Critical Care Nursing Diagnosis and Management PDF

14 Cardiovascular Disorders Annette Haynes and Patricia Henry http://evolve.elsevier.com/Urden/CriticalCareNursing Cardiovascular disease remains the leading cause of death in the CORONARY ARTERY DISEASE United States. From 2006 to 2016, the overall rate of cardiovas- cular disease (CVD) mortal...

14 Cardiovascular Disorders Annette Haynes and Patricia Henry http://evolve.elsevier.com/Urden/CriticalCareNursing Cardiovascular disease remains the leading cause of death in the CORONARY ARTERY DISEASE United States. From 2006 to 2016, the overall rate of cardiovas- cular disease (CVD) mortality in the United States declined by Description and Etiology 31.8%.1 Globally, 17.6 million deaths occur secondary to CVD The biggest contributor to cardiovascular system related morbid- occur each year, which is a 14.5% increase worldwide.1 The ity and mortality is coronary artery disease (CAD). Atherosclerosis is American Heart Association (AHA) has evolved from focusing a progressive disease that affects arteries throughout the body. In only on prevention of disease to an emphasis on cardiovascular the heart, atherosclerotic changes are clinically known as CAD. health with a healthy lifestyle, maintaining health factors, and This disease process is also known by the term coronary heart dis- population-level health promotion. ease (CHD), because other heart structures ultimately become A healthy lifestyle includes a healthy diet, weight, physical involved in the disease process. The atherosclerotic vascular activity, and not smoking. Health factor goals throughout the changes that lead to CAD may begin in childhood. Research and life span include optimal cholesterol levels, blood pressure epidemiologic data collected during the past 50 years have demon- (BP), and glucose control. Population-level health promotion strated a strong association between preventable (modifiable) risk aims to improve the cardiovascular health of the public. The factors and nonpreventable (nonmodifiable) risk factors and the seven metrics of a healthy lifestyle and health factors are the development of CAD1,4 (Box 14.1). The nonmodifiable risk factors basis of the AHA’s 2020 Impact Goals to improve cardiovascu- include age, family history, race, and sex. The salient modifiable lar health for all Americans by 20% and decrease deaths from risk factors for CAD include diabetes (Table 14.1), hyperlipidemia CVD and stroke by 20% by 2020.2 The prevalence of athero- (Table 14.2), hypertension (Table 14.3), cigarette smoking, obesity, sclerotic cardiovascular disease (ASCVD), which includes cor- and physical inactivity (Box 14.2).1 16 Avoiding these behaviors onary heart disease (CHD), heart failure (HF), stroke, and demonstrated 80% prevention of CVD.4 Other risk factors include hypertension in adults (. 20 years old) was 48% (121.5 mil- elevated C-reactive protein (Table 14.4), which is a marker of lion) in 2016. Hypertension demonstrated the greatest effect inflammation, and two CAD disease-risk equivalents: chronic kid- on ASCVD, with 24.3 million.1 Treatments have evolved with ney disease and diabetes. See Box 14.3 for a summary of all of the age-specific and sex-specific guidelines and campaigns includ- currently recommended target levels to prevent and manage CAD ing Go Red for Women. The World Health Organization’s glo- risk. bal action plan targets preventable risk factors (tobacco and alcohol use, salt intake, obesity, elevated blood pressure and Women and Heart Disease glucose) to reduce premature mortality by 25% by 2025, also Substantial progress has been made in the awareness, treatment, known as the 25 by 25 campaign.3 and prevention of CVD in women.17 CVD still causes approxi- In 2014, there were more than 7.9 million cardiovascular mately more than one-third of female deaths in the United operations and procedures. The annual direct and indirect States.1 After age 65 years, a higher percentage of women than costs of CVD and stroke were more than $350 billion in 2014 men have hypertension. Average body weight continues to to 2015.1 The critical care nurse is in a unique position to increase. Nearly two out of every three women in the United assist with educating the public on a daily basis about CVD States older than age 20 years are overweight or obese.17 The and the risk factors that are modifiable with changes in habits average age for first acute myocardial infarction (MI) in men is or lifestyles. Current guidelines for primary prevention of 65 years; in women, it is 71.8 years.1 CVD include estimation of the 10-year Atherosclerotic The Nurses’ Health Study identified that early menarche Cardiovascular Disease risk (ASCVD). This measure allows (monthly period onset) younger than 10 years old increased team focus on promoting healthy behaviors and working CVD risk by up to 20%. Early menopause (less than 40 years within the individual’s social determinants of health. Social old) increased CVD risk by 32%.18 The incidence of CVD is two determinants of health, including housing instability, food to three times higher among postmenopausal women than insecurity, transportation, access to exercise activities, and among women who are premenopausal.1 In the past, it seemed personal safety, are all essential for CVD prevention.3 An logical to prescribe hormone replacement therapy (HRT) to treat understanding of the pathology of CVD processes and clini- the symptoms of menopause.18 Current guidelines do not cal management allows the critical care nurse to anticipate recommend the use of HRT for primary or secondary preven- and plan interventions. This chapter focuses on cardiac dis- tion of CVD.18 Diabetes, smoking, and hyperlipidemia all orders commonly seen in the critical care environment. increase the cardiovascular risk for women.19 Data from the 298  CHAPTER 14 Cardiovascular Disorders 299 BOX 14.1 Modifiable and Nonmodifiable TABLE 14.2 Treatment of Blood Cholesterol Coronary Artery Disease Risk Factors to Decrease Atherosclerotic Cardiovascular Nonmodifiable Risk Factors Risk Disease6,14 Age Patient Sex Characteristics Intensity of Statins Needed Family history Age 75 y or less and no High-intensity statin Race safety concerns Modifiable Risk Factors Age more than 75 y or Moderate-intensity statin Elevated serum lipids safety concerns Hypertension Primary Prevention for LDL-C.190 mg/dL Cigarette smoking Age.21 y High-intensity statins to achieve 50% Prediabetes or diabetes mellitus decrease in LDL-C; consider nonstatin Diet high in saturated fat, cholesterol, and calories therapy Elevated homocysteine level Metabolic syndrome Diabetes; age 40 75 y; Moderate-intensity statins; high-intensity Obesity LDL-C 70 189 mg/dL statins when 10-y ASCVD risk is greater Physical inactivity than 7.5% Postmenopause (modification is controversial) No diabetes; age 40 75 y; Moderate-intensity statins; if 10-y ASCVD risk LDL-C 70 189 mg/dL is more than 7.5%, moderate- to high- intensity statins; if 10-y ASCVD risk is 0.5% 7.5%, moderate-intensity steroids Other Factors to Consider TABLE 14.1 Fasting Blood Glucose and Risk LDL-C $ 160 mg/dL Family history; premature ASCVD; hs-CRP 2 or for Coronary Artery Disease greater; CAC Agatston score.300; ABI Blood Glucose Fasting Plasma Glucose ,0.9; or lifetime ASCVD risk Level Levela (mg/dL) LDL-C ,190 mg/dL Age less than 40 y or greater than 75 y; or Normal 70 100 ,5% 10-y ASCVD risk Prediabetes 101 125 Clinical ASCVD Risk Factors Diabetes 126 or greater ACS a History of MI Values greater than normal increase the risk for coronary artery Stable or unstable angina disease and kidney failure. Coronary or other arterial revascularization Stroke Framingham Heart Study indicate the lifetime risk for CVD is TIA more than one in two for women.19,20 Optimum prevention PAD strategies for women following the AHAs Life’s Simple 7 model ABI, Ankle-brachial index; ACS, acute coronary syndrome; ASCVD, are often delayed or inadequate.20 Women lag 10 years behind