Care of the Patient with Acute Coronary Syndrome PDF

Chapter 6 Care of the Patient with Acute Coronary Syndrome Carrie Edgerly MacLeod, PhD, APRN-BC Abbreviations ACS Acute Coronary Syndrome NSTEMI Non-ST-Segment Elevation Myocardial CAB...

Chapter 6 Care of the Patient with Acute Coronary Syndrome Carrie Edgerly MacLeod, PhD, APRN-BC Abbreviations ACS Acute Coronary Syndrome NSTEMI Non-ST-Segment Elevation Myocardial CABG Coronary Artery Bypass Graft Infarction CAD Coronary Artery Disease PTCI Percutaneous Transluminal Coronary Intervention CK-MB Creatine phosphokinase–myocardial band PTCA Percutaneous Transluminal Coronary DAPT Dual antiplatelet therapy Angioplasty ECG Electrocardiogram STEMI ST-Segment Elevation Myocardial Infarction LIMA Left Internal Mammary Artery tPA Tissue Plasminogen Activator MI Myocardial Infarction USA Unstable Angina MIDCAB Minimally Invasive Direct Coronary Artery Bypass Learning Outcomes Upon completion of this chapter, the learner will be able to: myocardial infarction, and non–ST- elevation myocardial infarction. 1. Articulate the pathophysiology, classifications, and risk factors of acute 3. Compare invasive therapies/interventions coronary syndrome. and distinguish the nursing care associated with each. 2. Interpret the manifestations, diagnostic testing, and collaborative care of the patient 4. Detect the potential complications with angina pectoris, ST-elevation associated with acute coronary syndrome. Introduction myocardial infarction (STEMI) to non–ST-segment eleva- tion (NSTE) ACS, which includes the diagnosis of unstable Acute coronary syndrome (ACS) is an inclusive term for angina and non ST-segment elevation myocardial infarc- conditions that cause chest pain due to insufficient blood tion (NSTEMI). These life-threatening disorders are a supply to the heart muscle. ACS thus covers the spectrum major cause of emergency medical care and hospitalization of clinical conditions ranging from ST-segment elevation in the United States. 137 138 Chapter 6 Coronary artery disease (CAD) is the leading global ruptures or becomes u ­ nstable in the vasculature. The cause of death accounting for 17.3 million deaths annually unstable plaque is characteristically composed of a large (American Heart Association, 2015). In the past few years, lipid core, a large number of lipid-laden macrophages, and the death rate has started to decline, most likely due to a thin fibrous cap. Rupture of this cap exposes the throm- improved prevention and treatment. Despite this decline, bogenic contents of the plaque into a patient’s circulation. CAD is the number one cause of death in the United States This evolution of foreign material causes circulating plate- and is also the leading cause of death for women, account- lets to adhere to the subendocardial collagen, thus causing ing for the loss of more lives than all types of cancer com- more platelets to activate and aggregate at the site of injury bined (Mozaffarian et al., 2015). (Srikanth & Ambrose, 2012). Pathophysiology, Aorta Classifications, and Risk Right Left coronary Factors of Acute Coronary artery coronary artery Syndromes ACS is the clinical manifestation of coronary heart disease, Circumflex which includes the development of fatty plaques in the cor- artery onary arteries. The growth of the atherosclerotic plaques Right narrows the vasculature, which then limits the blood flow and atrium Anterior delivery of oxygen to the coronary muscle (2 Figures 6-1 descending and 2 6-2). In the early stage of atherosclerosis, small lipo- artery protein particles penetrate the vascular endothelium, Marginal artery Posterior where they are coalesced into the intimal lining. This leads interventricular to an accumulation of plaque in the coronary arteries artery resulting in a less serious condition known as stable angina. A more serious condition exists when the plaque Figure 6-1 Coronary circulation, coronary arteries. Coronary artery Adventitia Media Plaque Intima In atherosclerosis, lipids accumulate in the intimal layer of arteries. Fibroblasts in the area respond by producing collagen, and smooth muscle cells proliferate, together forming a complex lesion called plaque. Plaque consists mostly of cholesterol, triglycerides, Endothelium phospholipids, collagen, and smooth muscle cells. Collagen Plaque reduces the size of the lumen of the affected artery, impairing blood flow. In addition, plaque may ulcerate, Smooth muscle cell causing a thrombus to form that may completely occlude the Cholesterol crystal Plaque vessel. Lipid Internal elastic lamina (damaged) Fibrosis Figure 6-2 Atherosclerosis. P. Motta/G. Macchiarelli/S. Nottola/ Photo Researchers, Inc.  