23 Management of Patients with

Coronary Vascular Disorders

GLOSSARY

acute coronary syndrome (ACS): signs and symptoms that indicate unstable

angina or acute myocardial infarction

angina pectoris: chest pain brought about by myocardial ischemia atheroma: fibrous cap composed of smooth muscle cells that forms over lipid

deposits within arterial vessels and protrudes into the lumen of the vessel, narrowing the lumen and obstructing blood flow; also called plaque

atherosclerosis: abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and the lumen

contractility: ability of the cardiac muscle to shorten in response to an electrical impulse

coronary artery bypass graft (CABG): a surgical procedure in which a blood

vessel from another part of the body is grafted onto the occluded coronary artery below the occlusion in such a way that blood flow bypasses the blockage

high-density lipoprotein (HDL): a protein-bound lipid that transports cholesterol to the liver for excretion in the bile; composed of a higher proportion of protein to lipid than low-density lipoprotein; exerts a beneficial effect on the arterial wall

ischemia: insufficient tissue oxygenation low-density lipoprotein (LDL): a protein-bound lipid that transports

cholesterol to tissues in the body; composed of a lower proportion of protein to lipid than high-density lipoprotein; exerts a harmful effect on the arterial wall

metabolic syndrome: a cluster of metabolic abnormalities including insulin

resistance, obesity, dyslipidemia, and hypertension that increase the risk of cardiovascular disease

myocardial infarction (MI): death of heart tissue caused by lack of

oxygenated blood flow

percutaneous coronary intervention (PCI): a procedure in which a catheter

is placed in a coronary artery, and one of several methods is employed to reduce blockage within the artery

percutaneous transluminal coronary angioplasty (PTCA): a type of

percutaneous coronary intervention in which a balloon is inflated within a coronary artery to break an atheroma and open the vessel lumen, improving coronary artery blood flow

stent: a metal mesh that provides structural support to a coronary vessel, preventing its closure

sudden cardiac death: abrupt cessation of effective heart activity thrombolytic: a pharmacologic agent that breaks down blood clots; alternatively referred to as a fibrinolytic

troponin: a cardiac muscle biomarker; measurement is used as an indicator of heart muscle injury

Cardiovascular disease is the leading cause of death in the United States for men and women of all racial and ethnic groups (Arnett, Blumenthal, Albert, et al., 2019).

Research related to the identification of and treatment for cardiovascular disease includes all segments of the population affected by cardiac conditions, including women, children, and people of diverse racial and ethnic backgrounds. The results of ongoing research are used by nurses to identify specific prevention and treatment strategies in these populations.

Coronary Artery Disease

Coronary artery disease (CAD) is the most prevalent type of cardiovascular disease in adults. For this reason, nurses must recognize various manifestations of coronary artery conditions and evidence-based methods for assessing, preventing, and treating these disorders.

Coronary Atherosclerosis

The most common cause of cardiovascular disease in the United States is atherosclerosis, an abnormal accumulation of lipid, or fatty substances, and fibrous tissue in the lining of arterial blood vessel walls. These substances block and narrow the coronary vessels in a way that reduces blood flow to the myocardium. Atherosclerosis involves a repetitious inflammatory response to injury of the artery wall and subsequent alteration in the structural and biochemical properties of the arterial walls. New information that relates to the development of atherosclerosis has increased the understanding of treatment and prevention of this progressive and potentially life-threatening process.

Pathophysiology

The inflammatory response involved with the development of atherosclerosis begins with injury to the vascular endothelium and progresses over many years (Norris, 2019). 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 (Norris, 2019).

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 (see Fig. 23-1). Plaque may be stable or unstable, depending on the degree of inflammation and thickness of the fibrous cap. If the fibrous cap over the plaque is thick and the lipid pool remains relatively stable, it can resist the stress of blood flow and vessel movement. If the cap is thin and inflammation is ongoing, the lesion becomes what is called vulnerable plaque. At this point, the lipid core may grow, causing 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.

Figure 23-1 • A, B. Atherosclerosis begins as monocytes and lipids enter the intima of an injured vessel. Smooth muscle cells proliferate within the vessel wall (C), contributing to the development of fatty accumulations and atheroma (D). As the plaque enlarges, the vessel narrows and blood flow decreases (E). The plaque may rupture and a thrombus might form, obstructing blood flow.

The anatomic structure of the coronary arteries makes them particularly susceptible to atherosclerosis. As Figure 23-2 shows, the three major coronary arteries have multiple branches. Atherosclerotic lesions most often form where the vessels branch and with turbulent blood flow, suggesting a hemodynamic component is involved in their formation (Norris, 2019). Although heart disease is most often caused by atherosclerosis of the coronary arteries, other phenomena may also decrease blood flow to the heart. Examples include vasospasm (sudden constriction or narrowing) of a coronary artery and profound hypotension.

Figure 23-2 • The coronary arteries supply the heart muscle with oxygenated blood, adjusting the flow according to metabolic needs. A. Anterior view of the heart. B. Posterior view of heart.

Clinical Manifestations

CAD produces symptoms and complications according to the location and degree of narrowing of the arterial lumen, thrombus formation, and obstruction of blood flow to the myocardium. This impediment to blood flow is usually progressive, causing an inadequate blood supply that deprives the cardiac muscle cells of oxygen needed for their survival. The condition is known as ischemia. Angina pectoris refers to chest pain that is brought about by myocardial ischemia. Angina pectoris usually is caused by significant coronary atherosclerosis. If the decrease in blood supply is great enough, of long enough duration, or both, irreversible damage and death of myocardial cells may result. Over time, irreversibly damaged myocardium undergoes degeneration and is replaced by scar tissue, causing various degrees of myocardial dysfunction. Significant myocardial damage may result in persistently low cardiac output and heart failure where the heart cannot support the body’s needs for blood. A decrease in blood supply from CAD may cause the heart to abruptly stop beating; this is known as sudden cardiac death (see Chapter 25 for further discussion on CPR).

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 (Kannel, 1986). 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 (Davis, 2017). 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. Major risk factors are listed in Chart 23-1. 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. The Framingham Risk Calculator is a tool commonly used to estimate the risk for having a cardiac event within the next 10 years (Grundy, Stone, Bailey, et al., 2018). This tool is designed for adults 20 years and older. The calculation is performed using the individual’s risk factor data, including age, gender, total cholesterol, HDL, smoking status, systolic blood pressure, and need for antihypertensive medication.

In addition, a cluster of metabolic abnormalities known as metabolic syndrome has emerged as a major risk factor for cardiovascular disease (Grundy et al., 2018). 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)

•        Elevated fasting glucose (greater than or equal to 100 mg/dL on two separate occasions, or current drug treatment for elevated glucose)

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 tissue cytokines), free fatty acids, and other substances are known to modify insulin action and contribute to atherogenic changes in the cardiovascular system (see Fig. 23-3).

C-reactive protein (CRP) is known to be an inflammatory marker for cardiovascular risk, including acute coronary events and stroke. The liver produces CRP in response to a stimulus such as tissue injury, and high levels of this protein may occur in people with diabetes and those who are likely to have an acute coronary event (Norris, 2019). 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.

Figure 23-3 • Pathophysiology of cardiovascular disease in metabolic syndrome. Central adiposity plays a major role in the development of metabolic syndrome. Adipokines released from fat cells along with other hormones and metabolites are thought to contribute to the development of metabolic abnormalities. The eventual effect of these processes is the promotion of atherosclerosis.

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 (see Fig. 23-4). This is a physiologic process necessary for the formation of lipoprotein-based cell membranes and other important metabolic processes. When an excess of LDL is produced, LDL particles adhere to receptors in the arterial endothelium. Here, macrophages ingest them, contributing to plaque formation.

Figure 23-4 • Lipoproteins and the development of atherosclerosis. As dietary cholesterol and saturated fat are processed by the gastrointestinal tract, chylomicrons enter the blood. They are broken down into chylomicron remnants in the capillaries. The liver processes them into lipoproteins. When these are released into the circulation, excess low-density lipoproteins (LDLs) adhere to receptors on the intimal wall. Macrophages also ingest LDLs and transport them into the vessel wall, beginning the process of plaque formation. HDLs, high-density lipoproteins; VLDLs, very– low-density lipoproteins.

The American College of Cardiology and the American Heart Association (ACC/AHA) have developed clinical practice guidelines on the treatment of blood cholesterol to reduce cardiovascular risk in adults (Grundy et al., 2018). These guidelines address primary prevention (preventing the occurrence of CAD) and secondary prevention (preventing the progression of CAD). All adults 20 years and older should have a fasting lipid profile (total cholesterol, LDL, HDL, and triglycerides) performed at least once every 5 years, and more often if the profile is abnormal. Patients who have had an acute event (e.g., MI), a percutaneous coronary intervention (PCI), or a coronary artery bypass graft (CABG) require assessment of their LDL cholesterol level within a few months of the event or procedure, because LDL levels may be low immediately after the acute event or procedure. Subsequently, lipids should be monitored every 4 to 12 weeks until the desired level is achieved and then every 3 to 12 months as needed (Grundy et al., 2018). A fasting lipid profile should demonstrate the following values (Stone, Robinson, Lichtenstein, et al., 2014):

•        LDL cholesterol less than 100 mg/dL (less than 70 mg/dL for very high risk patients)

•        Total cholesterol less than 200 mg/dL

•        HDL cholesterol greater than 40 mg/dL for males and greater than 50 mg/dL for females

•        Triglyceride less than 150 mg/dL

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.

 Concept Mastery Alert

It is important to remember the different types of cholesterol and the role of each as a risk factor for heart disease. HDL is the “good cholesterol,” and higher levels are better; LDL is the “bad cholesterol,” and lower levels are better.

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 (Franquesa, Pujol-Busquets, García-Fernández, et al., 2019). 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 (Arnett et al., 2019). 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.

Many resources are available to assist people in controlling their cholesterol levels. The National Heart, Lung, and Blood Institute (NHLBI) and its National Cholesterol Education Program (NCEP), the AHA, and the American Diabetes Association (ADA), as well as CAD support groups and reliable Internet sources, are a few examples of the available resources (see Resources section at the end of this chapter). Cookbooks and recipes that include the nutritional contents of foods can be included as resources for patients. Dietary control has been made easier because food manufacturers are required to provide nutritional data on product labels. The label information of interest to a person attempting to eat a heart-healthy diet is as follows: serving size (expressed in household measures), amount of total fat per serving, amount of saturated fat and trans fat per serving, amount of cholesterol per serving, and amount of fiber per serving.

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 moderateintensity 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 (Arnett et al., 2019). 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

If diet alone cannot normalize serum cholesterol levels, medications can have a synergistic effect with the prescribed diet and control cholesterol levels (see Table 231). Lipid-lowering medications can reduce CAD mortality in patients with elevated lipid levels and in at-risk patients with normal lipid levels (Grundy et al., 2018). The various types of lipid-lowering agents affect the lipid components somewhat differently; these types include 3-hydroxy-3-methylglutaryl coenzyme A (HMGCoA) (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 (Grundy et al., 2018).

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 (Grundy et al., 2018).

Promoting Cessation of Tobacco Use

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 (Frandsen & Pennington, 2021). 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 (Lee, Ong, Zhou, et al., 2019). 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 (Frandsen & Pennington, 2021). Hemoglobin, the oxygen-carrying component of blood, combines more readily with carbon monoxide than with oxygen. Myocardial ischemia and reduced contractility can result.

↓ decrease, ↑ increase; ACS, acute coronary syndrome; CABG, coronary artery bypass graft; GI, gastrointestinal; HDL, high-density lipoprotein; HMG-CoA, 3-hydroxy3-methylglutaryl coenzyme A; LDL, low-density lipoprotein; MI, myocardial infarction; TGs, triglycerides.

Adapted from Frandsen, G., & Pennington, S. S. (2021). Abrams’ clinical drug therapy: Rationales for nursing practice (12th ed.). Philadelphia, PA: Wolters Kluwer Health.

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 (Benjamin, Muntner, Alonso, et al., 2019).

The use of medications such as the nicotine patch, nicotine lozenges, nicotine gum, varenicline, or bupropion may assist with stopping the use of tobacco (Barua, Rigotti, Benowitz, et al., 2018). 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.

Exposure to others’ smoke (passive or secondhand smoke) increases the risk for CAD by 25% to 30% and for stroke by 20% to 30% (Benjamin et al., 2019). Other forms of tobacco use are becoming increasingly common today. Use of electronic nicotine delivery systems (ENDS) including e-cigarettes, e-pens, e-pipes, e-hookah, and e-cigars has increased, particularly among adolescents and young adults. Specifically, e-cigarette use, which entails inhalation of a vaporized liquid that includes nicotine, solvents, and flavoring (“vaping”), has risen significantly in these groups. Use of cigarillos and other mass market cigars, hookahs, and water pipes are also on the rise. Short-term exposure to water pipe smoking is associated with an increase in systolic blood pressure and heart rate, but long-term effects remain unclear. The cardiovascular risks associated with e-cigarette use are not yet known (Benjamin et al., 2019).

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 (Whelton, Carey, Aronow, et al., 2018). 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 (Whelton et al., 2018). 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 (Whelton et al., 2018; see Chapter 27 for a detailed discussion of hypertension).

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 other therapeutic interventions that lower plasma glucose levels can lead to improved endothelial function and patient outcomes. See Chapter 46 for a detailed discussion of diabetes.

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 (Wada, Miyauchi, & Daida, 2019). 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 (Wada et al., 2019).

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 (Wada et al., 2019; see Chapter 21 for further discussion).