atherosclerotic cardiovascular disease; CAC, coronary artery calcium; men for total CHD risk and more than 20 years for MI and sud- hs-CRP, high-sensitivity C-reactive protein; LDL-C, low-density den death. lipoprotein cholesterol; MI, myocardial infarction; PAD, peripheral In the 2011 update of Effectiveness Based Guidelines for the artery disease; TIA, transient ischemic attack. Prevention of CVD in Women,17 a new algorithm for risk classi- fication in women was adopted that stratified women’s risk into the following three categories: Women at high risk: Documented CHD, CVD, peripheral TABLE 14.3 Hypertension Management artery disease (PAD), abdominal aortic aneurysm, diabetes Guidelines15 mellitus, end-stage or chronic kidney disease, or 10-year General Population predicted risk for CHD greater than 10% (No Diabetes or CKD) Diabetes or CKD Present Women at risk: Cigarette smoking; systolic BP 120 mm Hg Age $ 60 y Age , 60 y All ages; diabetes All ages; CKD or greater, diastolic BP 80 mm Hg or greater, or treated present; no CVD present with hypertension; total cholesterol 200 mg/dL or greater, high- or without diabetes density lipoprotein (HDL) C less than 50 mg/dL, or treated BP goala: BP goal: BP goal: BP goal: for dyslipidemia; obesity, particularly central adiposity; poor SBP , 150 SBP , 140 SBP , 140 SBP , 140 diet; physical inactivity; family history of premature CVD occur- DBP , 90 DBP , 90 DBP , 90 DBP , 90 ring in first-degree relatives in men younger than 55 years old BP, Blood pressure; CKD, chronic kidney disease; CVD, cardiovascular disease; or women younger than 65 years old; metabolic syndrome; evi- DBP, diastolic blood pressure; SBP, systolic blood pressure. dence of advanced subclinical atherosclerosis (e.g., coronary cal- a BP values greater than normal increase the risk for coronary artery disease and cification, carotid plaque, or thickened intimal mean thickness); heart failure. All BP values are reported in mm Hg. 300 UNIT II Cardiovascular Alterations BOX 14.2 Detailed Coronary Artery Disease Risk Factors Age If these are ineffective, lipid-lowering medications are indicated. Coronary artery disease (CAD) disease generally first manifests after age Less than 50% of patients prescribed reduction therapy take their 45 years. medications. Men tend to develop CAD symptoms 5 to 10 years earlier than women. Only one-third of treated patients reach their LDL target value. Rate of cardiovascular disease (CVD) in women increases after age 75 years. Hyperlipidemia CAD rate is two to three times greater in postmenopausal women Hyperlipidemia causes severe atherosclerosis and development of CAD. compared with premenopausal women. Total cholesterol is the sum of HDL, LDL, and VLDL cholesterol (goal ,200 mg/dL). Family History Positive family history is defined as a close blood relative who has a HDL (Goal.40 mg/dL for Men;.50 mg/dL for Women) myocardial infarction (MI) or stroke before age 60 years. HDL is known as good cholesterol; a higher serum level protects against Family history suggests genetic or lifestyle predisposition for development atherosclerotic events. of CAD. HDL promotes efflux of cholesterol from cells. Patients with CAD family history have a 50% greater risk of having an MI. HDL has antiinflammatory and antioxidant effects on the arterial wall.6 Diabetes Mellitus LDL (Goal ,100 mg/dL) Elevated blood glucose is a known risk factor for development of vascular LDL is known as bad cholesterol because high serum levels are associated inflammation associated with atherosclerosis. with increased risk of ACS, stroke, and peripheral artery disease. The American Diabetes Association recommends use of the hemoglobin A1c LDL initiates atherosclerosis by infiltrating the vessel wall and inflammatory test with a threshold of 6.5% or greater, fasting blood glucose 126 mg/dL vessel effects. or greater, or 2-hour plasma glucose 200 mg/dL during an oral glucose Initial efforts to decrease LDL are based on weight loss, smoking cessation, tolerance test to diagnose diabetes. low-fat diet, physical exercise, and maintaining normal body size. Diabetics have increased risk of developing CAD and worse clinical If lifestyle changes are not effective in decreasing LDL, the medication outcomes after acute coronary syndrome (ACS) events. category of choice is statins. See Table 14.1 for fasting blood glucose levels and risk for CAD. See Table 14.2 for lipid guidelines and risk for CAD. Physical Activity Triglycerides (Ideal Goal ,100 mg/dL) A sedentary lifestyle has negative effects regardless of age, sex, body Triglyceride level greater than 150 mg/dL increases risk for heart disease mass index (BMI), and smoking status. and stroke. Regular vigorous physical activity using large muscle groups promotes Mean triglyceride level in men older than 20 years is 108.8 mg/dL. adaptation to aerobic exercise, which can prevent development of CAD and reduce symptoms in patients with established CVD. Lipoprotein(a) (Goal ,30 mg/dL) Exercise, decreased low-density lipoprotein (LDL) and triglyceride levels, Lp(a) is one of the lipid particles that makes up total LDL value. and increased high-density lipoprotein (HDL) cholesterol reduce insulin Lp(a) is described verbally as “LP little a.” resistance at the cellular level, lowering the risk for developing type 2 It is manufactured in the liver and circulates bound to a large glycoprotein diabetes. called apolipoprotein A. Lifelong physical activity is necessary to prevent atherosclerotic CAD and It is elevated in the presence of inflammation. stroke. Lp(a) stimulates atheroma and clot formation in inflamed arteries. Elevated Lp(a) is the most frequently encountered genetic lipid disorder in Obesity families with premature CAD. Two-thirds of U.S. adults are overweight. Medication treatment is high doses (1500 2000 mg/day) of extended- BMI greater than 30 kg/m2 is considered obese. release nicotinic acid (niacin). Obesity is associated with a sedentary lifestyle, calories consumed, and portion size. Metabolic Syndrome Normal BMI is 18.5 25 kg/m2 (Weight/Height2) Metabolic syndrome refers to clustering of risk factors associated with CVD and type 2 diabetes. Fat Pattern Distribution Approximately one-third of people in the United States have metabolic Higher weight carried in the abdominal area has greater risk of CAD. syndrome. Large waist (apple body shape)—excess abdominal adiposity—indicates Risk factors include: added fat around the abdominal organs. Fasting plasma glucose greater than 100 mg/dL or taking medications to Smaller waist and larger hips (pear body shape) is associated with lower lower elevated blood glucose risk of CAD. HDL cholesterol less than 40 mg/dL in men and less than 50 mg/dL in Goal waist measurements are less than 40 inches for men and less than 35 women inches for women. Triglycerides greater than 150 mg/dL or taking medications to lower elevated triglycerides High-Fat Diet Waist circumference greater than 40 inches (102 cm) in men or greater A diet rich in saturated fats leads to elevated cholesterol levels. than 35 inches (88 cm) in women A low-fat, high-fiber diet and increased physical activity are the first line of Blood pressure (BP) greater than 130 mm Hg systolic or greater than 85 treatment. mm Hg diastolic or taking antihypertensive medications (Continued)  CHAPTER 14 Cardiovascular Disorders 301 BOX 14.2 Detailed Coronary Artery Disease Risk Factors—cont'd Cigarette Smoking Hypertension is known as the silent killer because 28% of patients without Smoking unfavorably alters lipid profile by decreasing HDL and increasing CAD and 51% of patients with CVD are unaware of having hypertension. LDL and triglyceride levels. Initial treatments aim at lifestyle changes including physical activity, low The greater number of cigarettes smoked per day, the greater risk of sodium diet, limiting alcohol intake, and achieving normal body weight. developing CAD, acute MI, and stroke. Most patients are started on a diuretic; if this