Care of the Patient with Acute Coronary Syndrome 139 The formation of platelet-rich thrombi is the underly- ing cause of adverse ischemic events across the full spec- trum of ACS. At first, the growth of the platelet-rich Box 6-2 Interventions to thrombi causes an occlusion, which leads to myocardial Achieve Goal Blood ischemia and the diagnosis of unstable angina (USA). As the platelets continue to aggregate, they can cause block- Pressure age of smaller blood vessels resulting in a NSTEMI. The Initiate lifestyle modification, including weight control; plaque rupture also induces the formation of thrombin, increased physical activity; alcohol moderation; sodium which converts fibrinogen into fibrin. This formation of restriction. fibrin along the area of ruptured plaque assists the throm- Include a diet of fresh fruits and vegetables and low-fat bus to stabilize and fully occlude the coronary vessel. The dairy products. result of this full occlusion is a STEMI. If blood pressure is elevated, control with medication— beta blockers and/or ACE inhibitors and diuretics. Risk Factors for Acute Coronary Syndrome Hypertension. Hypertension increases the heart’s work- Through extensive research the American Heart Associa- load, causing increased stress and oxygen consumption tion has articulated several factors that place a patient at by myocardial muscle. There is a definite correlation be- risk for developing CAD (Eckel et al., 2014). Some of these tween the degree of blood pressure (BP) elevation and risk factors can be modified, treated, or controlled, and CAD risk. The 20 mmHg average increase in systolic BP others c­ annot. The more risk factors a person has, the that comes with age increases the occurrence of CAD two greater the chance of developing an ACS sometime in the to three times for individuals between the ages of 30 and person’s lifetime. 65 years. Recent modifications in the AHA recommenda- tions for individuals with CAD call for maintenance of a Modifiable Risk Factors SBP < 140 mmHg and a DBP < 90 mmHg. However, an Modifiable risks are those that the patient has some control ­excessive lowering of the DBP for patients with ACS may over, for example, smoking, high blood pressure, seden- impair coronary blood flow and oxygen supply. In addi- tary life style, obesity, cholesterol level, and diabetes. tion, patients with ACS often have v ­ asomotor i­ nstability with an increased tendency to exaggerated responses to Tobacco Smoke. Cigarette smoking has an adverse effect antihypertensive therapy (Rosendorff et al., 2015) (Box 6-2). on the lipid profile, clotting factors, and platelet function. Physical Activity. Sedentary lifestyles are strong risk Smokers’ risk of coronary heart disease is two to four times factors for heart disease. Regular, moderate to vigorous that of nonsmokers. Cigarette smoking has been linked to physical activity has been shown to prevent heart and sudden cardiac death as well as ACS. People who smoke blood vessel disease. Exercise has also been demonstrated cigars and pipes also have a high risk of dying from CAD, to assist in controlling or eliminating other risk factors but it is still less than that of cigarette smokers. Exposure to such as hypertension, hyperlipidemia, diabetes, and obe- secondhand smoke for nonsmokers also increases the risk sity (Box 6-3). of having an ACS event. Cessation of smoking can reduce the risk of a coronary event by 50% within the first 1–2 years Obesity. The measurement commonly used to determine of quitting (U.S. Department of Health, 2014) (Box 6-1). whether a person is obese is the body mass index (BMI). A BMI of 25.9 kg/m2 to 29.9 kg/m2 is considered overweight, Box 6-1 Interventions to Achieve Tobacco use Box 6-3 Interventions Cessation to Achieve Physical Ask about tobacco status. Activity Goal Advise to quit if still smoking. Assess risk with physical activity history and/or exercise test. Assess willingness to quit. Encourage 30–60 minutes of activity every day. Assist in developing a plan for quitting. Encourage resistance training 2 days per week. Arrange for a smoking cessation class. Encourage cardiac rehabilitation program for people at Avoid environmental exposure. high risk. 140 Chapter 6 Bariatric Considerations Extreme obesity (EO), defined as BMI ≥ 40 kg/m2, is surgery (CABG). The results indicated that a higher BMI correlated with a higher risk of procedural and surgical and CABG surgery were associated with greater risk of complications. A recent study of 133 EO patients exam- major complications. Interestingly enough, both PCI and ined complications one year after percutaneous coro- CABG procedures demonstrated the same rates for stroke, nary intervention (PCI) and coronary artery bypass death and myocardial infarction (Ramirez et al., 2015). and a BMI of over 30 kg/m2 is considered obese. Excess weight causes added stress on the heart muscle, which increases coronary workload. Obesity is also linked to hy- Box 6-5 Interventions to pertension, hyperlipidemia, a decrease in high-density Achieve Goal Serum Lipid lipoproteins (HDL), impaired glucose metabolism, and inflammation. Numerous studies indicate the presence of Levels the “obesity paradox,” which is present when lean patients Start dietary therapy. Reduce intake of saturated fats to with established CAD have a worse clinical prognosis than 4 Source: Martin, S. S., et al. (2014). 2013 ACC/AHA cholesterol treatment guideline: What was done well and what could be done better. Journal of the American College of Cardiology, 63 (24), 2674–2678.  