Nursing Care of Clients with Altered Tissue Perfusion PDF

Nursing Care of Clients with Altered Tissue Perfusion Ischemic Heart Disease/Coronary Artery Disease Pathophysiology The inflammatory response involved with the development of atherosclerosis begins with injury to the vascular endothelium and progresses over many years. The injury may be initiate...

Nursing Care of Clients with Altered Tissue Perfusion Ischemic Heart Disease/Coronary Artery Disease Pathophysiology The inflammatory response involved with the development of atherosclerosis begins with injury to the vascular endothelium and progresses over many years. The injury may be initiated by smoking or tobacco use, hypertension, hyperlipidemia, and other factors. The endothelium undergoes changes and stops producing the normal antithrombotic and vasodilating agents. The presence of inflammation attracts inflammatory cells, such as macrophages. The macrophages ingest lipids, becoming “foam cells” that transport the lipids into the arterial wall. Some of the lipid is deposited on the arterial wall, forming fatty streaks. Activated macrophages also release biochemical substances that can further damage the endothelium by contributing to the oxidation of low-density lipoprotein (LDL). The oxidized LDL is toxic to the endothelial cells and fuels progression of the atherosclerotic process. Following the transport of lipid into the arterial wall, smooth muscle cells 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. 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 the fibrous plaque to rupture. A ruptured plaque attracts platelets and causes thrombus formation. A thrombus may then obstruct blood flow, leading to acute coronary syndrome (ACS), which may result in an acute myocardial infarction (MI). When an MI occurs, a portion of the heart muscle no longer receives blood flow and becomes necrotic. 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 pjdb–118l–m4-101124 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 cause the heart to abruptly stop beating; this is known as sudden cardiac death. The most common manifestation of myocardial ischemia is the onset of chest pain. However, the classic epidemiologic study of the people in Framingham, Massachusetts, showed that nearly 15% of men and women who had coronary events, which included unstable angina, MIs, or sudden cardiac death events, were totally asymptomatic prior to the coronary event. Patients with myocardial ischemia may present to an emergency department (ED) or clinic with a variety of symptoms other than chest pain. Some complain of epigastric distress and pain that radiates to the jaw or left arm. Patients who are older or have a history of diabetes or heart failure may report shortness of breath. Many women have been found to have atypical symptoms, including indigestion, nausea, palpitations, and numbness. Prodromal symptoms may occur (e.g., angina a few hours to days before the acute episode), or a major cardiac event may be the first indication of coronary atherosclerosis. Risk Factors Epidemiologic studies point to several factors that increase the probability that a person will develop heart disease. Although many people with CAD have one or more risk factors, some do not have classic risk factors. Elevated low-density lipoprotein (LDL), also known as bad cholesterol, is a well-known risk factor and the primary target of cholesterol-lowering therapy. People at the highest risk for having a cardiac event are those with known CAD or those with diabetes, peripheral arterial disease, abdominal aortic aneurysm, or carotid artery disease. The latter diseases are referred to as 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 is also affected by factors, such as age, gender, systolic blood pressure, smoking history, level of total cholesterol, 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 is made when a patient has three of the following five risk factors: Enlarged waist circumference (greater than 35.4 inches in males, greater than 31.4 inches in females) Elevated triglycerides (greater than or equal to 175 mg/dL, or currently on drug treatment for elevated triglycerides) Reduced HDL (less than 40 mg/dL in males, less than 50 mg/dL in females, or currently on drug treatment for reduced HDL) Hypertension (systolic blood pressure greater than or equal to 130 mm Hg and/or diastolic blood pressure greater than or equal to 80 mm Hg on an average of two to three measurements obtained on two to three separate occasions, or currently on antihypertensive drug treatment for a history of hypertension) Many people with type 2 diabetes fit this clinical picture. Theories suggest that in patients with obesity, excessive adipose tissue may secrete mediators that lead to metabolic changes. Adipokines (adipose pjdb–118l–m4-101124 tissue cytokines), free fatty acids, and other substances are known to modify insulin action and contribute to atherogenic changes in the cardiovascular system. 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 may view high sensitivity C-reactive protein (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—are established risk factors for CAD and its complications. As a result, they receive much attention in health promotion programs. Controlling Cholesterol Abnormalities The association of a high blood cholesterol level with heart disease is well established, and the metabolism of fats is known to be an important contributor to the development of heart disease. Fats, which are insoluble in water, are encased in water-soluble lipoproteins that allow them to be transported within the circulatory system. The various lipoproteins are categorized by their protein content, which is measured in density. The density increases when more protein is present. 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 (GI) tract into lipoprotein globules called chylomicrons. These are reprocessed by the liver as lipoproteins. 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 receptors in the arterial endothelium. Here, macrophages ingest them, contributing to plaque formation. LDL is the target of current therapy because of its strong association with advancing CAD. The total cholesterol level is also a clear predictor of coronary events. HDL is known as good cholesterol because it transports other lipoproteins such as LDL to the liver, where they can be degraded and excreted. Because of this, a high HDL level is a strong negative risk factor for heart disease (i.e., it protects against heart disease). Triglyceride is made up of fatty acids and is transported through the blood by a lipoprotein. Although an elevated triglyceride level (more than 200 mg/dL) may be genetic in origin, it also can be caused by obesity, physical inactivity, excessive alcohol intake, high-carbohydrate diets, diabetes, kidney disease, and certain medications, such as oral contraceptives and corticosteroids. Dietary Measures Adults who need to lower LDL (and blood pressure) should consider the AHA’s diet recommendations or the Mediterranean diet, which are reported to reduce mortality from cardiovascular disease. Both eating plans provide similar key elements: an emphasis on plant foods (fruits, vegetables, whole-grain breads or other forms of cereals, beans, nuts, and seeds), minimally processed foods, seasonally fresh foods, inclusion of fish, and minimal intake of red meat. Individuals needing to lower LDL and blood pressure. pjdb–118l–m4-101124 Dietary Measures Adults who need to lower LDL (and blood pressure) should consider the AHA’s diet recommendations or the Mediterranean diet, which are reported to reduce mortality from cardiovascular disease. Both eating plans provide similar key elements: an emphasis on plant foods (fruits, vegetables, whole-grain breads or other forms of cereals, beans, nuts, and seeds), minimally processed foods, seasonally fresh foods, inclusion of fish, and minimal intake of red meat. Individuals needing to lower LDL and blood pressure should also limit the intake of sweets and sugar sweetened beverages. Adopting a strict vegetarian diet can significantly reduce blood lipids, blood glucose, body mass index, and blood pressure; however, this type of intensive dietary program may not be acceptable to all patients who need to modify risk factors. Referral to a dietitian can help patients in following a diet that is appropriate. 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 adults is to engage in moderate-intensity aerobic activity of at least 150 minutes per week or vigorous-intensity aerobic activity of at least 75 minutes per week, or an equivalent combination. In addition, adults should engage in muscle-strengthening activities on 2 or more days each week that work all major muscle groups. The nurse helps the patient to 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. 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. Patients should stop any activity if chest pain, unexpected shortness of breath, dizziness, lightheadedness, or nausea occurs. Medications Lipid-lowering medications can reduce CAD mortality in patients with elevated lipid levels and in at-risk patients with normal lipid levels. The various types of lipid-lowering agents affect the lipid components somewhat differently; these types include 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) (or statins), fibric acids (or fibrates), bile acid sequestrants (or resins), cholesterol absorption inhibitors, and proprotein convertase subtilisin-kexin type 9 (PCSK9) agents. Because of their high cost, PCSK9 agents are prescribed on a limited basis, but may be considered for those at high cardiovascular risk or who have familial hypercholesterolemia. Before starting statin therapy, the provider and patient should discuss risk factors, adherence to a healthy lifestyle, benefits of risk-reduction, the potential of adverse effects and drug–drug interactions, as well as patient preferences for an individualized treatment plan. Promoting Cessation of Tobacco Use pjdb–118l–m4-101124 Tobacco use contributes to the development and severity of CAD in at least three ways: Nicotinic acid in tobacco triggers the release of catecholamines, which raise the heart rate and blood pressure. Nicotinic acid can also cause the coronary arteries to constrict. These effects lead to an increased risk of CAD and sudden cardiac death. Tobacco use can increase the oxidation of LDL, damaging the vascular endothelium. This increases platelet adhesion and leads to a higher probability of thrombus formation. Inhalation of smoke increases the blood carbon monoxide level and decreases the supply of oxygen to the myocardium. Hemoglobin, the oxygen-carrying component of blood, combines more readily with carbon monoxide than with oxygen. Myocardial ischemia and reduced contractility can result. A person at increased risk for heart disease is encouraged to stop tobacco use through any means possible: educational programs, counseling, consistent motivation and reinforcement messages, support groups, and medications. Some people have found complementary therapies (e.g., acupuncture, guided