In the past, women who possibly had coronary vascular events were less likely than men to be referred for coronary artery diagnostic procedures such as heart catheterization or treatment with invasive interventions (e.g., PCI). However, as a result of better education of health care professionals and the general public, gender differences now have less influence on diagnosis and treatment (Wada et al., 2019).

Unfolding Patient Stories: Carl Shapiro • Part 1

Angina Pectoris

Angina pectoris is a clinical syndrome usually characterized by episodes or paroxysms of pain or pressure in the anterior chest. The cause is insufficient coronary blood flow, resulting in a decreased oxygen supply when there is increased myocardial demand for oxygen in response to physical exertion or emotional stress. In other words, the need for oxygen exceeds the supply.

Pathophysiology

Angina is usually caused by atherosclerotic disease and most often is associated with a significant obstruction of at least one major coronary artery. Normally, the myocardium extracts a large amount of oxygen from the coronary circulation to meet its continuous demands. When demand increases, flow through the coronary arteries needs to be increased. When there is a blockage in a coronary artery, flow cannot be increased and ischemia results. The types of angina are listed in Chart 23-2. Several factors are associated with typical anginal pain:

•        Physical exertion, which precipitates an attack by increasing myocardial oxygen demand

•        Exposure to cold, which causes vasoconstriction and elevated blood pressure, with increased oxygen demand

•        Eating a heavy meal, which increases the blood flow to the mesenteric area for digestion, thereby reducing the blood supply available to the heart muscle; in a severely compromised heart, shunting of blood for digestion can be sufficient to induce anginal pain

•        Stress or any emotion-provoking situation, causing the release of catecholamines, which increases blood pressure, heart rate, and myocardial workload

Unstable angina is not closely associated with these listed factors. It may occur at rest (see later discussion).

Clinical Manifestations

Ischemia of the heart muscle may produce pain or other symptoms, varying from mild indigestion to a choking or heavy sensation in the upper chest. The severity ranges from discomfort to agonizing pain. The pain may be accompanied by severe apprehension and a feeling of impending death. It is often felt deep in the chest behind the sternum (retrosternal area). Typically, the pain or discomfort is poorly localized and may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms, usually the left arm. The patient often feels tightness or a heavy choking or strangling sensation that has a viselike, insistent quality. The patient with diabetes may not have severe pain with angina because autonomic neuropathy can blunt nociceptor transmission, dulling the perception of pain (Norris, 2019).

A feeling of weakness or numbness in the arms, wrists, and hands, as well as shortness of breath, pallor, diaphoresis, dizziness or lightheadedness, and nausea and vomiting, may accompany the pain. An important characteristic of angina is that it subsides with rest or administration of nitroglycerin. In many patients, anginal symptoms follow a stable, predictable pattern.

Unstable angina is characterized by attacks that increase in frequency and severity and are not relieved by rest and administration of nitroglycerin. Patients with unstable angina require medical intervention.

 Gerontologic Considerations

The older adult with angina may not exhibit a typical pain profile because of the diminished pain transmission that can occur with aging. Often the presenting symptom in older adults is dyspnea. Sometimes there are no symptoms (“silent” CAD), making recognition and diagnosis a clinical challenge. Older patients should be encouraged to recognize their chest pain–like symptom (e.g., weakness) as an indication that they should rest or take prescribed medications. Pharmacologic stress testing and cardiac catheterization may be used to diagnose CAD in older patients. Medications used to manage angina are given cautiously in older adults because they are associated with an increased risk of adverse reactions (Frandsen & Pennington, 2021). Invasive procedures (e.g., PCI) that were once considered too risky in older adults are now being performed successfully, and many older adults benefit from symptom relief and longer survival (Lattuca, Kerneis, & Zeitouni, 2019).

Assessment and Diagnostic Findings

The diagnosis of angina begins with the patient’s history related to the clinical manifestations of ischemia. A 12-lead electrocardiogram (ECG) may show changes indicative of ischemia, such as T-wave inversion, ST-segment elevation, or the development of an abnormal Q wave (Norris, 2019). Laboratory studies are performed; these generally include cardiac biomarker testing to rule out ACS (see later discussion). The patient may undergo an exercise or pharmacologic stress test in which the heart is monitored continuously by an ECG, echocardiogram, or both. The patient may also be referred for a nuclear scan or invasive procedure (e.g., cardiac catheterization, coronary angiography).

Medical Management

The objectives of the medical management of angina are to decrease the oxygen demand of the myocardium and to increase the oxygen supply. Medically, these objectives are met through pharmacologic therapy and control of risk factors. Alternatively, reperfusion procedures may be used to restore the blood supply to the myocardium. These include PCI procedures (e.g., percutaneous transluminal coronary angioplasty [PTCA] and intracoronary stents) and CABG (see later discussion).

Pharmacologic Therapy

Table 23-2 summarizes drug therapy.

Nitroglycerin

Nitrates are a standard treatment for angina pectoris. Nitroglycerin is a potent vasodilator that improves blood flow to the heart muscle and relieves pain. Nitroglycerin dilates primarily the veins and, to a lesser extent, the arteries. Dilation of the veins causes venous pooling of blood throughout the body. As a result, less blood returns to the heart, and filling pressure (preload) is reduced. If the patient is hypovolemic (does not have adequate circulating blood volume), the decrease in filling pressure can cause a significant decrease in cardiac output and blood pressure (Frandsen & Pennington, 2021).

Nitrates also relax the systemic arteriolar bed, lowering blood pressure and decreasing afterload. These effects decrease myocardial oxygen requirements, bringing about a more favorable balance between supply and demand.

Nitroglycerin may be given by several routes: sublingual tablet or spray, oral capsule, topical agent, and intravenous (IV) administration. Sublingual nitroglycerin is generally placed under the tongue or in the cheek (buccal pouch) and ideally alleviates the pain of ischemia within 3 minutes. Chart 23-3 provides more information on self-administration of sublingual nitroglycerin. Oral preparations and topical patches are used to provide sustained effects. A regimen in which the patches are applied in the morning and removed at bedtime allows for a nitrate-free period to prevent the development of tolerance.

Adapted from Rousan, T. A., Mathew, S. T., & Thadani, U. (2017). Drug therapy for stable angina pectoris. Drugs, 77(3), 265–284.

A continuous or intermittent IV infusion of nitroglycerin may be given to the hospitalized patient with recurring signs and symptoms of ischemia or after a revascularization procedure. The rate of infusion is titrated to the patient’s pain level and blood pressure. It usually is not given if the systolic blood pressure is less than 90 mm Hg. Generally, after the patient is symptom-free, the nitroglycerin may be switched to an oral or topical preparation within 24 hours. A common adverse effect of nitroglycerin is headache, which may limit the use of this drug in some patients.

Beta-Adrenergic Blocking Agents

Beta-blockers such as metoprolol reduce myocardial oxygen consumption by blocking beta-adrenergic sympathetic stimulation to the heart. The result is a reduction in heart rate, slowed conduction of impulses through the conduction system, decreased blood pressure, and reduced myocardial contractility (force of contraction). Because of these effects, beta-blockers balance the myocardial oxygen needs (demands) and the amount of oxygen available (supply). This helps control chest pain and delays the onset of ischemia during work or exercise. Beta-blockers reduce the incidence of recurrent angina, infarction, and cardiac mortality. The dose can be titrated to achieve a resting heart rate of 50 to 60 bpm (Frandsen & Pennington, 2021).

Cardiac side effects and possible contraindications include hypotension, bradycardia, advanced atrioventricular block, and acute heart failure. If a beta-blocker is given IV for an acute cardiac event, the ECG, blood pressure, and heart rate are monitored closely after the medication has been given. Side effects include depressed mood, fatigue, decreased libido, and dizziness. Patients taking beta-blockers are cautioned not to stop taking them abruptly, because angina may worsen, and MI may develop. Beta-blocker therapy should be decreased gradually over several days before being discontinued. Patients with diabetes who take beta-blockers are instructed to monitor their blood glucose levels as prescribed because beta-blockers can mask signs of hypoglycemia. Beta-blockers that are not cardioselective also affect the betaadrenergic receptors in the bronchioles, causing bronchoconstriction, and therefore are contraindicated in patients with significant chronic pulmonary disorders, such as asthma.

Self-Administration of Nitroglycerin

Most patients with angina pectoris self-administer nitroglycerin on an as-needed basis. A key nursing role in such cases is educating patients about the medication and how to take it. Sublingual nitroglycerin comes in tablet and spray forms.

•        Instruct the patient to make sure that the mouth is moist, the tongue is still, and saliva is not swallowed until the nitroglycerin tablet dissolves. If the pain is severe, the patient can crush the tablet between the teeth to hasten sublingual absorption.

•        Advise the patient to carry the medication at all times as a precaution. However, because nitroglycerin is very unstable, it should be carried securely in its original container (e.g., capped dark glass bottle); tablets should never be removed and stored in metal or plastic pillboxes.

•        Explain that nitroglycerin is volatile and is inactivated by heat, moisture, air, light, and time. Instruct the patient to renew the nitroglycerin supply every 6 months.

•        Inform the patient that the medication should be taken in anticipation of any activity that may produce pain. Because nitroglycerin increases tolerance for exercise and stress when taken prophylactically (i.e., before anginaproducing activity, such as exercise, stair-climbing, or sexual intercourse), it is best taken before pain develops.

•        Recommend that the patient note how long it takes for the nitroglycerin to relieve the discomfort. Advise the patient that if pain persists after taking three sublingual tablets at 5-minute intervals, emergency medical services should be called.

•        Discuss possible side effects of nitroglycerin, including flushing, throbbing headache, hypotension, and tachycardia.

•        Advise the patient to sit down for a few minutes when taking nitroglycerin to avoid hypotension and syncope.

Adapted from Comerford, K. C., & Durkin, M. T. (Eds.) (2020). Nursing2020 Drug Handbook. Philadelphia, PA: Wolters Kluwer.

Calcium Channel Blocking Agents

Calcium channel blockers have a variety of effects on the ischemic myocardium. These agents decrease sinoatrial node automaticity and atrioventricular node conduction, resulting in a slower heart rate and a decrease in the strength of myocardial contraction (negative inotropic effect). These effects decrease the workload of the heart. Calcium channel blockers also increase myocardial oxygen supply by dilating the smooth muscle wall of the coronary arterioles; they decrease myocardial oxygen demand by reducing systemic arterial pressure and the workload of the left ventricle (Frandsen & Pennington, 2021). The calcium channel blockers most commonly used are amlodipine and diltiazem. In addition to their use to treat angina, they are commonly prescribed for hypertension. Hypotension may occur after the administration of any of the calcium channel blockers, particularly when administered IV. Other side effects may include atrioventricular block, bradycardia, and constipation.

Antiplatelet and Anticoagulant Medications

Antiplatelet medications are given to prevent platelet aggregation and subsequent thrombosis, which impedes blood flow through the coronary arteries.

Aspirin

Aspirin prevents platelet aggregation and reduces the incidence of MI and death in patients with CAD (Frandsen & Pennington, 2021). A 162- to 325-mg dose of aspirin should be given to the patient with a new diagnosis of angina and then continued with 81 to 325 mg daily. Patients should be advised to continue aspirin even if they concurrently take other analgesics such as acetaminophen. Because aspirin may cause GI upset and bleeding, the use of histamine-2 (H₂) blockers (e.g., famotidine) or proton pump inhibitors (e.g., omeprazole) should be considered concomitant with continued aspirin therapy (Ibanez, James, Agewall, et al., 2018).

Adenosine Diphosphate Receptor Antagonists (P2Y₁₂)

These medications act on different pathways than aspirin to block platelet activation. However, unlike aspirin, these agents may take a few days to achieve antiplatelet effects. Clopidogrel is commonly prescribed in addition to aspirin in patients at high risk for MI. Newer oral agents such as prasugrel and ticagrelor may be used in place of clopidogrel during coronary events and interventions (Frandsen & Pennington, 2021). Both carry the risk of bleeding from the GI tract or other sites.

Heparin

Unfractionated IV heparin prevents the formation of new blood clots (i.e., it is an anticoagulant). Treating patients with unstable angina with heparin reduces the occurrence of MI. If the patient’s signs and symptoms indicate a significant risk for a cardiac event, the patient is hospitalized and may be given an IV bolus of heparin and started on a continuous infusion. The dose of heparin given is based on the results of the activated partial thromboplastin time (aPTT). Heparin therapy is usually considered therapeutic when the aPTT is 2 to 2.5 times the normal aPTT value.

A subcutaneous injection of low-molecular-weight heparin (LMWH; enoxaparin or dalteparin) may be used instead of IV unfractionated heparin to treat patients with unstable angina or non–ST-segment elevation myocardial infarction (NSTEMI) (Frandsen & Pennington, 2021). LMWH provides effective and stable anticoagulation, potentially reducing the risk of rebound ischemic events, and eliminating the need to monitor aPTT results. LMWHs may be beneficial before and during PCIs as well as for ACS.

Because unfractionated heparin and LMWH increase the risk of bleeding, the patient is monitored for signs and symptoms of external and internal bleeding, such as low blood pressure, increased heart rate, and decreased serum hemoglobin and hematocrit. The patient receiving heparin is placed on bleeding precautions, which include:

•        Applying pressure to the site of any needle puncture for a longer time than usual

•        Avoiding intramuscular (IM) injections

•        Avoiding tissue injury and bruising from trauma or use of constrictive devices (e.g., continuous use of an automatic blood pressure cuff)

A decrease in platelet count or evidence of thrombosis may indicate heparininduced thrombocytopenia (HIT), an antibody-mediated reaction to heparin that may result in thrombosis. Patients who have received heparin within the past 3 months and those who have been receiving unfractionated heparin for 4 to 14 days are at high risk for HIT (Frandsen & Pennington, 2021). As an alternative to LMWH and unfractionated heparin, argatroban, a direct antithrombotic agent might be prescribed (Frandsen & Pennington, 2021; see Chapter 29 for further discussion of HIT).