Care of the Patient with Acute Coronary Syndrome 141 have a higher risk than Caucasians. Due to the obesity Box 6-6 Interventions to factor, it has been found that Mexican Americans, American Indians, and some Asian Americans are also Achieve Goal Serum at increased risk for developing a heart disease-related Glucose Levels syndrome (AHA, 2015). Stress: People who are under extreme stress tend to Initiate lifestyle and pharmacotherapy to achieve a normal ­participate in other unhealthy activities. This includes HbA1c. lack of exercise, overeating, and smoking. Stress also Lifestyle changes as indicated in other risk factors. increases the workload on the cardiovascular system. Coordinate care between other medical providers. Stress has the tendency to increase BP and heart rate (HR) and also contributes to the blood’s ability to form clots, putting the patient at increased risk for a coro- As this occurs, glucose cannot enter the cells in sufficient nary event. quantities. Initially, the pancreas responds by producing larger amounts of insulin. People with this condition are Alcohol Consumption: Alcohol, when taken in large often asymptomatic though they have both hyperglycemia quantities, has been attributed to increasing a person’s and hyperinsulinemia. Other abnormalities that are pres- BP. It also contributes to an increase in triglycerides, an ent in metabolic syndrome include central obesity, defined important component in the development of CAD. as a waist circumference larger than 40 inches in men or Menopause: Early menopause, at age 39 years or larger than 35 inches in women; high triglyceride levels, younger, and late menopause, at age 56 years or older, over 150 mg/dL; high LDL; and low HDL, less than increases cardiovascular risk. By age 75, a woman’s 40 mg/dL in men and less than 50 mg/dL in women. These risk of death from CAD is equal to or greater than the factors greatly increase the risk of heart disease. risk for a man. Women who are taking estrogen ther- apy and who have vascular disease can continue this Nonmodifiable and Other therapy if it is prescribed for other well-established indications. However, there is no clinical evidence for Contributing Risk Factors adding or continuing estrogens in postmenopausal women with CAD in an effort to prevent or retard pro- Age: Plaque builds up over time so the incidence of CAD gression of the disease (Whayne & Debabrata, 2015). occurs more as we age. The risk for women increases after age 55 years and the risk for men increases after age 45 years. Angina Pectoris Gender: Men have a greater risk of MIs than women, Angina pectoris literally means “strangling of the chest.” It and they tend to experience MIs earlier in life. In the is a general medical term used to define types of chest pain 35 to 44 year old age group, white men are 6.1 times caused by myocardial ischemia. Due to plaque buildup and more likely to die of CAD than white women. There is atherosclerosis, the myocardium can become deprived of less difference among nonwhites. blood and oxygen. Thrombus formation and further plaque Heredity: Children of parents with heart disease are at formation eventually narrow the coronary arteries, causing greater risk for developing it themselves. African ischemia and death of myocardial tissue. Ischemia occurs if Americans, due to the comorbidity of hypertension, the demand for oxygen exceeds its ­supply. Demand for Angina Variant Stable Unstable Prinzmetals STEMI NSTEMI Visual Map 6-1 Relationship Among Types of Angina 142 Chapter 6 myocardial oxygen increases with isometric and isotonic Variant (Prinzmetal’s) Angina exercise, stress, exposure to cold, cigarette smoking, and Variant angina is a less common form of angina. It is char- sympathetic nervous system stimulation (Visual Map 6-1). acterized by episodes of chest pain that occur at rest. Unlike stable and unstable angina, variant angina is caused by Classification coronary artery vasospasms, which can cause an increase Angina can be classified into three different phases: stable, in myocardial oxygen demand and a transient ST-segment unstable, and variant. The angina that is of the most con- elevation. This type of angina is often treated with calcium cern to the development of ACS is the unstable angina pro- channel blockers and long-acting nitrate preparations. totype. The stable and variant types are included to assist Patients with Prinzmetal’s angina are younger and have in the differentiation of the major anginal prototypes. fewer risk factors, so a cardiac examination is often unre- Many factors can precipitate anginal pain (Box 6-7). markable in the absence of ischemia. Cardiac catheteriza- tion may or may not d ­ emonstrate transient coronary Stable Angina. Stable angina is chest pain that occurs pre- spasms, with minimal plaque formation (Cannon & dictably on exertion. This type of angina is associated with Braunwald, 2012). stable plaque buildup in the coronary arteries. The stenotic coronary vessel reduces coronary artery blood flow to a criti- Unstable Angina cal level. Symptoms of stable angina, although caused by decreased myocardial oxygen, can change from time to time Unstable angina is pain that occurs more often and in depending on stress, oxygen consumption, and tempera- unpredictable patterns. It can occur while the patient is ture extremes. Stable angina is often treated with short term at rest, as well as with minimal exertion, and often ­nitroglycerin preparations