imagery, hypnosis) to be helpful. People who stop smoking reduce their risk of heart disease within the first year, and the risk continues to decline as long as they refrain from smoking. The use of medications such as the nicotine patch, nicotine lozenges, nicotine gum, varenicline, or bupropion may assist with stopping the use of tobacco. Products containing nicotine have some of the same effects as smoking: catecholamine release (increasing heart rate and blood pressure) and increased platelet adhesion. These medications should be used for a short time and at the lowest effective doses. Managing Hypertension Hypertension is defined as systolic blood pressure measurements of greater than 130 mm Hg and/or diastolic blood pressure levels greater than 80 mm Hg. A single reading is not adequate to make a diagnosis. Averaging two or three measurements obtained on two to three different occasions will provide a more accurate measurement. The risk of cardiovascular disease increases as blood pressure increases, and current guidelines support treating hypertension with a goal of keeping the blood pressure under 130/80 for all adults. Long-standing elevated blood pressure may result in increased stiffness of the vessel walls, leading to vessel injury and a resulting inflammatory response within the intima. Inflammatory mediators then lead to the release of growth-promoting factors that cause vessel hypertrophy and hyperresponsiveness. These changes result in acceleration and aggravation of atherosclerosis. Hypertension also increases the work of the left ventricle, which must pump harder to eject blood into the arteries. Over time, the increased workload causes the heart to enlarge and thicken (i.e., hypertrophy) and may eventually lead to heart failure. Early detection of high blood pressure and adherence to a therapeutic regimen can prevent the serious consequences associated with untreated elevated blood pressure, including CAD. Intensive management of hypertension lowers the risk of cardiovascular events, including heart attack and stroke, and lowers the risk of death. Controlling Diabetes Diabetes is known to accelerate the development of heart disease. Hyperglycemia fosters dyslipidemia, increased platelet aggregation, and altered red blood cell function, which can lead to thrombus formation. These metabolic alterations may impair endothelial cell–dependent vasodilation and smooth muscle function, promoting the development of atherosclerosis. Treatment with insulin, metformin, and pjdb–118l–m4-101124 other therapeutic interventions that lower plasma glucose levels can lead to improved endothelial function and patient outcomes. Gender Heart disease has long been recognized as a cause of morbidity and mortality in men, but it has not always been as readily recognized in women. Cardiovascular events in women occur an average of 10 years later in life than they do in men. Women tend to have a higher incidence of complications from cardiovascular disease and a higher mortality. In addition, women tend to not recognize the symptoms of CAD as early as men, and they wait longer to report their symptoms and seek medical assistance. The age difference between women and men who were newly diagnosed with CAD was traditionally thought to be related to estrogen. Menopause is now recognized as a milestone in the aging process, during which risk factors tend to accumulate. Cardiovascular disease may be well developed by the time of menopause, and although hormone therapy (HT) (formerly referred to as hormone replacement therapy) for menopausal women was once promoted as preventive therapy for CAD, research does not support HT as an effective means of prevention. HT decreases menopausal symptoms and the risk of osteoporosis- related bone fractures; however, it also has been associated with an increased incidence of CAD, breast cancer, deep vein thrombosis, stroke, and pulmonary embolism. Current guidelines do not recommend HT for primary or secondary prevention of CAD. Heart Failure Heart failure (HF) is a clinical syndrome resulting from structural or functional cardiac disorders so that the heart is unable to pump enough blood to meet the body’s metabolic demands or needs. The term heart failure indicates myocardial disease in which impaired contraction of the heart (systolic dysfunction) or filling of the heart (diastolic dysfunction) may cause pulmonary or systemic congestion. Some cases of HF are reversible, depending on the cause. Most often, HF is a chronic, progressive condition that is managed with lifestyle changes and medications to prevent episodes of acute decompensated heart failure. These episodes are characterized by increased symptoms of respiratory distress, decreased cardiac output (CO), and poor perfusion. These episodes are also associated with increased hospitalizations, increased health care costs, and decreased quality of life. HF is more prevalent among African Americans and Hispanics than among Caucasians. The risk for having HF increases with advancing age. For adults over 60 years of age, HF is more prevalent among men than women. As typical for other major cardiovascular diseases and disorders, cigarette smoking, obesity, poorly managed diabetes, and metabolic syndrome are all risks for HF. The onset of HF is typically a morbid consequence of another disease or disorder, including coronary artery disease (CAD), hypertension, cardiomyopathy, valvular disorders, and renal dysfunction with volume overload. Atherosclerosis of the coronary arteries is a primary cause of HF, and CAD is found in the majority of patients with HF. Ischemia causes myocardial dysfunction because it deprives heart cells of oxygen and causes cellular damage. Myocardial infarction (MI) causes focal heart muscle necrosis, the death of myocardial cells, and a loss of contractility; the extent of the infarction correlates with the severity of HF. Revascularization of the coronary artery by a percutaneous coronary intervention (PCI) or by coronary pjdb–118l–m4-101124 artery bypass surgery (coronary artery bypass graft [CABG]) may improve myocardial oxygenation and ventricular function and prevent more extensive myocardial necrosis that can lead to HF. Systemic or pulmonary hypertension increases afterload (resistance to ejection), increasing the cardiac workload and leading to the hypertrophy of myocardial muscle fibers. This can be considered a compensatory mechanism because it initially increases contractility. However, sustained hypertension eventually leads to changes that impair the heart’s ability to fill properly during diastole, and the hypertrophied ventricles may dilate and fail. Cardiomyopathy is a disease of the myocardium. The various types of cardiomyopathy lead to HF and arrhythmias. Dilated cardiomyopathy (DCM), the most common type of cardiomyopathy, causes diffuse myocyte necrosis and fibrosis, and commonly leads to progressive HF. DCM can be idiopathic (unknown cause), or it can result from an inflammatory process, such as myocarditis, or from a cytotoxic agent, such as alcohol or certain antineoplastic drugs. Usually, HF due to cardiomyopathy is chronic and progressive. However, cardiomyopathy and HF may resolve following removal of the causative agent. Genetic testing may be recommended for idiopathic cardiomyopathy. Valvular heart disease is also a cause of HF. The valves ensure that blood flows in one direction. With valvular dysfunction, it becomes increasingly difficult for blood to move forward, increasing pressure within the heart and increasing cardiac workload, leading to HF. Several systemic conditions, including progressive kidney failure, contribute to the development and severity of HF. Nearly 30% of patients with chronic HF also have chronic kidney disease. In addition, cardiac arrhythmias such as atrial fibrillation may either cause or result from HF; in both instances, the altered electrical stimulation impairs myocardial contraction and decreases the overall efficiency of myocardial function. Other factors, such as hypoxia, acidosis, and electrolyte abnormalities, can worsen myocardial function. Pathophysiology Regardless of the etiology, the pathophysiology of HF results in similar changes and clinical manifestations. Significant myocardial dysfunction usually occurs before the patient experiences signs and symptoms of HF such as shortness of breath, edema, or fatigue. As HF develops, the body activates neurohormonal compensatory mechanisms. These mechanisms represent the body’s attempt to cope with the HF and are responsible for the signs and symptoms that develop. Understanding these mechanisms is important because the treatment for HF is aimed at correcting them and relieving symptoms. The most common type of HF is systolic HF, also called Heart Failure with reduced Ejection Fraction (HFrEF). Systolic heart failure results in decreased blood ejected from the ventricle. The decreased blood flow is sensed by baroreceptors in the aortic and carotid bodies, and the sympathetic nervous system is then stimulated to release epinephrine and norepinephrine. The purpose of this initial response is to increase heart rate and contractility and support the failing myocardium, but the continued response has multiple negative effects. Sympathetic stimulation causes vasoconstriction in the skin, gastrointestinal tract, and kidneys. A decrease in renal perfusion due to low CO and vasoconstriction then causes the release of renin by the kidneys. Renin converts the plasma protein angiotensinogen to angiotensin I, which then circulates to the lungs. Angiotensin-converting enzyme (ACE) in the lumen of pulmonary blood pjdb–118l–m4-101124 vessels converts angiotensin I to angiotensin II, a potent vasoconstrictor, which then increases the blood pressure and afterload. Angiotensin II also stimulates the release of aldosterone from the adrenal cortex, resulting in sodium and fluid retention by the renal tubules and an increase in blood volume. These mechanisms lead to the fluid volume overload commonly seen in HF. Angiotensin, aldosterone, and other neurohormones (e.g., endothelin) lead to an increase in preload and afterload, which increases stress on the ventricular wall, causing an increase in cardiac workload. A counterregulatory mechanism is attempted through the release of natriuretic peptides. Atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP; brain type) are released from the overdistended cardiac chambers. These substances promote vasodilation and diuresis. However, their effect is usually not strong enough to overcome the negative effects of the other mechanisms. pjdb–118l–m4-101124 As the heart’s workload increases, contractility of the myocardial muscle fibers decreases. Decreased contractility results in an increase in end-diastolic blood volume in the ventricle, stretching the myocardial muscle fibers and increasing the size of the ventricle (ventricular dilation). The heart compensates for the increased workload by increasing the thickness of the heart muscle (ventricular hypertrophy). Hypertrophy results in abnormal changes in the structure and function of myocardial cells, a process known