the patient s pulse for strength and rhythm (ie, regular or irregular) and asks if the patient has experienced palpitations or felt forceful heartbeats (see Chap. 27). The nurse also assesses for dizziness, syncope, increased weakness, or angina pectoris (see Chap. 28). The nurse collaborates with the patient to develop a medication schedule and teaches about the name, dosage, actions, side effects, and any drug-drug or drug-food interactions of the prescribed medications for heart failure, dysrhythmias, angina pectoris, or other symptoms. The nurse teaches the patient to weigh daily and report the gain of 2 pounds in 1 day or 5 pounds in 1 week to the health care provider. The nurse may assist the patient with planning activity and rest periods to achieve a lifestyle acceptable to the patient. If the patient is to have surgical valve replacement or valvuloplasty, the nurse teaches the patient about the procedure and anticipated recovery. Valve Repair and Replacement Procedures VALVULOPLASTY The repair, rather than replacement, of a cardiac valve is referred to as valvuloplasty. The type of valvuloplasty depends on the cause and type of valve dysfunction. Repair may be made to the commissures between the leaflets in a procedure known as commissurotomy, to the annulus of the valve by annuloplasty, to the leaflets, or to the chordae by chordoplasty. Most valvuloplasty procedures require general anesthesia and often require cardiopulmonary bypass. Some procedures, however, can be performed in the cardiac catheterization laboratory; these procedures do not always require general anesthesia or cardiopulmonary bypass. Percutaneous partial cardiopulmonary bypass is used in some cardiac catheterization laboratories. The cardiopulmonary bypass is achieved by inserting a large catheter (ie, cannula) into two peripheral blood vessels, usually a femoral vein and an artery. Blood is diverted from the body through the venous catheter to the cardiopulmonary bypass machine (see Chap. 28) and returned to the patient through the arterial catheter. The patient is usually managed in a critical care unit for the first 24 to 72 hours after surgery. Care focuses on hemodynamic stabilization and recovery from anesthesia. Vital signs are assessed every 5 to 15 minutes and as needed until the patient recovers from anesthesia or sedation and then every 2 to 4 hours and as needed. Intravenous medications to increase or decrease blood pressure and to treat dysrhythmias or altered heart rates are administered, and their effects are monitored. The intravenous medications are gradually decreased until they are no longer re-

7 Chapter 29 Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders 769 quired or the patient takes needed medication by another route (eg, oral, topical). Patient assessments are conducted every 1 to 4 hours and as needed, with particular attention to neurologic, respiratory, and cardiovascular assessments. After the patient has recovered from anesthesia and sedation, is hemodynamically stable without intravenous medications, and assessments are stable, the patient is usually transferred to a telemetry or surgical unit for continued postsurgical care and teaching. The nurse provides wound care and patient teaching regarding diet, activity, medications, and self-care. Patients are discharged from the hospital in 1 to 7 days. In general, valves that have undergone valvuloplasty function longer than replacement valves, and the patients do not require continuous anticoagulation. Commissurotomy The most common valvuloplasty procedure is commissurotomy. Each valve has leaflets; the site where the leaflets meet is called the commissure. The leaflets may adhere to one another and close the commissure (ie, stenosis). Less commonly, the leaflets fuse in such a way that, in addition to stenosis, the leaflets are also prevented from closing completely, resulting in a backward flow of blood (ie, regurgitation). A commissurotomy is the procedure performed to separate the fused leaflets. CLOSED COMMISSUROTOMY Closed commissurotomies do not require cardiopulmonary bypass. The valve is not directly visualized. The patient receives a general anesthetic, a midsternal incision is made, a small hole is cut into the heart, and the surgeon s finger or a dilator is used to break open the commissure. This type of commissurotomy has been performed for mitral, aortic, tricuspid, and pulmonary valve disease. Balloon Valvuloplasty. Balloon valvuloplasty (Fig. 29-3) is another type of closed commissurotomy beneficial for mitral valve stenosis in younger patients, for aortic valve stenosis in elderly patients, and for patients with complex medical conditions that place them at high risk for the complications of more extensive surgical procedures. Most commonly used for mitral and aortic valve stenosis, balloon valvuloplasty also has been used for tricuspid and pulmonic valve stenosis. The procedure is performed in the cardiac catheterization laboratory, and the patient may receive a local anesthetic. Patients remain in the hospital 24 to 48 hours after the procedure. Mitral valvuloplasty is contraindicated for patients with left atrial or ventricular thrombus, severe aortic root dilation, significant mitral valve regurgitation, thoracolumbar