is insufficient, an Smoking fewer than five cigarettes per day increases risk. angiotensin-converting enzyme inhibitor, angiotensin receptor blocker, beta- Smokers are two to four times more likely to develop CAD compared with blocker, or calcium channel blocker may be added. nonsmokers.1 Most patients require at least two medications from different Passive secondhand smoke exposure also increases CVD risk for classifications to normalize their BP. nonsmoking adults with up to 30% increased risk of coronary heart disease. See Table 14.3 for BP guidelines and CAD risk. Of US adults, 20% are current smokers. Within 1 year of giving up cigarettes, an ex-smoker’s risk of developing Risk Equivalents for CAD CAD decreases significantly. Medical conditions in which patients have as much risk of experiencing a Nicotine is addictive, and giving up smoking is difficult. coronary event as if they already had CAD include: People need tremendous support to be able to “kick the habit.” Chronic kidney disease—risk for death from acute MI rises as serum creatinine level increases Hypertension Diabetes mellitus Hypertension is defined as systolic BP greater than 120 mm Hg and/or Peripheral artery disease diastolic BP greater than 90 mm Hg. Cerebrovascular disease Increased systolic pressure damages endothelium, leading to vascular inflammation and plaque development. TABLE 14.4 C-Reactive Protein and Risk for Adherence to healthy behaviors Coronary Artery Disease Lean body mass index less than 25 kg/m2 Participation in physical activity at recommended levels Category hs-CRP Levela (mg/L) Cessation of smoking Low risk (normal) ,1 Pursuit of eating pattern as suggested by Dietary Approaches to Stop Hypertension (DASH diet)20 Moderate risk 1 3 Almost 400,000 women die of CVD annually in the United High risk.3 States. Mortality rates for women after an acute MI are higher than for men: 26% compared with 14.9%.21 The risk factors hs-CRP, High-sensitivity C-reactive protein. hypertension, diabetes mellitus, alcohol intake, and physical a Values.1 mg/dL increase the risk for coronary artery disease, but inactivity are more strongly associated with acute MI in women test results are not valid in the presence of infection or other than in men.17,20 Many reasons contribute to the higher mortal- inflammatory condition. Normal values may vary slightly between ity from acute MI in women, including waiting longer to seek clinical laboratories; however, values ,1 mg/dL are usually considered normal. A test result.10 mg/L suggests a noncoronary medical care, having smaller coronary arteries, being older source of inflammation or infection. when symptoms occur, and experiencing very different symp- Based on data from Ramasamy I. Biochemical markers in acute toms from those of men of similar age.19,20 coronary syndrome. Clin Chim Acta. 2011;412:1279. Increased focus on sex differences with CVD led to more female enrollment in studies and female-focused studies. Female-specific predictors of increased risk include pregnancy-related outcomes systemic autoimmune collagen vascular disease (e.g., lupus or such as: preeclampsia, gestational diabetes, gestational hyperten- rheumatoid arthritis); history of preeclampsia, gestational dia- sion, preterm delivery, and low birth weight for estimated age. betes, or pregnancy-induced hypertension; or poor exercise tol- Collaboration between the American College of Obstetrics and erance with treadmill testing Gynecology (ACOG) and AHA led to guidelines to address female Women’s ideal cardiovascular health: Framingham risk score CV risk across the lifespan. These guidelines include recognition of less than 10%, absence of major CVD risk factors, and engage- the female-specific risk profile and identify the need for early and ment in a healthy lifestyle1,17 continued healthy heart behaviors as primary prevention. Most In 2011, these guidelines added several 10-year risk equa- women use their obstetrician/gynecologist as a primary care provi- tions for the prediction of 10-year global CVD risk, such as the der. This collaborative emphasis on healthy heart behaviors for updated Framingham CVD risk profile and the Reynolds Risk women across the lifespan are essential for all health care providers. Score for women.17,19 The future of successful prevention and CVD treatment for women The AHA defined a new concept of ideal cardiovascular depends on collaborative work across physician specialties with health in women as follows: ongoing studies and preventive treatment plans.21 Absence of clinical CVD and presence of all ideal levels of total cholesterol (less than 200 mg/dL) Vascular Inflammation BP less than 120/80 mm Hg The link between vascular inflammation and atherosclerotic dis- Fasting blood glucose less than 100 mg/dL ease is well established22 (see the later section Pathophysiology 302 UNIT II Cardiovascular Alterations BOX 14.3 Characteristics of Angina Pectoris Location Shortness of breath, with feeling of suffocation Beneath sternum, radiating to neck and jaw Most severe pain ever experienced Upper chest Beneath sternum, radiating down left arm Radiation Epigastric Medial aspect of left arm Epigastric, radiating to neck, jaw, and arms Jaw Neck and jaw Left shoulder Left shoulder, inner aspect of both arms Right arm Intrascapular Precipitating Factors Duration Exertion or exercise Less than 5 min (stable) Cold weather Longer than 5 min or worsening symptoms without relief from rest or sublingual Exercising after large, heavy meal nitroglycerin indicates preinfarction symptoms (unstable) Walking against the wind Emotional upset Quality Fright, anger Sensation of pressure or heavy weight on the chest Coitus Feeling of tightness like a vise Visceral quality (deep, heavy, squeezing, aching) Medication Relief Burning sensation Usually within 45 s to 5 min after sublingual nitroglycerin administration of Coronary Artery Disease). Research to identify prognostic lifestyle change.26 The major risk factors for developing CAD and sensitive inflammatory markers is ongoing. have been extensively documented in large epidemiologic stu- dies and include smoking, family history, adverse lipid profile, C-Reactive Protein and elevated BP. The inflammatory marker most frequently cited is C-reactive pro- tein (CRP). It is measured as high-sensitivity CRP (hs-CRP).22 Primary Versus Secondary Prevention of Coronary CRP is associated with an increased risk for development of other Artery Disease cardiovascular risk factors, including diabetes, hypertension, and If a person has symptoms of CAD or has previously had an ACS weight gain. The higher the hs-CRP value, the greater the risk of a event, the goal of any lifestyle change or medication is called sec- coronary event, especially if all other potential causes of systemic ondary prevention, or preventing another heart attack.11 If an inflammation, such as infection, can be ruled out. Value ranges for individual matches the risk profile described previously but does hs-CRP are shown in Table 14.4. If other systemic inflammatory not have symptoms of CAD or has not had an acute MI, the conditions such as bronchitis or urinary tract infection are present, treatment plan is described as primary prevention. The constella- the hs-CRP test loses all predictive value. CRP and other inflam- tion of cardiac risk factors is well established and can predict matory markers are used to estimate the probability of future acute development of CAD for most populations in the developed coronary events.22 25 During acute coronary syndrome (ACS) world. events, there is widespread activation of neutrophils in the cardiac circulation (measured from the coronary sinus), which suggests Pathophysiology of Coronary Artery Disease that inflammation is not limited to one unstable plaque.22 CAD is a progressive atherosclerotic disorder of the coronary arteries that results in narrowing or complete occlusion. Coronary Artery Disease Risk Equivalents Atherosclerosis affects the medium-sized