as ventricular remodeling. Under the influence of neurohormones (e.g., angiotensin II), enlarged myocardial cells become dysfunctional and die early (a process called apoptosis), leaving the other, functional myocardial cells struggling to maintain CO. As cardiac cells die and the heart muscle becomes fibrotic, diastolic heart failure, also called Heart Failure with preserved Ejection Fraction (HFpEF), can develop, leading to further dysfunction. A stiff ventricle resists filling, and less blood in the ventricles causes a further decrease in CO. All of these compensatory mechanisms of HF have been referred to as the “vicious cycle of heart failure” because low CO leads to multiple mechanisms that make the heart work harder, worsening the HF. Clinical Manifestations The cardinal manifestations of HF are dyspnea; fatigue, which may limit exercise tolerance; and fluid retention, which may lead to congestion, evidenced by pulmonary and peripheral edema. The signs and symptoms of HF are related to the ventricle that is most affected. Left-sided heart failure, also referred to as left ventricular failure because of the inability of the left ventricle to fill or eject sufficient blood into the systemic circulation, causes different manifestations than right-sided heart failure, also referred to as right ventricular failure because of the inability of the right ventricle to fill or eject sufficient blood into the pulmonary circulation. In chronic HF, particularly congestive heart failure, patients may have signs and symptoms of both left- and right-sided heart failure. The patient with pulmonary edema manifests signs and symptoms of acute decompensation, warranting expeditious treatment. Left-Sided Heart Failure Pulmonary congestion occurs when the left ventricle cannot effectively pump blood out of the ventricle into the aorta and the systemic circulation. The increased left ventricular end-diastolic blood volume increases the left ventricular end-diastolic pressure, which decreases blood flow from the left atrium into the left ventricle during diastole. The blood volume and pressure build up in the left atrium, decreasing flow through the pulmonary veins into the left atrium. Pulmonary venous blood volume and pressure increase in the lungs, forcing fluid from the pulmonary capillaries into the pulmonary tissues and alveoli, causing pulmonary interstitial edema and impaired gas exchange. The clinical manifestations of pulmonary congestion include dyspnea, cough, pulmonary crackles, and low oxygen saturation levels. An extra heart sound, the S3, or “ventricular gallop,” may be detected on auscultation. It is caused by abnormal ventricular filling. Dyspnea, or shortness of breath, may be precipitated by minimal to moderate activity (dyspnea on exertion [DOE]), yet dyspnea may also occur at rest. The patient may report orthopnea, difficulty breathing when lying flat. Patients with orthopnea may use multiple pillows to prop themselves up in bed, or they may sleep sitting up or in a high, reclined position. Some patients have sudden attacks of dyspnea at pjdb–118l–m4-101124 night, a condition known as paroxysmal nocturnal dyspnea (PND). Fluid accumulating in the dependent extremities during the day may be reabsorbed into the circulating blood volume when the patient lies down. Because the impaired left ventricle cannot eject the increased circulating blood volume, the pressure in the pulmonary circulation increases, shifting fluid into the alveoli. The fluid-filled alveoli cannot exchange oxygen and carbon dioxide. Without sufficient oxygen, the patient experiences dyspnea and has difficulty sleeping. The cough associated with left ventricular failure is initially dry and nonproductive. Most often, patients complain of a dry hacking cough that may be mislabeled as asthma or chronic obstructive pulmonary disease (COPD). Over time, the cough may begin to accumulate secretions. Large quantities of frothy sputum, sometimes pink or tan, may be produced, indicating acute decompensated HF and pulmonary edema. Adventitious breath sounds may be heard in various areas of the lungs. Usually, bibasilar crackles that do not clear with coughing are detected in the early phase of left ventricular failure. As the failure worsens and pulmonary congestion increases, crackles may be auscultated throughout the lung fields. At this point, oxygen saturation may decrease. In addition to pulmonary manifestations, the decreased amount of blood ejected from the left ventricle can lead to inadequate tissue perfusion. The diminished CO has widespread manifestations because not enough blood reaches all of the tissues and organs (low perfusion) to provide the necessary oxygen. The decrease in stroke volume (SV) can also stimulate the sympathetic nervous system to release catecholamines, which further impedes perfusion to many organs, including the kidneys. As reduced CO and catecholamines decrease blood flow to the kidneys, urine output drops. Renal perfusion pressure falls, and the renin–angiotensin–aldosterone system is stimulated to increase blood pressure and intravascular volume. While the patient sleeps, the cardiac workload decreases, improving renal perfusion. This may cause nocturia (i.e., frequent urination at night). As HF progresses, decreased output from the left ventricle may cause other symptoms. Decreased gastrointestinal perfusion causes altered digestion. Decreased brain perfusion causes dizziness, lightheadedness, confusion, restlessness, and anxiety due to decreased oxygenation and blood flow. As anxiety increases, so does dyspnea, increasing anxiety and creating a vicious cycle. Stimulation of the sympathetic system also causes the peripheral blood vessels to constrict, so the skin appears pale or ashen and feels cool and clammy. A decrease in SV causes the sympathetic nervous system to increase the heart rate (tachycardia), often causing the patient to complain of palpitations. The peripheral pulses become weak. Without adequate CO, the body cannot respond to increased energy demands, and the patient becomes easily fatigued and has decreased activity tolerance. Fatigue also results from the increased energy expended in breathing and the insomnia that results from respiratory distress, coughing, and nocturia. Right-Sided Heart Failure When the right ventricle fails, congestion in the peripheral tissues and the viscera predominates. This occurs because the right side of the heart cannot eject blood effectively and cannot accommodate all of the blood that normally returns to it from the venous circulation. Increased venous pressure leads to jugular venous distention (JVD) and increased capillary hydrostatic pressure throughout the venous pjdb–118l–m4-101124 system. Systemic clinical manifestations include dependent edema (edema of the lower extremities), hepatomegaly (enlargement of the liver), ascites (accumulation of fluid in the peritoneal cavity), and weight gain due to retention of fluid. Edema usually affects the feet and ankles and worsens when the patient stands or sits for a long period. The edema may decrease when the patient elevates the legs. Edema can gradually progress up the legs and thighs and eventually into the external genitalia and lower trunk. Ascites is evidenced by increased abdominal girth and may accompany lower body edema or may be the only edema present. Sacral edema is common in patients who are on bed rest, because the sacral area is dependent. Pitting edema, in which indentations in the skin remain after even slight compression with the fingertips, is generally obvious after retention of at least 4.5 kg (10 lb) of fluid (4.5 L). Hepatomegaly and tenderness in the right upper quadrant of the abdomen result from venous engorgement of the liver. The increased pressure may interfere with the liver’s ability to function (secondary liver dysfunction). As hepatic dysfunction progresses, increased pressure within the portal vessels may force fluid into the abdominal cavity, causing ascites. Ascites may increase pressure on the stomach and intestines and cause gastrointestinal distress. Hepatomegaly may also increase pressure on the diaphragm, causing respiratory distress. Anorexia (loss of appetite), nausea, or abdominal pain may result from the venous engorgement and venous stasis within the abdominal organs. The generalized weakness that accompanies right-sided HF results from reduced CO and impaired circulation. Congestive Heart Failure Right-sided heart failure can sometimes occur as a result of left-sided failure. The failure of these dual mechanisms is sometimes referred to as congestive heart failure. When the left ventricle fails, increased fluid pressure is transferred back through the lungs, leading to damage of the right side of the heart. When the right side loses pumping power, the blood backs up in the body’s venous system. This may cause swelling or congestion in the legs, ankles, and swelling within the abdomen such as the GI tract and liver. Increased venous pressure may also lead to JVD and increased capillary hydrostatic pressure throughout the venous system. Edema may be present in the periphery as well as within the pulmonary vascular bed. Without appropriate treatment, this may progress to pulmonary edema. Pulmonary Edema Pulmonary edema is an acute event, reflecting a breakdown of physiologic compensatory mechanisms; hence, it is sometimes referred to as acute decompensated heart failure. It can occur following acute MI or as an exacerbation of chronic HF. When the left ventricle begins to fail, blood backs up into the pulmonary circulation, causing pulmonary interstitial edema. This may occur quickly in some patients, a condition sometimes called flash pulmonary edema. Pulmonary edema can also develop slowly, especially when it is caused by noncardiac disorders such as kidney injury and other conditions that cause fluid overload. The left ventricle cannot handle the volume overload, and blood volume and pressure build up in the left atrium. The rapid increase in atrial pressure results in an acute increase in pulmonary venous pressure, which produces an increase in hydrostatic pressure that forces fluid out of the pulmonary capillaries and into the interstitial spaces and alveoli. As a result of decreased cerebral oxygenation, the patient may become increasingly restless and anxious. Along with a sudden onset of breathlessness and a sense of suffocation, the patient may be tachypneic with low oxygen saturation pjdb–118l–m4-101124 levels. The skin and mucous membranes may be pale to cyanotic, and the hands may be cool and clammy. Tachycardia and JVD may be present. Incessant coughing may occur, producing increasing quantities of foamy sputum. The patient may become progressively confused. The situation demands emergent action before oxygenation and perfusion levels become critical. Assessment and Diagnostic Findings HF may go undetected until the patient presents with signs and symptoms of pulmonary and peripheral edema. Some of the physical signs that suggest HF may also occur with other diseases, such as kidney injury and COPD; therefore, diagnostic testing is essential