scoliosis, rotation of the great vessels, and other cardiac conditions that require open heart surgery. Mitral balloon valvuloplasty involves advancing one or two catheters into the right atrium, through the atrial septum into the left atrium, across the mitral valve into the left ventricle, and out into the aorta. A guide wire is placed through each catheter, and the original catheter is removed. A large balloon catheter is then placed over the guide wire and positioned with the balloon across the mitral valve. The balloon is then inflated with a dilute angiographic solution. When two balloons are used, they are inflated simultaneously. The advantage of two balloons is that they are each smaller than the one large balloon often used, making smaller atrial septal defects. As the balloons are inflated, they usually do not completely occlude the mitral valve, thereby permitting some forward flow of blood during the inflation period. Guide wire Dilation catheter Mitral valve Atrial transseptal puncture FIGURE 29-3 Balloon valvuloplasty: cross-section of heart illustrating guide wire and dilation catheter placed through an atrial transseptal puncture and across the mitral valve. The guide wire is extended out from the aortic valve into the aorta for catheter support. All patients have some degree of mitral regurgitation after the procedure. Other possible complications include bleeding from the catheter insertion sites, emboli resulting in complications such as strokes, and rarely, left-to-right atrial shunts through an atrial septal defect caused by the procedure. Aortic balloon valvuloplasty also may be performed by passing the balloon or balloons through the atrial septum, but it is performed more commonly by introducing a catheter through the aorta, across the aortic valve, and into the left ventricle. The oneballoon or the two-balloon technique can be used for treating aortic stenosis. The aortic procedure is not as effective as the procedure for the mitral valve, and the rate of restenosis is nearly 50% in the first 12 to 15 months after the procedure (Braunwald et al., 2001). Possible complications include aortic regurgitation, emboli, ventricular perforation, rupture of the aortic valve annulus, ventricular dysrhythmias, mitral valve damage, and bleeding from the catheter insertion sites. OPEN COMMISSUROTOMY Open commissurotomies are performed with direct visualization of the valve. The patient is under general anesthesia, and a median sternotomy or left thoracic incision is made. Cardiopulmonary bypass is initiated, and an incision is made into the heart. A finger, scalpel, balloon, or dilator may be used to open the commissures. An added advantage of direct visualization of the valve is that thrombus may be identified and removed, calcifications can be seen, and if the valve has chordae or papillary muscles, they may be surgically repaired (chordoplasty is discussed later in this chapter).

8 770 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION Annuloplasty Annuloplasty is the repair of the valve annulus (ie, junction of the valve leaflets and the muscular heart wall). General anesthesia and cardiopulmonary bypass are required for all annuloplasties. The procedure narrows the diameter of the valve s orifice and is useful for the treatment of valvular regurgitation. There are two annuloplasty techniques. One technique uses an annuloplasty ring (Fig. 29-4). The leaflets of the valve are sutured to a ring, creating an annulus of the desired size. When the ring is in place, the tension created by the moving blood and contracting heart is borne by the ring rather than by the valve or a suture line, and progressive regurgitation is prevented by the repair. The other technique involves tacking the valve leaflets to the atrium with sutures or taking tucks to tighten the annulus. Because the valve s leaflets and the suture lines are subjected to the direct forces of the blood and heart muscle movement, the repair may degenerate more quickly than with the annuloplasty ring technique. Leaflet Repair Damage to cardiac valve leaflets may result from stretching, shortening, or tearing. Leaflet repair for elongated, ballooning, or other excess tissue leaflets is removal of the extra tissue. The elongated tissue may be folded over onto itself (ie, tucked) and sutured (ie, leaflet plication). A wedge of tissue may be cut from the middle of the leaflet and the gap sutured closed (ie., leaflet resection) (Fig. 29-5). Short leaflets are most often repaired by chordoplasty. After the short chordae are released, the leaflets often unfurl and can resume their normal function of closing the valve during systole. A piece of pericardium may also be sutured to extend the leaflet. A pericardial patch may be used to repair holes in the leaflets. Chordoplasty Chordoplasty is the repair of the chordae tendineae. The mitral valve is involved with chordoplasty (because it has the chordae tendineae); seldom is chordoplasty required for the tricuspid valve. Regurgitation may be caused by stretched, torn, or shortened chordae tendineae. Stretched chordae tendineae can be shortened, torn ones can be reattached to the leaflet, and shortened ones can be elongated. Regurgitation may also be caused by stretched papillary