arteries that perfuse Certain medical conditions are risk equivalents of CAD. A risk the heart and other major organs. Normal arterial walls are equivalent means the person has the same risk of having an composed of three layers: (1) the intima (inner lining), (2) the acute MI as if he or she already had CHD. Two noncardiac med- media (middle muscular layer), and (3) the adventitia (outer ical conditions considered risk equivalents for CAD are diabetes coat). mellitus and chronic kidney disease.26 PAD and cerebrovascular disease are atherosclerotic conditions that are also considered Development of Atherosclerosis CAD risk equivalents.26 Atherosclerosis is a chronic inflammatory disorder that is char- acterized by an accumulation of macrophages and T lympho- Multifactorial Risk cytes in the arterial intimal wall. One of the triggers of vascular CAD has multifactorial causation; the greater the number of inflammation is a high low-density lipoprotein (LDL) cholester- risk factors, the greater the risk of developing CAD. The best ol concentration. The inflammation injures the wall, allowing time for an individual to make lifestyle changes is before the the LDL cholesterol to move into the vessel wall below the symptoms of CAD occur. Patients with two or more risk factors endothelial surface. Blood monocytes adhere to endothelial cells or with one or more CAD risk-equivalent diseases have the and migrate into the vessel wall. Within the artery wall, some greatest potential to benefit from risk factor reduction and monocytes differentiate into macrophages that unite with and  CHAPTER 14 Cardiovascular Disorders 303 then internalize LDL cholesterol. The foam cells that result are back, but the most commonly described location is pain or pres- the marker cells of atherosclerosis. sure behind the sternum. The pain often radiates to the left arm Elevated LDL cholesterol levels promote low-level endothe- but can also radiate down both arms and to the back, shoulder, lial inflammation, which allows lipoproteins to infiltrate the jaw, or neck (Fig. 14.2). Angina symptoms are not the same for intimal vessel wall. After it has infiltrated under the endothe- all individuals. Many patients may describe pressure or discom- lium, LDL cholesterol tends to stay within the vessel wall rather fort rather than pain, and presenting symptoms can be highly than return to the circulation. This contrasts with the actions of individualized, as described in Box 14.3. Patients and families HDL cholesterol, which enters the vessel wall, helps efflux cho- must be taught that angina does not always present in the dra- lesterol from cells, and then returns to the circulation.7 The matic heart attack scenario as often portrayed on television and actions of HDL cholesterol may help minimize the number of in movies, in which the person clutches the throat or chest and foam cells in the artery wall.7 exhibits extreme distress.26,28 Angina symptom equivalents. Men and women should be Atherosclerotic Plaque Rupture informed of angina symptom equivalents, such as unexpected When a mature atherosclerotic plaque develops, it is not uni- shortness of breath; breaking out in a cold sweat; or sudden fa- form in composition. It has a lipid liquid center filled with pro- tigue, nausea, or lightheadedness.28 coagulant factors. A connective tissue fibrous cap covers the top Women and angina. Many women experience a variety of of the fluid lipid center.27 The abrupt rupture of this cap allows symptoms before an acute MI and during the acute event, as procoagulant lipids to flood into the vessel lumen and rapidly shown in Box 14.4.19,20 The recognition and publicity about the form a coronary thrombosis, as shown in Table 14.5. As the fact that many women have atypical symptoms but do not experi- enlarging clot blocks blood flow through the coronary artery, an ence “crushing chest pain” is important to understand to avoid a MI will occur unless adequate collateral circulation from other woman’s symptoms being trivialized by health care clinicians.19 It coronary vessels occurs. Symptoms and suggested cardiac inter- is vital that women are made aware of the angina symptom equiva- ventions at appropriate stages in development of CAD are listed lents of unexplained shortness of breath; breaking out in a cold in Table 14.5. sweat; or sudden fatigue, nausea, or lightheadedness.26,28 More Plaques that are likely to rupture are saturated with macro- women die every year in the United States of ACS compared with phages and other inflammatory cells. These vulnerable plaques men, a fact that is largely unknown by health care providers.19,20 are usually not obstructive and are situated at bends or branch Stable angina. Stable angina is predictable and caused by points in the arterial tree.26 It is unknown what factors increase similar precipitating factors each time; typically, it is exercise erosion or rupture of the fibrous cap. As deep fissures in the cap induced. Patients become used to the pattern of this type of expose the procoagulant factors to the blood plasma, an unstop- angina and may describe it as “my usual chest pain.” Pain con- pable cycle is put into motion. When platelets in the blood- trol should be achieved within 5 minutes of rest and by taking stream are exposed to collagen, necrotic debris, von Willebrand sublingual nitroglycerin. Ischemia and chest pain occur when factor, and thromboxane, a clot is formed and can occlude the myocardial demand from exertion exceeds the fixed blood oxy- coronary artery. Highly fibrotic plaques do not rupture. The gen supply. Additional information on CAD and stable angina type of atherosclerotic plaque that is prone to rupture has a is provided in Box 14.5. weak fibrous cap and a large amount of liquid cholesterol within Unstable angina. Unstable angina is defined as a change in a the core (see Table 14.5). previously established stable pattern of angina. It is part of the continuum of ACS. Unstable angina usually is more intense Plaque Regression than stable angina, may awaken the person from sleep, or may A reduction in blood cholesterol decreases atherosclerotic necessitate more than nitrates for pain relief. A change in the plaque size by decreasing the amount of liquid cholesterol with- level or frequency of symptoms requires immediate medical in the plaque core.6 Lowering cholesterol levels does not change evaluation. Severe angina that persists for more than 5 minutes, the dimensions of the fibrous or calcified portions of the plaque. worsens in intensity, and is not relieved by one nitroglycerin However, lower cholesterol levels reduce vascular inflammation tablet is a medical emergency, and the patient or a family mem- and make vulnerable plaque less likely to rupture. ber must call 911 immediately.27 The 911 (Emergency Medical Services [EMS]) system is available to 98% of the population of Acute Coronary Syndrome the United States.28 Family and friends are discouraged from The term acute coronary syndrome (ACS) is used to describe the driving a person experiencing unstable angina to the hospital array of clinical presentations of CAD that range from and instead are urged to call 911. Patients should be instructed unstable angina to acute MI (Fig. 14.1).1,26 An acute MI is gen- never to drive themselves but to contact the EMS by calling 911. erally described by patients as a “heart attack.” This section dis- Delay in reperfusion, cardiac arrest in personal car, and mortal- cusses stable manifestations of CAD (stable angina) and acute ity are all increased when EMS is not called.28 manifestations described as an ACS (unstable angina and acute Unstable angina is an indication of atherosclerotic plaque MI). Fig. 14.1 is a concept map of ACS. instability. It can signal atherosclerotic plaque rupture and thrombus formation that can lead to MI. A patient who comes Angina to the emergency department with recent-onset unstable angina Angina pectoris, or chest pain, caused by myocardial ischemia is but