to confirm a diagnosis of HF. Assessment of ventricular function is an essential part of the initial diagnostic workup. An echocardiogram is performed to determine the ejection fraction (EF), identify anatomic features such as structural abnormalities and valve malfunction, and confirm the diagnosis of HF. The ejection fraction is a measure of ventricular contractility; it is the percentage of the end-diastolic blood volume that is ejected with each heartbeat. An expected EF is 55% to 65% of the ventricular volume; the ventricle does not completely empty between contractions. There are two recognized main types of left-sided HF, with a third, emerging category. In heart failure with reduced ejection fraction (HFrEF), or systolic heart failure, the left ventricle loses the ability to contract effectively, manifesting as EFs of less than 40%, reflecting decreased CO and pump failure. Heart failure with preserved ejection fraction (HFpEF), or diastolic heart failure, is diagnosed when the left ventricular function measures greater than or equal to 50%, yet the ventricle loses its ability to relax due to myocardial stiffness. Because of the noncompliance of the ventricular wall, the chamber is unable to fill at normal capacity during the relaxation phase of diastole. Heart failure with midrange ejection fraction (HFmrEF) is a third and emerging classification category, with EFs typically between 40% and 49%. Diagnosing a patient with HFpEF is more challenging than diagnosing a patient with HFrEF, because the diagnosis of HFpEF is a diagnosis of exclusion. That is, it is made by excluding other potential noncardiac causes suggestive of HF. The incidence of HFpEF is increasing and is becoming more commonplace among older adult women with a history of hypertension; indeed, hypertension is the most common underlying cause of HFpEF. Comorbid conditions such as obesity, CAD, diabetes, atrial fibrillation, and hyperlipidemia are also common in patients with HFpEF. In addition to the echocardiogram, a chest x-ray and a 12-lead electrocardiogram (ECG) are obtained to assist in the diagnosis. Laboratory studies usually performed during the initial workup include serum electrolytes, blood urea nitrogen (BUN), creatinine, liver function tests, thyroid-stimulating hormone, complete blood count (CBC), BNP, and routine urinalysis. The results of these laboratory studies assist in determining the underlying cause and can also be used to establish a baseline to assess effects of treatment. The BNP level is a key diagnostic indicator of HF; high levels are a sign of high cardiac filling pressure and can aid in both the diagnosis and management of HF; in particular, rising levels may suggest an acute exacerbation of HF. BNP levels are best used for diagnostic purposes when there is a baseline measurement and a measurement obtained at the time of treatment (e.g., hospital discharge) to help in determining a posttreatment prognosis. American College of Cardiology and American Heart Association (ACC/AHA) Classification of Heart Failure pjdb–118l–m4-101124  Classification Criteria Patient Treatment Characteristics Recommendations for Appropriate Patients Stage A At high risk for developing left Hypertension Heart healthy lifestyle ventricular dysfunction but without Atherosclerotic Risk factor control of structural heart disease or disease hypertension, lipids, symptoms of HF Diabetes diabetes, obesity Metabolic syndrome Stage B With left ventricular dysfunction or History of myocardial Implement stage A structural heart disease who have infarction recommendations, not developed symptoms of HF Left ventricular plus: hypertrophy ACE inhibitor, or Low ejection fraction ARB, or ARNI for low EF or history of MI Beta-blocker Statin Stage C With left ventricular dysfunction or Shortness of breath Implement stage A and structural heart disease with current Fatigue B recommendations, or prior symptoms of heart disease Decreased exercise plus: tolerance Diuretics Aldosterone antagonist Sodium restriction Implantable defibrillator Cardiac resynchronization therapy Stage D With refractory end-stage HF Symptoms despite Implement stage A, B, requiring maximal medical and C specialized interventions therapy recommendations, Recurrent plus: hospitalizations Fluid restriction End-of-life care Extraordinary measures: Inotropes Cardiac transplantation Mechanical support Medical Management Improvement of cardiac function with optimal pharmacologic management Reduction of symptoms and improvement of functional status Stabilization of patient condition and lowering of the risk of hospitalization pjdb–118l–m4-101124  Delay of the progression of HF and extension of life expectancy Promotion of a lifestyle conducive to cardiac health Treatment options vary according to the severity of the patient’s condition, comorbidities, and cause of the HF, and may include oral and intravenous (IV) medications, lifestyle modifications, supplemental oxygen, and surgical interventions, including implantation of cardiac devices, and cardiac transplantation. Managing the patient with HF begins with providing comprehensive education and counseling to the patient and family. The patient and family must understand the nature of HF and the importance of their participation in the treatment regimen, including side and adverse effects of pharmacologic therapies. Lifestyle recommendations include restriction of dietary sodium; avoidance of smoking, including secondhand smoke; avoidance of excessive fluid and alcohol intake; weight reduction when indicated; and regular exercise. The patient must also know how to recognize signs and symptoms that need to be reported to the primary provider. Pharmacologic Therapy The cornerstone of therapy for patients with HFrEF (systolic HF), which is the most common type of HF, includes a diuretic, an angiotensin system blocker, and a beta-blocker. Many of these medications, particularly angiotensin system blockers and beta-blockers, improve symptoms and extend survival. Others, such as diuretics, improve symptoms but may not affect survival. The patient with HFpEF (diastolic HF) may be prescribed a diuretic, most commonly an aldosterone antagonist, and may also be prescribed an angiotensin system blocker and/or a beta-blocker and find symptomatic relief; however, these drugs are not necessarily associated with improved survival in those patients. Target doses for these medications and alternative medications for treating heart failure are identified in the ACC/AHA guidelines. Nurses, primary providers, and pharmacists work collaboratively toward achieving effective dosing of these medications. Diuretics are prescribed to remove excess extracellular fluid by increasing diuresis in patients with signs and symptoms of fluid overload. ACC/AHA guidelines advocate using the smallest dose of diuretic necessary to control fluid volume. The type and dose of diuretic prescribed depend on clinical signs and symptoms and renal function. Careful patient monitoring and dose adjustments are necessary to balance the effectiveness of these medications with the side effects. Loop, thiazide, and aldosterone-blocking diuretics may be prescribed; these medications differ in their site of action in the kidney and their effects on renal electrolyte excretion and reabsorption. Loop diuretics, such as furosemide, inhibit sodium and chloride reabsorption mainly in the ascending loop of Henle. Patients with HF and with severe volume overload are generally treated with a loop diuretic first. Thiazide diuretics, such as metolazone, inhibit sodium and chloride reabsorption in the early distal tubules. Both of these classes of diuretics increase potassium excretion; therefore, patients treated with these medications must have their serum potassium levels closely monitored. Diuretics can also lead to orthostatic hypotension and kidney injury. Both a loop and a thiazide diuretic may be used in patients with severe HF who are unresponsive to a single diuretic. The need for diuretics can be decreased if the patient avoids excessive fluid intake (e.g., more than 2000 mL/day) and adheres to a low sodium diet (e.g., no more than 2 g/day). Aldosterone antagonists, such as spironolactone, are potassium-sparing diuretics that block the effects of aldosterone in the distal tubule and collecting duct (Yancy et al., 2016). As noted previously, they are frequently prescribed for patients with HFpEF. Serum creatinine and potassium levels are monitored pjdb–118l–m4-101124 frequently (e.g., within the first week and then every 4 weeks) when spironolactone is first given. These drugs are not prescribed for patients with an elevated serum creatinine. Loop diuretics are administered IV for exacerbations of HF when rapid diuresis is necessary, as when pulmonary edema is present. Diuretics improve the patient’s symptoms, provided that renal function is adequate. As HF progresses, cardiorenal syndrome may develop or worsen. Cardiorenal syndrome is a type of prerenal acute kidney injury characterized by a disruption in adequate blood flow to the kidneys. Patients with this syndrome are resistant to diuretics and may require other interventions to deal with congestive signs and symptoms. Angiotensin System Blockers Angiotensin system blockers include classes of medications such as the ACE inhibitors, angiotensin receptor blockers (ARBs), and angiotensin receptor-neprilysin inhibitors (ARNIs). Angiotensin-Converting Enzyme Inhibitors ACE inhibitors, such as lisinopril, have been found to relieve clinical manifestations of HF and significantly decrease mortality and morbidity in patients with HFrEF. Specifically, they slow the progression of HF, improve exercise tolerance, and decrease the number of hospitalizations in patients with HFrEF. ACE inhibitors are also appropriate for hypertension management in patients with HFpEF. Available as oral and IV medications, ACE inhibitors promote vasodilation and diuresis, ultimately decreasing both afterload and preload. Vasodilation reduces resistance to left ventricular ejection of blood, diminishing the heart’s workload and improving ventricular emptying. ACE inhibitors decrease the secretion of aldosterone, a hormone that causes the kidneys to retain sodium and water. ACE inhibitors also promote renal excretion of sodium and fluid (while retaining potassium), thereby reducing left ventricular filling pressure and decreasing pulmonary congestion. These agents are also recommended for prevention of HF in patients at risk due to vascular disease and diabetes. Patients receiving ACE inhibitors are monitored for hypotension, hyperkalemia (increased potassium in the blood), and alterations in renal function, especially if they are also receiving diuretics. Because ACE inhibitors cause the kidneys to retain potassium, the patient who is also receiving a loop diuretic or a thiazide diuretic may not need to take oral potassium supplements. However, the patient receiving a potassium-sparing diuretic, such as an aldosterone antagonist, which does not cause potassium loss with diuresis, must be carefully monitored for hyperkalemia. ACE inhibitors may be