muscles, which can be shortened. VALVE REPLACEMENT Prosthetic valve replacement began in the 1960s. When valvuloplasty or valve repair is not a viable alternative, such as when the annulus or leaflets of the valve are immobilized by calcifications, valve replacement is performed. General anesthesia and cardiopulmonary bypass are used for all valve replacements. Most procedures are performed through a median sternotomy (ie, incision through the sternum), although the mitral valve may be approached through a right thoracotomy incision. After the valve is visualized, the leaflets and other valve structures, such as the chordae and papillary muscles, are removed. Some surgeons leave the posterior mitral valve leaflet, its chordae, and papillary muscles in place to help maintain the shape and function of the left ventricle after mitral valve replacement. Sutures are placed around the annulus and then into the valve prosthesis. The replacement valve is slid down the suture into position and tied into place (Fig. 29-6). The incision is closed, and the surgeon evaluates the function of the heart and the quality of the prosthetic repair. The patient is weaned from cardiopulmonary bypass, and surgery is completed. Before surgery, the heart gradually adjusted to the pathology, but the surgery abruptly corrects the way blood flows through the heart. Complications unique to valve replacement are related to the sudden changes in intracardiac blood pressures. All prosthetic valve replacements create a degree of stenosis when they are implanted in the heart. Usually, the stenosis is mild and does not effect heart function. If valve replacement was for a stenotic valve, blood flow through the heart is often improved. The signs and symptoms of the backward heart failure resolve in a few hours or days. If valve replacement was for a regurgitant valve, it may take months for the chamber into which blood had been regurgitat- A B C FIGURE 29-4 Annuloplasty ring insertion. (A) Mitral valve regurgitation; leaflets do not close. (B) Insertion of an annuloplasty ring. (C) Completed valvuloplasty; leaflets close.

9 Chapter 29 Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders 771 A B C FIGURE 29-5 Valve leaflet resection and repair with a ring annuloplasty. (A) Mitral valve regurgitation; the section indicated by dashed lines is excised. (B) Approximation of edges and suturing. (C) Completed valvuloplasty, leaflet repair, and annuloplasty ring. ing to achieve its optimal postoperative function. The signs and symptoms of heart failure resolve gradually as the heart function improves. The patient is at risk for many postoperative complications, such as bleeding, thromboembolism, infection, congestive heart failure, hypertension, dysrhythmias, hemolysis, and mechanical obstruction of the valve. Types of Valve Prostheses Two types of valve prostheses may be used: mechanical and tissue (ie, biologic) valves. Figure 29-7 shows mechanical and tissue valves. MECHANICAL VALVES The mechanical valves are of the ball-and-cage or disk design. Mechanical valves are thought to be more durable than tissue prosthetic valves and often are used for younger patients. Mechanical valves are used if the patient has renal failure, hypercalcemia, endocarditis, or sepsis and requires valve replacement. The mechanical valves do not deteriorate or become infected as easily as the tissue valves used for patients with these conditions. Thromboemboli are significant complications associated with mechanical valves, and long-term anticoagulation with warfarin is required. TISSUE OR BIOLOGIC VALVES Tissue (ie, biologic) valves are of three types: xenografts, homografts, and autografts. Tissue valves are less likely to generate thromboemboli, and long-term anticoagulation is not required. Tissue valves are not as durable as mechanical valves and require replacement more frequently. Prosthetic tissue valve A Sutures ready to be placed through valve's ring Sutures already placed through valve's ring Valve orifice B Sutures placed around annulus to anchor prosthetic valve FIGURE 29-6 Valve replacement. (A) The native valve is excised and the prosthetic valve is sutured in place. (B) Once all sutures are placed through the ring, the surgeon slides the prosthetic valve down the sutures and into the natural orifice. The sutures are then tied off and trimmed. Prosthetic valve in place at the completion of the procedure

10 772 Unit 6 CARDIOVASCULAR, CIRCULATORY, AND HEMATOLOGIC FUNCTION A C FIGURE 29-7 Common mechanical and tissue valve replacements. (A) Caged ball valve (Starr-Edwards, mechanical). (B) Tilting-disk valve (Medtronic-Hall, mechanical). (C) Porcine heterograft valve (Carpenter- Edwards, tissue). Xenografts. Xenografts are tissue valves (eg, bioprostheses, heterografts); most are from pigs (porcine), but valves from cows (bovine) may also be used. Their viability is 7 to 10 years. They do not generate thrombi, thereby eliminating the need for longterm anticoagulation. They are used for women of childbearing age because the potential complications of long-term anticoagulation associated with menses, placental transfer to a fetus, and delivery of a child do not exist. Xenografts also are used for patients older than 70 years of age, patients with