who has nonspecific or nonelevated ST segment changes on not a separate disease but rather a symptom of CAD. It is caused a 12-lead electrocardiogram (ECG) may be admitted to the criti- by a blockage or spasm of a coronary artery, leading to dimin- cal care unit to rule out MI. If the symptoms are typical of MI, it ished myocardial blood supply. The lack of oxygen causes myo- is important to treat the patient according to the latest published cardial ischemia, which is felt as chest discomfort, pressure, or guidelines, because not all patients who experience MI have ST pain. Angina may occur anywhere in the chest, neck, arms, or segment elevation on the 12-lead ECG.17,27 304 UNIT II Cardiovascular Alterations TABLE 14.5 Coronary Artery Disease: Pathogenesis, Symptoms, Diagnosis and Management Timeline Management of Pathology of CAD Symptoms of CAD Diagnosis of CAD CAD Normal coronary artery seen in No symptoms None Healthy lifestyle young healthy children Obesity prevention Fatty streaks on intima of No symptoms None Preventive measures aorta and coronary arteries with a focus on a in many young adults. healthy lifestyle Atherosclerotic plaque No symptoms None Cardiac risk factor increases in size but does Most adults are unaware management not occlude blood flow. they have CAD Atherosclerotic plaque Stable Angina ECG stress test Aggressive risk factor occludes more than 70% of Chest pain or pressure with Elective coronary management coronary artery lumen. exertion or exercise arteriogram Sublingual Stable cap on lipid plaque nitroglycerin for interior. angina Elective PCI with stent Atherosclerotic plaque Unstable angina/ACS 12-lead ECG Emergency PCI with becomes fibrous and Change in chest pain/ Coronary arteriogram stent calcified. Plaque has a large pressure symptoms Biomarkers Aggressive risk factor procoagulant lipid core. Cap Chest pain/pressure at rest management has thinned with cracks, Symptoms not relieved by Aggressive risk factor allowing platelets and fibrin NTG management to aggregate. Atherosclerotic cap ruptures STEMI or NSTEMI Emergency 12-lead ECG Emergency PCI with and the procoagulant lipid Abrupt onset of chest pain Emergency coronary stent core is released forming a or pressure or symptoms at arteriogram Aggressive risk factor thrombosis that blocks blood rest Biomarkers management flow. Angina not relieved by NTG Sudden shortness of breath, cold sweat ACS, Acute coronary syndrome; ECG, electrocardiogram; CAD, coronary artery disease; NSTEMI, non ST segment elevation myocardial infarction; NTG, nitroglycerin; PCI, percutaneous coronary intervention; STEMI, ST segment elevation myocardial infarction.  ASSESSMENT DATA ST SEGMENT ELEVATION ac tors MYOCARDIAL INFARCTION Smoker, hypertension, obesity, Risk F (STEMI) hyperglycemia, hyperlipidemia, high-stress job, sedentary lifestyle. Changes Changes seen seen on 12-Lead 12-lead EKG DIAGNOSTIC CONFIRMATION ST-segment elevation > 0.1 mV in two contiguous precordial leads, new LBBB with onset of symptoms < 12 hours ago. nt Re - Vital Signs: HR, BP, RR, T, SpO2, continuous me ess pe n 30 ECG to detect dysrhythmias. wit s rfu - Assess for warm or cool skin, color, capillary As Confirm diagnosis with cardiac biomarkers hi al sio minu refill, peripheral pulses. y sic Ph n w tes - Auscultate heart for cardiac murmur or new S3 or S4. 62-year-old Mike Hayes admitted ith Troponin I or T are elevated. - Auscultate breath sounds plus crackles to ICU with an acute STEMI IV f arri & wheezes. receiving fibrinolytic therapy. fibr o - Observe for breathlessness and frothy pink ino al sputum (pulmonary edema). lys - Ask patient, family, significant others for v is relevant history. NURSING INTERVENTIONS SAVE THE LIFE OF n to Increase supply & decrease the demand e ctio THE PATIENT WITH STEMI det to arly ns E tio CHAPTER 14 Cardiovascular Disorders New murmur may indicate rupture of Before administration rule out contraindications, including ica papillary muscle, severe damage, impending stroke or cognitive defects, facial trauma, uncontrolled HTN. pl heart failure and pulmonary edema. m co PATIENT OUTCOMES - Provide O2 to maintain O2 sat > 90%, elevate HOB. or - Monitor VS and hemodynamics for ongoing rf cardiac evaluation. to The patient will - Fluid management: urine output, I/O, daily ni Mo 1) Have cardiac output within normal range to weight, IVs. Bradycardia, bundle branch blocks, heart - Continuous cardiac monitoring, antidysrhythmics blocks, heart failure, pulmonary edema, maintain tissue perfusion. 2) Will be pain-free. as needed. and cardiogenic shock. - Administer nitroglycerin immediately. 3) Have adequate coping skills to deal with situational crisis. - Provide morphine for pain relief. DIAGNOSIS AND PATIENT CARE MANAGEMENT 4) Demonstrate adequate knowledge of disease - Monitor for signs of bleeding, especially when management. administering fibrinolytic therapy. - Assess for signs of continued ischemic pain. - Positive inotropic medications (dobutamine, Low cardiac output due to dopamine, milrinone). Early beta-blockade and alterations in preload, afterload, ACEI therapy. contractility, heart rate, or rhythm. - Bed rest, reposition & frequent skin assessment, bedside commode when stable, stool softeners. FIG. 14.1 Concept Map for Acute Coronary Syndrome. ACEI, Angiotensin receptor blockers I; BP, blood pressure; CO, cardiac output; ECG, electrocar- diogram; HOB, head of bed; HR, heart rate; HTN, hypertension; I/O, intake and output; IV, intravenous; LBBB, left bundle branch block; O2 Sat, oxygen satura- tion; RR, respiratory rate; R/T, related to; S/S, signs and symptoms; SPO2, saturation of hemoglobin with oxygen measured by pulse oximetry; STEMI, ST segment elevation myocardial infarction; T, temperature; U/O, urine output; VS, vital signs. (Concept maps created by Deanne A. Blach, MSN, RN.) 305 306 UNIT II Cardiovascular Alterations A B C D E F G H FIG. 14.2 Common Sites for Anginal Pain. (A) Upper part of chest. (B) Beneath sternum, radiating to neck and jaw. (C) Beneath sternum, radiating down left arm. (D) Epigastric. (E) Epigastric, radiating to neck, jaw, and arms. (F) Neck and jaw. (G) Left shoulder. (H) Intrascapular. BOX 14.4 Cardiovascular Symptoms methamphetamine) use may precipitate spasm. A definitive diag- nosis of variant angina is made during a cardiac catheterization Experienced by Women Before Acute study. Signs of spasm include ST segment elevation and chest pain. Myocardial Infarction Coronary artery spasm can occur with or without CAD. The prog- Generalized Symptoms Discomfort/Pain Symptoms nosis is excellent when no significant coronary artery stenosis exists. Before Acute Myocardial During Acute Myocardial Coronary artery spasm is treated with nitroglycerin or calcium Infarction Infarction channel blockers to vasodilate the coronary arteries. Silent ischemia. Silent ischemia describes a situation in which Unusual fatigue Centered high in chest Dizzy or faint Left breast objective evidence of ischemia is observed on an ECG monitor, but Hot, flushed Back/between shoulder blades the person does not complain of anginal symptoms. Silent ischemia Indigestion Neck/throat can occur in many clinical situations, as described in Box 14.6. Heart racing Generalized chest One-third of patients who are having an MI do not report chest Numbness in hands/fingers Leg(s) pain as a symptom.26 Patients with diabetes are at particular risk for Vomiting Both arms silent ischemia. Many patients who had type 2 diabetes for more Loss of appetite Top of shoulders than 10 years have developed autonomic neuropathy, which New vision problems Right arm or shoulder decreases their ability to experience chest pain. Patients with dia- Headache Jaw/teeth betes may misinterpret angina symptom equivalents such as nau- Coughing sea, vomiting, and diaphoresis as signaling a disruption in glucose Choking sensation control rather than a sign of myocardial ischemia. From McSweeney JC. Preventing and experiencing ischemic heart Medical Management disease as a woman: state of the science. A scientific statement from Accurate assessment of chest pain symptoms is essential if the American Heart Association. Circulation. 