and rest. Beta blockers are rec- causes the patient to limit his activity. The 2014 AHA key ommended as the initial agent to relieve symptoms in most recommendations emphasize the continuum between patients with stable angina. If beta blockers are not well tol- unstable angina and NSTEMI (Amsterdam & Wenger, erated, patients may be placed on calcium channel blockers 2014) (Table 6-2). or long-acting nitrates. If the patient is known to have had a previous myocardial infarction or concurrent coronary artery Myocardial Infarction (MI) disease, treatment should also include antiplatelet therapy, An MI occurs when the heart muscle is abruptly deprived of such as aspirin, clopidogrel, or a combination of the two. oxygen. When the heart is deprived of oxygen, it proceeds ACE inhibitors should be prescribed for patients with through several phases of tissue injury (2 Figure 6-3). The ­diabetes or left ventricular dysfunction unless contraindi- first phase is the area of ischemia. If treatment is not imme- cated (Fihn et al., 2012) Risk factor modification and lifestyle diate, the tissue damage will continue on to injury and changes are also included in the management of stable angina. then necrosis. Coronary plaque rupture initiates the events Reflect On A patient starts experiencing left-sided chest pain. He associates it with “heartburn” and does not seek further evaluation. As the nurse, what would you suggest to this patient? What could be the conse- quences of the patient’s actions? Box 6-7 Precipitating Ischemia causes Causes of Anginal Pain T wave inversion Injury causes e Physical exertion on ST elevation i c z ne Temperature extremes m zo he ne Infarction causes Isc jury n zo q waves Emotions (stress and anger) In tio rc Consumption of a large meal fa In Tobacco use Opposite from Sexual activity the site of infarction the leads show Stimulants (caffeine, cocaine, amphetamines) reciprocal changes Circadian rhythm patterns Figure 6-3 The evolution changes in acute MI.  Care of the Patient with Acute Coronary Syndrome 143 Table 6-2 Classification and Treatment of Anginal Prototypes Classification Etiology Symptoms Treatment Stable Myocardial ischemia ACS Episodic pain lasting 5–10 minutes NTG Aggravated by exertion, exposure to cold, Aspirin eating, emotional stress Beta adrenergic blockers Relieved by rest or nitroglycerin Calcium channel blockers ACE inhibitors Unstable Ruptured or thickened plaque Angina of increasing intensity, frequency, NTG with platelet and fibrin throm- or duration Beta blockers tissue plasminogen bus, causing an increase in Occurs at rest or with minimal activity activators (tPA), oxygen coronary obstruction Pain unresponsive to NTG Clopidogrel Morphine Statins Aspirin Variant Coronary vasospasm Occurs at rest without provocation Calcium channel blockers Triggered by smoking Transient ST-segment elevation during pain. Often with associated AV block or ventricular arrhythmias Occurs with or without the presence of CAD of an acute MI. Myocardial cells become ischemic within 10 A lateral wall MI usually occurs with an occlusion of seconds of coronary occlusion. During ischemia, cells the circumflex artery or the diagonal branch of the LAD. experience a temporary shortage of oxygen, hypoxia, and Muscle damage occurs in the free, lateral wall of the left downgrade their activity to conserve energy. Several min- ventricle. Because the circumflex artery also supplies a utes after the loss of contractile ability, the myocardium is portion of the sinoatrial (SA) node and atrioventricular deprived of its glucose source necessary for aerobic metab- (AV) node, patients often present with the complications olism. This causes anaerobic processes to take over, and a of sinus dysrhythmias. An inferior wall MI is most com- buildup of lactic acid ensues. During this period the cells of monly due to an occlusion of the right coronary artery the myocardium do not fully polarize. If this buildup con- (RCA). The muscle damage is seen in the right ventricle tinues without restoration of aerobic processes, an MI and posterior and inferior left ventricle. More than half of occurs. Because infarcted cells cannot respond to electrical all inferior wall MIs are associated with an occlusion impulses, they cannot help the heart contract. The buildup of the proximal portion of the RCA, which can lead to of scar tissue from the ensuing necrotic heart tissue can ­significant damage to the right ventricle. (Further infor- lead to ventricular remodeling, which changes the shape mation can be found later in the chapter in the discussion and function of the heart muscle. of the anatomical location of MIs.) Myocardial injury to the posterior wall of the left ven- Location of Infarction tricle is uncommon due to the dual blood supply from the RCA and circumflex artery. If an infarction occurs in this Myocardial injury and infarction occur mostly in the left portion of the heart muscle, it will also cause significant ventricle because it has the greatest oxygen demand and is damage to the right ventricle. therefore more affected by occlusions of the coronary arter- ies. An MI is categorized by the wall of the ventricle on which it occurs. This can be the anterior, lateral, septal, inferior, or