Nursing Care Management 112 Midterm Module PDF

COLEGIO DE SAN ANTONIO DE PADUA Supervised by the Lasallian School Supervision Office Ramon M. Durano Foundation Compound Guinsay, Danao City Tel. No. (032)344-4709 **Nursing Care Management 112:** **Care of Clients with Problems in Oxygenation, Fluid and Electrolyte, Infe...

COLEGIO DE SAN ANTONIO DE PADUA Supervised by the Lasallian School Supervision Office Ramon M. Durano Foundation Compound Guinsay, Danao City Tel. No. (032)344-4709 **Nursing Care Management 112:** **Care of Clients with Problems in Oxygenation, Fluid and Electrolyte, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations, Acute and Chronic** This course deals with the principles and techniques of nursing care management of sick clients across lifespan with emphasis on the adult person and population group in any setting with alterations/problems in oxygenation, fluid and electrolyte balance, infectious, inflammatory and immunologic, and cellular aberration function. ***Learning Outcomes: After reading this chapter, the student should be able to:*** 1. **Describe the pathophysiology, clinical manifestations, and treatment of coronary atherosclerosis.** 2. **Describe the pathophysiology, clinical manifestations, and treatment of angina pectoris.** 3. **Define valvular disorders of the heart and describe the pathophysiology, clinical manifestations, and management of patients with mitral and aortic disorders.** 4. **Describe the pathophysiology, clinical manifestations, and management of patients with cardiomyopathies.** 5. **Describe the pathophysiology, clinical manifestations, and management of patients with infections of the heart.** 6. Use the nursing process as a framework for care of patients with HF. 7. Describe the management of patients with pulmonary edema. 8. **Identify risk factors for hypertension.** 9. **Explain the differences between normal blood pressure and hypertension and discuss the significance of hypertension.** Prepared by: **NURSE FAITH I. MANINGO** **CHAPTER 1** **MANAGEMENT OF PATIENTS WITH CORONARY VASCULAR DISORDERS** Cardiovascular disease is the leading cause of death for men and women of all racial and ethnic groups (American Heart Association \[AHA\], 2007). Research related to the identification and treatment of cardiovascular disease includes all segments of the population affected by cardiac conditions, including women, children, and people of diverse racial and ethnic backgrounds. This research aims to identify specific prevention and treatment strategies in these populations. ***1.1 Coronary Artery Disease*** Coronary artery disease (CAD) is the most prevalent type of cardiovascular disease in adults. For this reason, it is important for nurses to become familiar with various manifestations of coronary artery conditions and methods for assessing, preventing, and treating these disorders. *1.1.1 Coronary Atherosclerosis* The most common cause of cardiovascular disease is atherosclerosis, an abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls. These substances block and narrow the coronary vessels in a way that reduces blood flow to the myocardium. Atherosclerosis involves a repetitious inflammatory response to injury of the artery wall and subsequent alteration in the structural and biochemical properties of the arterial walls. *Pathophysiology* Atherosclerosis is thought to begin as fatty streaks of lipids that are deposited in the intima of the arterial wall. These lesions commonly begin early in life, perhaps even in childhood. Not all fatty streaks later develop into advanced lesions. Genetics and environmental factors are involved in the progression of these lesions. The development of atherosclerosis over many years involves an inflammatory response, which begins with injury to the vascular endothelium. The injury may be initiated by smoking, hypertension, and other factors. The presence of inflammation has multiple effects on the arterial wall, including the attraction of inflammatory cells, such as monocytes (macrophages). The macrophages ingest lipids, becoming "foam cells" that transport the lipids into the arterial wall. Activated macrophages also release biochemical substances that can further damage the endothelium, attracting platelets and initiating clotting. Smooth muscle cells within the vessel wall subsequently proliferate and form a fibrous cap over a core filled with lipid and inflammatory infiltrate. These deposits, called atheromas or plaques, protrude into the lumen of the vessel, narrowing it and obstructing blood flow (Fig. 28-1). Plaque may be stable or unstable, depending on the degree of inflammation and thickness of the fibrous cap. If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can resist the stress of blood flow and vessel movement. If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable plaque. At this point, the lipid core may grow, causing it to rupture and hemorrhage into the plaque. A ruptured plaque is a focus for thrombus formation. The thrombus may then obstruct blood flow, leading to acute coronary syndrome (ACS), which may result in an acute myocardial infarction (MI) if quick, decisive action is not taken. When an MI occurs, a portion of the heart muscle becomes necrotic. The anatomic structure of the coronary arteries makes them particularly susceptible to the mechanisms of atherosclerosis. As Figure 28-2 shows, the three major coronary arteries have multiple branches. Atherosclerotic lesions most often form where the vessels branch, suggesting a hemodynamic component that favors their formation. Although heart disease is most often caused by atherosclerosis of the coronary arteries, other phenomena may also decrease blood flow to the heart. Examples include vasospasm (sudden constriction or narrowing) of a coronary artery, myocardial trauma from internal or external forces, structural disease, congenital anomalies, decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure), and increased oxygen demand (eg, from rapid heart rate, thyrotoxicosis, or use of cocaine). *Clinical Manifestations* CAD produces symptoms and complications according to the location and degree of narrowing of the arterial lumen, thrombus formation, and obstruction of blood flow to the myocardium. This impediment to blood flow is usually progressive, causing an inadequate blood supply that deprives the cardiac muscle cells of oxygen needed for their survival. The condition is known as ischemia. Angina pectoris refers to chest pain that is brought about by myocardial ischemia. Angina pectoris usually is caused by significant coronary atherosclerosis. If the decrease in blood supply is great enough, of long enough duration, or both, irreversible damage and death of myocardial cells may result. Over time, irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardial dysfunction. Significant myocardial damage may result in persistently low cardiac output and heart failure where the heart cannot support the body's needs for blood. A decrease in blood supply from CAD may even cause the heart to abruptly stop beating (sudden cardiac death). *Risk Factors* Epidemiologic studies point to several factors that increase the probability that a person will develop heart disease. Major risk factors are listed in Chart 28-1. Some people do not have classic risk factors. Elevated low-density lipoprotein (LDL) cholesterol, also known as bad cholesterol, is the primary target of cholesterol-lowering therapy. People at highest risk for having a cardiac event within 10 years are those with known CAD or those with diabetes, peripheral arterial disease, abdominal aortic aneurysm, or carotid artery disease. The latter diseases are called CAD risk equivalents, because patients with these diseases have the same risk for a cardiac event as patients with CAD. The likelihood of having a cardiac event within 10 years is also affected by factors such as age, systolic blood pressure, smoking history, level of total cholesterol, level of LDL, and level of high-density lipoprotein (HDL), also known as good cholesterol. In addition, a cluster of metabolic abnormalities known as metabolic syndrome has emerged as a major risk factor for cardiovascular disease. A diagnosis of this syndrome includes three of the following conditions: Insulin resistance (fasting plasma glucose more than 100 mg/dL or abnormal glucose tolerance test) Central obesity (waist circumference more than 35 inches in women, more than 40 inches in men) Dyslipidemia (triglycerides more than 150 mg/dL, HDL less than 50 mg/dL in women, less than 40 mg/dL in men) Blood pressure persistently greater than 130/85 mm Hg Proinflammatory state (high levels of C-reactive protein) Prothrombotic state (high fibrinogen level) Many people with type 2 diabetes mellitus fit this clinical picture. It is theorized that in obese patients, excessive adipose tissue may secrete mediators that lead to metabolic changes. Adipokines (adipose tissue cytokines), free fatty acids, and other substances are known to modify insulin action and contribute to atherogenic changes in the cardiovascular system (Fig. 28-3). C-reactive protein (CRP) is known to be an inflammatory marker for cardiovascular risk, including acute coronary events and stroke. The liver produces CRP in response to a stimulus such as tissue injury, and high levels of this protein may occur in people with diabetes and those who are likely to have an acute coronary event. To determine overall cardiovascular risk, clinicians view high sensitivity (hs-CRP) test results together with other screening tools such as measurements of lipid levels. *Prevention* Four modifiable risk factors---cholesterol abnormalities, tobacco use, hypertension, and diabetes mellitus---have been cited as major risk factors for complications. As a result, they receive much attention in health promotion programs. *Controlling Cholesterol Abnormalities* Four elements of fat metabolism---total cholesterol, LDL, HDL, and triglycerides---are known to affect the development of heart disease. Cholesterol is processed by the gastrointestinal tract into lipoprotein globules called chylomicrons. These are reprocessed by the liver as lipoproteins (Fig. 28-4). This is a physiologic process necessary for the formation of lipoprotein-based cell membranes and other important metabolic processes. When an excess of LDL is produced, LDL particles adhere to vulnerable points in the arterial endothelium. Here macrophages ingest them, contributing to plaque formation. A fasting lipid profile should demonstrate the following values: LDL cholesterol less than 100 mg/dL (less than 70 mg/dL for very high-risk patients) Total cholesterol less than 200 mg/dL HDL cholesterol greater than 60 mg/dL Triglyceride less than 150 mg/dL *Dietary Measures* Table 28-1 provides recommendations of the Therapeutic Lifestyle Changes (TLC) diet (Lichtenstein, Appel, Brands, et al., 2006). These general