a history of peptic ulcer disease, and others who cannot tolerate long-term anticoagulation. Xenografts are used for all tricuspid valve replacements. Homografts. Homografts, or allografts (ie, human valves), are obtained from cadaver tissue donations. The aortic valve and a portion of the aorta or the pulmonic valve and a portion of the pulmonary artery are harvested and stored cryogenically. Homografts are not always available and are very expensive. Homografts last for about 10 to 15 years, somewhat longer than xenografts. Homografts are not thrombogenic and are resistant to subacute bacterial endocarditis. They are used for aortic and pulmonic valve replacement. Autografts. Autografts (ie, autologous valves) are obtained by excising the patient s own pulmonic valve and a portion of the pulmonary artery for use as the aortic valve. Anticoagulation is unnecessary because the valve is the patient s own tissue and is not thrombogenic. The autograft is an alternative for children (it may grow as the child grows), women of childbearing age, young adults, patients with a history of peptic ulcer disease, and those who cannot tolerate anticoagulation. Aortic valve autografts have remained viable for more than 20 years. Most aortic valve autograft procedures are double valvereplacement procedures, because a homograft also is performed for pulmonic valve replacement. If pulmonary vascular pressures are normal, some surgeons elect not to replace the pulmonic valve. The patient can recover without a valve between the right ventricle and the pulmonary artery. B VALVULOPLASTY AND REPLACEMENT: NURSING MANAGEMENT Patients who have had valvuloplasty or valve replacements are admitted to the intensive care unit; care focuses on recovery from anesthesia and hemodynamic stability. Vital signs are assessed every 5 to 15 minutes and as needed until the patient recovers from anesthesia or sedation and then assessed every 2 to 4 hours and as needed. Intravenous medications to increase or decrease blood pressure and to treat dysrhythmias or altered heart rates are administered and their effects monitored. The intravenous medications are gradually decreased until they are no longer required or the patient takes needed medication by another route (eg, oral, topical). Patient assessments are conducted every 1 to 4 hours and as needed, with particular attention to neurologic, respiratory, and cardiovascular systems. (See Plan of Nursing Care 28-2: Care of the Patient After Cardiac Surgery, in Chap. 28). After the patient has recovered from anesthesia and sedation, is hemodynamically stable without intravenous medications, and assessment values are stable, the patient is usually transferred to a telemetry unit, typically within 24 to 72 hours after surgery. Nursing care continues as for most postoperative patients, including wound care and patient teaching regarding diet, activity, medications, and self-care. The nurse educates the patient about long-term anticoagulant therapy, explaining the need for frequent follow-up appointments and blood laboratory studies, and provides teaching about any prescribed medication: the name of the medication, dosage, its actions, prescribed schedule, potential side effects, and any drug-drug or drug-food interactions. Patients with a mechanical valve prosthesis require education to prevent bacterial endocarditis with antibiotic prophylaxis, which is prescribed before all dental and surgical interventions. Patients are discharged from the hospital in 3 to 7 days. Home care and office or clinic nurses reinforce all new information and self-care instructions with the patient and family for 4 to 8 weeks after the procedure. Septal Repair The atrial or ventricular septum may have an abnormal opening between the right and left sides of the heart (ie, septal defect). Although most septal defects are congenital and are repaired during infancy or childhood, adults may not have undergone early repair or may develop septal defects as a result of myocardial infarctions or diagnostic and treatment procedures. Repair of septal defects requires general anesthesia and cardiopulmonary bypass. The heart is opened, and a pericardial or synthetic (usually polyester or Dacron) patch is used to close the opening. Atrial septal defect repairs have low morbidity and mortality rates. When the mitral or tricuspid valve is involved, however, the procedure is more complicated because valve repair or replacement may be required and the heart failure may be more severe. Generally, ventricular septal repairs are uncomplicated, but the proximity of the defect to the intraventricular conduction system and the valves may make this repair more complex. (See Chapter 28, Plan of Nursing Care: Care of the Patient After Cardiac Surgery.) Cardiomyopathies Cardiomyopathy is a heart muscle disease associated with cardiac dysfunction. It is classified according to the structural and functional abnormalities of the heart muscle: dilated cardiomyopathy