Glycoprotein IIb/IIIa Agents

IV administration of glycoprotein (GP) IIb/IIIa agents, such as abciximab or eptifibatide, is indicated for hospitalized patients with unstable angina and as adjunct therapy for PCI. These agents prevent platelet aggregation by blocking the GP IIb/IIIa receptors on the platelets, preventing adhesion of fibrinogen and other factors that crosslink platelets to each other and thus form intracoronary clots (Urden, Stacy, & Lough, 2019). As with heparin, bleeding is the major side effect, and bleeding precautions should be initiated.

Oxygen Administration

Oxygen therapy is usually initiated at the onset of chest pain in an attempt to increase the amount of oxygen delivered to the myocardium and to decrease pain. The therapeutic effectiveness of oxygen is determined by observing the rate and rhythm of respirations and the color of skin and mucous membranes. Blood oxygen saturation is monitored by pulse oximetry; the normal oxygen saturation (SpO₂) level is >95% on room air (Urden et al., 2019).

NURSING PROCESS

The Patient with Angina Pectoris

Assessment

The nurse gathers information about the patient’s symptoms and activities, especially those that precede and precipitate attacks of angina pectoris. Appropriate questions are listed in Chart 23-4. The answers to these questions form the basis for designing an effective program of treatment and prevention. In addition to assessing angina pectoris or its equivalent, the nurse also assesses the patient’s risk factors for CAD, the patient’s response to angina, the patient’s and family’s understanding of the diagnosis, and adherence to the current treatment plan.

Diagnosis NURSING DIAGNOSES

Based on the assessment data, major nursing diagnoses may include:

•        Risk for impaired cardiac function

•        Anxiety associated with cardiac symptoms and possible death

•        Lack of knowledge about the underlying disease and methods for avoiding complications

•        Able to perform self care

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS Potential complications may include the following:

•        ACS and/or MI (described later in this chapter)

•        Arrhythmias and cardiac arrest (see Chapters 22 and 25)

•        Heart failure (see Chapter 25)

•        Cardiogenic shock (see Chapter 11)

Planning and Goals

Major patient goals include immediate and appropriate treatment when angina occurs, prevention of angina, reduction of anxiety, awareness of the disease process and understanding of the prescribed care, adherence to the self-care program, and absence of complications.

Nursing Interventions TREATING ANGINA

If the patient reports pain (or cardiac ischemia is suggested by prodromal symptoms, which may include sensations of indigestion or nausea, choking, heaviness, weakness or numbness in the upper extremities, dyspnea, or dizziness), the nurse takes immediate action. The patient experiencing angina is directed to stop all activities and sit or rest in bed in a semi-Fowler position to reduce the oxygen requirements of the ischemic myocardium. The nurse assesses the patient’s angina, asking questions to determine whether the angina is the same as the patient typically experiences. A change may indicate a worsening of the disease or a different cause. The nurse then continues to assess the patient, measuring vital signs and observing for signs of respiratory distress. If the patient is in the hospital, a 12-lead ECG is usually obtained and assessed for ST-segment and Twave changes. If the patient has been placed on cardiac monitoring with continuous ST-segment monitoring, the ST segment is assessed for changes.

Nitroglycerin is given sublingually, and the patient’s response is assessed (relief of chest pain and effect on blood pressure and heart rate). If the chest pain is unchanged or is lessened but still present, nitroglycerin administration is repeated up to three doses. Each time blood pressure, heart rate, and the ST segment (if the patient is on a monitor with ST-segment monitoring capability) are assessed. The nurse administers oxygen therapy if the patient’s respiratory rate is increased or if the oxygen saturation level is decreased. Oxygen is usually given at 2 L/min by nasal cannula, even without evidence of desaturation, although there is no current evidence of a positive effect on patient outcome. If the pain is significant and continues after these interventions, the patient is further evaluated for acute MI and may be transferred to a higher-acuity nursing unit (Ibanez et al., 2018).

REDUCING ANXIETY

Patients with angina often fear loss of their roles within society and the family. They may also fear that the pain (or the prodromal symptoms) may lead to an MI or death. Exploring the implications that the diagnosis has for the patient and providing information about the illness, its treatment, and methods of preventing its progression are important nursing interventions. Various stress reduction methods, such as guided imagery or music therapy, should be explored with the patient (Meghani, 2017). Addressing the spiritual needs of the patient and family may also assist in allaying anxieties and fears.

PREVENTING PAIN

The nurse reviews the assessment findings, identifies the level of activity that causes the patient’s pain or prodromal symptoms, and plans the patient’s activities accordingly. If the patient has pain frequently or with minimal activity, the nurse alternates the patient’s activities with rest periods. Balancing activity and rest is an important aspect of the educational plan for the patient and family.

PROMOTING HOME, COMMUNITY-BASED, AND TRANSITIONAL CARE

 Educating Patients About Self-Care. The program for educating the

patient with angina is designed so that the patient and family understand the illness, identify the symptoms of myocardial ischemia, state the actions to take when symptoms develop, and discuss methods to prevent chest pain and the advancement of CAD. The goals of education are to reduce the frequency and severity of anginal attacks, to delay the progress of the underlying disease if possible, and to prevent complications. The factors outlined in Chart 23-5 are important in educating the patient with angina pectoris.

The self-care program is prepared in collaboration with the patient and family or friends. Activities should be planned to minimize the occurrence of anginal episodes. The patient needs to understand that any pain unrelieved within 15 minutes by the usual methods, including nitroglycerin (see Chart 23-3), should be treated at the closest ED; the patient should call 911 for assistance.

Continuing and Transitional Care. For patient with disability or special needs, arrangements are made for transitional, home, or community care when appropriate. A home health or transitional care nurse can assist the patient with scheduling and keeping follow-up appointments. The patient may need reminders about follow-up monitoring, including periodic laboratory testing. In addition, the home health nurse may monitor the patient’s adherence to dietary restrictions and to prescribed antianginal medications, including nitroglycerin. If the patient has severe anginal symptoms, the nurse may assess the home environment and recommend modifications that diminish the occurrence of anginal episodes. For instance, if a patient cannot climb stairs without experiencing ischemia, the home health nurse may help the patient plan daily activities that minimize stair-climbing.

Evaluation

Expected patient outcomes may include:

1.      Reports that pain is relieved promptly

a.      Recognizes symptoms

b.      Takes immediate action

c.      Seeks medical assistance if pain persists or changes in quality

2.      Reports decreased anxiety

a.      Expresses acceptance of diagnosis

b.     Expresses control over choices within medical regimen

c.      Does not exhibit signs and symptoms that indicate a high level of anxiety

3.      Understands ways to avoid complications and is free of complications

a.      Describes the process of angina

b.     Explains reasons for measures to prevent complications

c.      Exhibits stable ECG

d.     Experiences no signs and symptoms of acute MI

4.      Adheres to self-care program

a.      Takes medications as prescribed

b.     Keeps health care appointments

c.      Implements plan to reduce risk factors

 Acute Coronary Syndrome and Myocardial Infarction

Acute coronary syndrome (ACS) is an emergent situation characterized by an acute onset of myocardial ischemia that results in myocardial death (i.e., MI) if definitive interventions do not occur promptly. (Although the terms coronary occlusion, heart attack, and myocardial infarction are used synonymously, the preferred term is myocardial infarction.) The spectrum of ACS includes unstable angina, NSTEMI, and ST-segment elevation myocardial infarction (STEMI).

Pathophysiology

In unstable angina, there is reduced blood flow in a coronary artery, often due to rupture of an atherosclerotic plaque. A clot begins to form on top of the coronary lesion, but the artery is not completely occluded. This is an acute situation that can result in chest pain and other symptoms that may be referred to as preinfarction angina because the patient will likely have an MI if prompt interventions do not occur.

In an MI, plaque rupture and subsequent thrombus formation result in complete occlusion of the artery, leading to ischemia and necrosis of the myocardium supplied by that artery. Vasospasm (sudden constriction or narrowing) of a coronary artery, decreased oxygen supply (e.g., from acute blood loss, anemia, or low blood pressure), and increased demand for oxygen (e.g., from a rapid heart rate, thyrotoxicosis, or ingestion of cocaine) are other causes of MI. In each case, a profound imbalance exists between myocardial oxygen supply and demand.

The area of infarction develops over minutes to hours. As the cells are deprived of oxygen, ischemia develops, cellular injury occurs, and the lack of oxygen results in infarction, or the death of cells. The expression “time is muscle” reflects the urgency of appropriate treatment to improve patient outcomes. Approximately every 40 seconds, an American will have an MI (Benjamin et al., 2019), and many of these people will die as a result. Early recognition and treatment of patients presenting with an MI will improve their chances of survival.

Various descriptions are used to further identify an MI: the type (NSTEMI, STEMI), the location of the injury to the ventricular wall (anterior, inferior, posterior, or lateral wall), and the point in time within the process of infarction (acute, evolving, or old). The differentiation between NSTEMI and STEMI is determined by diagnostic tests and is explained later in this chapter.

The 12-lead ECG identifies the type and location of the MI, and other ECG indicators, such as a Q wave, and patient history, identify the timing. Regardless of the location, the goals of medical therapy are to relieve symptoms, prevent or minimize myocardial tissue death, and prevent complications. The pathophysiology of CAD and the risk factors involved were discussed earlier in this chapter.

Clinical Manifestations

Chest pain that occurs suddenly and continues despite rest and medication is the presenting symptom in most patients with ACS. Some of these patients have prodromal symptoms or a previous diagnosis of CAD, but others report no previous symptoms. Patients may present with a combination of symptoms, including chest pain, shortness of breath, indigestion, nausea, and anxiety. They may have cool, pale, and moist skin. Their heart rate and respiratory rate may be faster than normal. These signs and symptoms, which are caused by stimulation of the sympathetic nervous system, may be present for only a short time or may persist. In many cases, the signs and symptoms of MI cannot be distinguished from those of unstable angina; hence, the evolution of the term acute coronary syndrome.

Assessment and Diagnostic Findings

The diagnosis of ACS is generally based on the presenting symptoms (see Chart 236); the 12-lead ECG and laboratory tests (e.g., serial cardiac biomarkers) are performed to clarify whether the patient has unstable angina, NSTEMI, or STEMI (Ibanez et al., 2018). The prognosis depends on the severity of coronary artery obstruction and the presence and extent of myocardial damage. Physical examination is always conducted, but the examination alone does not confirm the diagnosis.

Patient History

The patient history includes the description of the presenting symptom (e.g., pain), the history of previous cardiac and other illnesses, and the family history of heart disease. The history should also include information about the patient’s risk factors for heart disease.

Electrocardiogram

The 12-lead ECG provides information that assists in ruling out or diagnosing an acute MI. It should be obtained within 10 minutes from the time a patient reports pain or arrives in the ED. By monitoring serial ECG changes over time, the location, evolution, and resolution of an MI can be identified and monitored.

The ECG changes that occur with an MI are seen in the leads that view the involved surface of the heart. The expected ECG changes are T-wave inversion, STsegment elevation, and development of an abnormal Q wave (see Fig. 23-5). Because infarction evolves over time, the ECG also changes over time. The first ECG signs of an acute MI are usually seen in the T wave and ST segment (Urden et al., 2019). As the area of injury becomes ischemic, myocardial repolarization is altered and delayed, causing the T wave to invert. Myocardial injury also causes ST-segment changes. The ST segment is normally flat on the ECG tracing. The injured myocardial cells depolarize normally but repolarize more rapidly than normal cells, causing the ST segment to rise at least 1 mm above the isoelectric line (the area between the T wave and the next P wave is used as the reference for the isoelectric line). This change is measured 0.06 to 0.08 seconds after the end of the QRS—a point called the J point (Urden et al., 2019) (see Fig. 23-6). An elevation in the ST segment in two contiguous leads is a key diagnostic indicator for MI (i.e., STEMI).

Assessing for Acute Coronary Syndrome or Acute Myocardial Infarction

Be alert for the following signs and symptoms:

Cardiovascular

•       Chest pain or discomfort not relieved by rest or nitroglycerin; palpitations. Heart sounds may include S₃, S₄, and new onset of a murmur.

•       Increased jugular venous distention may be seen if the myocardial infarction (MI) has caused heart failure.

•       Blood pressure may be elevated because of sympathetic stimulation or decreased because of decreased contractility, impending cardiogenic shock, or medications.

•       Irregular pulse may indicate atrial fibrillation.

•       In addition to ST-segment and T-wave changes, the electrocardiogram may show tachycardia, bradycardia, or other arrhythmias.

Respiratory

Shortness of breath, dyspnea, tachypnea, and crackles if MI has caused pulmonary congestion. Pulmonary edema may be present.

Gastrointestinal

Nausea, indigestion, and vomiting.

Genitourinary

Decreased urinary output may indicate cardiogenic shock.

Skin

Cool, clammy, diaphoretic, and pale appearance due to sympathetic stimulation may indicate cardiogenic shock.

Neurologic

Anxiety, restlessness, and lightheadedness may indicate increased sympathetic stimulation or a decrease in contractility and cerebral oxygenation. The same symptoms may also herald cardiogenic shock.

Psychological

Fear with feeling of impending doom, or denial that anything is wrong.

The appearance of abnormal Q waves is another indication of MI. Q waves develop within 1 to 3 days because there is no depolarization current conducted from necrotic tissue (Urden et al., 2019). A new and significant Q wave is 0.04 seconds or longer and 25% of the R wave depth. An acute MI may also cause a significant decrease in the height of the R wave. During an acute MI, injury and ischemic changes are usually present. An abnormal Q wave may be present without STsegment and T-wave changes, which indicates an old, not acute, MI. For some patients, there is no persistent ST elevation or other ECG changes; therefore, an NSTEMI is diagnosed by blood levels of cardiac biomarkers.