posterior wall, or a combination of these walls. Non-ST-Segment Elevation Myocardial An anterior wall MI is caused by occlusion of the Infarction (NSTEMI) left anterior descending artery (LAD). The higher or NSTEMI (previously termed subendocardial infarction or more proximal the occlusion, the more muscle damage non-Q-wave myocardial infarction) and unstable angina ensues. Occlusion to the LAD can also cause an antero- occur as a result of a subtotal occluding thrombus. This lateral or anteroseptal MI. Damage for this particular MI type of infarction is associated with ST segment depression includes the anterior wall and anterior portion of the or T wave inversion on the ECG (2 Figure 6-4). There are septal wall. Anterior wall MIs account for 25% of MIs no acute ST-segment elevations or Q waves. NSTEMI and and have the highest mortality rate. These patients often unstable angina may be undistinguishable with ECG suffer from serious complications of ACS, elaborated on ­studies. They differentiate only by the serologic evidence later in the chapter. of myocardial necrosis. 144 Chapter 6 ○○ Oral beta blockers should be instituted to decrease heart rate, blood pressure, and myocardial oxygen demand ○○ Calcium antagonists are used for patients unre- NSTEMI: non-ST sponsive to NTG and beta blockers -elevation myocardial ○○ Aspirin, P2Y12 inhibitor, anticoagulation with infarction unfractionated heparin or bivalirudin STEMI, ST elevation ○○ High intensity statin therapy myocardial ○○ Urgent/immediate invasive strategy infarction Figure 6-4 ECG and myocardial findings in Q-wave ST-Segment Elevation Myocardial and non-Q-wave MIs. Infarction (STEMI) (Courtesy Barbara Ritter, EdD, FNP-BS, CS.) The most common cause of STEMI, formerly known as Initial Focused Assessment and treatment includes Q-wave MI, is reduced myocardial perfusion from an (Amsterdam & Wenger, 2014): occlusive thrombus that developed on a ruptured por- tion of atherosclerotic plaque. Associated ECG changes Hospital admission will be discussed later in this chapter but briefly include Serial ECGs and cardiac enzymes ST segment elevation, Q waves, and a new left bundle Rest for 24–48 hours branch block. Nursing actions are similar to the NSTEMI Continuous bedside ECG actions and will be further elaborated upon in the next Analgesics session (Abid et al., 2015). Reperfusion therapy should be administered to all eligible patients with STEMI with Supplemental oxygen symptom onset within the prior 12 hours, and PCI is the Pharmacological therapy recommended method of reperfusion when it can be ○○ Sublingual nitroglycerin to start, if pain reoccurs performed in a timely fashion by experienced operators should be placed on a NTG intravenous drip (O’Gara et al., 2013). Anginal Pain + Cardiac EKG Changes Markers + Exercise Test Cardiac PTCA CABG Catherization Risk Factor modification Medication Management Cardiac Rehabilitation Visual Map 6-2 Assessment and Management of the Patient with Anginal Pain  Care of the Patient with Acute Coronary Syndrome 145 Manifestations, Diagnostic Table 6-4 S  ymptoms of Heart Disease in Special Populations Testing, and Collaborative Women The most commonly encountered symptom is Care of the Patient with shortness of breath. Other atypical signs and symptoms include nausea or vomiting, diaphoresis, palpitations, gastrointestinal problems Acute Coronary Syndrome Diabetics Atypical and silent signs and symptoms due to autonomic dysfunction The classic symptom a patient experiences during a cardiac Elderly Generalized weakness, stroke or cerebral vascular event is pain. It is important for the nurse to differentiate accident, syncope or change in mental status, silent ischemia, especially if having a history of the pain of an MI or angina attack from a multitude of other heart failure. pain syndromes that can mimic a coronary event. Noncar- Source: Adapted from Fihn, S. D., et al. (2012). ACCF/AHA/ACP/AATS/PCNA/SCAI/ diac chest pain (NCCP) may be caused by other cardiovas- STS guideline for the diagnosis and management of patients with stable ischemic heart disease: A report of the American College of Cardiology Foundation/American Heart cular issues including pericarditis, aortic aneurysm or Association Task Force on Practice Guidelines, and the American College of Physicians, American Association for Thoracic Surgery, Preventive Cardiovascular Nurses dissection. Non-cardiovascular causes may originate from Association, Society for Cardiovascular Angiography and Interventions, and Society of Thoracic Surgeons. Journal of the American College of Cardiology, 60(24), e44–e164. organs in close proximity to the heart. Gastrointestinal causes may include peptic ulcer disease, reflux, pancreatitis or esophageal rupture. Pulmonary causes may include pul- experience chest discomfort but may present with only monary embolus, pneumothorax, pleuritis or pneumonia. dyspnea and palpitations. Women often arrive in the ED Musculokeletal causes may include costochondritis, rib complaining of shortness of breath, fatigue, lethargy, indi- fracture or disc injury. Patients commonly describe the dis- gestion, and anxiety. Women also tend to experience pain comfort as crushing, oppressive, or constricting