2016;133:1302. unstable angina is to be recognized and treated effectively. Factors to consider when assessing chest pain are listed in Box 14.7. An important reason to ask questions about the chest pain is to differ- Variant angina. Variant angina, or Prinzmetal angina, is caused entiate between stable and unstable angina. The change from by a dynamic obstruction from intense vasoconstriction of a coron- stable to unstable angina is potentially life threatening for the ary artery.29 Spasm can occur with or without atherosclerotic patient. If the ST segments are elevated or a newly documented left lesions. Variant angina commonly occurs when the individual is bundle branch block (LBBB) is seen on the 12-lead ECG, the at rest, and it is often cyclic, occurring at the same time every patient should be treated for acute MI.28 However, if these classic day. Smoking, alcohol use, and illegal stimulant drug (cocaine, ECG signs are missing and the chest pain continues, the current  CHAPTER 14 Cardiovascular Disorders 307 BOX 14.5 Evidence-Based Practice Coronary Artery Disease and Stable Angina Strong evidence exists that the following lifestyle interventions help prevent and to less than 130/80 mm Hg if diabetes or kidney disease is coronary artery disease (CAD). present. Diet: C—Cholesterol and cigarettes: Obtain a fasting lipid profile. Recommend Diet low in salt and high in fiber, fruit, vegetables, and grains diet or lipid reduction medication therapy (statin) to lower low-density All dietary fat less than 30% of total calories; saturated fat less lipoprotein cholesterol (LDL-C) to less than 100 mg/dL (,70 mg/dL if than 7% achievable), increase high-density lipoprotein cholesterol to more than Limit glucose in diet (simple sugars) 40 mg/dL for men or more than 50 mg/dL for women, and reduce Limit calories if overweight triglycerides to less than 150 mg/dL. Recommend adding plant stanols Omega-3 fatty acids included in diet or sterols (2 g/day) or viscous fiber (. 10 g/day), or both, to diet to Exercise: further lower LDL-C; add dietary omega-3 fatty acids in the form of Start by walking more often and increase physical exercise from there. fish or capsule (1 g/day). Always ask about tobacco use, and strongly Refer to cardiac rehabilitation program. recommend smoking cessation; encourage nicotine replacement Obesity: therapy (nicotine patches or gum) as needed. Achieve healthy body weight. D—Diet and diabetes: Prescribe a low-fat, calorie-appropriate diet and Addiction: provide nutritional consultation as needed to achieve a fasting Stop cigarette smoking. blood glucose level of 70 to 100 mg/dL and hemoglobin A1c of less Avoid exposure to environmental (secondhand) tobacco smoke at home than 6.5%. and at work. E—Education and exercise: Provide education about risk factor Limit alcohol intake. modification and the CAD disease process; recommend daily Strong evidence exists that the following diagnostic procedures help exercise for 30 to 60 min (ideal) or at least seven times each week the patient with angina. (minimum of 5 days per week). A body mass index between 18.5 When a patient presents with chest pain, quickly obtaining a detailed history kg/m2 and 24.9 kg/m2 and waist circumference less than 40 inches of symptoms, focused physical examination, and risk factor assessment can for men or less than 35 inches for women should be recommended. help determine whether the probability of CAD is low, intermediate, or high. Treat depression, if present. Hormone replacement therapy is not Initial laboratory tests include hemoglobin, fasting blood glucose, lipid recommended as a treatment for symptoms of coronary heart panel, and cardiac enzymes. disease. Influenza vaccination is recommended. Obtain a baseline 12-lead electrocardiogram (ECG) at rest, even if chest pain is not present. Interventional and Surgical Recommendations for Obtain a 12-lead ECG during an episode of chest pain. Stable High-Risk Patients Obtain a chest radiograph if symptoms of heart failure are present. Patients are risk stratified according to their symptoms and the results of car- Obtain an exercise 12-lead ECG if the patient’s condition is stable and diac diagnostic tests. symptoms suggest CAD or if the patient’s condition is stable with complete Percutaneous catheter intervention (PCI): left bundle branch block or right bundle branch block that makes the ECG PCI is more frequently performed than open heart surgery for relief of difficult to interpret for ischemia. anginal symptoms. Obtain cardiac echocardiography for a patient with a systolic murmur Coronary artery bypass graft surgery: suggestive of aortic stenosis. For patients with left main occlusion or multivessel disease Use cardiac echocardiography to determine the extent of left ventricular For patients with two-vessel disease who have significant proximal left (LV) hypertrophy or dysfunction. anterior descending coronary artery stenosis and an LV ejection fraction Stress cardiac echocardiography is recommended for patients with greater less than 50% than 1 mm of ST segment depression at rest (stress may be induced by References physical exercise or by pharmacologic stimulation). Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC Guideline for Coronary angiography (typically as part of a cardiac catheterization the management of patients with non-ST elevation acute coronary syndromes. procedure) is recommended for patients at high risk for adverse coronary A report of the American College of Cardiology/American Heart Association events. Task Force on practice guidelines. Circulation. 2014;130:e344 e426. Initial Pharmacologic and Lifestyle Treatment Fihn SD, Gardin JM, Abrams J, et al. 2012 ACCF/AHA/ACP/AATS/PCNA/SCAI/STS Recommendations guideline for the diagnosis and management of patients with stable ischemic heart The goal of treatment is to eliminate chest pain. disease: a report of the American College of Cardiology Foundation/American The 10 most important elements of CAD and stable angina management Heart Association Task Force on Practice Guidelines, and the American College of can be remembered using the following A-to-E mnemonic: Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular A—Aspirin and antianginal medications: Prescribe daily low-dose Nurses Association, Society for Cardiovascular Angiography and Interventions, and (75 325 mg) aspirin, oral nitrates, and sublingual nitroglycerin for Society of Thoracic Surgeons. Circulation. 2012;126(25):e354. episodes of angina. O’Gara PT, Kushner FG, Ascheim DD, et al. 2013 ACCF/AHA guideline for the B—Beta-blockers and blood pressure: Use angiotensin-converting management of ST-elevation myocardial infarction: a report of the American enzyme inhibitors and beta-blockers to decrease blood pressure to College of Cardiology Foundation/American Heart Association Task Force on less than 140/90 mm Hg if no other CAD risk factors are present Practice Guidelines. Circulation. 2013;127(4):e362. 