discontinued if the potassium level remains greater than 5.5 mEq/L or if the serum creatinine rises. An adverse effect of ACE inhibitors includes a dry, persistent cough that may not respond to cough suppressants due to the inhibition of the enzyme kininase, which inactivates bradykinin. The nurse should carefully assess any cough in a patient taking an ACE inhibitor, as this symptom can also indicate a worsening of ventricular function and failure. In less than 1% of patients, ACE inhibitors may cause an allergic reaction accompanied by angioedema. This reaction tends to occur more frequently in African Americans and women. If angioedema affects the oropharyngeal area and impairs breathing, the ACE inhibitor must be stopped immediately and appropriate emergency care must be provided. If the patient cannot continue taking an ACE inhibitor because of development of cough, an elevated creatinine level, or hyperkalemia, an ARB, an ARNI, or a combination of hydralazine and isosorbide dinitrate is prescribed. pjdb–118l–m4-101124 Angiotensin Receptor Blockers Whereas ACE inhibitors block the conversion of angiotensin I to angiotensin II, ARBs, such as valsartan, block the vasoconstricting effects of angiotensin II at the angiotensin II receptors. ARBs are commonly prescribed as an alternative to ACE inhibitors, as they are associated with reduced morbidity and mortality in patients with HFrEF and can provide symptomatic relief in patients with HFpEF who are intolerant of ACE inhibitors. ARBs do not inhibit kininase; therefore, ARBs are not associated with the bothersome cough that occurs with some patients prescribed an ACE inhibitor. Angiotensin Receptor-Neprilysin Inhibitors An ARNI combines an ARB with a neprilysin inhibitor. Neprilysin is an enzyme that breaks down natriuretic peptides. Participants with HFrEF enrolled in clinical trials who were prescribed an ARNI demonstrated a significant reduction in cardiovascular death or hospitalization as compared with participants prescribed an ACE inhibitor. Based on these findings, updated ACC/AHA guidelines advocate prescribing an ARNI as first-line angiotensin system blocker therapy for most patients with symptomatic HFrEF. However, an ARNI is reportedly a costlier option than most ACE inhibitors and ARBs, which may preclude its practical use. For patients unable to take an ARNI, an ACE inhibitor or ARB is a good alternative. An ARNI should not be administered concurrently or within 36 hours of an ACE inhibitor as concomitant dosing with both agents is associated with angioedema. Adverse effects associated with use of an ARNI are similar to those associated with ACE inhibitor or ARB use; therefore, the nurse should assess for hypotension, renal insufficiency, and angioedema in patients taking an ARNI. Beta-Blockers Beta-blockers block the adverse effects of the sympathetic nervous system. They relax blood vessels, lower blood pressure, decrease afterload, and decrease cardiac workload. Beta-blockers, such as carvedilol, have been found to improve functional status and reduce mortality and morbidity in patients with HF. In addition, beta-blockers have been recommended for patients with asymptomatic HFrEF to prevent progression and the onset of symptoms of HF, even if patients do not have a history of MI. The therapeutic effects of these drugs may not be seen for several weeks or even months. Beta-blockers can produce a number of side effects, including dizziness, hypotension, bradycardia, fatigue, and depression. Side effects are most common in the initial few weeks of treatment. Because of the potential for side effects, beta-blockers are started at a low dose. The dose is titrated up slowly (every few weeks), with close monitoring after each dosage increase. Nurses educate patients about potential symptoms during the early phase of treatment and stress that adjustment to the drug may take several weeks. Nurses must also provide support to patients going through this symptom-provoking phase of treatment. Because beta-blockade can cause bronchiole constriction, these drugs are used with caution in patients with a history of bronchospastic diseases such as asthma. Ivabradine pjdb–118l–m4-101124 Ivabradine is a new agent that is a hyperpolarization-activated cyclic nucleotide channel blocker. It is a medication with unique electrophysiologic effects, characterized by its negative chronotropic effect on the sinoatrial node, thereby decreasing the heart rate without targeting the neurohormonal system. It is indicated as an adjunct agent to beta-blockers in patients with symptomatic HFrEF and with high resting heart rates of at least 70 bpm. It may also be beneficial for patients with HFrEF who cannot tolerate beta- blockers. Adverse effects of ivabradine include bradycardia resulting in dizziness and fatigue; it is also associated with an increased risk of atrial fibrillation. Hydralazine and Isosorbide Dinitrate A combination of hydralazine and isosorbide dinitrate may be an alternative medication for patients who cannot take any of the three angiotensin system blockers (i.e., ACE inhibitor, ARB, and ARNI), so long as the patient’s systolic BP is at least 90 mm Hg. Nitrates (e.g., isosorbide dinitrate) cause venous dilation, which reduces the amount of blood return to the heart and lowers preload. Hydralazine lowers systemic vascular resistance and left ventricular afterload. Hydralazine-isosorbide dinitrate is associated with decreased hospitalizations and improved survival in patients with HFrEF; however, these improvements are not as robust as those associated with angiotensin system blockers. Adverse effects may include hypotension, and rarely, a lupus-type reaction. Digitalis For many years, digitalis (i.e., digoxin) was considered an essential agent for the treatment of HF. With the introduction of newer medications, it is not prescribed as often. Digoxin increases the force of myocardial contraction and slows conduction through the atrioventricular node. It improves contractility, increasing left ventricular output. Although the use of digoxin does not result in decreased mortality rates among patients with HFrEF, it can be effective in decreasing the symptoms of HF and may help prevent hospitalization. Patients with renal dysfunction and older patients should receive smaller doses of digoxin, as it is excreted through the kidneys. A key concern associated with digoxin therapy is digitalis toxicity. Clinical manifestations of toxicity include anorexia, nausea, visual disturbances, confusion, and bradycardia. The serum potassium level is monitored because the effect of digoxin is enhanced in the presence of hypokalemia and digoxin toxicity may occur. A serum digoxin level is obtained if the patient’s renal function changes or there are symptoms of toxicity. Intravenous Infusions IV inotropes (e.g., dopamine, dobutamine, milrinone) increase the force of myocardial contraction; as such, they may be indicated for hospitalized patients with pulmonary edema (i.e., acute decompensated HF). These agents are used for patients who do not respond to routine pharmacologic therapy and are reserved for patients with severe ventricular dysfunction, low blood pressure, or impaired perfusion and evidence of significantly depressed CO, with or without congestion. They are used with caution, as some studies have associated their use with increased mortality. Patients usually require admission to the intensive care unit (ICU) and may also have hemodynamic monitoring with a pulmonary artery catheter or alternative technology. Hemodynamic data are used to assess cardiac function and volume status and to pjdb–118l–m4-101124 guide therapy with inotropes, vasodilators, and diuretics. Patients with end-stage HF who cannot be weaned from IV inotropes may be candidates for continuous therapy at home. Dopamine Dopamine is a vasopressor given to increase BP and myocardial contractility. Given at low doses, a dopamine infusion may be helpful as an adjunct therapy along with loop diuretics in improving diuresis, preserving renal function, and improving renal blood flow. Dobutamine Dobutamine is given to patients with significant left ventricular dysfunction and hypoperfusion. A catecholamine, dobutamine stimulates the beta-1 adrenergic receptors. Its major action is to increase cardiac contractility and renal perfusion to enhance urine output. However, it also increases the heart rate and can precipitate ectopic beats and tachyarrhythmias. Milrinone Milrinone is a phosphodiesterase inhibitor that leads to an increase in intracellular calcium within myocardial cells, increasing their contractility. This agent also promotes vasodilation, resulting in decreased preload and afterload and reduced cardiac workload. Milrinone is administered IV to patients with severe HF, including patients who are waiting for heart transplantation. Because the drug causes vasodilation, the patient’s blood pressure is monitored prior to administration; if the patient is hypovolemic, the blood pressure could drop quickly. The major side effects are hypotension and increased ventricular arrhythmias. Blood pressure and ECG are monitored closely during and following infusions of milrinone. Vasodilators Intravenous vasodilators such as IV nitroglycerin, nitroprusside, or nesiritide may enhance symptom relief for acutely decompensated HF. Their use is contraindicated in patients who are hypotensive. Blood pressure is continually assessed in patients receiving IV vasodilator infusions. Adjunct Medications for Heart Failure Target blood pressures should be less than 130/80 mm Hg. Maintaining BPs at these levels is associated with reduced likelihood of morbid progression to symptomatic HF in patients who are asymptomatic. It is also associated with improved morbidity in patients who are symptomatic with both HFrEF and HFpEF. Anemia is independently associated with HF disease severity, and iron deficiency appears to be uniquely associated with reduced exercise capacity. IV iron repletion in patients with HF may improve functional capacity and quality of life; however, there is mixed evidence to support the use of oral iron supplementation. Erythropoietin-stimulating agents, such as darbepoetin alfa, are not recommended in patients with both HF and anemia as a risk of thromboembolic events associated with their use has been pjdb–118l–m4-101124 observed during clinical trials. Anticoagulants may be prescribed, especially if the patient has a history of atrial fibrillation or a thromboembolic event. Antiarrhythmic drugs such as amiodarone may be prescribed for patients with arrhythmias, along with an evaluation for device therapy with an implantable cardioverter defibrillator (ICD). Medications to manage hyperlipidemia (e.g., statins) are also routinely prescribed, in tandem with guidance on nutritional therapy. It is recommended that patients with HF avoid nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen because the risk of decreased renal perfusion is higher, especially in older adults. Adjunct Therapies for Heart Failure Additional therapies that may be indicated in the treatment of patients with HF include