or as a pres- in the back rather than substernally or in the left side of the sure that may radiate to the left arm, neck, jaw, infrascapular chest and do not characterize it as pain, but as a numbness area, or epigastric region. Transient symptoms that last less or tingling sensation (Fihn et al., 2012). Refer to Table 6-4, than 15 minutes and disappear at rest are classified as “Symptoms of Heart Disease in Specialized Populations.” angina. The discomfort associated with an MI typically lasts more than 30 minutes, is not relieved by rest or nitro- Focused Assessment and glycerin, and may or may not be severe. The patient is asked to evaluate the level of pain using the universal 0 to Management 10 scale, with 10 being the highest level of discomfort. A mnemonic device used for the evaluation of chest pain is Additional signs and symptoms of an MI include nau- “APQRST” (Table 6-5). A history must be ascertained from sea, vomiting, diaphoresis, palpitations, and dyspnea. The the patient. This should include symptomatology of the patient may have cool, clammy skin due to vasoconstric- ­anginal pain, history of CAD, and presence of CAD risk tion and a low-grade fever caused by the systemic response ­factors (Loscalzo, 2012). Therapeutic hypothermia should be to inflammation (Table 6-3). started as soon as possible in comatose patients with STEMI Special populations may be challenging to assess cor- and out-of-hospital cardiac arrest caused by ventricular fibril- rectly. The elderly and patients with diabetes may not lation or pulseless ventricular tachycardia (O’Gara et al., 2013). Table 6-3 Differentiation Between Cardiac and Noncardiac Pain Characteristics Cardiac Noncardiac Timing Usually occurs in the AM End of day Pain Quality Pressure, heaviness, constricting, burning, squeezing. Sharp, more localized. Deep pain, not superficial. Easy to pinpoint Radiates to arms, jaw, back, below diaphragm. Cannot pinpoint; described as diffuse pain Etiology Pain preceded by exertion: exercise, heavy meals, “out of the blue” pain directly associated with injury extreme weather. May awaken patient from sound sleep Associated Symptoms Dyspnea, nausea/vomiting, diaphoresis, palpitations. Feelings of impending doom. Pain Duration Lasts with exertion but declines or stops with rest. May be fleeting or last several hours. Pain Relief Stops with rest. Rest or exercise Nitroglycerin Simple analgesics Sitting and leaning forward Antacids Laying down increases pain Reassurance Risk Factors Hypertension, diabetes, obesity, dyslipidemia, smoking 146 Chapter 6 Vital Signs—should be taken at frequent intervals. Nursing Actions Ace Inhibitor—should be started, especially for Upon arrival to the emergency department (ED), the nurse patients with STEMI in the anterior location, heart fail- needs to perform the following interventions to alleviate ure, or ejection fraction less than or equal to 40. pain and anxiety and increase the myocardial oxygen level. The patient is placed in a semi-Fowler’s position to allow for comfort and proper cardiovascular functioning. Diagnostic Criteria An ECG and cardiac enzymes should be assessed Diagnostic criteria are extremely important for the patient within 10 minutes. with an MI and ACS. This information helps to determine the location of the muscle damage as well as the extent of An intravenous line should be started to keep the vein the damage. Several diagnostic tests are included as the open for immediate access for the administration of mainstay of MI or ACS diagnosis. emergency drugs. Medications and treatments are then started in a stan- dard progression. Electrocardiogram Aspirin is given first and consists of four “baby strength” The 12-lead electrocardiogram (ECG) is one of the most aspirin or the equivalent of 325 mg. Baby aspirin is the crucial diagnostic tools available for ACS. In a normal treatment of choice because the patient can chew or have ECG, the ST segment is level with the tracing’s isoelectric the medication dissolve in the mouth without a bitter line. Any deviation of the ST segment from this isoelectric taste. It is used to prevent platelet aggregation and the line will determine the amount of damage to the heart formation of blood clots in the coronary vasculature. A muscle. Patients presenting to an ED with chest discomfort loading dose of a P2Y12 receptor inhibitor, clopidogrel, should have a 12-lead ECG performed within 10 minutes ticagrelor, or prasugrel, should be given as early as pos- of arrival and should also be evaluated with telemetry mon- sible or at time of primary PCI (O’Gara et al., 2013). itoring. The presence of severe and prolonged elevation of the ST segment, or, less frequently, new Q waves, or new left Nitroglycerin—May be administered in either the sub- bundle branch block (LBBB) indicates that the patient is lingual tablet or translingual spray, which will reduce likely experiencing a STEMI. Patients with NSTEMI may the pain that is currently present, or the intravenous present with ST depression, T-wave inversion, transient ST- form to prevent future episodes. segment elevation, or with any ischemic ECG abnormalities. Supplemental oxygen—According ACLS Guidelines (AHA, 2015), oxygen should be applied only