Figure 23-5 • Effects of ischemia, injury, and infarction on an electrocardiogram recording. Ischemia causes inversion of the T wave because of altered repolarization. Cardiac muscle injury causes elevation of the ST segment. Later, Q waves develop because of the absence of depolarization current from the necrotic tissue and opposing currents from other parts of the heart.

Figure 23-6 • Using the electrocardiogram to diagnose acute myocardial infarction (MI). (ST-segment elevation is measured 0.06 to 0.08 seconds after the J point. An elevation of more than 1 mm in contiguous leads is indicative of acute MI.)

Using the information presented, patients are diagnosed with one of the following forms of ACS:

•        Unstable angina: The patient has clinical manifestations of coronary ischemia, but ECG and cardiac biomarkers show no evidence of acute MI.

•        STEMI: The patient has ECG evidence of acute MI with characteristic changes in two contiguous leads on a 12-lead ECG. In this type of MI, there is a significant damage to the myocardium.

•        NSTEMI: The patient has elevated cardiac biomarkers (e.g., troponin) but no definite ECG evidence of acute MI. In this type of MI, there may be less damage to the myocardium.

During recovery from an MI, the ST segment often is the first ECG indicator to return to normal. Q-wave alterations are usually permanent. An old STEMI is usually indicated by an abnormal Q wave or decreased height of the R wave without STsegment and T-wave changes.

Echocardiogram

The echocardiogram is used to evaluate ventricular function. It may be used to assist in diagnosing an MI, especially when the ECG is nondiagnostic. The echocardiogram can detect hypokinetic and akinetic wall motion and can determine the ejection fraction (see Chapter 21).

Laboratory Tests

Cardiac enzymes and biomarkers, which include troponin, creatine kinase (CK), and myoglobin, are used to diagnose an acute MI. Cardiac biomarkers can be analyzed rapidly, expediting an accurate diagnosis. These tests are based on the release of cellular contents into the circulation when myocardial cells die.

Troponin

Troponin, a protein found in myocardial cells, regulates the myocardial contractile process. There are three isomers of troponin: C, I, and T. Troponins I and T are specific for cardiac muscle, and these biomarkers are currently recognized as reliable and critical markers of myocardial injury (Norris, 2019). An increase in the level of troponin in the serum can be detected within a few hours during acute MI. It remains elevated for a long period, often as long as 2 weeks, and it therefore can be used to detect recent myocardial damage. It should be noted that cardiac troponin levels may rise during inflammation and other forms of mechanical stress on the myocardium. These include sepsis, heart failure, and respiratory failure (Felker & Fudim, 2018).

Creatine Kinase and Its Isoenzymes

There are three CK isoenzymes: CK-MM (skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue). CK-MB is the cardiac-specific isoenzyme; it is found mainly in cardiac cells and therefore increases when there has been damage to these cells. Elevated CK-MB is an indicator of acute MI; the level begins to increase within a few hours and peaks within 24 hours of an infarct.

Myoglobin

Myoglobin is a heme protein that helps transport oxygen. Like the CK-MB enzyme, myoglobin is found in cardiac and skeletal muscle. The myoglobin level starts to increase within 1 to 3 hours and peaks within 12 hours after the onset of symptoms. An increase in myoglobin is not very specific in indicating an acute cardiac event; however, negative results can be used to rule out an acute MI.

Chart 23-7

Medical Management

The goals of medical management are to minimize myocardial damage, preserve myocardial function, and prevent complications. These goals are facilitated by the use of guidelines developed by the ACC and the AHA (see Chart 23-7).

The goal for treating patients with acute MI is to minimize myocardial damage by reducing myocardial oxygen demand and increasing oxygen supply with medications, oxygen administration, and bed rest. The resolution of pain and ECG changes indicate that demand and supply are in equilibrium; they may also indicate reperfusion. Visualization of blood flow through an open vessel in the catheterization laboratory is evidence of reperfusion.

Initial Management

The patient with suspected MI should immediately receive supplemental oxygen, aspirin, nitroglycerin, and morphine. Morphine is the drug of choice to reduce pain and anxiety. It also reduces preload and afterload, decreasing the work of the heart. The response to morphine is monitored carefully to assess for hypotension or decreased respiratory rate. Nurses should be aware that evolving research has suggested an association between morphine and potential adverse outcomes, including larger infarct size, increased length of hospital stay, and mortality, and should stay abreast of changes to clinical guidelines impacting its use (McCarthy, Bhambhani, Pomerantsev, et al., 2018; Neto, 2018). A beta-blocker may also be used if arrhythmias occur. If a beta-blocker is not needed in the initial management period, it should be introduced within 24 hours of admission, once hemodynamics have stabilized and it is confirmed that the patient has no contraindications (Ibanez et al., 2018). Unfractionated heparin or LMWH may also be prescribed along with plateletinhibiting agents to prevent further clot formation.

Emergent Percutaneous Coronary Intervention

The patient with STEMI is taken directly to the cardiac catheterization laboratory for an immediate PCI (if a cardiac catheterization laboratory is on site). The procedure is used to open the occluded coronary artery and promote reperfusion to the area that has been deprived of oxygen. Superior outcomes have been reported with the use of PCI when compared to thrombolytic agents (Urden et al., 2019) (also called fibrinolytic agents; see the Thrombolytics section). Thus, PCI is preferred as the initial treatment method for acute MI in all age groups (Urden et al., 2019). The procedure treats the underlying atherosclerotic lesion. Because the duration of oxygen deprivation determines the number of myocardial cells that die, the time from the patient’s arrival in the ED to the time PCI is performed should be less than 60 minutes. This is frequently referred to as door-to-balloon time. A cardiac catheterization laboratory and staff must be available if an emergent PCI is to be performed within this short time. The nursing care related to PCI is presented later in this chapter.

Thrombolytics

Thrombolytic therapy is initiated when primary PCI is not available or the transport time to a PCI-capable hospital is too long. These agents are administered IV according to a specific protocol (see Chart 23-8). The thrombolytic agents used most often are alteplase, reteplase, and tenecteplase. The purpose of thrombolytics is to dissolve (i.e., lyse) the thrombus in a coronary artery (thrombolysis), allowing blood to flow through the coronary artery again (reperfusion), minimizing the size of the infarction and preserving ventricular function. However, although thrombolytics may dissolve the thrombus, they do not affect the underlying atherosclerotic lesion. The patient may be referred for a cardiac catheterization and other invasive procedures following the use of thrombolytic therapy. Thrombolytics should not be used if the patient is bleeding or has a bleeding disorder. They should be given within 30 minutes of symptom onset for best results (Norris, 2019). This is frequently referred to as door-to-needle time.

Inpatient Management

Following PCI or thrombolytic therapy, continuous cardiac monitoring is indicated, preferably in a cardiac intensive care unit (ICU). Continuing pharmacologic management includes aspirin, a beta-blocker, and an angiotensin-converting enzyme

(ACE) inhibitor. ACE inhibitors prevent the conversion of angiotensin I to angiotensin II. In the absence of angiotensin II, the blood pressure decreases and the kidneys excrete sodium and fluid (diuresis), decreasing the oxygen demand of the heart. The use of ACE inhibitors in patients after MI decreases mortality rates and prevents remodeling of myocardial cells that is associated with the onset of heart failure. Blood pressure, urine output, and serum sodium, potassium, and creatinine levels need to be monitored closely. If an ACE inhibitor is not suitable, an angiotensin receptor blocker (ARB) should be prescribed (Ibanez et al., 2018). Nicotine replacement therapy and tobacco cessation counseling should also be initiated for all tobacco users.

Administration of Thrombolytic Therapy

Indications

•        Chest pain lasting more than 20 minutes, unrelieved by nitroglycerin

•        ST-segment elevation in at least two leads that face the same area of the heart

•        Less than 12 hours from onset of pain

Absolute Contraindications

•        Active bleeding

•        Known bleeding disorder

•        History of hemorrhagic stroke

•        History of intracranial vessel malformation

•        Recent major surgery or trauma

•        Uncontrolled hypertension

•        Pregnancy

Nursing Considerations

•        Minimize the number of times the patient’s skin is punctured.

•        Avoid intramuscular injections.

•        Draw blood for laboratory tests when starting the IV line.

•        Start IV lines before thrombolytic therapy; designate one line to use for blood draws.

•        Avoid continual use of noninvasive blood pressure cuff.

•        Monitor for acute arrhythmias and hypotension.

•        Monitor for reperfusion: resolution of angina or acute ST-segment changes.

•        Check for signs and symptoms of bleeding: decrease in hematocrit and hemoglobin values, decrease in blood pressure, increase in heart rate, oozing or bulging at invasive procedure sites, back pain, muscle weakness, changes in level of consciousness, complaints of headache.

•        Treat major bleeding by discontinuing thrombolytic therapy and any anticoagulants; apply direct pressure and notify the primary provider immediately.

•        Treat minor bleeding by applying direct pressure if accessible and appropriate; continue to monitor.

Adapted from Urden, L. D., Stacy, K. M., & Lough, M. E. (2019). Priorities in critical care nursing (8th ed.). St. Louis, MO: Elsevier.

Cardiac Rehabilitation

After the patient with an MI is in a stable condition, an active rehabilitation program is initiated. Cardiac rehabilitation is an important continuing care program for patients with CAD that targets risk reduction by providing patient and family education, offering individual and group support, and encouraging physical activity and physical conditioning. The goals of rehabilitation for the patient who has had an MI are to extend life and improve the quality of life. The immediate objectives are to limit the effects and progression of atherosclerosis, return the patient to work and a pre-illness lifestyle, enhance the patient’s psychosocial and vocational status, and prevent another cardiac event. Cardiac rehabilitation programs increase survival, reduce recurrent events and the need for interventional procedures, and improve quality of life (Dickins & Braun, 2017).

Physical conditioning is achieved gradually over time. Many times, patients will “overdo it” in an attempt to achieve their goals too rapidly. Patients are observed for chest pain, dyspnea, weakness, fatigue, and palpitations and are instructed to stop exercise if any of these occur. Patients may also be monitored for an increase in heart rate above the target heart rate, an increase in systolic or diastolic blood pressure of more than 20 mm Hg, a decrease in systolic blood pressure, onset or worsening of arrhythmias, or ST-segment changes on the ECG.

Cardiac rehabilitation programs are categorized into three phases (Dickins & Braun, 2017). Phase I begins with the diagnosis of atherosclerosis, which may occur when the patient is admitted to the hospital for ACS. Because of brief hospital lengths of stay, mobilization occurs early and patient education focuses on the essentials of self-care rather than instituting behavioral changes for risk reduction. Priorities for inhospital education include the signs and symptoms that indicate the need to call 911 (seek emergency assistance), the medication regimen, rest–activity balance, and follow-up appointments with the primary provider. The patient is reassured that although CAD is a lifelong disease and must be treated as such, they can likely resume a normal life after an MI. The amount and type of activity recommended at discharge depend on the patient’s age, his or her condition before the cardiac event, the extent of the disease, the course of the hospital stay, and the development of any complications.

Phase II occurs after the patient has been discharged. The patient attends sessions three times a week for 4 to 6 weeks but may continue for as long as 6 months. The outpatient program consists of supervised, often ECG-monitored, exercise training that is individualized. At each session, the patient is assessed for the effectiveness of and adherence to the treatment. To prevent complications and another hospitalization, the cardiac rehabilitation staff alerts the referring primary provider to any problems. Phase II cardiac rehabilitation also includes educational sessions for patients and families that are given by cardiologists, exercise physiologists, dietitians, nurses, and other health care professionals. These sessions may take place outside a traditional classroom setting. For instance, a dietitian may take a group of patients to a grocery store to examine labels and meat selections or to a restaurant to discuss menu offerings for a heart-healthy diet.

Phase III is a long-term outpatient program that focuses on maintaining cardiovascular stability and long-term conditioning. The patient is usually selfdirected during this phase and does not require a supervised program, although it may be offered. The goals of each phase build on the accomplishments of the previous phase.

NURSING PROCESS

The Patient with Acute Coronary Syndrome

Assessment

One of the most important aspects of care of the patient with ACS is the assessment. It establishes the patient’s baseline, identifies the patient’s needs, and helps determine the priority of those needs. Systematic assessment includes a careful history, particularly as it relates to symptoms: chest pain or discomfort, dyspnea (difficulty breathing), palpitations, unusual fatigue, syncope (faintness), or other possible indicators of myocardial ischemia. Each symptom must be evaluated with regard to time, duration, and the factors that precipitate the symptom and relieve it, and in comparison with previous symptoms. A focused physical assessment is critical to detect complications and any change in patient status. Chart 23-6 identifies important assessments and possible findings.