recommendations may need to be adjusted for the individual patient who has other nutritional needs, such as the patient who has diabetes. To assist in following the appropriate TLC diet, the patient should be referred to a registered dietitian. Other TLC recommendations include weight loss, cessation of tobacco use, and increased physical activity. *Physical Activity* Management of an elevated triglyceride level focuses on weight reduction and increased physical activity. Regular, moderate physical activity increases HDL levels and reduces triglyceride levels, decreasing the incidence of coronary events and reducing overall mortality risk. The goal for most people is a total of 30 minutes of moderate exercise (such as brisk walking) on most days. The nurse helps patients set realistic goals for physical activity. For example, inactive patients can start with activity that lasts 3 minutes, such as parking farther from a building to increase daily walking time. For sustained activity, patients should begin with a 5-minute warm-up period to stretch and prepare the body for exercise. They should end the exercise with a 5-minute cool-down period in which they gradually reduce the intensity of the activity to prevent a sudden decrease in cardiac output. Patients should be instructed to engage in an activity or variety of activities that interest them to maintain motivation. They should also be taught to exercise to an intensity that does not preclude their ability to talk; if they cannot have a conversation while exercising, they should slow down or switch to a less intensive activity. When the weather is hot and humid, patients should exercise during the early morning, or indoors, and wear loose-fitting clothing. When the weather is cold, they should layer clothing and wear a hat. The nurse can also suggest walking in large stores or shopping malls in inclement weather. Patients should stop any activity if chest pain, unusual shortness of breath, dizziness, lightheadedness, or nausea occurs. *Medications* If diet alone cannot normalize serum cholesterol levels, medications can have a synergistic effect with the prescribed diet and control cholesterol levels. Lipid-lowering medications can reduce CAD mortality in patients with elevated lipid levels and in at-risk patients with normal lipid levels. The lipid-lowering agents affect the lipid components somewhat differently and can be grouped into six types: 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) (or statins), nicotinic acids, fibric acids (or fibrates), bile acid sequestrants (or resins), cholesterol absorption inhibitor, and omega-3 acid-ethyl esters. *1.1.2 Angina Pectoris* Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical exertion or emotional stress. In other words, the need for oxygen exceeds the supply. In general, the severity of the symptoms of angina is based on the magnitude of the precipitating activity and its effect on activities of daily living. *Pathophysiology* Angina is usually caused by atherosclerotic disease. Almost invariably, angina is associated with a significant obstruction of at least one major coronary artery. Normally, the myocardium extracts a large amount of oxygen from the coronary circulation to meet its continuous demands. When there is an increase in demand, flow through the coronary arteries needs to be increased. When there is blockage in a coronary artery, flow cannot be increased, and ischemia results. The types of angina are listed in Chart 28-2. Several factors are associated with typical anginal pain: Physical exertion, which can precipitate an attack by increasing myocardial oxygen demand Exposure to cold, which can cause vasoconstriction and elevated blood pressure, with increased oxygen demand Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle; in a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain Stress or any emotion-provoking situation, causing the release of catecholamines, which increases blood pressure, heart rate, and myocardial workload Unstable angina is not associated with these listed factors. It may occur at rest. *Clinical Manifestations* Ischemia of the heart muscle may produce pain or other symptoms, varying in severity from mild indigestion to a choking or heavy sensation in the upper chest that ranges from discomfort to agonizing pain accompanied by severe apprehension and a feeling of impending death. The pain is often felt deep in the chest behind the sternum (retrosternal area). Typically, the pain or discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the left arm. The patient often feels tightness or a heavy choking or strangling sensation that has a viselike, insistent quality. The patient with diabetes mellitus may not have severe pain with angina because diabetic neuropathy can blunt nociceptor transmission, dulling the perception of pain. Women may have different symptoms than men, possibly because coronary disease in women tends to be more diffuse and affects long segments of the artery rather than discrete segments. A feeling of weakness or numbness in the arms, wrists, and hands, as well as shortness of breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting may accompany the pain. Anxiety may occur with angina. An important characteristic of angina is that it subsides with rest or administering nitroglycerin. In many patients, anginal symptoms follow a stable, predictable pattern. Unstable angina is characterized by attacks that increase in frequency and severity and are not relieved by rest and administering nitroglycerin. Patients with unstable angina require medical intervention. *1.1.3 Acute Coronary Syndrome and Myocardial Infarction* (MI) ACS is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death if definitive interventions do not occur promptly. (Although the terms coronary occlusion, heart attack, and MI are used synonymously, the preferred term is MI.) The spectrum of ACS includes unstable angina, non--ST-segment elevation MI (NSTEMI), and ST-segment elevation MI (STEMI). *Pathophysiology* In unstable angina, there is reduced blood flow in a coronary artery, often due to rupture of an atherosclerotic plaque, but the artery is not completely occluded. This is an acute situation that is sometimes referred to as preinfarction angina because the patient will likely have an MI if prompt interventions do not occur. In an MI, an area of the myocardium is permanently destroyed, typically because plaque rupture and subsequent thrombus formation result in complete occlusion of the artery. Vasospasm (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (eg, from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (eg, from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine) are other causes of MI. In each case, a profound imbalance exists between myocardial oxygen supply and demand. The area of infarction develops over minutes to hours. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and the lack of oxygen results in infarction, or the death of cells. The expression "time is muscle" reflects the urgency of appropriate treatment to improve patient outcomes. Various descriptions are used to further identify an MI: the type (NSTEMI, STEMI), the location of the injury to the ventricular wall (anterior, inferior, posterior, or lateral wall), and the point in time within the process of infarction (acute, evolving, or old). *Clinical Manifestations* Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients with ACS. Some of these patients have prodromal symptoms or a previous diagnosis of CAD, but about half report no previous symptoms (AHA, 2007). Patients may present with a combination of symptoms, including chest pain, shortness of breath, indigestion, nausea, and anxiety. They may have cool, pale, and moist skin. Their heart rate and respiratory rate may be faster than normal. These signs and symptoms, which are caused by stimulation of the sympathetic nervous system, may be present for only a short time or may persist. In many cases, the signs and symptoms of MI cannot be distinguished from those of unstable angina; hence, the evolution of the term ACS. *Assessment and Diagnostic Findings* The diagnosis of ACS is generally based on the presenting symptoms (Chart 28-6); the 12-lead ECG and laboratory tests (eg, serial cardiac biomarkers) are performed to clarify whether the patient has unstable angina, NSTEMI, or STEMI. The prognosis depends on the severity of coronary artery obstruction and the presence and extent of myocardial damage. Physical examination is always conducted, but the examination alone does not confirm the diagnosis. *Patient History* The patient history includes the description of the presenting symptom (eg, pain), the history of previous cardiac and other illnesses, and the family history of heart disease. The history should also include information about the patient's risk factors for heart disease. *Electrocardiogram* The 12-lead ECG provides information that assists in ruling out or diagnosing an acute MI. It should be obtained within 10 minutes from the time a patient reports pain or arrives in the emergency department. By monitoring serial ECG changes over time, the location, evolution, and resolution of an MI can be identified and monitored. The ECG changes that occur with an MI are seen in the leads that view the involved surface of the heart. The classic ECG changes are T-wave inversion, ST-segment elevation, and development of an abnormal Q wave (Fig. 28-5). Because infarction evolves over time, the ECG also changes over time. The first ECG signs of an acute MI occur as a result of myocardial ischemia and injury. Myocardial injury causes the T wave to become enlarged and symmetric. As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert. The ischemic region may remain depolarized while adjacent areas of the myocardium return to the resting state. Myocardial injury also causes ST-segment changes. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line (the area between the T wave and the next P wave is used as the reference for the isoelectric line) when measured 0.06 to 0.08 seconds after the end of the QRS, a point called the J point (Fig. 28-6). This elevation in the ST segment in two contiguous leads is a key diagnostic indicator for MI (ie, STEMI). The appearance of abnormal Q waves is another indication of MI. Q waves develop within 1 to 3 days because there is no depolarization current conducted from necrotic tissue. The lead system then views the flow of current from other parts of the heart. A new and significant Q wave is 0.04 seconds or longer and 25% of the R-wave depth (provided the R wave exceeds a depth of 5 mm). An acute MI may also cause a significant decrease in the height of the R wave. During an acute MI, injury and ischemic changes are usually present. An abnormal Q wave may be present without STsegment and T-wave changes, which indicates an old, not acute, MI. For some patients, there are no persistent ECG changes, and the MI is diagnosed by blood levels of cardiac biomarkers. Using the above information, patients are diagnosed with one of the following forms of ACS: Unstable angina: The patient has clinical manifestations of coronary ischemia, but ECG and cardiac biomarkers show no evidence of acute MI. STEMI: The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12-lead ECG. In this type of MI, there is significant damage to the myocardium. NSTEMI: The patient has elevated cardiac biomarkers but no definite ECG evidence of acute MI. *Echocardiogram* The echocardiogram is used to evaluate ventricular function. It may be used to assist in diagnosing an MI, especially when the ECG is nondiagnostic. The echocardiogram can detect hypokinetic and akinetic wall motion and can determine the ejection fraction. *Laboratory Tests* Cardiac enzymes and biomarkers are used to diagnose an acute MI. Cardiac biomarkers, which include myoglobin and troponin, can be analyzed rapidly, expediting an accurate diagnosis. These tests are based on the release of cellular contents into the circulation when myocardial cells die. Figure 28-7 shows the time courses of cardiac enzymes and biomarkers. *Creatine Kinase and Its Isoenzymes* There are three creatine kinase (CK) isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue). CK-MB is the cardiac-specific isoenzyme; it is found mainly in cardiac cells and therefore increases only when there has been damage to these cells. Elevated CKMB assessed by mass assay is an indicator of acute MI; the level begins to increase within a few hours and peaks within 24 hours of an MI. If the area is reperfused (eg, due to thrombolytic therapy or PCI), it peaks earlier. *Myoglobin* is a heme protein that helps transport oxygen. Like CK-MB enzyme, myoglobin is found in cardiac and skeletal muscle. The myoglobin level starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms. An increase in myoglobin is not very specific in indicating an acute cardiac event; however, negative results are an excellent parameter for ruling out an acute MI. *Troponin*, a protein found in the myocardium, regulates the myocardial contractile process. There are three isomers of troponin: C, I, and T. Troponins I and T are specific for cardiac muscle, and these biomarkers are currently recognized as reliable and critical markers of myocardial injury. An increase in the level of troponin in the serum can be detected within a few hours during acute MI. It remains elevated for a long period, often as long as 3 weeks, and it therefore can be used to detect recent myocardial damage. *Medical Management* The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications. These goals are facilitated by the use of guidelines developed by the American College of Cardiology (ACC) and the AHA (Chart 28-7). These goals may be achieved by reperfusing the area with the emergency use of thrombolytic medications or by PCI. Minimizing myocardial damage is also accomplished by reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest. The resolution of pain and ECG changes indicate that demand and supply are in equilibrium; they may also indicate reperfusion. Visualization of blood flow through an open vessel in the catheterization laboratory is evidence of reperfusion. ***1.2 Invasive Coronary Artery Procedures*** *1.2.1 Percutaneous Coronary Interventions* Invasive interventional procedures to treat CAD include PTCA, intracoronary stent implantation, atherectomy, and brachytherapy. All of these procedures are classified as PCIs. *Percutaneous Transluminal Coronary Angioplasty* In PTCA, a balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia. It is used in patients with angina and as an intervention for ACS. Catheterbased interventions can also be used to open blocked CABGs. The purpose of PTCA is to improve blood flow within a coronary artery by compressing and "cracking" the atheroma. The procedure is attempted when the interventional cardiologist believes that PTCA can improve blood flow to the myocardium. PTCA is carried out in the cardiac catheterization laboratory. Hollow catheters called sheaths are inserted, usually in the femoral artery (and sometimes femoral vein), providing a conduit for other catheters. Catheters are then threaded through the femoral artery, up through the aorta, and into the coronary arteries. Angiography is performed using injected radiopaque contrast agents (commonly called dye) to identify the location and extent of the blockage. A balloon-tipped dilation catheter is passed through the sheath and positioned over the lesion. The physician determines the catheter position by examining markers on the balloon that can be seen with fluoroscopy. When the catheter is properly positioned, the balloon is inflated with high pressure for several seconds and then deflated. The pressure compresses and often "cracks" the atheroma (Fig. 28-8). The media and adventitia of the coronary artery are also stretched. *Coronary Artery Stent* After PTCA, the area that has been treated may close off partially or completely, a process called restenosis. The intima of the coronary artery has been injured and responds by initiating an acute inflammatory process. This process may include release of mediators that leads to vasoconstriction, clotting, and scar tissue formation. A coronary artery stent may be placed to overcome these risks. A stent is a metal mesh that provides structural support to a vessel at risk of acute closure. The stent is positioned over the angioplasty balloon. When the balloon is inflated, the mesh expands and presses against the vessel wall, holding the artery open. The balloon is withdrawn, but the stent is left permanently in place within the artery (Fig. 28-8). *Atherectomy* is an invasive interventional procedure that involves the removal of the atheroma, or plaque, from a coronary artery by cutting, shaving, or grinding. It may be used in conjunction with PTCA. Directional coronary atherectomy and transluminal extraction catheter procedures involve the use of a catheter that removes the lesion and its fragments. *Brachytherapy* PTCA and stent implantation cause a cellular reaction in the coronary artery that promotes proliferation of the intima of the artery, increasing the possibility of arterial obstruction. Brachytherapy reduces the recurrence of obstruction, preventing vessel restenosis by inhibiting smooth muscle cell proliferation. Brachytherapy involves the delivery of gamma or beta radiation by placing a radioisotope close to the lesion. The radioisotope may be delivered by a catheter or implanted with the stent. However, drug-eluting stents are used more commonly to prevent restenosis, because they are typically more effective and less expensive than brachytherapy. *1.2.2 Surgical Procedures: Coronary Artery Revascularization* Advances in diagnostics, medical management, surgical and anesthesia techniques, as well as the care provided in critical care and surgical units, home care, and rehabilitation programs have continued to make surgery an effective treatment option for patients with CAD. CAD has been treated by myocardial revascularization since the 1960s, and the most common CABG techniques have been performed for more than 35 years. CABG is a surgical procedure in which a blood vessel is grafted to an occluded coronary artery so that blood can flow beyond the occlusion; it is also called a bypass graft. The major indications for CABG are: Alleviation of angina that cannot be controlled with medication or PCI Treatment of left main coronary artery stenosis or multivessel CAD Prevention and treatment of MI, dysrhythmias, or heart failure Treatment for complications from an unsuccessful PCI A vessel commonly used for CABG is the greater saphenous vein, followed by the lesser saphenous vein (Fig. 28-9). Cephalic and basilic veins are also used. The vein is removed from the leg (or arm) and grafted to the ascending aorta and to the coronary artery distal to the lesion. Traditionally, a skin incision was made over the length of vein segment, but new techniques allow small incisions on the affected extremity. A common adverse effect of vein removal is edema in the extremity from which the vein was taken. The degree of edema varies and usually diminishes over time. Within 5 to 10 years, atherosclerotic changes often develop in saphenous vein grafts. *Traditional Coronary Artery Bypass Graft* CABG procedures are performed with the patient under general anesthesia. In the traditional CABG procedure, the surgeon performs a median sternotomy and connects the patient to the cardiopulmonary bypass (CPB) machine. Next, a blood vessel from another part of the patient's body (eg, saphenous vein, left internal mammary artery) is grafted distal to the coronary artery lesion, bypassing the obstruction (Fig. 28-10). CPB is then discontinued, chest tubes and epicardial pacing wires are placed, and the incision is closed. The patient is then admitted to a critical care unit. *Cardiopulmonary Bypass* Many cardiac surgical procedures are possible because of CPB (ie, extracorporeal circulation). The procedure mechanically circulates and oxygenates blood for the body while bypassing the heart and lungs. CPB maintains perfusion to body organs and tissues and allows the surgeon to complete the anastomoses in a motionless, bloodless surgical field. CPB is accomplished by placing a cannula in the right atrium, vena cava, or femoral vein to withdraw blood from the body. The cannula is connected to tubing filled with an isotonic crystalloid solution. Venous blood removed from the body by the cannula is filtered, oxygenated, cooled or warmed by the machine, and then returned to the body. The cannula used to return the oxygenated blood is usually inserted in the ascending aorta, or it may be inserted in the femoral artery (Fig. 28-11). The heart is stopped by the injection of a potassium-rich cardioplegia solution into the coronary arteries. The patient receives heparin to prevent clotting and thrombus formation in the bypass circuit when blood comes in contact with the surfaces of the tubing. At the end of the procedure when the patient is disconnected from the bypass machine, protamine sulfate is administered to reverse the effects of heparin. *Alternative Coronary Artery Bypass Graft Techniques* A number of alternative CABG techniques have been developed that may have fewer complications for some groups of patients. Off-pump CABG (OPCAB) surgery has been used successfully in many patients since the 1990s. OPCAB involves a standard median sternotomy incision, but the surgery is performed without CPB. A beta-adrenergic blocker may be used to slow the heart rate. The surgeon also uses a myocardial stabilization device to hold the site still for the anastomosis of the bypass graft into the coronary artery while the heart continues to beat (Fig. 28-12). *Complications