if the oxy- Ischemia. Myocardial ischemia is the result of an imbal- hemoglobin concentration is less than or equal to 94%. ance between the myocardial oxygen supplies versus the Morphine—Morphine sulfate is given in a dose of 2 to myocardial oxygen demand. If this supply and demand 5 mg intravenous every 5 to 30 minutes as needed. scenario is not corrected in a timely fashion, cell death will Morphine is used for both pain management and as an occur. There are several key ECG changes that coincide antianxiety medication. If this medication is given with myocardial ischemia. The first is a T-wave inversion. first, it can mask the patient’s perception of pain and Other ECG changes are ST-segment depression of greater mask the underlying cause of ischemia. than 0.5 mm, an ST segment that remains on the baseline Beta blockers—should be promptly instituted because longer than 0.12 second, and inverted U waves. they decrease heart rate and blood pressure levels. These drugs will also decrease left ventricular contrac- Injury. Myocardial injury is most often indicated by ­ST-­ tility, thereby reducing myocardial oxygen demand. segment elevation of 1 mm or more above the baseline. Table 6-5 “APQRST” Mnemonic for the Evaluation of Chest Pain A = Associated symptoms Dyspnea, nausea/vomiting, diaphoresis, palpitations, feelings of impending doom P = Precipitating factors Exertion; exposure to cold; following meals; movement; relieved by rest, nitroglycerin, or positional changes Q = Quality Heaviness; tightness; pressure; sharp, stabbing, burning R = Region, radiation, risk factors Radiates to arm, jaw, back, below diaphragm Region is substernal, left lateral, right chest Risk factors include hypertension, diabetes, obesity, dyslipidemia, smoking S = Severity Pain scale of 0–10 T = Timing Onset and duration: nocturnal, constant or intermittent Source: Adapted from Reigle, J. (2005). Evaluating the patient with chest pain: The value of a comprehensive history. Journal of Cardiovascular Nursing, 20(4), 226–231.  Care of the Patient with Acute Coronary Syndrome 147 The T wave may also become taller and pointed in con- When a Q wave appears on an ECG, the MI tends to be trans- figuration. There is also symmetric T-wave inversion. ST mural or through the entire thickness of the myocardium. T- segment elevation of greater than 0.2mmV in more than wave inversion occurs within hours of an infarction and can two chest leads, ST segment elevation more than 0.1mmV last for several months after the complete evolution of the MI. in more than two contiguous limb leads or a new complete left bundle branch block (LBBB) are indications for imme- diate coronary intervention. Specific 12-Lead Changes An anterior MI is correlated to ST elevation in leads V2 through Infarction. Infarction is suspected when the ECG shows V4. An MI caused by the occlusion of the left main artery is ­either new Q waves or a deepening of existing Q waves. A characterized by ST-segment elevation in leads V1 through Q wave on an ECG is the first negative deflection in a QRS V6. Elevation in V1 through V6 represents a large amount of ­complex. Q waves appear within hours of pain onset and ­damage to the myocardium. An anterior lateral MI caused usually remain for the remainder of a patient’s lifetime. A Q by an occlusion of the LAD shows ST-segment elevations in wave that is either 0.04-second-wide or that has a depth of at V3 through V6 and leads I and aVL. An anteroseptal MI shows least 25% of the size of the R wave is considered pathologic. ST elevations in leads V1 through V4 (2 Figure 6-5). I Standard Leads aVR Augmented Leads V1 Chest Leads V4 II aVL V2 V5 III aVF V3 V6 Rhythm Strip I Standard Leads aVR Augmented Leads V1 Chest Leads V4 II aVL V2 V5 III aVF V3 V6 Rhythm Strip Figure 6-5 12-lead ECG of patient with an anterior MI before and after reperfusion. 148 Chapter 6 Table 6-6 ECG Changes in MI Site Of Infarction Changes Seen Possible Occlusion Large anterior wall V1–V6: ST-segment elevation Left main coronary artery II, III, aVF: ST-segment depression Anterior wall V2–V4: ST-segment elevation Left anterior descending artery II, III, aVF: ST-segment depression Anteroseptal V1–V4: ST-segment elevation LAD and branches supplying blood II, III, aVF: ST-segment depression to the septal wall Anterolateral I, aVL, V3–V6: ST-segment elevation LAD and branches supplying blood II, III, aVF: ST-segment depression to the lateral wall Lateral wall V5, V6, I, aVL: Pathologic Q wave, ST-segment elevation, Left circumflex (LCx) and/or LAD inverted T wave III, aVF-segment depression Inferior wall II, III, aVF: Pathologic Q wave, ST-segment elevation, RCA and/or LCx inverted T wave ST-depression AVL + Lead 1 Posterior wall V1–V3: ST-segment depression, tall, upright, symmetrical R wave, and tall, RCA and/or LCx symmetrical T wave Source: Adapted from Ellis, K. (2007). EKG plain and simple. Upper Saddle River, NJ. Prentice Hall. ST-segment changes in leads I and aVL indicate a high values of 0.1 ng/mL as markedly elevated and indicating a lateral wall infarct, whereas elevations in leads V5 and V6 high risk of death. Cardiac troponins may not be released reveal a lower lateral infarct. Inferior wall MI is shown until 6 hours after