Two IV lines are typically placed for any patient with ACS to ensure that access is available for administering emergency medications. Medications are administered IV to achieve rapid onset and to allow for timely adjustment. After the patient’s condition stabilizes, IV lines may be changed to a saline lock to maintain IV access. Diagnosis NURSING DIAGNOSES

Based on the clinical manifestations, history, and diagnostic assessment data, major nursing diagnoses may include:

•        Acute pain associated with increased myocardial oxygen demand and decreased myocardial oxygen supply

•        Risk for impaired cardiac function associated with reduced coronary blood flow

•        Risk for hypovolaemia

•        Impaired peripheral tissue perfusion associated with impaired cardiac output from left ventricular dysfunction

•        Anxiety associated with cardiac event and possible death

•        Lack of knowledge about post-ACS self-care

COLLABORATIVE PROBLEMS/POTENTIAL COMPLICATIONS Potential complications may include the following:

•        Acute pulmonary edema (see Chapter 25)

•        Heart failure (see Chapter 25)

•        Cardiogenic shock (see Chapter 11)

•        Arrhythmias and cardiac arrest (see Chapters 22 and 25)

•        Pericardial effusion and cardiac tamponade (see Chapter 25)

Planning and Goals

The major goals for the patient include relief of pain or ischemic signs (e.g., STsegment changes) and symptoms, prevention of myocardial damage, maintenance of effective respiratory function, maintenance or attainment of adequate tissue perfusion, reduced anxiety, adherence to the self-care program, and early recognition of complications. Care of the patient with ACS who has an uncomplicated MI is summarized in the Plan of Nursing Care (see Chart 23-9).

Nursing Interventions

RELIEVING PAIN AND OTHER SIGNS AND SYMPTOMS OF ISCHEMIA

Balancing myocardial oxygen supply with demand (e.g., as evidenced by the relief of chest pain) is the top priority in the care of the patient with an ACS. Although administering medications as described previously is required to accomplish this goal, nursing interventions are also important. Collaboration among the patient, nurse, and primary provider is critical in evaluating the patient’s response to therapy and in altering the interventions accordingly.

Oxygen should be given along with medication therapy to assist with relief of symptoms. Administration of oxygen raises the circulating level of oxygen to reduce pain associated with low levels of myocardial oxygen. The route of administration (usually by nasal cannula) and the oxygen flow rate are documented. A flow rate of 2 to 4 L/min is usually adequate to maintain oxygen saturation levels of at least 95% unless chronic pulmonary disease is present.

Vital signs are assessed frequently as long as the patient is experiencing pain and other signs or symptoms of acute ischemia. Physical rest in bed with the head of the bed elevated or in a supportive chair helps decrease chest discomfort and dyspnea. Elevation of the head and torso is beneficial for the following reasons:

•        Tidal volume improves because of reduced pressure from abdominal contents on the diaphragm and better lung expansion.

•        Drainage of the upper lung lobes improves.

•        Venous return to the heart (preload) decreases, reducing the work of the heart.

The pain associated with an acute MI reflects an imbalance in myocardial oxygen supply and demand or ineffective myocardial tissue perfusion. The pain also results in increases in heart rate, respiratory rate, and blood pressure. Promptly relieving the pain helps to reestablish this balance, thus decreasing the workload of the heart and minimizing damage to the myocardium. Relief of pain also helps to reduce the patient’s anxiety level, which in turn reduces the sympathetic stress response, leading to a decrease in workload of the already stressed heart.

IMPROVING RESPIRATORY FUNCTION

Regular and careful assessment of respiratory function detects early signs of pulmonary complications. The nurse monitors fluid volume status to prevent fluid overload and encourages the patient to breathe deeply and change position frequently to maintain effective ventilation throughout the lungs. Pulse oximetry guides the use of oxygen therapy.

PROMOTING ADEQUATE TISSUE PERFUSION

Bed or chair rest during the initial phase of treatment helps reduce myocardial oxygen consumption. This limitation on mobility should remain until the patient is pain free and hemodynamically stable. Skin temperature and peripheral pulses must be checked frequently to monitor tissue perfusion.

REDUCING ANXIETY

Alleviating anxiety and decreasing fear are important nursing functions that reduce the sympathetic stress response. Less sympathetic stimulation decreases the workload of the heart, which may relieve pain and other signs and symptoms of ischemia.

The development of a trusting and caring relationship with the patient is critical in reducing anxiety. Providing information to the patient and family in an honest and supportive manner encourages the patient to be a partner in care and greatly assists in developing a positive relationship. Other interventions that can be used to reduce anxiety include ensuring a quiet environment, preventing interruptions that disturb sleep, and providing spiritual support consistent with the patient’s beliefs. The nurse provides frequent opportunities for the patient to privately share concerns and fears. An atmosphere of acceptance helps the patient know that these concerns and fears are both realistic and normal. Alternative therapies such as pet therapy can help certain patients relax and reduce anxiety (Waite, Hamilton, & O’Brien, 2018). Many hospitals have developed infection control and safety procedures pertaining to the animals, their handlers, and the patients eligible for pet therapy.

MONITORING AND MANAGING POTENTIAL COMPLICATIONS

Complications that can occur after acute MI are caused by the damage that occurs to the myocardium and to the conduction system from reduced coronary blood flow. Because these complications can be life-threatening, close monitoring for and early identification of their signs and symptoms are critical (see Chart 23-9).

The nurse monitors the patient closely for changes in cardiac rate and rhythm, heart sounds, blood pressure, chest pain, respiratory status, urinary output, skin color and temperature, mental status, ECG changes, and laboratory values. Any changes in the patient’s condition must be reported promptly to the primary provider and emergency measures instituted when necessary.

PROMOTING HOME, COMMUNITY-BASED, AND TRANSITIONAL CARE

 Educating Patients About Self-Care. The most effective way to increase

the probability that the patient will implement a self-care regimen after discharge is to identify the patient’s priorities, provide adequate education about hearthealthy living, and facilitate the patient’s involvement in a cardiac rehabilitation program (Ibanez et al., 2018). Patient participation in the development of an individualized program enhances the potential for an effective treatment plan (see Chart 23-10).

Continuing and Transitional Care. Depending on the patient’s condition and the availability of family assistance, home, community-based, or transitional, care may be indicated. The nurse making a home visit can assist the patient with scheduling and keeping follow-up appointments and with adhering to the prescribed cardiac rehabilitation regimen. The patient may need reminders about follow-up monitoring, including periodic laboratory testing, as well as ongoing assessment of cardiac status. In addition, the home health nurse monitors the patient’s adherence to dietary restrictions and to prescribed medications. If the patient is receiving home oxygen, the nurse ensures that the patient is using the oxygen as prescribed and that appropriate home safety measures are maintained. If the patient has evidence of heart failure secondary to an MI, appropriate home care guidelines for the patient with heart failure are followed (see Chapter 25).

Evaluation

Expected patient outcomes may include:

1.      Experiences relief of angina

2.      Has stable cardiac and respiratory status

3.      Maintains adequate tissue perfusion

4.      Exhibits decreased anxiety

5.      Adheres to a self-care program

6.      Has no complications

INVASIVE CORONARY ARTERY PROCEDURES

Methods to reperfuse ischemic myocardial tissue when patients are refractory to more conservative management methods include PCIs and CABG surgery, as noted previously. The following sections discuss specific indications for each of these and the nursing management of patients who are having either PCIs or CABGs.

Percutaneous Coronary Interventions

Invasive interventional procedures to treat CAD include PTCA and intracoronary stent implantation. These procedures are classified as percutaneous coronary interventions (PCIs), as they are performed through a skin puncture rather than a surgical incision.

Percutaneous Transluminal Coronary Angioplasty

In percutaneous transluminal coronary angioplasty (PTCA), a balloon-tipped catheter is used to open blocked coronary vessels and resolve ischemia. It is used in patients with angina and as an intervention for ACS. Catheter-based interventions can also be used to open blocked CABGs (see later discussion). The purpose of PTCA is to improve blood flow within a coronary artery by compressing the atheroma. The procedure is attempted when the interventional cardiologist determines that PTCA can improve blood flow to the myocardium.

PTCA is carried out in the cardiac catheterization laboratory. Hollow catheters called sheaths are inserted, usually in the femoral artery (and sometimes the radial artery), providing a conduit for other catheters. Catheters are then threaded through the femoral or radial artery, up through the aorta, and into the coronary arteries. Angiography is performed using injected radiopaque contrast agents (commonly called dye) to identify the location and extent of the blockage. A balloon-tipped dilation catheter is passed through the sheath and positioned over the lesion. The physician determines the catheter position by examining markers on the balloon that can be seen with fluoroscopy. When the catheter is properly positioned, the balloon is inflated with high pressure for several seconds and then deflated. The pressure compresses and often “cracks” the atheroma (see Fig. 23-7). The media and adventitia of the coronary artery are also stretched.

Several inflations with different balloon sizes may be required to achieve the goal, usually defined as an improvement in blood flow and a residual stenosis of less than 10% (Urden et al., 2019). Other measures of the success of PTCA are an increase in the artery’s lumen and no clinically obvious arterial trauma. Because the blood supply to the coronary artery decreases while the balloon is inflated, the patient may complain of chest pain and the ECG may display ST-segment changes. Intracoronary stents are usually positioned in the intima of the vessel to maintain patency of the artery after the balloon is withdrawn.

If thick, deep, or concentric calcification is present, the lesion may require the use of devices such as cutting, scoring, or high pressure balloons, rotational atherectomy, orbital atherectomy and excimer lasers to prepare the lesion for stenting (Shlofmitz, Shlofmitz, & Lee, 2019).

In addition to these approaches, intravascular lithotripsy (IVL) is currently being investigated to treat calcified artery blockages with sonic pressure waves in a similar way that is used to treat kidney stones. Pulsatile sonic pressure waves are used during balloon inflation to fracture both intimal and medial calcium in the artery wall but pass through the surrounding soft vascular tissue in a safe manner. This technology is approved for use in peripheral arteries at this time. Further studies are being done to assess their efficacy in coronary arteries (Riley, Corl, & Kereiakes, 2019).

Coronary Artery Stent

After PTCA, the area that has been treated may close off partially or completely—a process called restenosis. The intima of the coronary artery has been injured and responds by initiating an acute inflammatory process. This process may include release of mediators that leads to vasoconstriction, clotting, and scar tissue formation. A coronary artery stent may be placed to overcome these risks. A stent is a metal mesh that provides structural support to a vessel at risk of acute closure. The stent is initially positioned over the angioplasty balloon. When the balloon is inflated, the mesh expands and presses against the vessel wall, holding the artery open. The balloon is withdrawn, but the stent is left permanently in place within the artery (see Fig. 23-7). Eventually, endothelium covers the stent and it is incorporated into the vessel wall. The original stents do not contain medications and are known as bare metal stents. Some stents are coated with medications, such as sirolimus or paclitaxel, which may minimize the formation of thrombi or scar tissue within the coronary artery lesion. These drug-eluting stents (DES) have increased the success of PCI (Mishra, Edla, Tripathi, et al., 2019). Because of the risk of thrombus formation within the stent, the patient receives antiplatelet medications, usually aspirin and clopidogrel. Aspirin should be continued indefinitely and clopidogrel is continued for 1 year following stent placement (Urden et al., 2019).

Figure 23-7 • Percutaneous transluminal coronary angioplasty. A. A balloon-tipped catheter is passed into the affected coronary artery and placed across the area of the atheroma (plaque). B. The balloon is then rapidly inflated and deflated with controlled pressure. C. A stent is placed to maintain patency of the artery, and the balloon is removed.

Complications

Complications that can occur during a PCI procedure include coronary artery dissection, perforation, abrupt closure, or vasospasm. Additional complications include acute MI, serious arrhythmias (e.g., ventricular tachycardia), and cardiac arrest. Some of these complications may require emergency surgical treatment. Complications after the procedure may include abrupt closure of the coronary artery and a variety of vascular complications, such as bleeding at the insertion site, retroperitoneal bleeding, hematoma, and arterial occlusion (Urden et al., 2019). In addition, there is a risk of acute kidney injury from the contrast agent used during the procedure (see Table 23-3).

Postprocedure Care

Patient care is similar to that for a diagnostic cardiac catheterization (see Chapter 21). Patients who are not already hospitalized are admitted the day of the PCI. Those with no complications go home the same day. When the PCI is performed emergently to treat ACS, patients typically go to a critical care unit and stay in the hospital for a few days. During the PCI, patients receive IV heparin or a thrombin inhibitor (e.g., bivalirudin) and are monitored closely for signs of bleeding. Patients may also receive a GP IIb/IIIa agent (e.g., eptifibatide) for several hours following the PCI to prevent platelet aggregation and thrombus formation in the coronary artery (Urden et al., 2019). Hemostasis is achieved, and femoral sheaths may be removed at the end of the procedure by using a vascular closure device (e.g., Angio-Seal, VasoSeal) or a device that sutures the vessels. Hemostasis after sheath removal may also be achieved by direct manual pressure, a mechanical compression device (e.g., C-shaped clamp), or a pneumatic compression device (e.g., FemoStop).

Patients may return to the nursing unit with the large peripheral vascular access sheaths in place. The sheaths are then removed after blood studies (e.g., activated clotting time) indicate that the heparin is no longer active and the clotting time is within an acceptable range. This usually takes a few hours, depending on the amount of heparin given during the procedure. The patient must remain flat in bed and keep the affected leg straight until the sheaths are removed and then for a few hours afterward to maintain hemostasis. Because immobility and bed rest may cause discomfort, treatment may include analgesics and sedation. Nonpharmacologic interventions include repositioning and heat application for back pain. Sheath removal and the application of pressure on the vessel insertion site may cause the heart rate to slow and the blood pressure to decrease (vasovagal response). A dose of IV atropine is usually given to treat this response.

BUN, blood urea nitrogen; ECG, electrocardiogram; IV, intravenous.

Adapted from Urden, L. D., Stacy, K. M., & Lough, M. E. (2019). Priorities in critical care nursing (8th ed.). St. Louis, MO: Elsevier.

Some patients with unstable lesions and at high risk for abrupt vessel closure are restarted on heparin after sheath removal, or they receive an IV infusion of a GP IIb/IIIa inhibitor. These patients are monitored closely and may have a delayed recovery period.