308 UNIT II Cardiovascular Alterations BOX 14.6 Clinical Characteristics of Silent BOX 14.8 DIAGNOSIS AND PATIENT Ischemia CARE MANAGEMENT Objective electrocardiogram (ECG) evidence of myocardial ischemia Coronary Artery Disease and Angina without any chest pain or symptoms. Acute Pain due to transmission and perception of cutaneous, visceral, No anginal symptoms after previous myocardial infarction (MI), but muscular, or ischemic impulses objective ECG evidence of myocardial ischemia continues. Ineffective Tissue Perfusion due to decreased myocardial blood flow Symptoms of angina with some episodes of ischemia and no symptoms Activity Intolerance due to cardiopulmonary dysfunction with other ischemic events; patient may or may not have had previous MI. Powerlessness due to lack of control over current situation or disease progression Anxiety due to threat to biologic, psychologic, or social integrity BOX 14.7 Factors to Consider When Lack of Knowledge of Treatment Regime due to lack of previous Assessing Chest Pain exposure to information (see Box 14.9, Patient and Family Education Onset: Was onset of pain sudden or gradual? Plan: Coronary Artery Disease and Angina) Duration: Did pain last seconds or minutes? How soon after onset did the Patient Care Management plans are located in Appendix A. patient call for help? Precipitating factors: Was the patient up and moving around? Location: Was pain substernal? Was it located in the same area as previous pain? (see Box 14.7). The patient is asked to rate the intensity of the Radiation: Did pain radiate to the jaw, neck, arm, or shoulder? chest discomfort on a scale of 0 to 10. Pain levels must be Quality: Was pain similar to previous anginal pain? Was pain more assessed with sensitivity to differences in cultural manifestations intense or less intense? of pain. The term chest pain is not to be used exclusively, because Intensity: On a scale of 1 to 10, where would the patient rate the pain? some patients describe their angina as “pressure” or “heaviness.” Relieving factors: What made the pain better—changing position, It is important to document the characteristics of the pain and the nitroglycerin, oxygen, the presence of the nurse? patient’s heart rate and rhythm, BP, respirations, temperature, skin Aggravating factors: Did things such as the environment, telephone calls, color, peripheral pulses, urine output, mentation, and overall tissue or waiting for help worsen the pain? perfusion. A 12-lead ECG is used to identify the area of ischemic Associated symptoms: Was the pain accompanied by nausea, vomiting, myocardium. The major concern is that the chest pain may represent diaphoresis, or dyspnea? preinfarction angina, and early identification is essential so that the Emotional response: Was there an emotional response that intensified patient can be immediately treated. Treatment may include transfer the pain—anxiety, fear, anger? to the cardiac catheterization laboratory for a coronary arteriogram and opening of a blocked artery. If the hospital does not have a cardi- ac catheterization laboratory, GP IIb/IIIa receptor blockers may be pharmacologic treatment of choice is aspirin (if the patient cannot infused to prevent the evolution of the acute MI before transfer.27,28 tolerate aspirin, a thienopyridine such as clopidogrel can be given). Patients with definite unstable angina or non ST segment ele- Relieving Chest Pain vation myocardial infarction (NSTEMI) should receive dual anti- In the critical care unit, control of angina is achieved by a com- platelet therapy on admission if an invasive strategy is imminent. A bination of supplemental oxygen, nitrates, analgesia, and sur- glycoprotein (GP) IIb/IIIa inhibitor or direct thrombin inhibitor veillance of angina and of the effects of pharmacologic therapy. such as bivalirudin is administered; a loading dose of clopidogrel is Oxygen: All patients with acute ischemic pain are administered given at least 6 hours before the procedure. Patients undergoing supplemental oxygen to increase myocardial oxygenation. Pulse noninvasive treatment should receive aspirin and a thienopyridine oximetry is used to guide therapy and maintain oxygen satura- (clopidogrel, prasugrel, or ticagrelor) for 1 month and ideally up to tion above 90% unless the patient has a history of chronic 1 year. If symptoms persist, diagnostic angiography is performed. A obstructive pulmonary disease and is a carbon dioxide retainer. stress test should be performed on patients who are not undergoing Nitrates: A combination of intravenous and sublingual nitro- invasive therapy for unstable angina or NSTEMI; if the stress test is glycerin is used to vasodilate the coronary arteries and decrease negative, the GP IIb/IIIa inhibitor can be discontinued and unfrac- pain. After nitrate administration, the critical care nurse closely tionated heparin (UFH) administered for 48 hours. observes the patient for relief of chest pain, for return of the ST segment to baseline, and for the potential development of Nursing Management unwanted side effects such as hypotension and headache. Care management for a patient with CAD and angina incorpo- Administration of a nitrate is avoided if the systolic BP is less rates a variety of patient care diagnoses (Box 14.8). Nursing than 90 mm Hg. Medication interactions with nitrates are interventions focus on early identification of myocardial ische- another potential cause for concern. The phosphodiesterase mia, control of chest pain, recognition of complications, main- inhibitor medication sildenafil is prescribed for several condi- tenance of a calm environment, and patient and family tions including pulmonary hypertension (PH) (Revatio) and education. See Appendix A for patient care management plans erectile dysfunction (Viagra). Sildenafil and nitrates in combi- specific to patients with CAD. nation may contribute to a precipitous fall in BP.3 Analgesia: Morphine (2 to 4 mg given intravenously) is the Recognizing Myocardial Ischemia analgesic opiate of choice for preinfarction angina. It relieves Complaints of chest discomfort (angina) must be evaluated pain and decreases fear and anxiety. After administration, quickly, because angina is an indicator of myocardial ischemia the critical care nurse assesses the patient for pain relief and  CHAPTER 14 Cardiovascular Disorders 309 PATIENT-CENTERED CRITICAL CARE Bedside Rounds With Family in the Critical Care Unit Morning bedside rounds are vitally important in development of the daily plan of care for critically ill patients in the critical care unit. Rounds can involve large or small numbers of health care professionals depending on the size of the hospital and whether it is an academic/teaching hospital or a community hospital. In larger teaching hospitals, the team at morning rounds will include multiple professionals. These may include med- ical staff (attending physician, fellows, residents, medical students) and the primary nurse. The team may also include advanced practice providers (nurse practitioners, physician assistants, clinical nurse specialists) respiratory therapists, pharmacists, dietitians, rehabilitation therapists, and medical social workers. Consulting teams for specialty care may also participate in morning rounds when care needs are complex. Consequently, for some patients, the rounding teams will have 10 to 20 people at the bedside. In an academic/teaching hospital, the morning rounds often include educa- tion about disease processes and interventions so that rounds are also a learning opportunity. Typically the interprofes- sional dialogue uses medical technical language versus everyday language for teaching during rounds. In a smaller hospital, the team has fewer members and may include the attending physician (medicine or surgical speci- alty), advanced practice providers, and the bedside nurse. A respiratory therapist or other professionals may also be present. With the national movement toward patient-centered care and greater family involvement in the critical care unit, it is natural that this would include family participation in bedside rounds, especially when the patient is unable to com- municate because of intubation, sedation, critical illness, or cognitive impairment. When family members are present, it is helpful to begin with introductions in which everyone present at rounds states their name and role. Although the discussion is often rapid and includes technical medical terms, there is generally time at the end of rounds to answer family questions and explain the plan for the day in everyday language. Team rounds may be a few minutes longer with the family present. However, when patients and family members under- stand the plan for the day and are in agreement with the plan, this is beneficial for communication and patient outcomes. the development of unwanted side