of Coronary Artery Bypass Graft* CABG may result in complications such as hemorrhage, dysrhythmias, and MI. The patient may require interventions for more than one complication at a time. Collaboration among nurses, physicians, pharmacists, respiratory therapists, and dietitians is necessary to achieve the desired patient outcomes. Although most patients improve symptomatically following surgery, CABG is not a cure for CAD, and angina, exercise intolerance, or other symptoms experienced before CABG may recur. Medications required before surgery may need to be continued. Lifestyle modifications recommended before surgery remain important to treat the underlying CAD and for the continued viability of the newly implanted grafts. *Nursing Management* Cardiac surgery patients have many of the same needs and require the same perioperative care as other surgical patients, plus some special needs. Preoperative teaching is important; patients and their families may be very anxious as the association of the heart with life and death intensifies their emotions. Before surgery, physical and psychological assessments establish a baseline for future reference. In addition, it is necessary to evaluate the patient's understanding of the surgical procedure, informed consent, and adherence to treatment protocols. Questions may be asked to obtain the following information: Knowledge and understanding of the surgical procedure, postoperative course, and recovery Meaning of the surgery to the patient and family Fears regarding the present and future Coping mechanisms that are being used Support systems in effect Specific information about the surgical procedure and important factors about postoperative management are communicated by the surgical team and anesthesia personnel to the critical care or PACU nurse, who then assumes responsibility for the patient's care. Figure 28-13 presents an overview of the many aspects of postoperative care of the cardiac surgical patient. *Assessing the Patient* When the patient is admitted to the critical care unit or PACU, and hourly for at least every 8 hours thereafter, nursing and medical personnel perform a complete assessment of all systems. It is necessary to assess the following parameters: Neurologic status: level of responsiveness, pupil size and reaction to light, reflexes, facial symmetry, movement of the extremities, and hand grip strength Cardiac status: heart rate and rhythm, heart sounds, pacemaker status, arterial blood pressure, central venous pressure (CVP), and in selected patients, hemodynamic parameters: pulmonary artery pressure, pulmonary artery wedge pressure (PAWP), cardiac output and index, systemic and pulmonary vascular resistance, mixed venous oxygen saturation (SvO2) Respiratory status: chest movement, breath sounds, ventilator settings (eg, rate, tidal volume, oxygen concentration, mode such as synchronized intermittent mandatory ventilation, positive end-expiratory pressure, pressure support), respiratory rate, peak inspiratory pressure, arterial oxygen saturation (SaO2), percutaneous oxygen saturation (SpO2), end-tidal CO2, pleural chest tube drainage, arterial blood gases Peripheral vascular status: peripheral pulses; color of skin, nail beds, mucosa, lips, and earlobes; skin temperature; edema; condition of dressings and invasive lines Renal function: urinary output; urine specific gravity and osmolality Fluid and electrolyte status: intake, output from all drainage tubes, all cardiac output parameters, and indications of electrolyte imbalance Pain: nature, type, location, and duration; apprehension; response to analgesics Assessment also includes checking all equipment and tubes to ensure that they are functioning properly: endotracheal tube, ventilator, end-tidal CO2 monitor, SpO2 monitor, pulmonary artery catheter, SvO2 monitor, arterial and IV lines, IV infusion devices and tubing, cardiac monitor, pacemaker, chest tubes, and urinary drainage system. As the patient regains consciousness and progresses through the postoperative period, the nurse also assesses indicators of psychological and emotional status. The patient may exhibit behavior that reflects denial or depression or may experience postcardiotomy delirium. Characteristic signs of delirium include transient perceptual illusions, visual and auditory hallucinations, disorientation, and paranoid delusions. It is also necessary to assess the family's needs. The nurse ascertains how family members are coping with the situation; determines their psychological, emotional, and spiritual needs; and finds out whether they are receiving adequate information about the patient's condition. **MODULE 2: CHAPTER 1 LEARNING ACTIVITIES** **LEARNING ACTIVITY 1: ESSAY** Answer the following questions in a minimum of 3 sentences and a maximum of 5. Use extra sheets of bond paper. (5 POINTS PER ITEM) 1. A 72-year-old man is admitted to the surgical intensive care unit following four-vessel CABG surgery. Initially, his blood pressure is high at 164/88, but it drops to 92/60 mm Hg, his ECG shows sinus tachycardia, and his cardiac output is decreased. What are the most likely reasons for the drop in blood pressure? What other parameters should be assessed? Describe your interventions for this postoperative CABG patient with hypotension and low cardiac output. Identify your expected outcomes for these interventions. 2. You are caring for a patient who has been hospitalized with a diagnosis of unstable angina. His condition is stable and he will be discharged later in the day. He is anxious to go home, but agrees to an educational session with you prior to discharge. The patient is obese and has a history of hypertension and cigarette smoking. Knowing that multiple lifestyle changes are recommended, how will you prioritize your teaching strategies? What type of follow-up care is available to assist this patient following discharge? **LEARNING ACTIVITY 2: CASE STUDY.** Read, analyze, and encircle the letter of the correct answer or supply what is being asked in the case study. (1 point per item) CASE STUDY: Angina Pectoris Ermelina, a 64-year-old retired secretary, is admitted to the medical--surgical area for management of chest pain caused by angina pectoris. 1\. The nurse knows that the basic cause of angina pectoris is believed to be: a\. dysrhythmias triggered by stress. c. minute emboli discharged through the narrowed lumens of the coronary vessels. b\. insufficient coronary blood flow. d. spasms of the vessel walls owing to excessive secretion of epinephrine (adrenaline). 2\. The medical record lists a probable diagnosis of chronic stable angina. The nurse knows that Ermelina's pain: a\. has increased progressively in frequency and duration. c. is relieved by rest and is predictable. b\. is incapacitating. d. usually occurs at night and may be relieved by sitting upright. 3\. Ermelina has nitroglycerin at her bedside to take PRN. The nurse knows that nitroglycerin acts in all of the following ways except: a\. causing venous pooling throughout the body. c. dilating the coronary arteries to increase the oxygen supply. b\. constricting arterioles to lessen peripheral blood flow. d. lowering systemic blood pressure. 4\. Ermelina took a nitroglycerin tablet at 10:00 AM, after her morning care. It did not relieve her pain, so, 5 minutes later, she repeated the dose. Ten minutes later and still in pain, she calls the nurse, who should: c\. help her to a comfortable position, give her oxygen at 2 L/min, and call her physician. CASE STUDY: Decreased Myocardial Tissue Perfusion Mr. Lillis, a 46-year-old bricklayer, is brought to the emergency department by ambulance with a suspected diagnosis of myocardial infarction. He appears ashen, is diaphoretic and tachycardiac, and has severe chest pain. The nursing diagnosis is decreased cardiac output, related to decreased myocardial tissue perfusion. 1\. The nurse knows that the most critical time period for his diagnosis is: a\. the first hour after symptoms begin. c. within the first 48 hours after the attack. b\. within 24 hours after the onset of symptoms. d. between the third and fifth day after the attack. 2\. Because the area of infarction develops over minutes to hours, the nurse knows to interpret the following ECG results as indicative of initial myocardial injury: a\. abnormal Q waves. b. enlarged T wave. c. inverted T wave. d. ST segment depression. 3\. The nurse evaluates a series of laboratory tests within the first few hours. She knows that a positive indicator of cell damage is: a\. decreased level of troponin. c. lower level of myoglobin. b\. elevated creatine kinase (CK-MB). d. all of the above. 4\. On the basis of assessment data, the physician diagnoses an acute myocardial infarction. List the drug classification that the nurse knows should be given within 3 to 6 hours of diagnosis: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. List two common examples: \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ and \_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_. 5\. The nurse needs to look for symptoms associated with one of the major causes of sudden death during the first 48 hours, which is: a\. cardiogenic shock. b. pulmonary edema. c. pulmonary embolism. d. ventricular rupture. 6\. The nurse is aware that ischemic tissue remains sensitive to oxygen demands, because scar formation is not seen until the: a\. second week. b. third week. c. sixth week. d. eighth week. 7\. Mr. Lillis needs to be advised that myocardial healing will not be complete for about: a\. 2 months. b. 4 months. c. 6 months. d. 8 months. 8\. For discharge planning, Mr. Lillis is advised to: a\. avoid large meals. c. restrict caffeine-containing beverages. b\. exercise daily. d. do all of the above. 9\. The nurse can advise Mr. Lillis that sexual activities can be resumed after what activity tolerance has been achieved?\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ MULTIPLE CHOICE: Select the best answer for each question. Answers are provided at the end of this module. 1\. The most common heart disease for adults in the United States is: a\. angina pectoris. b. coronary artery disease. c. myocardial infarction. d. valvular heart disease. 2\. Lumen narrowing with atherosclerosis is caused by: a\. atheroma formation on the intima. b. scarred endothelium. c. thrombus formation. d. all of the above. 3\. A healthy level of serum cholesterol would be a reading of: a\. 160 to 190 mg/dL. b. 210 to 240 mg/dL. c. 250 to 275 mg/dL. d. 280 to 300 mg/dL. 4\. Which of the following findings is not a significant risk factor for heart disease? a\. Cholesterol, 280 mg/dL c. High-density lipoproteins (HDL), 80 mg/dL b\. LDL, 160 mg/dL d. A ratio of low-density lipoproteins (LDL) to HDL, 4.5 to 1.0 5\. Hypertension is repeated blood pressure measurements exceeding: a\. 110/80 mm Hg. b. 120/80 mm Hg. c. 130/90 mm Hg. d. 140/90 mm Hg. 6\. The incidence of coronary artery disease tends to be equal for men and women after the age of: a\. 