nutritional therapy, supplemental oxygen, management of sleep disorders, and procedural or surgical interventions. Nutritional Therapy Following a low sodium (no more than 2 g/day) diet and avoiding excessive fluid intake are usually recommended, although studies differ regarding the effectiveness of sodium restriction. Decreasing dietary sodium reduces fluid retention and the symptoms of peripheral and pulmonary congestion. The purpose of sodium restriction is to decrease the amount of circulating blood volume, which decreases myocardial work. A balance should be achieved between the patient’s ability to adhere to the diet and the recommended guidelines. Nutritional supplements, such as vitamins and antioxidants, are not recommended for patients with HF as no benefits are associated with their use. Omega-3 polyunsaturated fatty acid (PUFA) supplementation is associated with decreased fatal cardiovascular events and is recommended for patients with either HFrEF or HFpEF, unless contraindicated. Any change in eating patterns should consider good nutrition as well as the patient’s likes, dislikes, and cultural food patterns. Patient adherence is important because dietary indiscretions may result in exacerbations of HF symptoms. However, behavioral changes in eating patterns are difficult for many patients to achieve. Supplemental Oxygen Oxygen therapy may become necessary as HF progresses based on the degree of pulmonary congestion and resulting hypoxia. Some patients require supplemental oxygen only during periods of activity. Management of Sleep Disorders Sleep disorders, including sleep apnea, are common in patients with HF. It is estimated that 61% of patients with HF have either central or obstructive sleep apnea (OSA). A formal sleep study should be performed. Continuous positive airway pressure (CPAP) might be recommended if results from the sleep study suggest OSA. CPAP has been shown to improve sleep quality, reduce apneic episodes and excessive daytime sleepiness, and improve nocturnal oxygenation in patients with OSA and HF. Procedural and Surgical Interventions pjdb–118l–m4-101124 Patients with HF are at high risk for arrhythmias, and sudden cardiac death is common among patients with advanced HF. In patients with severe left ventricular dysfunction and the possibility of life-threatening arrhythmias, placement of an ICD can prevent sudden cardiac death and extend survival. Candidates for an ICD include those with an EF less than 35%, including those with and without a history of ventricular arrhythmias. Patients with HF who do not improve with standard therapy may benefit from cardiac resynchronization therapy (CRT). CRT involves the use of a biventricular pacemaker to treat electrical conduction defects and to synchronize ventricular contractions. A prolonged QRS duration on ECG indicates left bundle branch block, which is a type of delayed conduction that is frequently seen in patients with HF. This problem results in asynchronous conduction and contraction of the right and left ventricles, which can further decrease EF. The use of a pacing device with leads placed in the right atrium, right ventricle, and left ventricular cardiac vein can synchronize the contractions of the right and left ventricles. This intervention improves CO, optimizes myocardial energy consumption, reduces mitral regurgitation, and slows the ventricular remodeling process. For patients with a CRT, improvement of left ventricular EF is associated with reduced rates of ventricular arrhythmias. There are combination devices available for patients who require CRT and an ICD. Ultrafiltration is an alternative intervention for patients with severe fluid overload. It is reserved for patients with advanced HF who are resistant to diuretic therapy. A dual-lumen central IV catheter is placed, and the patient’s blood is circulated through a small bedside filtration machine. Liters of excess fluid and plasma are removed slowly from the patient’s intravascular circulating volume over a number of hours. The patient’s output of filtration fluid, blood pressure, and hemoglobin (analyzed for hemoconcentration) are monitored as indicators of volume status. Research on ultrafiltration is ongoing, and targets comparisons of its efficacy to diuretics and the optimal fluid removal target. For some patients with end-stage HF, cardiac transplantation is one of the few options for long-term survival. Patients with ACC/AHA stage D HF who may be eligible are referred for consideration of transplantation. Some of these patients require mechanical circulatory assistance with an implanted ventricular assist device as a bridge therapy to cardiac transplantation. A left ventricular assist device may also be implanted as destination therapy (permanent therapy) for select patients. Cardiogenic Shock Cardiogenic shock occurs when decreased CO leads to inadequate tissue perfusion and initiation of the shock syndrome. Cardiogenic shock most commonly occurs following acute MI when a large area of myocardium becomes ischemic and hypokinetic. It also can occur as a result of end-stage HF, cardiac tamponade, pulmonary embolism (PE), cardiomyopathy, and arrhythmias. Cardiogenic shock is a life- threatening condition with a high mortality rate. Thromboembolism Patients with cardiovascular disorders are at risk for the development of arterial thromboemboli and venous thromboemboli (VTE). Intracardiac thrombi can form in patients with atrial fibrillation because the atria do not contract forcefully, resulting in slow and turbulent flow, and increasing the likelihood of pjdb–118l–m4-101124 thrombus formation. Mural thrombi can also form on ventricular walls when contractility is poor. Intracardiac thrombi can break off and travel through the circulation to other structures, including the brain, where they cause a stroke. Clots within the cardiac chambers can be detected by an echocardiogram and treated with anticoagulant agents, such as heparin and warfarin. Decreased mobility and other factors in patients with cardiac disease also can lead to clot formation in the deep veins of the legs. Although signs and symptoms of deep vein thrombosis (DVT) can vary, patients may report leg pain and swelling and the leg may appear erythematous and feel warm. These clots can break off and travel through the inferior vena cava and through the right side of the heart into the pulmonary artery, where they can cause a pulmonary embolus. Pericardial Effusion and Cardiac Tamponade Pericardial effusion (accumulation of fluid in the pericardial sac) may accompany advanced HF, pericarditis, metastatic carcinoma, cardiac surgery, or trauma. Normally, the pericardial sac contains about 20 mL of fluid, which is needed to decrease friction for the beating heart. An increase in pericardial fluid raises the pressure within the pericardial sac and compresses the heart. This has the following effects: Elevated pressure in all cardiac chambers Decreased venous return due to atrial compression Inability of the ventricles to distend and fill adequately Pericardial fluid may build up slowly without causing noticeable symptoms until a large amount (1 to 2 L) accumulates. However, a rapidly developing effusion (e.g., hemorrhage into the pericardial sac from chest trauma) can quickly stretch the pericardium to its maximum size and cause an acute problem. As pericardial fluid increases, pericardial pressure increases, reducing venous return to the heart and decreasing CO. This can result in cardiac tamponade, which causes low CO and obstructive shock. Clinical Manifestations The signs and symptoms of pericardial effusion can vary according to whether the problem develops quickly or slowly. In acute cardiac tamponade, the patient suddenly develops chest pain, tachypnea, and dyspnea. JVD results from poor right atrial filling and increased venous pressure. Hypotension occurs from low CO, and heart sounds are often muted. The subacute presentation of a pericardial effusion is less dramatic. The patient may report chest discomfort or a feeling of fullness. The feeling of pressure in the chest may result from stretching of the pericardial sac. These patients also develop dyspnea, JVD, and hypotension over time. Patients with cardiac tamponade typically have tachycardia in response to low CO. In addition to hypotension, patients with cardiac tamponade may develop pulsus paradoxus, a systolic blood pressure that is markedly lower during inhalation. Also known as paradoxical pulse, this finding is characterized by an abnormal difference of at least 10 mm Hg in systolic pressure between the point that it is heard during exhalation and the point that it is heard during inhalation. This difference is caused by the variation in cardiac filling that occurs with changes in intrathoracic pressure during breathing. Assessment and Diagnostic Findings pjdb–118l–m4-101124 An echocardiogram is performed to confirm the diagnosis and quantify the amount of pericardial fluid. A chest x-ray may show an enlarged cardiac silhouette due to pericardial effusion. The ECG shows tachycardia and may also show low voltage. Medical Management Pericardiocentesis If cardiac function becomes seriously impaired, pericardiocentesis (puncture of the pericardial sac to aspirate pericardial fluid) is performed. During this procedure, the patient is monitored by continuous ECG and frequent vital signs. Catheter pericardiocentesis is performed using echocardiography to guide placement of the drainage catheter. A resulting decrease in central venous pressure and an associated increase in blood pressure after withdrawal of pericardial fluid indicate that the cardiac tamponade has been relieved. The patient almost always feels immediate relief. If there is a substantial amount of pericardial fluid aspirated, a small catheter may be left in place to drain recurrent accumulation of blood or fluid. Pericardial fluid is sent to the laboratory for examination for tumor cells, bacterial culture, chemical and serologic analysis, and differential blood cell count. Pericardiotomy Recurrent pericardial effusions, usually associated with neoplastic disease, may be treated by a pericardiotomy (pericardial window). Under general anesthesia, a portion of the pericardium is excised to permit the exudative pericardial fluid to drain into the lymphatic system. The nursing care following the procedure includes routine postsurgical care in addition to observation for recurrent tamponade. Hypertensive Crisis Two classes of hypertensive crisis that require immediate intervention include hypertensive emergency and hypertensive urgency, which occur when the SBP exceeds 180 mm Hg or the DBP exceeds 120 mm Hg. Hypertensive emergencies and urgencies may occur in patients with secondary hypertension, and in those whose hypertension has been poorly controlled, whose hypertension has been undiagnosed, or in those who have abruptly discontinued their medications (i.e., rebound hypertension). Once the hypertensive crisis has been managed, a complete evaluation is performed to review the patient’s ongoing treatment plan, and strategies to prevent the occurrence of