After hemostasis is achieved, a pressure dressing is applied to the site. Patients resume self-care and ambulate unassisted within a few hours of the procedure. The duration of immobilization depends on the size of the sheath inserted, the type of anticoagulant given, the method of hemostasis, the patient’s condition, and the physician’s preference. On the day after the procedure, the site is inspected and the dressing removed. The patient is instructed to monitor the site for bleeding or development of a hard mass indicative of hematoma.

 Surgical Procedures: Coronary Artery Revascularization

Advances in diagnostics, medical management, and surgical and anesthesia techniques, as well as the care provided in critical care and surgical units, home care, and rehabilitation programs, have continued to make surgery an effective treatment option for patients with CAD. CAD has been treated by myocardial revascularization since the 1960s, and the most common CABG techniques have been performed for more than 40 years. Coronary artery bypass graft (CABG) is a surgical procedure in which a blood vessel is grafted to an occluded coronary artery so that blood can flow beyond the occlusion; it is also called a bypass graft. The major indications for CABG are:

•        Alleviation of angina that cannot be controlled with medication or PCI

•        Treatment for left main coronary artery stenosis or multivessel CAD

•        Prevention of and treatment for MI, arrhythmias, or heart failure

•        Treatment for complications from an unsuccessful PCI

The recommendation for CABG is determined by a number of factors, including the number of diseased coronary vessels, the degree of left ventricular dysfunction, the presence of other health problems, the patient’s symptoms, and any previous treatment. CABG and PCI have shown similar results in outcomes, such as MI rate, mortality, and improvement of angina post-intervention. However, the requirement of a second reperfusion intervention has been shown to be lower with CABG compared to PCI therapy (Gaudino, Spadaccio, & Taggart, 2019).

CABG is performed less frequently in women (Angraal, Khera, Wang, et al., 2018). Compared with men, women referred for this surgery tend to be older and have more comorbidities such as diabetes. In addition, they have a higher risk of surgical complications and increased mortality (Angraal et al., 2018). Although some women have good outcomes following CABG, men generally have a better rate of graft patency and symptom relief.

For a patient to be considered for CABG, the coronary arteries to be bypassed must have at least a 70% occlusion, or at least a 50% occlusion in the left main coronary artery (Urden et al., 2019). If significant blockage is not present, flow through the artery will compete with flow through the bypass, and circulation to the ischemic area of myocardium may not improve. The artery also must be patent beyond the area of blockage or the flow through the bypass will be impeded.

Current guidelines recommend use of the internal thoracic arteries (formerly called the internal mammary arteries) for CABG, because of their histologic characteristics and increased production of vasoactive molecules and anti-inflammatory cytokines which improve arterial patency. Recent studies demonstrate increased survival when using internal thoracic artery grafting. The left internal thoracic artery graft has been shown to have greater than 90% patency after 20 years and is the recommended conduit to use first (Gaudino et al., 2019). Arterial grafts are preferred to venous grafts because they do not develop atherosclerotic changes as quickly and remain patent longer. The surgeon leaves the proximal end of the thoracic artery intact and detaches the distal end of the artery from the chest wall. This end of the artery is then grafted to the coronary artery distal to the occlusion. The internal thoracic arteries may not be long enough to use for multiple bypasses. Because of this, many CABG procedures are performed with a combination of venous and arterial grafts.

A vein commonly used for CABG is the greater saphenous vein, followed by the lesser saphenous vein (see Fig. 23-8). The vein is removed from the leg and grafted to the ascending aorta and to the coronary artery distal to the lesion. Traditionally, a skin incision was made over the length of vein segment, but new techniques allow small leg incisions. Endovascular methods of vein harvesting have reduced complications such as infection and wound dehiscence, which are associated with longer leg incisions (Gaudino et al., 2019). Lower extremity edema continues to be a common adverse effect of vein removal. The degree of edema varies and usually diminishes over time. The patency of vein grafts can be limited. Within 5 to 10 years, atherosclerotic changes often develop in saphenous vein grafts.

Figure 23-8 • The greater and lesser saphenous veins are commonly used in bypass graft procedures.

Traditional Coronary Artery Bypass Graft

CABG procedures are performed with the patient under general anesthesia. In the traditional CABG procedure, the surgeon performs a median sternotomy and connects the patient to the cardiopulmonary bypass (CPB) machine. Next, a blood vessel from another part of the patient’s body (e.g., saphenous vein, left internal thoracic artery) is grafted distal to the coronary artery lesion, bypassing the obstruction (see Fig. 23-9). CPB is then discontinued, chest tubes and epicardial pacing wires are placed, and the incision is closed. The patient is then admitted to a critical care unit.

Cardiopulmonary Bypass

Many cardiac surgical procedures are possible because of CPB (i.e., extracorporeal circulation). The procedure mechanically circulates and oxygenates blood for the body while bypassing the heart and lungs. CPB maintains perfusion to body organs and tissues and allows the surgeon to complete the anastomoses in a motionless, bloodless surgical field.

CPB is accomplished by placing a cannula in the right atrium, vena cava, or femoral vein to withdraw blood from the body. The cannula is connected to tubing filled with an isotonic crystalloid solution. Venous blood removed from the body by the cannula is filtered, oxygenated, cooled or warmed by the machine, and then returned to the body. The cannula used to return the oxygenated blood is usually inserted in the ascending aorta, or it may be inserted in the femoral artery (see Fig. 23-10). The heart is stopped by the injection of a potassium-rich cardioplegia solution into the coronary arteries. The patient receives heparin to prevent clotting and thrombus formation in the bypass circuit when blood comes in contact with the surfaces of the tubing. At the end of the procedure when the patient is disconnected from the bypass machine, protamine sulfate is given to reverse the effects of heparin.

Figure 23-9 • Coronary artery bypass grafts. One or more procedures may be performed using various veins and arteries. A. Left internal thoracic artery (formerly called the left internal mammary artery), used frequently because of its functional longevity. B. Saphenous vein, also used as bypass graft.

During the procedure, hypothermia is maintained at a temperature of about 28°C (82.4°F) (Urden et al., 2019). The blood is cooled during CPB and returned to the body. The cooled blood slows the body’s basal metabolic rate, thereby decreasing the demand for oxygen. Cooled blood usually has a higher viscosity, but the crystalloid solution used to prime the bypass tubing dilutes the blood. When the surgical procedure is completed, the blood is rewarmed as it passes through the CPB circuit. Urine output, arterial blood gases, electrolytes, and coagulation studies are monitored to assess the patient’s status during CPB.

Figure 23-10 • The cardiopulmonary bypass system, in which cannulas are placed through the right atrium into the superior and inferior vena cavae to divert blood from the body and into the bypass system. The pump system creates a vacuum, pulling blood into the venous reservoir. The blood is cleared of air bubbles, clots, and particulates by the filter and then is passed through the oxygenator, releasing carbon dioxide and obtaining oxygen. Next, the blood is pulled to the pump and pushed out to the heat exchanger, where its temperature is regulated. The blood is then returned to the body via the ascending aorta.

Alternative Coronary Artery Bypass Graft Techniques

A number of alternative CABG techniques have been developed that may have fewer complications for some groups of patients. Off-pump coronary artery bypass (OPCAB) surgery has been used successfully in many patients. OPCAB involves a standard median sternotomy incision, but the surgery is performed without CPB. A beta-adrenergic blocker may be used to slow the heart rate. The surgeon also uses a myocardial stabilization device to hold the site still for the anastomosis of the bypass graft into the coronary artery while the heart continues to beat (see Fig. 23-11). Research suggests that OPCAB is associated with reduced short-term postoperative morbidity, including stroke and other complications. However, with on-pump CABG, graft patency rate is higher and long-term mortality may be lower (Gaudino et al., 2019).

Minimally invasive surgical techniques that eliminate median sternotomy have also been developed. These endoscopic techniques use smaller incisions via a right or left thoracotomy approach and a robotic system to place bypass grafts. The patient may or may not require CPB (Snyder, 2018). Minimally invasive heart surgery may be considered an acceptable alternative to conventional CABG for select patients, such as those who do not require bypass grafts to several vessels. It is most commonly used to bypass occlusions in the left anterior descending artery (Snyder,

2018). It has allowed patients to recover earlier, require fewer blood transfusions, experience fewer respiratory complications, and be less likely to experience acute kidney injury (Urden et al., 2019).

The most important criterion when deciding whether a patient needs a CABG or a PCI is the predicted surgical mortality, which takes into consideration the patient’s individual characteristics, the anatomic complexity of the coronary lesions, and the ability to achieve revascularization. The cardiac surgeon will assess the following factors to determine risk and the ability to revascularize: clinical history (age, sex, diabetes, hypertension, left ventricular function, arrhythmias), previous cardiovascular events (previous cardiovascular surgery, PCI, MI, or stroke), and disease complexity (number of diseased vessels, concomitant valve disease). In some cases, CABG may still be recommended over PCI for only one lesion to achieve better revascularization (Gaudino et al., 2019).

Figure 23-11 • Stabilizer device for off-pump coronary artery bypass surgery.

Complications of Coronary Artery Bypass Graft

CABG may result in complications such as hemorrhage, arrhythmias, and MI (see Table 23-4). The patient may require interventions for more than one complication at a time. Collaboration among nurses, physicians, pharmacists, respiratory therapists, and dietitians is necessary to achieve the desired patient outcomes. Although most patients improve symptomatically following surgery, CABG is not a cure for CAD, and angina, exercise intolerance, or other symptoms experienced before CABG may recur. Medications required before surgery may need to be continued. Lifestyle modifications recommended before surgery remain important to treat the underlying CAD and for the continued viability of the newly implanted grafts.

 Nursing Management

Cardiac surgery patients have many of the same needs and require the same perioperative care as other surgical patients (see Unit 3), as well as some special needs.

Preoperative Management

Comprehensive preoperative medical management prevents complications and improves outcomes. This is particularly important because patients undergoing CABG surgery tend to be older and often have multiple comorbidities. The use of aspirin, beta-blockers, and statins during the preoperative period is associated with better outcomes. Preoperative use of aspirin is associated with a reduction in perioperative morbidity and mortality (Aboul-Hassan, Stankowski, Marczak, et al., 2017). Beta-blockers, when given at least 24 hours before CABG, reduce the incidence of postoperative atrial fibrillation (Urden et al., 2019). Perioperative use of statins has been shown to reduce the rates of postoperative MI, atrial fibrillation, neurologic dysfunction, renal dysfunction, infection, and death (Katsiki, Triposkiadis, Giannoukas, et al., 2018).

Assessing the Patient

Patients are frequently admitted to the hospital the day of the procedure. Therefore, most of the preoperative evaluation is completed in the physician’s office and during preadmission testing.

Nursing and medical personnel perform a history and physical examination. Preoperative testing consists of a chest x-ray; ECG; laboratory tests, including coagulation studies; and blood typing and cross-matching. The preoperative history and health assessment should be thorough and well documented because they provide a basis for postoperative comparison. The nurse assesses the patient for disorders that could complicate or affect the postoperative course, such as diabetes, hypertension, and lung disease.

Potential Complications of Cardiac Surgery

↑, increased; CVP, central venous pressure; IV, intravenous; MI, myocardial infarction; PAWP, pulmonary artery wedge pressure.

Adapted from Urden, L. D., Stacy, K. M., & Lough, M. E. (2019). Priorities in critical care nursing (8th ed.). St. Louis, MO: Elsevier.

The health assessment focuses on obtaining baseline physiologic, psychological, and social information. Cognitive status is carefully assessed, as patients with impaired cognitive status will need more assistance after surgery and may require subacute care prior to returning home. Older adults are at a high risk for suffering adverse cognitive outcomes following cardiac surgery (Jones, Matalanis, Mårtensson, et al., 2019). The patient’s and family’s education needs are identified and addressed. Of particular importance are the patient’s usual functional level, coping mechanisms, and available support systems. These factors affect the patient’s postoperative course, discharge plans, and rehabilitation.

The status of the cardiovascular system is determined by reviewing the patient’s symptoms, including past and present experiences with chest pain, palpitations, dyspnea, intermittent claudication (leg pain that occurs with walking), and peripheral edema. The patient’s history of major illnesses; previous surgeries; medication; and the use of illicit and over-the-counter drugs, herbal supplements, alcohol, and tobacco is also obtained. Particular attention is paid to blood glucose control in patients with diabetes because there is a higher incidence of postoperative complications when glycemic control is poor (Gordon, Lauver, & Buck, 2018).

The psychosocial assessment and the assessment of the patient’s and family’s learning needs are also important. Anticipation of cardiac surgery is a source of great stress to the patient and family, and patients with high anxiety levels have poorer outcomes (Ramesh, Nayak, Pai, et al., 2017). However, some anxiety is expected, and the work of worrying can help patients identify priorities and find coping strategies that help them face the threat of surgery. Questions may be asked to obtain the following information:

•        Knowledge and understanding of the surgical procedure, postoperative course, and recovery

•        Fears and concerns regarding the surgery and future health status

•        Coping mechanisms helpful to the patient

•        Support systems available during and following hospitalization

Reducing Fear and Anxiety

The nurse gives the patient and family time and opportunity to express their fears. Topics of concern may be pain, changes in body image, fear of the unknown, and fear of disability or death. It may be helpful to describe the sensations that the patient can expect, including the preoperative sedation, surgical anesthesia, and postoperative pain management. The nurse reassures the patient that the fear of pain is normal, that some pain will be experienced, that medication to relieve pain will be provided, and that the patient will be closely monitored. In addition, the nurse instructs the patient to request analgesic medication before the pain becomes severe. If the patient has concerns about scarring from surgery, the nurse encourages them to discuss this issue and corrects any misconceptions. The patient and family may want to discuss their fear of the patient dying. After the fear is expressed, the nurse can assure the patient and family that this fear is normal and further explore their feelings. For patients with extreme anxiety or fear and for whom emotional support and education are not successful, antianxiety medication such as lorazepam may be helpful.