45 years. b. 50 years. c. 55 years. d. 65 years. 7\. The pain of angina pectoris is produced primarily by: a\. coronary vasoconstriction. c. myocardial ischemia. b\. movement of thromboemboli. d. the presence of atheromas. 8\. The nurse advises a patient that sublingual nitroglycerin should alleviate angina pain within: a\. 3 to 4 minutes. b. 10 to 15 minutes. c. 30 minutes. d. 60 minutes. 9\. Patient education includes telling someone who takes nitroglycerin sublingually that he or she should take 1, then go quickly to the nearest emergency department if no relief has been obtained after taking \_\_\_\_\_\_ tablet(s) at 5-minute intervals. a\. 1 b. 2 c. 3 d. 4 to 5 10\. The scientific rationale supporting the administration of beta-adrenergic blockers is the drugs' ability to: a\. block sympathetic impulses to the heart. c. increase myocardial contractility. b\. elevate blood pressure. d. induce bradycardia. 11\. An antidote for propranolol hydrochloride (a beta-adrenergic blocker) that is used to treat bradycardia is: a\. digoxin. b. atropine. c. protamine sulfate. d. sodium nitroprusside. 12\. Calcium channel blockers act by: a\. decreasing SA node automaticity. c. increasing the heart rate. b\. increasing AV node conduction. d. creating a positive inotropic effect. 13\. In the United States, about 1 million people will have an acute myocardial infarction each year. Of these 1 million, what percentage will die? a\. 10% to 15% b. 25% c. 30% to 40% d. 60% 14\. The classic ECG changes that occur with an MI include all of the following except: a\. an absent P wave. b. an abnormal Q wave. c. T-wave inversion. d. ST-segment elevation. 15\. The most common site of myocardial infarction is the: a\. left atrium. b. left ventricle. c. right atrium. d. right ventricle. 16\. Which of the following statements about myocardial infarction pain is incorrect? a\. It is relieved by rest and inactivity. c. It is sudden in onset and prolonged in duration. b\. It is substernal in location. d. It is viselike and radiates to the shoulders and arms. 17\. Myocardial cell damage can be reflected by high levels of cardiac enzymes. The cardiac-specific isoenzyme is: a\. alkaline phosphatase. b. creatine kinase (CK-MB). c. myoglobin. d. troponin. 18\. The most common vasodilator used to treat myocardial pain is: a\. amyl nitrite. b. Inderal. c. nitroglycerine. d. Pavabid HCl. 19\. An intravenous analgesic frequently administered to relieve chest pain associated with myocardial infarction is: a\. meperidine hydrochloride. c. morphine sulfate. b\. hydromorphone hydrochloride. d. codeine sulfate. 20\. The need for surgical intervention in coronary artery disease (CAD) is determined by the: a\. amount of stenosis in the coronary arteries. c. occurrence of previous infarction related to the affected artery. b\. myocardial area served by the stenotic artery. d. all of the above. 21\. A candidate for percutaneous transluminal coronary angioplasty (PTCA) is a patient with coronary artery disease who: a\. has compromised left ventricular function. c. has at least 70% occlusion of a major coronary artery. b\. has had angina longer than 3 years. d. has questionable left ventricular function. 22\. A goal of dilation in PTCA is to increase blood flow through the artery's lumen and achieve a residual stenosis of less than: a\. 20%. b. 35%. c. 60%. d. 80%. 23\. The nurse expects a postoperative PTCA patient to be discharged: a\. the same day as surgery. b. within 24 hours of the procedure. c. 3 days later. d. after 1 week. 24\. The nurse needs to be alert to assess for clinical symptoms of possible postoperative complications of PTCA, which include: a\. abrupt closure of the artery. c. coronary artery vasospasm. b\. arterial dissection. d. all of the above. 25\. A candidate for coronary artery bypass grafting (CABG) must meet which of the following criteria? a\. A blockage that cannot be treated by PTCA c. Unstable angina. b\. Greater than 60% blockage in the left main coronary artery. d. All of the above. 26\. The most common nursing diagnosis for patients awaiting cardiac surgery is: a\. activity intolerance. c. decreased cardiac output. b\. fear related to the surgical procedure. d. anginal pain. 27\. Extremity paresthesia, dysrhythmias (peaked T waves), and mental confusion after cardiac surgery are signs of electrolyte imbalance related to the level of: a\. calcium. b. magnesium. c. potassium. d. sodium. 28\. A complication after cardiac surgery that is associated with an alteration in preload is: a\. cardiac tamponade. c. hypertension. b\. elevated central venous pressure. d. hypothermia. **CHAPTER 2** **MANAGEMENT OF PATIENTS WITH STRUCTURAL, INFECTIOUS, AND INFLAMMATORY CARDIAC DISORDERS** Structural, infectious, and inflammatory disorders of the heart present many challenges for the patient, family, and health care team. Problems with the heart valves, holes in the intracardiac septum, cardiomyopathies, and infectious diseases of the heart muscle alter cardiac output. Treatments for these disorders may be noninvasive, such as medication therapy and activity and dietary modification. Invasive treatments also may be used, such as valve repair or replacement, septal repair, ventricular assist devices, total artificial hearts, cardiac transplantation, and other procedures. Nurses have an integral role in the care of patients with structural, infectious, and inflammatory cardiac conditions. ***2.1 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 of the ventricles. 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, a condition 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 may require surgical repair or replacement of the valve to correct the problem, depending on severity of symptoms (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. *2.1.1 Mitral valve prolapse* is a deformity that usually produces no symptoms. Rarely, it progresses and can result in sudden death. This condition occurs more frequently in women than in men and is being diagnosed more frequently than it once was, probably because of improved diagnostic methods. The cause is usually an inherited connective tissue disorder resulting in enlargement of one or both of the mitral valve leaflets. The annulus often dilates. The chordae tendineae and papillary muscles may elongate. *Pathophysiology* In mitral valve prolapse, a portion of one or both mitral valve leaflets 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. About 15% of patients who develop murmurs eventually experience heart enlargement, atrial fibrillation, pulmonary hypertension, or heart failure. *Clinical Manifestations* Most people who have mitral valve prolapse never have symptoms. A few have symptoms of fatigue, shortness of breath, lightheadedness, dizziness, syncope, palpitations, chest pain, and anxiety. Fatigue may occur regardless of 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 palpitations have been reported while the heart has been beating normally. Chest pain, which is often localized to the chest, is not correlated with activity and may last for days. Anxiety may be a response to the symptoms; 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 that results in increased excretion of catecholamines). *Assessment and Diagnostic Findings* Often the first and only sign of mitral valve prolapse is identified when a physical examination of the heart reveals an extra heart sound, referred to as a mitral click. A systolic click is an early sign that a valve leaflet is ballooning into the left atrium. *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. Most patients do not require any medications; prophylactic antibiotics are no longer recommended prior to dental or invasive procedures, although antiarrhythmic medications may be prescribed. 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. Most patients do not require any medications; prophylactic antibiotics are no longer recommended prior to dental or invasive procedures, although antiarrhythmic medications may be prescribed. Chest pain that does not respond to nitrates may respond to calcium channel blockers or beta-blockers. *Nursing Management* The nurse educates the patient about the diagnosis and the possibility that the condition is hereditary. First-degree relatives (eg, parents, siblings) may be advised to have echocardiograms. Patients with mitral valve prolapse may be at risk for infectious endocarditis that results from bacteria entering the bloodstream and adhering to the abnormal valve structures. The nurse teaches the patient how to minimize this risk: practicing good oral hygiene, obtaining routine dental care, avoiding body piercing and body branding, and not using toothpicks or other sharp objects in the oral cavity. 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. To minimize symptoms, the nurse teaches the patient to avoid caffeine and alcohol. The nurse encourages the patient to read product labels, particularly on 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. In addition, the nurse also explores possible diet, activity, sleep, and other lifestyle factors that may correlate with symptoms. Women diagnosed with mitral valve prolapse without mitral regurgitation or other complications may complete pregnancies and have vaginal deliveries. *2.1.2 Mitral regurgitation* involves blood flowing back from the left ventricle into the left atrium during systole. Often the edges of the mitral valve leaflets do not close during systole. The leaflets cannot close completely because the leaflets and chordae tendineae have thickened and fibrosed, resulting in their contraction. The most common causes of mitral valve regurgitation in developed countries are degenerative changes of the mitral valve (eg, mitral valve prolapse) and ischemia of the left ventricle. The most common causes in developing countries are rheumatic heart disease and its sequelae. Other conditions that lead to mitral regurgitation include myxomatous changes, which enlarge and stretch the left atrium and ventricle, causing leaflets and chordae tendineae to stretch or rupture. Infective endocarditis may cause perforation of a leaflet, or the scarring following the infection may cause retraction of the leaflets or chordae tendineae. Collagen-vascular diseases (eg, systemic lupus erythematosus), cardiomyopathy, and ischemic heart disease may also result in changes in the left ventricle, causing the papillary muscles, chordae tendineae, or leaflets to stretch, shorten, or rupture. *Pathophysiology* Mitral regurgitation may result from problems with one or more of the leaflets, the chordae tendineae, the annulus, or the papillary muscles. As previously stated, a mitral valve leaflet may shorten or tear, and 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 myocardial infarction or ventricular dilation). The papillary muscles may be unable to contract because of ischemia. Regardless of the cause, blood regurgitates into the atrium during systole. With each beat of the left ventricle, some of the blood is forced back into the left atrium, adding to the blood flowing in from the lungs. This causes the left atrium to stretch and eventually hypertrophy and dilate. 