subsequent hypertensive crises are implemented. Hypertensive Emergency Hypertensive emergency is severe BP elevation (SBP greater than 180 mm Hg or DBP greater than 120 mm Hg) with new or worsening target organ damage. Some examples of target organ damage that may occur include hypertensive encephalopathy, ischemic stroke, MI, heart failure with pulmonary edema, dissecting aortic aneurysm, and renal failure. The 1-year mortality rate is more than 79% and median survival is 10.4 months if left untreated. The patient needs to be admitted to the intensive care unit for pjdb–118l–m4-101124 continuous monitoring of BP and parenteral administration of an appropriate antihypertensive medication. Hypertensive Urgency Hypertensive urgency is severe BP elevation (SBP greater than 180 mm Hg or DBP greater than 120 mm Hg) in stable patients without target organ damage as evidenced based on clinical examination and results of laboratory studies. Many times, patients with a hypertensive urgency are nonadherent with antihypertensive therapy, resulting in rebound hypertension. The underlying reason for nonadherence should be explored (e.g., finances, anxiety, misunderstandings, miscommunication, drug side effects, or recreational drug use) and the team approach used and resources mobilized to prevent nonadherence from continuing or recurring. Restarting antihypertensive medication therapy or increasing dosages are indicated in treating these patients. Cardiomyopathy Cardiomyopathy is disease of the heart muscle that is 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 cardiomyopathy (RCM), arrhythmogenic right ventricular cardiomyopathy/dysplasia (ARVC/D), and unclassified cardiomyopathy. A patient may have pathology representing more than one of these classifications, such as a patient with HCM with restrictive physiology. Ischemic cardiomyopathy is a term frequently used to describe an enlarged heart caused by coronary artery disease, which is usually accompanied by heart failure. In 2006, the American Heart Association proposed a set of Contemporary Classifications for cardiomyopathies, which continues to be in widespread use. Under this classification system, cardiomyopathies are divided into two major groups based on predominant organ involvement. These include primary cardiomyopathies (genetic, nongenetic, and acquired), which are focused primarily on the heart muscle, and secondary cardiomyopathies, which show myocardial involvement secondary to the influence of a vast list of disease processes that include, but are not limited to, amyloidosis, Fabry disease, sarcoidosis, and scleroderma. 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 place an increased workload on the heart. Often, the decrease in cardiac output can be seen on echocardiogram as a decrease in ejection fraction, expressed as a percentage of the end- diastolic blood volume ejected from the ventricle with each heartbeat. These alterations can lead to heart failure. Dilated Cardiomyopathy pjdb–118l–m4-101124 DCM is the most common form of cardiomyopathy, with a general prevalence of between 1 in 250 and 1 in 2500. DCM is distinguished by significant dilation of the ventricles without simultaneous hypertrophy and systolic dysfunction. The ventricles have elevated systolic and diastolic volumes but a decreased ejection fraction. Microscopic examination of the muscle tissue shows diminished contractile elements (actin and myosin filaments) of the muscle fibers and diffuse necrosis of myocardial cells. The result is poor systolic function. The structural changes decrease the amount of blood ejected from the ventricle with systole, increasing the amount of blood remaining in the ventricle after contraction. Less blood is then able to enter the ventricle during diastole, increasing end-diastolic pressure and eventually increasing pulmonary and systemic venous pressures. Altered valve function, usually regurgitation, can result from an enlarged stretched ventricle. Poor blood flow through the ventricle may also cause ventricular or atrial thrombi, which may embolize to other locations in the body. More than 75 conditions and diseases may cause DCM, including pregnancy, hypertension, heavy alcohol intake, viral infection (e.g., influenza), chemotherapeutic medications (e.g., daunorubicin, doxorubicin), thyrotoxicosis, myxedema, persistent tachycardia, and Chagas disease. When the causative factor cannot be identified, the diagnosis is idiopathic DCM which accounts for 20% to 30% of nonischemic DCM cases. Familial DCM accounts for approximately 30% to 50% of all DCM cases and approximately 40% of familial DCM cases have a definitive genetic etiology. An elucidation of family history by the nurse is therefore a very important component of the assessment process. Early diagnosis and treatment can prevent or delay significant symptoms and sudden death from DCM. Hypertrophic Cardiomyopathy The estimated prevalence of HCM is 0.16% to 0.29% of the adult population. HCM is an autosomal dominant genetic disorder that leads to increased heart muscle size and mass, especially along the septum but can involve other areas of the heart. The phenotypic expression of the disease is age dependent. HCM is the leading cause of sudden death in adolescents and young adults, particularly in athletes. 12-lead ECGs, physical examinations, and echocardiograms are used to screen for the disease. Patients with a suspected diagnosis of HCM should undergo genetic testing; if negative, the diagnosis is not completely ruled out. If genetic testing is positive for known HCM genetic mutations, first-degree relatives should also be tested for the genetic mutation found in the patient. In patients that have positive pjdb–118l–m4-101124 genetic testing, but are asymptomatic for cardiomyopathy, annual screening with an ECG, physical examination and echocardiogram should be done, as the likelihood of clinical progression increases with increasing age. The phenotype typically manifests sometime between adolescence and the fifth decade of life. Cardiac muscle cells normally lie parallel to and end to end with each other. The hypertrophied cardiac muscle cells are disorganized, oblique, and perpendicular to each other, decreasing the effectiveness of contractions. In HCM, the coronary arteriole walls are thickened, which decrease the internal diameter of the arterioles. The narrow arterioles restrict the blood supply to the myocardium, causing numerous small areas of ischemia and necrosis. The necrotic areas of the myocardium ultimately fibrose and scar, further impeding ventricular contraction and possibly increasing the risk of arrhythmias such as ventricular tachycardia and ventricular fibrillation. Increased thickness of the heart muscle reduces the size of the ventricular cavities and causes the ventricles to take a longer time to relax after systole. During the first part of diastole, it is more difficult for the ventricles to fill with blood. The atrial contraction at the end of diastole becomes critical for ventricular filling and systolic contraction. HCM can lead to obstruction of the left ventricular outflow tract (LVOT) if there is systolic anterior motion of the mitral valve that abuts the mitral valve against the hypertrophied septum during systole. LVOT obstruction is a dynamic process that is dependent on both the volume of blood in the left ventricle as well as the ability of the myocytes to contract. Approximately one third of patients with HCM have LVOT obstruction at rest that worsens with provocation, another one third do not have obstruction at rest, but can get obstruction with provocation (e.g., exercise or the Valsalva maneuver), and roughly one third of patients have no LVOT obstruction even with provocation. Obstruction of the LVOT can lead to syncope, ventricular arrhythmias, dyspnea, and heart failure. The presence of a systolic ejection murmur can be indicative of LVOT, and echocardiography is then indicated to confirm its presence. Hydration, beta- blockers, calcium channel blockers, and lifestyle modification can be used to minimize LVOT obstruction. In particular, patients should avoid activities that can cause rapid alterations to preload (e.g., hot tubs, saunas, prolonged hot showers). However, patients that do not respond to medical therapy should be considered for surgical myectomy or alcohol septal ablation to decrease the size of the hypertrophied septum and thereby eliminate LVOT obstruction. Restrictive Cardiomyopathy RCM is the least common type of cardiomyopathy. RCM is characterized by diastolic dysfunction caused by rigid ventricular walls that impair diastolic filling and ventricular stretch. A rigid ventricle alters the curve in the Frank–Starling law and leads to the rapid rise of filling pressures despite only small increases in blood volume. However, chamber size and systolic function are usually normal. Arrhythmias and conduction disturbances are common. Signs and symptoms are similar to constrictive pericarditis and include dyspnea, nonproductive cough, and chest pain. Echocardiography may be useful in differentiating between these two conditions. Generally, RCM is either due to an inherited or acquired disease that may be systemic. There are four general categories for the causes of RCM: infiltrative disease, storage disease, noninfiltrative, and endomyocardial. An example of an infiltrative disease that may cause RCM is amyloidosis, in which amyloid, a misfolded protein, is deposited between cardiomyocytes. An inherited storage disease that can lead to RCM is hemochromatosis, in which iron deposits in the heart lead to cardiac stiffness. Scleroderma is a noninfiltrative connective tissue disorder that can cause RCM. Certain cancer treatments, such as pjdb–118l–m4-101124 radiation and use of various chemotherapeutic agents (e.g., anthracyclines) can cause endomyocardial damage that leads to RCM. Often, endomyocardial biopsy is needed to determine the etiology; treatment is then directed at the underlying cause. Arrhythmogenic Right Ventricular Cardiomyopathy/Dysplasia ARVC/D is an uncommon form of inherited heart muscle disease. The prevalence is estimated to be between 1 in 2000 and 1 in 5000 people in the general population. ARVC/D occurs when the myocardium is progressively infiltrated and replaced by fibrous scar and adipose tissue. Infiltration of fibrous and adipose tissue leads to ventricle dilatation, poor contractility, and arrhythmias. Initially, only localized areas of the right ventricle are affected, but as the disease progresses, the entire heart is affected. Because of this typical pathologic progression, there is a move to change the name of this cardiomyopathy to a more general term of arrhythmogenic cardiomyopathy (ACM) to recognize the left ventricular involvement. In patients with ARVC/D, palpitations or syncope may develop between 15 and 40 years of age. Sudden cardiac death may also be the first presentation. Diagnosis is made based on the ECG, echocardiogram, cardiac MRI, and family history. Since this is a genetic disorder, patients that are diagnosed are referred to a genetic counselor for testing. However, genetic testing can be negative in up to 50% of patients. If a genetic mutation is identified, first-degree relatives of the patient should undergo genetic testing. Patients affected by arrhythmias may benefit from having an implantable cardioverter defibrillator (ICD) placed. Unclassified Cardiomyopathies Unclassified cardiomyopathies are different from or have characteristics of more than one of the previously described types and are caused by fibroelastosis, noncompacted myocardium, systolic dysfunction with minimal dilation, and mitochondrial diseases. Examples of unclassified cardiomyopathies can include left ventricular noncompaction and stress-induced (Takotsubo) cardiomyopathy. 