effects such as hypoten- emergency such as a cardiac arrest or to assist with emergency sion and respiratory depression.26 intubation or insertion of hemodynamic monitoring catheters. Aspirin: Chewing an oral non enteric-coated aspirin (162 to 325 mg) at the beginning of chest pain has been shown to Educate the Patient and Family reduce mortality. The nonenteric formulation is preferred In the critical care unit, the patient’s ability to retain educational because it increases absorption in the mouth when chewed, information is severely affected by stress and pain. Education topics not swallowed.26,28 that should be discussed when the clinical condition has stabilized are listed in Box 14.9. It is essential to teach avoidance of the Maintaining a Calm Environment Valsalva maneuver, which is defined as forced expiration against a Patients admitted to a critical care unit with unstable angina closed glottis. This can be explained to the patient as “bearing down” experience extreme anxiety and fear of death. The critical care during defecation or breath holding when repositioning in bed. The nurse is faced with the challenge of ensuring that the elements of Valsalva maneuver causes an increase in intrathoracic pressure, a calm environment to alleviate the patient’s fear and anxiety are which decreases venous return to the right side of the heart and can maintained while being ready at all times to respond to an acute be associated with low BP and symptomatic bradycardia. 310 UNIT II Cardiovascular Alterations BOX 14.9 PATIENT AND FAMILY After the anginal pain is controlled, longer-term education of the patient and the family can begin. Points to cover include (1) risk fac- EDUCATION tor modification, (2) signs and symptoms of angina, (3) when to call Coronary Artery Disease and Angina the physician, (4) medications, and (5) dealing with emotions and Before discharge, the patient should be able to teach back the following stress. However, because the acute hospital length of stay for uncom- topics: plicated angina is usually less than 3 days, referral to a cardiac rehabi- Angina: Describe signs and symptoms such as pain, pressure, and heaviness litation program for a controlled exercise program and risk factor in chest, arms, or jaw. modification after discharge may be the most helpful teaching inter- Preinfarction or unstable angina: Any chest pain that is not relieved by a vention a critical care nurse can provide. Clinical practice guidelines sublingual nitroglycerin (NTG) tablet taken 5 min apart times three doses for the management of CAD and stable angina are listed in Box 14.6. provides a reason to call 911 (emergency services). Use of the 0-to-10 pain scale: Notify critical care nurse or emergency personnel of any changes in pain intensity. MYOCARDIAL INFARCTION Use of sublingual NTG for angina: Pain intensity should decrease on pain Description and Etiology scale after NTG administration. At home, NTG must be kept in a dark, airtight container, or it loses its potency. To ensure potency, the NTG supply must be Myocardial infarction is the term used to describe irreversible replaced approximately every 6 months. Active NTG has a slight burning myocardial necrosis (cell death) that results from an abrupt sensation when placed under the tongue. decrease or total cessation of coronary blood flow to a specific Avoid Valsalva maneuver. area of the myocardium. In the hospital, this is often referred to Risk factor modification tailored to the patient’s individual risk factor as an acute MI, indicating the sudden onset and the life- profile: threatening nature of the event. Increasingly, an acute MI is Decrease fat intake to 30% of total calories a day. described in relation to whether ST segment elevation is seen on Stop smoking. a diagnostic 12-lead ECG. It may be labeled an acute NSTEMI27 Reduce salt intake. or an acute STEMI (ST segment elevation MI).28 Control hypertension. Three mechanisms can block the coronary artery and are Treat diabetes and control blood glucose levels (if patient has responsible for the acute reduction in oxygen delivery to the myo- diabetes). cardium: (1) plaque rupture, (2) new coronary artery thrombosis, Increase physical activity; achieve ideal body weight. and (3) coronary artery spasm close to the ruptured plaque. Intention to attend a cardiac rehabilitation program Myocardial tissue can best be salvaged within the first 2 Medication teaching about indications and side effects hours after the onset of anginal symptoms, as illustrated in Follow-up care after discharge Fig. 14.3.30 The earlier the myocardium is revascularized, the Symptoms to report to a health care professional better the chances of survival. However, many people do not Discussion of how to handle emotional stress and anger seek treatment until the acute phase has passed or delay seeking treatment because of denial of symptoms. Non-PCI Capable Hospital Immediate interhospital transport to a PCI-capable hospital for patients with STEMI Goal is FMC-to-PCI device time of 120 minutes. When unavoidable time delays will make the FMC-to-PCI device time longer than EMS on Scene 120 minutes, fibrinolysis should be EMS arrival on scene as FMC selected as the method of reperfusion Prehospital 12-lead ECG by for patients without contraindications. · Onset of symptoms EMS to diagnose STEMI IV fibrinolysis should start within 30 · Call 911 minutes of arrival. EMS transport directly to a PCI- capable hospital with FMC-to- PCI device goal of 90 minutes PCI-capable Hospital Activate hospital PCI team when When a patient is initially seen at a PCI- en route to hospital capable hospital, the goal is a door-to- PCI device time of under 90 minutes. Goal is Total Ischemic Time 120 Minutes FIG. 14.3 Evaluation of Prehospital Chest Pain and Acute Coronary Syndrome and Treatment Options. The first step is to call 911 (green arrow). Transport to a PCI-capable hospital is always the optimal first choice when available (red arrows). Transport to a non PCI-capable hospital is considered when other options are una- vailable (yellow arrow and yellow box). ECG, Electrocardiogram; EMS, emergency medical services; FMC, first medical contact; PCI, percutaneous coronary intervention; STEMI, ST segment elevation myocardial infarction.  CHAPTER 14 Cardiovascular Disorders 311 Pathophysiology depolarization from the cardiac surface involved in the MI Ischemia (Fig. 14.5D). As healing takes place, the cells in this area are replaced The outer region of the infarcted myocardial area is the zone of by scar tissue. ischemia, or penumbra, as illustrated in Fig. 14.4. It is composed of viable cells. Priority interventions are targeted to save this viable Q Wave Myocardial Infarction muscle. Repolarization in this zone is temporarily impaired but MIs are classified according to the location on the myocardial sur- eventually is restored to normal. Repolarization of the cells in this face and the muscle layers affected. Not all infarctions cause necro- area manifests as T-wave inversion on the ECG (Fig. 14.5). sis in all layers, as shown in Fig. 14.6. A transmural MI involves all three cardiac layers: endocardium, myocardium, and epicardium. Injury A transmural (full-thickness) MI usually provokes significant ECG The infarcted zone is surrounded by injured but still potentially changes (see Fig. 14.5). This is also described as a Q wave MI. Not viable tissue in an area known as the zone of injury (see every acute MI produces a recognizable series of Q waves on the Fig. 14.4). Cells in this area do not fully repolarize because of the 12-lead ECG. Some patients who had a demonstrated Q wave on a deficient blood supply. This is recorded on the ECG as elevation 12-lead ECG as a result of an acute MI lose the Q wave months or of the ST segment (Fig. 14.5C). years later. The reasons for this are unknown, but it may represent the development of collateral circulation. Infarction The area of dead muscle (necrosis) in the myocardium is known as Twelve-Le