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. *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. Doppler echocardiography is used to diagnose and monitor the progression of mitral regurgitation. Transesophageal echocardiography (TEE) provides the best images of the mitral valve. *Medical Management* of mitral regurgitation is the same as that for heart failure. Patients with mitral regurgitation and heart failure benefit from afterload reduction (arterial dilation) by treatment with angiotensin-converting enzyme (ACE) inhibitors, such as captopril (Capoten), enalapril (Vasotec), lisinopril (Prinivil, Zestril), ramipril (Altace), or hydralazine (Apresoline); angiotensin receptor blockers (ARBs), such as losartan (Cozar) or valsartan (Diovan); and beta-blockers, such as carvedilol (Coreg). Once symptoms of heart failure develop, the patient needs to restrict his or her activity level to minimize symptoms. Surgical intervention consists of mitral valvuloplasty (ie, surgical repair of the valve) or valve replacement. *2.1.3 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. *Pathophysiolog*y 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. Poor left ventricular filling can cause decreased cardiac output. The increased blood volume in the left atrium causes it to dilate and hypertrophy. 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 dyspnea on exertion as a result of pulmonary venous hypertension. Symptoms usually develop after the valve opening is reduced by one-third to one-half its usual size. Patients are likely to show progressive fatigue as a result of low cardiac output. The enlarged left atrium may create pressure on the left bronchial tree, resulting in a dry cough or wheezing. Patients may expectorate blood (ie, hemoptysis) or experience palpitations, orthopnea, paroxysmal nocturnal dyspnea (PND), and 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 lowpitched, 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 patients experience atrial dysrhythmias. Doppler echocardiography is used to diagnose mitral stenosis. Electrocardiography (ECG) and cardiac catheterization with angiography may be used to help determine the severity of the mitral stenosis. *Medical Management* 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 and may also require treatment for anemia. Patients with mitral stenosis are advised to avoid strenuous activities and competitive sports, both of which increase the heart rate. Mitral stenosis decreases the amount of blood that can flow from the left atrium to the left ventricle during diastole. When the heart rate increases, diastole is shortened, and thus the amount of time for the forward flow of blood is less. Therefore, as the heart rate increases, cardiac output decreases and pulmonary pressures increase with the backup of blood from the left atrium into the pulmonary veins. 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. *2.1.4 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 infective or rheumatic endocarditis, congenital abnormalities, diseases such as syphilis, a dissecting aneurysm that causes dilation or tearing of the ascending aorta, blunt chest trauma, or deterioration of an aortic valve replacement. In many cases, the cause is unknown and is classified as idiopathic. *Pathophysiology* 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 in an attempt to accommodate the increased volume of blood. It also hypertrophies in an attempt to increase muscle strength to expel more blood with above-normal force, thus increasing 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. Marked arterial pulsations that are visible or palpable at the carotid or temporal arteries may be present as a result of the increased force and volume of the blood ejected from the hypertrophied left ventricle. Exertional dyspnea and fatigue follow. Signs and symptoms of progressive left ventricular failure include breathing difficulties (eg, orthopnea, PND). *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 (Corrigan's) pulse, in which the pulse strikes the palpating finger with a quick, sharp stroke and then suddenly collapses. The diagnosis may be confirmed by Doppler echocardiography (preferably transesophageal), radionuclide imaging, ECG, magnetic resonance imaging (MRI), and cardiac catheterization. Patients with symptoms usually have echocardiograms every 4 to 6 months, and those without symptoms have echocardiograms every 2 to 3 years. *Medical Management* The patient is advised to avoid physical exertion, competitive sports, and isometric exercise. The medications usually prescribed first for patients with symptoms of aortic regurgitation are vasodilators such as calcium channel blockers (eg, nifedipine \[Adalat, Procardia\]) and ACE inhibitors (eg, captopril, enalapril, lisinopril, ramipril), or hydralazine. The treatment of choice is aortic valvuloplasty or valve replacement, preferably performed before left ventricular failure occurs. Surgery is recommended for any patient with left ventricular hypertrophy, regardless of the presence or absence of symptoms. *2.1.5 Aortic valve stenosis* is narrowing of the orifice between the left ventricle and the aorta. In adults, the stenosis is often a result of degenerative calcifications. Calcifications may be caused by inflammatory changes that occur in response to years of normal mechanical stress. Diabetes mellitus, hypercholesterolemia, hypertension, and low levels of high-density lipoprotein cholesterol may be risk factors for degenerative changes of the valve. Congenital leaflet malformations or an abnormal number of leaflets (ie, one or two rather than three) may be involved. Rarely rheumatic endocarditis may cause adhesions or fusion of the commissures and valve ring, stiffening of the cusps, and calcific nodules on the cusps. However, the cause of cusp calcification may be unknown. *Pathophysiology* Progressive narrowing of the valve orifice occurs, usually over 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 smaller orifice. The obstruction to left ventricular outflow increases pressure on the left ventricle, and the ventricular wall thickens, or 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. When symptoms develop, patients usually first have exertional dyspnea, caused by increased pulmonary venous pressure due to left ventricular failure. Orthopnea, PND, and pulmonary edema may also occur, along with dizziness and syncope because of reduced blood flow to the brain. Angina pectoris is a frequent symptom; it 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 is usually normal but may be low. Pulse pressure may be low (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. An S4 sound may be heard. If the examiner rests a hand over the base of the heart (second intercostal space next to the sternum and above the suprasternal notch up along the carotid arteries), a vibration may be felt. The vibration is caused by turbulent blood flow across the narrowed valve orifice. By having the patient lean forward during auscultation and palpation, especially during exhalation, it is possible to accentuate the signs of aortic stenosis. *Medical Management* 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-balloon or two-balloon percutaneous valvuloplasty procedures. *2.1.6 Nursing Management: Valvular Heart Disorders* The nurse teaches the patient with valvular heart disease about the diagnosis, the progressive nature of valvular heart disease, and the treatment plan. The patient is taught to report new symptoms or changes in symptoms to the health care provider. The nurse also teaches the patient 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. In addition, the nurse teaches the patient how to minimize the risk of developing infectious endocarditis. The nurse measures the patient's heart rate, blood pressure, and respiratory rate, compares these results with previous data, and notes any changes. Heart and lung sounds are auscultated and peripheral pulses palpated. The nurse assesses the patient with valvular heart disease for the following conditions: Signs and symptoms of heart failure, such as fatigue, dyspnea on exertion, an increase in coughing, hemoptysis, multiple respiratory infections, and orthopnea. Dysrhythmias, by palpating the patient's pulse for strength and rhythm (ie, regular or irregular) and asking whether the patient has experienced palpitations or felt forceful heartbeats Symptoms such as dizziness, syncope, increased weakness, or angina pectoris The nurse collaborates with the patient to develop a medication schedule and teaches about the name, dosage, actions, adverse effects, and any drug--drug or drug--food interactions of the prescribed medications for heart failure, dysrhythmias, angina pectoris, or other symptoms. Specific precautions are emphasized, such as the risk to patients with aortic stenosis who experience angina pectoris and take nitroglycerin. The venous dilation that results from nitroglycerin decreases blood return to the heart, thus decreasing cardiac output and increasing the risk of syncope and decreased coronary artery blood flow. The nurse teaches the patient about the importance of attempting to relieve the symptoms of angina with rest and relaxation before taking nitroglycerin and to anticipate the potential adverse effects. In addition, the nurse teaches the patient to weigh daily and report gains 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 an acceptable lifestyle. The patient may need to be advised to rest and sleep sitting in a chair or bed with the head elevated when experiencing symptoms of pulmonary congestion. Care of patients treated with valvuloplasty or surgical valve replacement is described later in this chapter. *2.1.7 Valve Repair and Replacement Procedures* The repair, rather than replacement, of a cardiac valve is referred to as valvuloplasty. In general, valves that undergo valvuloplasty function longer than prosthetic valve replacements, and patients do not require continuous anticoagulation. 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. TEE is usually performed at the conclusion of a valvuloplasty to evaluate the effectiveness of the procedure. 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. Balloon valvuloplasty (Fig. 29-3) is performed in the cardiac catheterization laboratory. The patient may receive light or moderate sedation or just a local anesthetic. *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), which may be preshaped (rigid/semirigid) or flexible. 