11 Chapter 29 Management of Patients With Structural, Infectious, and Inflammatory Cardiac Disorders 773 (DCM), hypertrophic cardiomyopathy (HCM), restrictive or constrictive cardiomyopathy, arrhythmogenic right ventricular cardiomyopathy (ARVC), and unclassified cardiomyopathy (Richardson et al., 1996). Ischemic cardiomyopathy is a term frequently used to describe an enlarged heart caused by coronary artery disease, which is usually accompanied by heart failure (see Chap. 30). Regardless of the category and the cause, cardiomyopathy may lead to severe heart failure, lethal dysrhythmias, and death. Cardiomyopathy causes more than 27,000 deaths each year in the United States (American Heart Association, 2001). The mortality rate is highest for African Americans and the elderly (American Heart Association, 2001). Pathophysiology The pathophysiology of all cardiomyopathies is a series of progressive events that culminate in impaired cardiac output. Decreased stroke volume stimulates the sympathetic nervous system and the renin-angiotensin-aldosterone response, resulting in increased systemic vascular resistance and increased sodium and fluid retention, which places an increased workload on the heart. These alterations can lead to heart failure (see Chap. 30). DILATED CARDIOMYOPATHY DCM is the most common form of cardiomyopathy, with an incidence of 5 to 8 cases per 100,000 people per year and increasing (Braunwald et al., 2001). DCM occurs more often in men and African Americans, who also experience higher mortality rates (Braunwald et al., 2001). DCM is distinguished by significant dilation of the ventricles (Fig. 29-8) without significant concomitant hypertrophy (ie, increased muscle wall thickness) and systolic dysfunction. DCM was formerly named congestive cardiomyopathy, but DCM may exist without signs and symptoms of congestion. Microscopic examination of the muscle tissue shows diminished contractile elements of the muscle fibers and diffuse necrosis of myocardial cells. The result is poor systolic function. These structural changes decrease the amount of blood ejected from the ventricle with systole, increasing the amount of blood remaining in the ventricle after contraction. Less blood is then able to enter the ventricle during diastole, increasing end-diastolic pressure and eventually increasing pulmonary pressures. Altered valve function can result from the enlarged stretched ventricle, usually resulting in regurgitation. Embolic events caused by ventricular and atrial thrombi as a result of the poor blood flow through the ventricle may also occur. More than 75 conditions and diseases may cause DCM, including pregnancy, heavy alcohol intake, and viral infection (eg, influenza). When the causative factor cannot be identified, the term used is idiopathic DCM. Idiopathic DCM accounts for approximately 25% of all heart failure cases (Braunwald et al., 2001). Early diagnosis and treatment can prevent or delay significant symptoms and sudden death from DCM. Echocardiography and ECG are used to diagnose DCM and should be conducted for all first-degree relatives (eg, parents, siblings, children) of patients with DCM (Braunwald et al., 2001). HYPERTROPHIC CARDIOMYOPATHY In HCM, the heart muscle increases in size and mass, especially along the septum (see Fig. 29-8). The increased thickness of the heart muscle reduces the size of the ventricular cavities and causes the ventricles to take a longer time to relax, making it more difficult for the ventricles to fill with blood during the first part of diastole and making them more dependent on atrial contraction for FIGURE 29-8 Cardiomyopathies that lead to congestive heart failure. A O, aorta; LA, left atrium; LV, left ventricle. With permission from Braunwald, E., et al. (Eds.) (2001). Heart disease: A textbook of cardiovascular medicine (6th ed.). Philadelphia: W. B. Saunders. filling. The increased septal size may misalign the papillary muscles so that the septum and mitral valve obstruct the flow of blood from the left ventricle into the aorta during ventricular contraction. Hence, HCM may be obstructive or nonobstructive. Because of the structural changes, HCM had also been called idiopathic hypertrophic subaortic stenosis (IHSS) or asymmetric septal hypertrophy (ASH). Structural changes may also result in a smaller than normal ventricular cavity and a higher velocity flow of blood out of the left ventricle into the aorta, which may be detected by echocardiography (Braunwald et al., 2001). HCM may cause significant diastolic dysfunction, but systolic function can be normal or high, resulting in a higher than normal ejection fraction. Because HCM is a genetic disease, family members are observed closely for signs and symptoms indicating development of the disease (Fuster et al., 2001). HCM is rare, occurring in men, women, and children (often detected after puberty) (Oakley, 1997) with an estimated prevalence rate of 0.05% to 0.2% (Berul & Zevitz, 2002). It may also be idiopathic (ie, no cause can be found). RESTRICTIVE CARDIOMYOPATHY Restrictive cardiomyopathy (RCM) is characterized by diastolic dysfunction caused by rigid ventricular walls that impair ventricular stretch and diastolic filling (see Fig. 29-8). Systolic function is usually normal. Because RCM is the least common cardiomyopathy, representing approximately 5% of pediatric cardiomyopathies, its pathogenesis is the least understood (Shaddy, 2001). Restrictive cardiomyopathy can be associated with amyloidosis (in which amyloid, a protein substance, is deposited within the