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 (e.g., DOE, fatigue, PND, cough [especially with exertion or at night], orthopnea, peripheral edema, early satiety, nausea). The patient also may experience chest pain, palpitations, dizziness, nausea, and syncope with exertion. Assessment and Diagnostic Findings Physical examination at early stages may reveal tachycardia and extra heart sounds (e.g., 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 (e.g., crackles on pjdb–118l–m4-101124 pulmonary auscultation, jugular vein distention, pitting edema of dependent body parts, hepatomegaly [i.e., enlarged liver]). Diagnosis is usually made from findings disclosed by the patient history and by ruling out other causes of heart failure such as myocardial infarction. The echocardiogram is one of the most helpful diagnostic tools because the structure and function of the ventricles can be observed easily. Cardiac MRI may also be used, particularly to assist with the diagnosis of HCM and ARCV/D. ECG may demonstrate arrhythmias (atrial fibrillation, ventricular arrhythmias) and changes consistent with left ventricular hypertrophy (left axis deviation, wide QRS, ST changes, inverted T waves). In ARVC/D, the ECG may show QRS widening, T- wave inversions in leads V1–V4, and ventricular ectopy. Additionally, there is often a small epsilon wave at the end of the QRS. The chest x-ray reveals heart enlargement and possibly pulmonary congestion. Cardiac catheterization, coronary CT, or stress testing is often used to rule out coronary artery disease as a causative factor. Endomyocardial biopsy may be performed to analyze myocardial cells, particularly in RCM. Medical Management 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 arrhythmias with antiarrhythmic medications and possibly with an implanted electronic device, such as an ICD. If the patient has signs and symptoms of congestion, fluid intake may be limited to 2 L each day. However, patients with HCM should avoid dehydration and may need beta-blockers to maintain cardiac output and minimize the risk of LVOT obstruction during systole. Anticoagulants are no longer routinely prescribed. For some patients with DCM, biventricular pacing (also known as cardiac resynchronization therapy or CRT) increases the ejection fraction and reverses some of the structural changes in the myocardium. 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 VAD is implanted to support the failing heart until a suitable donor heart becomes available. Left Ventricular Outflow Tract Surgery When patients with HCM and LVOT obstruction become symptomatic despite optimal medical therapy or cannot tolerate medical therapy, surgery is considered. The most common procedure done is a myectomy (sometimes referred to as a myotomy–myectomy or the Morrow procedure), in which some of the heart tissue is excised. Septal tissue approximately 1 cm wide and deep is cut from the enlarged septum below the aortic valve. The length of septum removed typically extends to the papillary muscles. Possible complications include complete heart block and subsequent pacemaker dependence, ventricular septal defects, or failure to adequately alleviate the obstruction. Surgical mortality rates are reportedly between less than 1% and as high as 16%. pjdb–118l–m4-101124 Heart Transplantation Because of advances in surgical techniques and immunosuppressive therapies, heart transplantation is now a therapeutic option for patients with end-stage heart disease. Cyclosporine and tacrolimus are some of the more common immunosuppressants that decrease the body’s rejection of foreign proteins, such as transplanted organs. Unfortunately, these drugs also decrease the body’s ability to resist infections and increase the risk of various cancers, and a satisfactory balance must be achieved between suppressing rejection and avoiding infection. Cardiomyopathy, ischemic heart disease, valvular disease, rejection of previously transplanted hearts, and congenital heart disease are the most common indications for transplantation. Typical candidates have severe symptoms uncontrolled by medical therapy, no other surgical options, and a prognosis of less than 1 to 2 years to live. A multidisciplinary team screens the candidate before recommending the transplantation procedure. The person’s age, pulmonary status, other chronic health conditions, psychosocial status, family support, infections, history of other transplantations, adherence to therapeutic regimens, and current health status are considered. Arrhythmias Arrhythmias are disorders of the formation or conduction (or both) of the electrical impulse within the heart. These disorders can cause disturbances of the heart rate, the heart rhythm, or both. Arrhythmias may initially be evidenced by the hemodynamic effect they cause (e.g., a change in conduction may change the pumping action of the heart and cause decreased blood pressure), and are diagnosed by analyzing the electrocardiographic (ECG) waveform. Their treatment is based on the frequency and severity of symptoms produced. Arrhythmias are named according to the site of origin of the electrical impulse and the mechanism of formation or conduction involved. For example, an impulse that originates in the sinoatrial (SA) node and at a slow rate is called sinus bradycardia. Types 1. Sinus Node Arrhythmias Sinus node arrhythmias originate in the SA node; these include sinus bradycardia, sinus tachycardia, and sinus arrhythmia. a. Sinus Bradycardia Sinus bradycardia occurs when the SA node creates an impulse at a slower-than-normal rate. Causes include lower metabolic needs (e.g., sleep, athletic training, hypothyroidism), vagal stimulation (e.g., from vomiting, suctioning, severe pain), medications (e.g., calcium channel blockers [e.g., nifedipine, amiodarone], beta-blockers [e.g., metoprolol]), idiopathic sinus node dysfunction, increased intracranial pressure, and coronary artery disease, especially myocardial infarction (MI) of the inferior wall. Unstable and symptomatic bradycardia is frequently due to hypoxemia. Other possible causes include acute altered mental status (e.g., delirium) and acute decompensated heart failure. pjdb–118l–m4-101124 All characteristics of sinus bradycardia are the same as those of normal sinus rhythm, except for the rate. The patient is assessed to determine the hemodynamic effect and the possible cause of the arrhythmia. If the decrease in heart rate results from stimulation of the vagus nerve, such as with bearing down during defecation or vomiting, attempts are made to prevent further vagal stimulation. If the bradycardia is caused by a medication such as a beta-blocker, the medication may be withheld. If the slow heart rate causes significant hemodynamic changes resulting in shortness of breath, acute alteration of mental status, angina, hypotension, ST-segment changes, or premature ventricular complexes (PVCs), treatment is directed toward increasing the heart rate. Slow heart rate may be due to sinus node dysfunction (previously known as sick sinus syndrome), which has a number of risk factors including increased body mass index, presence of right and left bundle branch block, history of a major cardiovascular event, increased age, and hypertension. Tachy-brady syndrome is the term used when bradycardia alternates with tachycardia. Medical Management Management depends on the cause and symptoms. Resolving the causative factors may be the only treatment needed. If the bradycardia produces signs and symptoms of clinical instability (e.g., acute alteration in mental status, chest discomfort, or hypotension), 0.5 mg of atropine may be given rapidly as an intravenous (IV) bolus and repeated every 3 to 5 minutes until a maximum dosage of 3 mg is given. Rarely, if the bradycardia is unresponsive to atropine, emergency transcutaneous pacing can be instituted, or medications, such as dopamine, isoproterenol, or epinephrine, are given. b. Sinus Tachycardia Sinus tachycardia occurs when the sinus node creates an impulse at a faster-than-normal rate. Causes may include the following: Physiologic or psychological stress (e.g., acute blood loss, anemia, shock, hypervolemia, hypovolemia, heart failure, pain, hypermetabolic states, fever, exercise, anxiety) Medications that stimulate the sympathetic response (e.g., catecholamines, aminophylline, atropine), stimulants (e.g., caffeine, nicotine), and illicit drugs (e.g., amphetamines, cocaine, ecstasy) Enhanced pjdb–118l–m4-101124  automaticity of the SA node and/or excessive sympathetic tone with reduced parasympathetic tone that is out of proportion to physiologic demands, a condition called inappropriate sinus tachycardia Autonomic dysfunction, which results in a type of sinus tachycardia referred to as postural orthostatic tachycardia syndrome (POTS). POTS is characterized by tachycardia without hypotension, and by presyncopal symptoms such as palpitations, lightheadedness, weakness, and blurred vision, which occur with sudden posture changes All aspects of sinus tachycardia are the same as those of normal sinus rhythm, except for the rate. Sinus tachycardia does not start or end suddenly (i.e., it is nonparoxysmal). As the heart rate increases, the diastolic filling time decreases, possibly resulting in reduced cardiac output and subsequent symptoms of syncope (fainting) and low blood pressure. If the rapid rate persists and the heart cannot compensate for the decreased ventricular filling, the patient may develop acute pulmonary edema. Medical Management Medical management of sinus tachycardia is determined by the severity of symptoms and directed at identifying and abolishing its cause. Vagal maneuvers, such as carotid sinus massage, gagging, bearing down against a closed glottis (as if having a bowel movement), forceful and sustained coughing, and applying a cold stimulus to the face (such as applying an ice-cold wet towel to the face), or administration of adenosine should be considered to interrupt the tachycardia. If the tachycardia is persistent and causing hemodynamic instability (e.g., acute alteration in mental status, chest discomfort, hypotension), synchronized cardioversion (i.e., electrical current given in synchrony with the patient’s own QRS complex to stop an arrhythmia) is the treatment of choice, if vagal maneuvers and adenosine are unsuccessful or not feasible. IV beta-blockers (Class II antiarrhythmic) and calcium channel blockers (Clas