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. Progressive regurgitation is prevented by the repair. The second technique involves tacking the valve leaflets to the atrium with sutures or taking tucks to tighten the annulus. *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 (closing the valve during systole). A leaflet may be extended by suturing a piece of pericardium to it. A pericardial or synthetic patch may be used to repair holes in the leaflets. *Chordoplasty* is repair of the chordae tendineae. The mitral valve is involved with chordoplasty (because it has chordae tendineae); the tricuspid valve seldom requires chordoplasty. Stretched, torn, or shortened chordae tendineae may cause regurgitation. Stretched chordae tendineae can be shortened, transposed to the other leaflet, or replaced with synthetic chordae. Torn chordae can be reattached to the leaflet and shortened chordae can be elongated. Stretched papillary muscles, which may also cause regurgitation, can be shortened as well. *Valve Replacement* When valvuloplasty is not a viable alternative (eg, when the annulus or leaflets of the valve are immobilized by calcifications, severe fibrosis or fusion of the chordate tendineae, papillary muscles, and leaflets below the valve), valve replacement is performed. General anesthesia and cardiopulmonary bypass are used for 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. Mitral, and more rarely aortic, valve replacements may be performed with minimally invasive techniques that do not involve cutting through the length of the sternum. Instead, incisions are made in only the upper or lower half of the sternum or between ribs; these incisions are only 2 to 4 inches long. Some of these minimally invasive procedures are robot assisted; the surgical instruments are connected to a robot, and the surgeon, watching a video display, uses a joystick to control the robot and surgical instruments. With these procedures, patients have less bleeding, pain, risk of infection, and scarring. Hospital stays average 3 days, and recovery may be as short as 3 weeks. The replacement valve is slid down the suture into position and tied into place (Fig. 29-6). Two types of valve prostheses may be used: mechanical and tissue (ie, biologic) valves (Fig. 29-7). *Mechanical valves* are of the bileaflet, ball-and-cage, or tilting-disk design and are thought to be more durable than tissue prosthetic valves; therefore, they are often used for younger patients. These valves are used for patients with renal failure, hypercalcemia, endocarditis, or sepsis who require valve replacement. The mechanical valves do not deteriorate or become infected as easily as the tissue valves used for patients with these conditions. Significant complications associated with mechanical valves are thromboemboli requiring long-term use of anticoagulants. Some amount of hemolysis also occurs with these valves; usually it is not clinically significant. *Tissue (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. *2.1.8 Nursing Management: Valvuloplasty and Replacement* The nurse assists the patient and family to prepare for the procedure, reinforces and supplements explanations provided by the physician, and provides psychosocial support. Patients who have undergone percutaneous balloon valvuloplasty procedures may be admitted to a telemetry or intensive care unit. The nurse assesses for signs and symptoms of heart failure and emboli (see Chapter 30), listens for any changes in heart sounds at least every 4 hours, and provides the patient with the same care as for postprocedure cardiac catheterization or percutaneous transluminal coronary angioplasty (PTCA). After undergoing percutaneous balloon valvuloplasty, the patient usually remains in the hospital for 24 to 48 hours. Patients who have undergone surgical 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 are assessed every 2 to 4 hours and as needed. Intravenous (IV) medications to increase or decrease blood pressure and to treat dysrhythmias or altered heart rates are administered and their effects monitored. The medications are gradually decreased until they are no longer required or the patient can take the 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. *2.1.9 Septal Defects* The atrial or ventricular septum may have an abnormal opening between the right and left sides of the heart (ie, septal defect). Most septal defects are congenital and are usually identified and repaired during infancy or childhood. Adults may not have undergone early repair or may develop septal defects as a result of myocardial infarction or trauma. In general, pressures in the left atria and ventricle are higher than those on the right, so blood initially flows from the left heart chamber into the right---a left-to-right shunt. With an atrial septal defect (ASD), ultimately the right atrial pressures become greater than the left atrial pressures, and blood begins to flow from the right atrium into the left atrium---a right-to-left shunt. With a ventricular septal defect (VSD), the extra blood volume causes the right ventricle to dilate, as well as pulmonary vascular congestion and hypertension. Patients with septal defects may not experience any symptoms, gradually develop symptoms, or rapidly develop heart failure. Patients with ASDs who gradually develop symptoms usually describe decreased exercise tolerance, dyspnea on exertion, palpitations, syncope, and symptoms of right ventricular or congestive heart failure. Cyanosis may result, or strokes (cerebrovascular accidents, brain attacks) may occur. Patients with VSDs who gradually develop symptoms describe shortness of breath, syncope, chest pain, and symptoms of left ventricular failure. *Medical Management* Treatment is individualized to the patient's symptoms. Vasodilators are often prescribed first to decrease resistance to ventricular ejection and minimize the left-to-right shunting. Many septal defects can be repaired percutaneously in a cardiac catheterization laboratory. A guidewire is advanced through a vein into the right side of the heart and through the septal defect. A special catheter is placed over the guidewire and positioned across the septal defect. Two connected mesh disks (one on each side of the septum) are then used to close the septal defect. *Nursing Management* Care for a patient recovering from a percutaneous septal defect repair is the same care as for postprocedure cardiac catheterization or PTCA. After undergoing percutaneous septal repair, the patient usually remains in the hospital for 24 to 48 hours. Care for a patient recovering from a surgical septal defect repair is the same as other cardiac surgeries. *2.1.10 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 (DCM), hypertrophic cardiomyopathy (HCM), restrictive or constrictive cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy (ARVC), and unclassified cardiomyopathy. A patient may have pathology representing more than one of these classifications, such as a patient with HCM developing dilation and symptoms of DCM. Ischemic cardiomyopathy is a term frequently used to describe an enlarged heart caused by coronary artery disease, which is usually accompanied by heart failure. *Pathophysiology* The pathophysiology of all cardiomyopathies is a series of 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. Dilated Cardiomyopathy DCM is the most common form of cardiomyopathy, with an incidence of 5 to 8 cases per 100,000 people per year. DCM is distinguished by significant dilation of the ventricles without simultaneous hypertrophy (ie, increased muscle wall thickness) and systolic dysfunction (Fig. 29-8). The ventricles have elevated systolic and diastolic volumes but a decreased ejection fraction. Hypertrophic Cardiomyopathy HCM is a rare autosomal dominant condition, occurring in men, women, and children (often detected after puberty). Echocardiograms may be performed every year from 12 to 18 years of age and then every 5 years from 18 to 70 years of age in susceptible individuals. Doppler echocardiography may also be used to detect the HCM and blood flow alterations. HCM also may be idiopathic (ie, no known cause). In HCM, the heart muscle asymmetrically increases in size and mass, especially along the septum (see Fig. 29-8). Restrictive Cardiomyopathy RCM is characterized by diastolic dysfunction caused by rigid ventricular walls that impair diastolic filling and ventricular stretch (see Fig. 29-8). Systolic function is usually normal. RCM may be associated with amyloidosis (amyloid, a protein substance, is deposited within cells) and other such infiltrative diseases. However, the cause is unknown (ie, idiopathic) in most cases. Signs and symptoms are similar to constrictive pericarditis: dyspnea, nonproductive cough, and chest pain. Arrhythmogenic Right Ventricular Cardiomyopathy ARVC occurs when the myocardium of the right ventricle is progressively infiltrated and replaced by fibrous scar and adipose tissue. Initially, only localized areas of the right ventricle are affected, but as the disease progresses, the entire heart is affected. Eventually, the right ventricle dilates and develops poor contractility, right ventricular wall abnormalities, and dysrhythmias. The prevalence of ARVC is unknown because many cases are not recognized. Palpitations or syncope may develop between 15 and 40 years of age. Unclassified Cardiomyopathies are different from or have characteristics of more than one of the previously described types. Examples of unclassified cardiomyopathies include fibroelastosis, noncompacted myocardium, systolic dysfunction with minimal dilation, and mitochondrial involvement. *Clinical Manifestations* Patients with cardiomyopathy may remain stable and without symptoms for many years. As the disease progresses, so do the symptoms. Frequently, dilated or restrictive cardiomyopathy is first diagnosed when the patient presents with signs and symptoms of heart failure (eg, dyspnea on exertion, fatigue). Patients with cardiomyopathy may also report PND, cough (especially with exertion), and orthopnea, which may lead to a misdiagnosis of bronchitis or pneumonia. Other symptoms include fluid retention, peripheral edema, and nausea, which is caused by poor perfusion of the gastrointestinal system. The patient also may experience chest pain, palpitations, dizziness, nausea, and syncope with exertion. However, with HCM, cardiac arrest (ie, sudden cardiac death) may be the initial manifestation in young people, including athletes. Regardless of type and cause, cardiomyopathy may lead to severe heart failure, lethal dysrhythmias, and death. *Assessment and Diagnostic Findings* Physical examination at early stages may reveal tachycardia and extra heart sounds (eg, S3, S4). Patients with DCM may have diastolic murmurs, and patients with DCM and HCM may have systolic murmurs. With disease progression, examination also reveals signs and symptoms of heart failure (eg, crackles on pulmonary auscultation, jugular vein