Monitoring and Managing Potential Complications

Angina may occur because of increased stress and anxiety related to the forthcoming surgery. The patient who develops angina usually responds to typical therapy for angina, most commonly nitroglycerin. Some patients require oxygen and IV nitroglycerin infusions. Physiologically unstable patients may require preoperative management in a critical care unit.

 Providing Patient Education

Prior to surgery, patients and their families are given specific instructions. This includes information on how the patient should take or stop specific medications, including anticoagulant agents, antihypertensive medications, and medications that control diabetes. The patient is instructed to shower with an antiseptic solution such as chlorhexidine gluconate and to apply mupirocin calcium 2% ointment to each nostril to help reduce the risk of surgical site infections (Reiser, Scherag, Forstner, et al., 2017). Cardiac surgical infections are often caused by Staphylococcus aureus which is found in the nasal passages. Studies have shown that decolonizing the nasal passage preoperatively is effective in reducing sternal wound infections associated with cardiac surgery (Lemaignen, Armand-Lefevre, Birgand, et al., 2018) (see Chapter 14 for further discussion of preoperative preparation).

Education also includes information about the hospitalization and surgery. The nurse informs the patient and family about the equipment, tubes, and lines that will be present after surgery and their purposes. They should expect monitors, several IV lines, chest tubes, and a urinary catheter. Explaining the purpose and the approximate time that these devices will be in place helps reassure the patient. Most patients remain intubated and on mechanical ventilation for several hours after surgery. It is important for patients to know that this will prevent them from talking, and the nurse should reassure them that the staff will be able to assist them with other means of communication.

The nurse takes care to answer the patient’s questions about postoperative care and procedures. After the nurse explains deep breathing and coughing, the use of the incentive spirometer, and foot exercises, the nurse practices these procedures with the patient. The benefit of early and frequent ambulation is discussed. The family’s questions at this time usually focus on the length of the surgery, who will discuss the results of the procedure with them after surgery, where to wait during the surgery, the visiting procedures for the critical care unit, and how they can support the patient before surgery and in the critical care unit.

Intraoperative Management

The perioperative nurse performs assessments and prepares the patient as described in Chapters 14 and 15. In addition to assisting with the surgical procedure, perioperative nurses are responsible for the comfort and safety of the patient.

Possible intraoperative complications include low cardiac output, arrhythmias, hemorrhage, MI, organ failure from shock, and thromboembolic events including stroke (Urden et al., 2019). Astute intraoperative nursing assessment is critical to prevent, detect, and initiate prompt intervention for these complications. Before the chest incision is closed, chest tubes are inserted to evacuate air and drainage from the mediastinum and the thorax.

Temporary epicardial pacemaker electrodes may be implanted on the surface of the right atrium and the right ventricle. These epicardial electrodes can be connected to an external pacemaker if the patient has persistent bradycardia perioperatively (see Chapter 22 for a discussion of pacemakers).

Postoperative Nursing Management

Initial postoperative care focuses on achieving or maintaining hemodynamic stability and recovery from general anesthesia. Care may be provided in the postanesthesia care unit (PACU) or ICU. The immediate postoperative period for the patient who has undergone cardiac surgery presents many challenges to the health care team. All efforts are made to facilitate the transition from the operating room to the ICU or PACU with minimal risk. Specific information about the surgical procedure and important factors about postoperative management are communicated by the surgical team and anesthesia personnel to the critical care or PACU nurse, who then assumes responsibility for the patient’s care. Figure 23-12 presents an overview of the many aspects of postoperative care of the cardiac surgical patient.

Figure 23-12 • Postoperative care of the patient who has undergone cardiac surgery requires the nurse to be proficient in interpreting hemodynamics, correlating physical assessment data with laboratory results, sequencing interventions, and evaluating progress toward desired outcomes.

After the patient’s cardiac status and respiratory status are stable, the patient is transferred to a surgical progressive care unit with telemetry. Care in both the ICU and progressive care unit focuses on monitoring of cardiopulmonary status, pain management, wound care, progressive activity, and nutrition. Education about medications and risk factor modification is emphasized.

A typical plan of postoperative nursing care is presented in Chart 23-11.

Assessing the Patient

When the patient is admitted to the critical care unit or PACU, nursing and medical personnel perform a complete assessment of all systems at least every 4 hours. It is necessary to assess the following parameters:

Neurologic status: level of responsiveness, pupil size and reaction to light, facial symmetry, movement of the extremities, and hand grip strength

Cardiac status: heart rate and rhythm, heart sounds, pacemaker status, arterial blood pressure, central venous pressure (CVP); in select patients, hemodynamic parameters: pulmonary artery pressure, pulmonary artery wedge pressure (PAWP), cardiac output and index, systemic and pulmonary vascular resistance, mixed venous oxygen saturation (Sv–O₂). A pulmonary artery catheter is often used to monitor these parameters. Alternatively, minimally invasive monitoring of stroke volume, systemic vascular resistance, and cardiac output are calculated through pressures obtained in the arterial line (e.g., Vigileo monitor with FloTrac sensor). (See Chapter

21 for a detailed description of hemodynamic monitoring.)

Respiratory status: chest movement, breath sounds, ventilator settings (e.g., rate, tidal volume, oxygen concentration, mode such as assist-control, positive endexpiratory pressure, pressure support), respiratory rate, peak inspiratory pressure, percutaneous oxygen saturation (SpO₂), end-tidal carbon dioxide (CO₂), pleural chest tube drainage, arterial blood gases. (See Chapters 17 and 19 for detailed descriptions of respiratory assessment and ventilatory management, respectively.)

Peripheral vascular status: peripheral pulses; color of skin, nail beds, mucosa, lips, and earlobes; skin temperature; edema; condition of dressings and invasive lines

Renal function: urinary output; serum creatinine and electrolytes

Fluid and electrolyte status: strict intake and output, including all IV fluids and blood products, output from all drainage tubes; clinical and laboratory indicators of imbalance

Pain: nature, type, location, and duration; apprehension; response to analgesics

Assessment also includes checking all equipment and tubes to ensure that they are functioning properly: endotracheal tube, ventilator, end-tidal CO₂ monitor, SpO₂ monitor, pulmonary artery catheter, Sv–O₂ monitor, arterial and IV lines, IV infusion devices and tubing, cardiac monitor, pacemaker, chest tubes, and urinary drainage system.

As the patient regains consciousness and progresses through the postoperative period, the nurse also assesses indicators of psychological and emotional status. The patient may exhibit behavior that reflects denial or depression or may experience postoperative delirium. Characteristic signs of delirium include transient perceptual illusions, visual and auditory hallucinations, disorientation, and paranoid delusions. Patients who have delirium after cardiac surgery have poorer outcomes than do similar patients without this complication (Jones et al., 2019).

The family’s needs also must be assessed. The nurse ascertains how family members are coping with the situation; determines their psychological, emotional, and spiritual needs; and finds out whether they are receiving adequate information about the patient’s condition.

Monitoring for Complications

The patient is continuously assessed for impending complications (see Table 23-4). The nurse and the surgical team function collaboratively to prevent complications, to identify early signs and symptoms of complications, and to institute measures to reverse their progression.

Decreased Cardiac Output

A decrease in cardiac output is always a threat to the patient who has had cardiac surgery, and it can have a variety of causes. Preload alterations occur when too little blood volume returns to the heart as a result of persistent bleeding and hypovolemia. Excessive postoperative bleeding can lead to decreased intravascular volume, hypotension, and low cardiac output. Bleeding problems are common after cardiac surgery because of the effects of CPB, trauma from the surgery, and anticoagulation. Preload can also decrease if there is a collection of fluid and blood in the pericardium (cardiac tamponade), which impedes cardiac filling. Cardiac output is also altered if too much volume returns to the heart, causing fluid overload.

Afterload alterations occur when the arteries are constricted as a result of postoperative hypertension or hypothermia, increasing the workload of the heart. Heart rate alterations from bradycardia, tachycardia, and arrhythmias can lead to decreased cardiac output, and contractility can be altered in cardiac failure, MI, electrolyte imbalances, and hypoxia.

Fluid Volume and Electrolyte Imbalance

Fluid and electrolyte imbalance may occur after cardiac surgery. Nursing assessment for these complications includes monitoring of intake and output, weight, hemodynamic parameters, hematocrit levels, neck vein distention, edema, breath sounds (e.g., fine crackles, wheezing), and electrolyte levels. The nurse reports changes in serum electrolytes promptly so that treatment can be instituted. Especially important are dangerously high or dangerously low levels of potassium, magnesium, sodium, and calcium. Elevated blood glucose levels are common in the postoperative period. Administration of IV insulin is recommended in patients both with and without diabetes to achieve the glycemic control necessary to promote wound healing, decrease infection, and improve survival after surgery (Gordon et al., 2018). Implementing an insulin infusion protocol that targets moderate glycemic control has been demonstrated as effective in treating acute hyperglycemia following cardiac surgery while also decreasing the incidence of hypoglycemia (Gordon et al., 2018).

Impaired Gas Exchange

Impaired gas exchange is another possible complication after cardiac surgery. All body tissues require an adequate supply of oxygen for survival. To achieve this after surgery, an endotracheal tube with ventilator assistance may be used for hours to days. The assisted ventilation is continued until the patient’s blood gas values are acceptable and the patient demonstrates the ability to breathe independently. Patients who are stable after surgery may be extubated as early as 2 to 4 hours after surgery, which reduces their discomfort and anxiety and facilitates patient–nurse communication.

While receiving mechanical ventilation, the patient is continuously assessed for signs of impaired gas exchange: restlessness, anxiety, cyanosis of mucous membranes and peripheral tissues, tachycardia, and fighting the ventilator. Breath sounds are assessed often to detect pulmonary congestion and monitor lung expansion. Arterial blood gases, SpO₂, and end-tidal CO₂ are assessed for decreased oxygen and increased CO₂. Following extubation, aggressive pulmonary interventions such as turning, coughing, deep breathing, and early ambulation are necessary to prevent atelectasis and pneumonia.

Impaired Cerebral Circulation

Hypoperfusion or microemboli during or following cardiac surgery may produce injury to the brain. Brain function depends on a continuous supply of oxygenated blood. The brain does not have the capacity to store oxygen and must rely on adequate continuous perfusion by the heart. The nurse observes the patient for signs and symptoms of cerebral hypoxia: restlessness, confusion, dyspnea, hypotension, and cyanosis. An assessment of the patient’s neurologic status includes the level of consciousness, response to verbal commands and painful stimuli, pupil size and reaction to light, facial symmetry, movement of the extremities, and hand grip strength. The nurse documents any indication of a change in status and reports abnormal findings to the surgeon because they may signal the onset of a complication such as a stroke.

Maintaining Cardiac Output

Ongoing evaluation of the patient’s cardiac status continues as the nurse monitors the effectiveness of cardiac output through clinical observations and routine measurements: serial readings of blood pressure, heart rate, CVP, arterial pressure, and pulmonary artery pressures.

Renal function is related to cardiac function, as blood pressure and cardiac output drive glomerular filtration; therefore, urinary output is measured and recorded. Urine output less than 0.5 mL/kg/h may indicate a decrease in cardiac output or inadequate fluid volume.

Body tissues depend on adequate cardiac output to provide a continuous supply of oxygenated blood to meet the changing demands of the organs and body systems. Because the buccal mucosa, nail beds, lips, and earlobes are sites with rich capillary beds, they are observed for cyanosis or duskiness as possible signs of reduced cardiac output. Distention of the neck veins when the head of the bed is elevated to 30 degrees or more may signal right-sided heart failure.

Arrhythmias may develop due to decreased perfusion to or irritation of the myocardium from surgery. The most common arrhythmias encountered during the postoperative period are atrial fibrillation, bradycardias, tachycardias, and ectopic beats (Urden et al., 2019). Continuous observation of the cardiac monitor for arrhythmias is essential.

The nurse reports any indications of decreased cardiac output promptly. The assessment data are used to determine the cause of the problem. After a diagnosis has been made, the primary provider and the nurse work collaboratively to restore cardiac output and prevent further complications. When indicated, blood components; fluids; and antiarrhythmics, diuretics, vasodilators, or vasopressors are prescribed. If additional interventions are necessary, such as the placement of an intra-aortic balloon pump, the patient and family are prepared for the procedure.

Promoting Adequate Gas Exchange

To ensure adequate gas exchange, the patency of the endotracheal tube is assessed and maintained. The tube must be secured to prevent it from slipping out or down into the right mainstem bronchus. Suctioning is necessary when crackles or coughing is present.

Arterial blood gas determinations are compared with baseline data, and changes are reported to the primary provider promptly.

When the patient’s hemodynamic parameters stabilize, body position is changed every 1 to 2 hours. Frequent changes of patient position provide for optimal pulmonary ventilation and perfusion, allowing the lungs to expand more fully.

Physical assessment and arterial blood gas results guide the process of weaning the patient from the ventilator. The nurse assists with the weaning process and eventually with the removal of the endotracheal tube. After extubation, the nurse encourages deep breathing and coughing at least every 1 to 2 hours to clear secretions, open the alveolar sacs, and promote effective ventilation. See Chapter 19 for discussion of weaning the patient from the ventilator.

Maintaining Fluid and Electrolyte Balance

To promote fluid and electrolyte balance, the nurse carefully assesses the intake and output to determine positive or negative fluid balance. It is necessary to record all fluid intake, including IV, nasogastric tube, and oral fluids, as well as all output, including urine, nasogastric drainage, and chest drainage.

Hemodynamic parameters (e.g., blood pressure, CVP, cardiac output) are correlated with intake, output, and weight to determine the adequacy of hydration and cardiac output. Serum electrolytes are monitored, and the patient is observed for signs of potassium, magnesium, sodium, or calcium imbalance (see Chapter 10).

Indications of dehydration, fluid overload, or electrolyte imbalance are reported promptly, and the primary provider and nurse work collaboratively to restore fluid and electrolyte balance and monitor the patient’s response to therapies.

Minimizing Confusion

Some patients exhibit abnormal behaviors and acute confusion that occur with varying intensity and duration. The risk of delirium is high in patients who have undergone cardiac surgery and increases with patients’ age (Jones et al., 2019; Smulter, Lingehall, Gustafson, et al., 2019; see the Nursing Research Profile in Chart 23-12). Clinical manifestations of postoperative delirium include restlessness, agitation, visual and auditory hallucinations, and paranoia. The delirium typically appears after a 2- to 5-day stay in an ICU. Patients are assessed for this problem with tools such as the Confusion Assessment Method for the ICU (CAM-ICU) (Price, Garvan, Hizel, et al., 2017) (see Chapter 8, Chart 8-7, for discussion of CAM). The CAMU-ICU scale assesses for key indicators of delirium such as disorganized thinking and inattention. When this testing is positive, further assessment of the patient’s physiologic and psychological status is required. Presumed causes of postoperative delirium include anxiety, sleep deprivation, increased sensory input, medications, and physiologic problems such as hypoxemia and metabolic imbalance (Blair, Mehmood, Rudnick, et al., 2019). Treatment includes correction of identified physiologic problems such as metabolic and electrolyte imbalances. In addition, behavioral interventions are used (e.g., frequent reorientation). Sedative medications such as haloperidol were once thought to reduce agitation and improve survival, but recent studies note that use of haloperidol causes oversedation and does not reliably treat or prevent delirium (Blair et al., 2019). The delirium often resolves after the patient is transferred from the unit, but nonetheless can be associated with negative outcomes including cognitive and functional decline, longer lengths of hospital stay, and higher mortality (Delaney, Hammond, & Litton, 2018).

Use of a Postoperative Delirium Screening Scale in Older Adults After Cardiac Surgery

Smulter, N., Lingehall, H. C., Gustafson, Y., et al. (2019). The use of a screening scale improves the recognition of delirium in older patients after cardiac surgery: A retrospective observational study. Journal of Clinical Nursing, 28(11-12), 2309–2318.

Purpose

Postoperative delirium (POD) is a frequent occurrence in older patients undergoing cardiac surgery. However, it is often not recognized by health care providers and therefore may go undiagnosed. The purpose of this study was to assess whether the use of a delirium screening tool by nurses postoperatively will improve the recognition and diagnosis of POD.

Design

This study was a retrospective observational analysis. Seventy eight patients aged 70 and older who had cardiac surgery were diagnosed with POD. Nurses used the Nursing Delirium Screening Scale (Nu-DESC) to screen for delirium symptoms. This scale uses five items to assess for delirium: disorientation, inappropriate behavior, inappropriate communication, illusions and hallucinations, and psychomotor retardation. Each item is graded from 0 to 2 with a maximum score of 10. A NuDESC score of 2 or greater is thought to indicate the presence of delirium. The screening was conducted three times daily, beginning post-op day 1 through discharge.

Data describing the incidence and nature of POD from the clinical database and discharge summaries were retrospectively collected. This information was compared to the results of symptom screening using the Nu-DESC.

Findings

POD was correctly identified in 41 of 78 (52.6%) patients. “Inappropriate behavior” was the most common descriptor used by nurses and physicians within discharge summaries. Terminology like “confused,” “aggressive/restless,” and “disoriented” were commonly used to describe delirium symptoms. The cause and specific treatment of delirium was not addressed within the discharge summaries

Screening using the Nu-DESC identified 56 of 78 (72%) patients with POD. Use of the Nu-DESC showed greater sensitivity in identifying symptoms of delirium than the information documented within the discharge summaries and database.

Nursing Implications

Delirium is a serious complication that is underdiagnosed in patients after cardiac surgery and, when present, not well documented. Use of a validated screening scale, such as the Nu-DESC, can improve the ability of nurses to recognize delirium in postoperative patients.

For all postoperative patients, basic comfort measures are used in conjunction with prescribed analgesics and sedatives to promote rest. Invasive lines and tubes are discontinued as soon as possible. Patient care is coordinated to provide undisturbed periods of rest. As the patient’s condition stabilizes and the patient is disturbed less frequently for monitoring and therapeutic procedures, rest periods can be extended.

Uninterrupted sleep is provided as much as possible, especially during the patient’s normal hours of sleep.

Careful explanations of all procedures and of the patient’s role in facilitating them help keep the patient positively involved throughout the postoperative course. Continuity of care is desirable; a familiar face and a nursing staff with a consistent approach help the patient feel safe. The patient’s family should be welcomed at the bedside. A well-designed and individualized plan of nursing care can assist the nursing team in coordinating its efforts for the emotional well-being of the patient.

Relieving Pain

Patients who have had cardiac surgery may have pain in the peri-incisional area or throughout the chest, shoulders, and back. Pain results from trauma to the chest wall and irritation of the pleura by the chest tubes as well as incisional pain from peripheral vein or artery graft harvest sites.

The nurse assesses patients for verbal and nonverbal indicators of pain and records the nature, type, location, and duration of the pain. To reduce the amount of pain, the nurse encourages the patient to accept medication on a regular basis. The addition of adjunctive pain relievers (anti-inflammatory agents, muscle relaxants) to opioids decreases the amount of opioids required for pain relief and increases patient comfort. Patients report the most pain during coughing, turning, and moving. Physical support of the incision with a folded bath blanket or small pillow during deep breathing and coughing helps minimize pain. The patient should then be able to participate in respiratory exercises and to progressively increase self-care. Patient comfort improves after removal of the chest tubes.

Pain produces distress, which may stimulate the central nervous system to release catecholamines, resulting in constriction of the arterioles and increased heart rate. This can cause increased afterload and decreased cardiac output. Opioids alleviate pain and induce sleep and feelings of well-being, which reduce the metabolic rate and oxygen demands. After the administration of opioids, it is necessary to document observations indicating relief of apprehension and pain in the patient’s record. The nurse observes the patient for any adverse effects of opioids, including respiratory depression, hypotension, constipation, ileus, or urinary retention. If respiratory depression occurs, an opioid antagonist (e.g., naloxone) may be required (see Chapter 9 for further discussion of nonpharmacologic pain interventions).

Maintaining Adequate Tissue Perfusion

The nurse routinely palpates peripheral pulses (e.g., pedal, tibial, femoral, radial, brachial) to assess for arterial obstruction. If a pulse is absent in any extremity, the cause may be prior catheterization of that extremity, chronic peripheral vascular disease, or a thromboembolic obstruction. The nurse immediately reports newly identified absence of any pulse.

Thromboembolic events can result from vascular injury, dislodgment of a clot from a damaged valve, loosening of mural thrombi, or coagulation problems. Air embolism can result from CPB or central venous cannulation. Symptoms of embolization vary according to site. The usual embolic sites are the lungs, coronary arteries, mesentery, spleen, extremities, kidneys, and brain. The patient is observed for the onset of the following:

•        Acute onset of chest pain and respiratory distress, as occur in pulmonary embolus or MI

•        Abdominal or back pain, as occur in mesenteric emboli

•        Pain, cessation of pulses, blanching, numbness, or coldness in an extremity

•        One-sided weakness and pupillary changes, as occur in stroke

The nurse promptly reports any of these symptoms.

Venous stasis, which can cause venous thromboembolism (e.g., deep vein thrombosis, pulmonary embolism), may occur after surgery. It can be prevented by using the following measures:

•        Apply sequential pneumatic compression devices as prescribed.

•        Discourage crossing of legs.

•        Avoid elevating the knees on the bed.

•        Omit pillows in the popliteal space.

•        Begin passive exercises followed by active exercises to promote circulation and prevent venous stasis.

Inadequate renal perfusion can occur as a complication of cardiac surgery. One possible cause is low cardiac output. Trauma to blood cells during CPB can cause hemolysis of red blood cells, which then occlude the renal glomeruli. The use of vasopressor agents to increase blood pressure may constrict the renal arterioles and reduce blood flow to the kidneys.

Nursing management includes accurate measurement of urine output. An output less than 0.5 mL/kg/h may indicate hypovolemia or renal insufficiency. The primary provider may prescribe fluids to increase cardiac output and renal blood flow, or IV diuretics may be given to increase urine output. The nurse should be aware of the patient’s blood urea nitrogen, serum creatinine, glomerular filtration rate, and serum electrolyte levels. The nurse should report abnormal levels promptly, because it may be necessary to adjust fluids and the dose or type of medication given. If efforts to maintain renal perfusion are ineffective, the patient may require continuous renal replacement therapy or dialysis (see Chapter 48).

Maintaining Normal Body Temperature

Patients are usually hypothermic when admitted to the critical care unit following the cardiac surgical procedure. Because induced hypothermia from CPB and anesthesia lower the patient’s core temperature, the patient must be gradually warmed to a normal temperature. This is accomplished partially by the patient’s own basal metabolic processes and often with the assistance of heated air blanket systems. While the patient is hypothermic, shivering and hypertension are common. Lowering the blood pressure with a vasodilator such as nitroprusside may be necessary. These problems typically resolve as warming occurs.

After cardiac surgery, the patient is at risk for developing elevated body temperature as a result of tissue inflammation or infection. The inflammatory/immune response to surgery includes the release of cytokines that cause fever (Norris, 2019). The resultant increase in metabolic rate increases tissue oxygen demands and increases cardiac workload. Antipyretics and other measures are used to lower body temperature.

Common sites of postoperative infection include the lungs, urinary tract, incisions, and intravascular catheters. Meticulous care is used to prevent contamination at the sites of catheter and tube insertions. Aseptic technique is used when changing dressings and when providing endotracheal tube and catheter care. Clearance of pulmonary secretions is accomplished by frequent repositioning of the patient, suctioning, and chest physical therapy, as well as educating and encouraging the patient to breathe deeply and cough. All invasive lines and tubes are discontinued as soon as possible after surgery to avoid infection.

Postpericardiotomy syndrome may occur in patients who undergo cardiac surgery. The syndrome is characterized by fever, pericardial pain, pleural pain, dyspnea, pericardial effusion, pericardial friction rub, and arthralgia. These signs and symptoms may occur days to weeks after surgery, often after the patient has been discharged from the hospital.

Postpericardiotomy syndrome must be differentiated from other postoperative complications (e.g., infection, incisional pain, MI, pulmonary embolus, bacterial endocarditis, pneumonia, atelectasis). Treatment depends on the severity of the signs and symptoms. Use of colchicine and anti-inflammatory agents may produce an improvement in symptoms (Lehto, Kiviniemi, Gunn, et al., 2018).

Promoting Home, Community-Based, and Transitional Care

 Educating Patients About Self-Care

Depending on the type of surgery and postoperative progress, the patient may be discharged from the hospital 3 to 5 days after surgery. Following recovery from the surgery, patients can expect fewer symptoms from CAD and an improved quality of life. CABG has been shown to increase the lifespan of high-risk patients, including those with left main artery blockages and left ventricular dysfunction with multivessel blockages (Urden et al., 2019).

Although the patient may be eager to return home, the patient and family usually are apprehensive about this transition. Family members often express the fear that they are not capable of caring for the patient at home or that they are unprepared to handle complications that may occur.

The nurse helps the patient and family set realistic, achievable goals. An education plan that meets the patient’s individual needs is developed with the patient and family. Specific instructions are provided about incision care; signs and symptoms of infection; diet; activity progression and exercise; deep breathing, incentive spirometry, and tobacco use cessation; weight and temperature monitoring; the medication regimen; and follow-up visits with home health nurses, the rehabilitation personnel, the surgeon, and the cardiologist or internist.

Some patients have difficulty learning and retaining information after cardiac surgery. The patient may experience recent memory loss, short attention span, difficulty with simple math, poor handwriting, and visual disturbances. Patients with these difficulties often become frustrated when they try to resume normal activities. The patient and family are reassured that the difficulty is almost always temporary and will subside, usually in 6 to 8 weeks. In the meantime, instructions are given to the patient at a slower pace than normal, and a family member assumes responsibility for making sure that the prescribed regimen is followed.

Continuing and Transitional Care

Arrangements are made for home, community-based, or transitional care when appropriate. Because the hospital stay is relatively short, it is particularly important for the nurse to assess the patient’s and family’s ability to manage care in the home. The nurse making a home visit continues the education process (see Chart 23-13), monitors vital signs and incisions, assesses for signs and symptoms of complications, and provides support for the patient and family. Additional interventions may include dressing changes, diet counseling, and tobacco use cessation strategies. Patients and families need to know that cardiac surgery did not cure the patient’s underlying heart disease process. Lifestyle changes for risk factor reduction are essential, and medications taken before surgery to control problems such as blood pressure and hyperlipidemia will still be necessary.

The nurse encourages the patient to contact the surgeon, cardiologist, or office nurse with problems or questions. This provides the patient and family with reassurance that professional support is available. The patient is expected to have at least one follow-up visit with the surgeon.

Education does not end at the time of discharge from the hospital, transitional, or home health care. Many patients and families benefit from supportive programs, including cardiac rehabilitation. These programs provide monitored exercise; instructions about diet and stress reduction; information about resuming work, driving, and sex; assistance with tobacco use cessation; and support groups for patients and families. Hospital or community-based support groups provide information as well as an opportunity for families to share experiences.