distention, pitting edema of dependent body parts, enlarged liver). *Medical Management* is directed toward identifying and managing possible underlying or precipitating causes; correcting the heart failure with medications, a low-sodium diet, and an exercise/rest regimen; and controlling dysrhythmias with antiarrhythmic medications and possibly with an implanted electronic device, such as an implantable cardioverter defibrillator. Systemic anticoagulation to prevent thromboembolic events is usually recommended. If the patient has signs and symptoms of congestion, fluid intake may be limited to 2 L each day. Patients with HCM should avoid dehydration and may need beta-blockers (atenolol \[Tenormin\], metoprolol \[Lopressor\], nadolol \[Corgard\], propranolol \[Inderal\]) to maintain cardiac output and minimize the risk of left ventricular outflow tract obstruction during systole. Patients with HCM or RCM may need to limit physical activity to avoid a life-threatening dysrhythmia. A pacemaker may be implanted to alter the electrical stimulation of the muscle and prevent the forceful hyperdynamic contractions that occur with HCM. Atrial-ventricular and biventricular pacing have been used to decrease symptoms and obstruction of the left ventricular outflow tract. For some patients with DCM and HCM, biventricular pacing increases the ejection fraction and reverses some of the structural changes in the myocardium. Nonsurgical septal reduction therapy, also called alcohol septal ablation, has been used to treat obstructive HCM. In the cardiac catheterization laboratory, a percutaneous catheter is positioned in one or more of the septal coronary arteries. *Surgical Management* When heart failure progresses and medical treatment is no longer effective, surgical intervention, including heart transplantation, is considered. However, because of the limited number of organ donors, many patients die waiting for transplantation. In some cases, a left ventricular assist device is implanted to support the failing heart until a suitable donor heart becomes available. Orthotopic transplantation is the most common surgical procedure for cardiac transplantation (Fig. 29-9). The recipient's heart is removed, and the donor heart is implanted at the vena cava and pulmonary veins. Some surgeons prefer to remove the recipient's heart, leaving a portion of the recipient's atria (with the vena cava and pulmonary veins) in place. The donor heart, which usually has been preserved in ice, is prepared for implant by cutting away a small section of the atria that corresponds with the sections of the recipient's heart that were left in place. The donor heart is implanted by suturing the donor atria to the residual atrial tissue of the recipient's heart. After the venous or atrial anastomoses are complete, the recipient's pulmonary artery and aorta are sutured to those of the donor heart. More complex devices that actually perform some or all of the pumping function for the heart also are being used. These more sophisticated ventricular assist devices (VADs) can circulate as much blood per minute as the heart, if not more (Fig. 29-10). Total artificial hearts are designed to replace both ventricles. Some require the removal of the patient's heart to implant the total artificial heart and others do not. - *Nursing Process: The Patient with Cardiomyopathy* *Nursing Diagnoses* Based on the assessment data, major nursing diagnoses may include: Decreased cardiac output related to structural disorders caused by cardiomyopathy or to dysrhythmia from the disease process and medical treatments Ineffective cardiopulmonary, cerebral, peripheral, and renal tissue perfusion related to decreased peripheral blood flow (resulting from decreased cardiac output) Impaired gas exchange related to pulmonary congestion caused by myocardial failure (resulting from decreased cardiac output) Activity intolerance related to decreased cardiac output or excessive fluid volume, or both Anxiety related to the change in health status and in role functioning Powerlessness related to disease process Noncompliance with medication and diet therapies *Collaborative Problems/Potential Complications* Based on the assessment data, potential complications include: Heart failure Ventricular dysrhythmias Atrial dysrhythmias Cardiac conduction defects Pulmonary or cerebral embolism Valvular dysfunction *Planning and Goals* The major goals for patients include improvement or maintenance of cardiac output, increased activity tolerance, reduction of anxiety, adherence to the self-care program, increased sense of power with decision making, and absence of complications. *Nursing Interventions* - Improving Cardiac Output - Increasing Activity Tolerance - Reducing Anxiety - Decreasing the Sense of Powerlessness - Promoting Home and Community-Based Care *Evaluation* Expected Patient Outcomes 1\. Maintains or improves cardiac function a\. Exhibits heart and respiratory rates within normal limits b\. Reports decreased dyspnea and increased comfort; maintains or improves gas exchange c\. Reports no weight gain; appropriate weight for height d\. Maintains or improves peripheral blood flow 2\. Maintains or increases activity tolerance a. Carries out activities of daily living (eg, brushes teeth, feeds self) b\. Reports increased tolerance to activity 3\. Is less anxious a\. Discusses prognosis freely b\. Verbalizes fears and concerns c\. Participates in support groups if appropriate 4\. Decreases sense of powerlessness a\. Identifies emotional response to diagnosis b\. Discusses control that he or she has 5\. Adheres to self-care program a\. Takes medications according to prescribed schedule b\. Modifies diet to accommodate sodium and fluid recommendations c\. Modifies lifestyle to accommodate activity and rest behavior recommendations d\. Identifies signs and symptoms to be reported to health care professionals ***2.2 Infectious Diseases of the Heart*** Any of the heart's three layers may be affected by an infectious process. The infections are named for the layer of the heart most involved in the infectious process: infective endocarditis (endocardium), myocarditis (myocardium), and pericarditis (pericardium). Rheumatic endocarditis is a unique infective endocarditis syndrome. The diagnosis of infection is made primarily on the basis of the patient's symptoms and echocardiography. The ideal management for all infectious diseases is prevention. IV antibiotics are usually necessary once an infection has developed in the heart. *2.2.1 Rheumatic Endocarditis* Acute rheumatic fever, which occurs most often in school-age children, may develop after an episode of group A betahemolytic streptococcal pharyngitis (Chart 29-2). Patients with rheumatic fever may develop rheumatic heart disease as evidenced by a new heart murmur, cardiomegaly, pericarditis, and heart failure. Prompt treatment of "strep" throat with antibiotics can prevent the development of rheumatic fever. The streptococcus is spread by direct contact with oral or respiratory secretions. Although the bacteria are the causative agents, malnutrition, overcrowding, poor hygiene, and lower socioeconomic status may predispose individuals to rheumatic fever. *2.2.2 Infective Endocarditis* is a microbial infection of the endothelial surface of the heart. It usually develops in people with prosthetic heart valves or structural cardiac defects (eg, valve disorders, HCM) (Chart 29-3). It is more common in older people, who are more likely to have degenerative or calcific valve lesions, reduced immunologic response to infection, and the metabolic alterations associated with aging. Staphylococcal endocarditis infections of the valves in the right side of the heart are common among IV injection drug users. Hospital-acquired infective endocarditis occurs most often in patients with debilitating disease or indwelling catheters and in patients who are receiving hemodialysis or prolonged IV fluid or antibiotic therapy. Patients taking immunosuppressive medications or corticosteroids are more susceptible to fungal endocarditis. Invasive procedures, particularly those involving mucosal surfaces, can cause a bacteremia, which rarely lasts for more than 15 minutes. However, if a patient has any anatomic cardiac defects, bacteremia can cause bacterial endocarditis. From 1950 to the mid-1980s, the incidence of infective endocarditis remained steady at about 3.6 cases per 100,000 patients. The incidence then increased, partially attributed to increased IV injection drug abuse and body piercing, especially oral, nasal, and nipple piercings. *Pathophysiology* A deformity or injury of the endocardium leads to accumulation on the endocardium of fibrin and platelets (clot formation). Infectious organisms, usually staphylococci, streptococci, enterococci, pneumococci, or chlamydia, invade the clot and endocardial lesion. Other causative micro-organisms include fungi (eg, Candida, Aspergillus) and Rickettsiae. The infection most frequently results in platelets, fibrin, blood cells, and microorganisms that cluster as vegetations on the endocardium. The vegetations may embolize to other tissues throughout the body. As the clot on the endocardium continues to expand, the infecting organism is covered by the new clot and concealed from the body's normal defenses. The infection may erode through the endocardium into the underlying structures (eg, valve leaflets), causing tears or other deformities of valve leaflets, dehiscence of prosthetic valves, deformity of the chordae tendineae, or mural abscesses. Usually the onset of infective endocarditis is insidious. The signs and symptoms develop from the toxic effect of the infection, from destruction of the heart valves, and from embolization of fragments of vegetative growths on the heart. Systemic emboli occur with left-sided heart infective endocarditis; pulmonary emboli occur with right-sided heart infective endocarditis. *Clinical Manifestations* The primary presenting symptoms of infective endocarditis are fever and a heart murmur. The fever may be intermittent or absent, especially in patients who are receiving antibiotics or corticosteroids, in those who are elderly, or those who have heart failure or renal failure. A heart murmur may be absent initially but develops in almost all patients. Murmurs that worsen over time indicate progressive damage from vegetations or perforation of the valve or the chordae tendineae. In addition to the fever and heart murmur, clusters of petechiae may be found on the body. Small, painful nodules (Osler nodes) may be present in the pads of fingers or toes. Irregular, red or purple, painless, flat macules (Janeway lesions) may be present on the palms, fingers, hands, soles, and toes. Hemorrhages with pale centers (Roth spots) caused by emboli may be observed in the fundi of the eyes. Splinter hemorrhages (ie, reddish-brown lines and streaks) may be seen under the fingernails and