symptoms begin; therefore, the ACC/ with elevations in leads II, III, and aVF. AHA (Amsterdam & Wegner, 2014) recommends that ECGs look primarily at the front of the heart; therefore, ­patients who have a negative troponin level within 6 hours in order to assess damage to the posterior wall, a nurse of symptom onset be retested at 8 to 12 hours after onset. needs to look for reciprocal changes in the pattern. These changes are italicized in Table 6-6, and include ST depres- Creatinine Kinase. Creatine kinase may not be help- sion in the contralateral leads. ful in i­mmediate diagnosis of an MI due to the 4 to 6 hours needed to see a significant rise. It is believed that the CK lev- els are more important in gauging the size and timing of an Reflect On acute MI than the actual diagnosis. Creatine phosphokinase– myocardial band (CK-MB) is used to determine myocardial A 65-year-old woman on the cardiac unit complains of chest pain. The ECG reveals changes indicative of acute anterior STEMI. What damage. These levels increase within 3 to 6 hours, peak at would be your nursing priorities? 24 hours, and return to normal within 36–72 hours after in- farction. The CK-MB is considered positive when it is greater than 3% of the ­total CK. This test can be an effective biomarker Laboratory Assessment in the ­detection of reinfarction (McLean & Huang, 2012). The patient who is suspected of having acute myocardial Myoglobin and C-Reactive Protein (CRP). Both of these bio- injury should have blood drawn to measure blood counts markers lack cardiac specificity and need to be used in con- including a CBC, metabolic profile and coagulation studies. junction with other definitive laboratory tests. A doubling Cardiac biomarkers are released when myocardial inflam- of the myoglobin level in 2 hours strongly suggests MI, and mation, injury, and necrosis are present. These biomarkers a negative myoglobin within 4 to 8 hours after the onset of are used to confirm diagnosis of an MI and assist with risk symptoms is used to rule out an MI. The CRP level corre- stratification and outcome prediction. Blood work should lates with peak levels of the MB isoenzyme. This peak usu- be performed within 10 minutes of arrival to the ED and ally occurs 1 to 3 days later. Failure of the CRP to normalize obtained serially as initial levels may be normal. may indicate ongoing damage to the heart. A baseline CRP is Troponin. Cardiac troponin assays are very useful in the a good marker for future cardiovascular events (Abid et al., diagnosis of an acute MI. These are highly sensitive tests 2015). Refer to Table 6-7 for comparison of these biomarkers. that can determine myocardial damage. There are two car- diac-specific troponin markers: Troponin T and ­troponin I. Reflect On Troponin I is the most accurate marker of myocardial in- jury. Data have suggested that a troponin T concentration A patient arrives at the emergency room complaining of chest pain. Cardiac enzymes 1 hour post the event are normal. Can you say the measured 72 hours after an acute MI may be predictive patient did not suffer from a STEMI? What else does the nurse need of MI size, independent of reperfusion. The guidelines to assess? consider values greater than 0.01 ng/mL as elevated and  Care of the Patient with Acute Coronary Syndrome 149 Diagnostic Imaging Table 6-7 Cardiac Biomarker Comparison In patients with a suspected STEMI, the two-dimension Initial Elevation echocardiography reveals abnormalities in wall motion Blood Levels and Peak Duration and determines left ventricular function. A TTE (transtho- Troponin I 1.5 ng/mL Peak: 12 hrs racic) or TEE (transesophageal) approach may be used. consistent with MI Doppler echocardiography allows assessment of both CPK-MB 3–6% Initial: 3–6 hrs Up to 48 hours direction and velocity of blood flow within the heart and Peak: 12–24 hrs great vessels. This can be used to evaluate valve integrity. The two-dimensional echocardiography and Doppler Chest X-ray echocardiography are often used in conjunction with exer- A chest x-ray upon admission can be used to determine cise or pharmacological stress testing to detect regional signs of impending heart failure. It can also be useful in rul- wall motion abnormalities during exercise. ing out pulmonary and vascular causes for chest pain such as pericardial effusion, pneumothorax, pulmonary effu- Cardiac Catheterization sions or consolidation, pulmonary vessel congestion from A cardiac catheterization or angiography is the gold pulmonary embolism and to evaluate for cardiomegaly. standard for diagnosis of cardiac pathology. It is used to determine the exact location of the myocardial injury and Exercise Testing specific obstructions to the coronary vasculature. A left Exercise testing with continuous electrocardiographic mon- heart catheterization permits the visualization of coronary itoring is a widely used and reliable method of evaluating artery anatomy, while a right heart catheterization patients who have or are at risk for developing an ACS. demonstrates intracardiac pressures. This test determines This type of evaluation focuses on the changes in the if coronary artery occlusion is amenable to nonsurgical ­electrocardiograph tracing during exercise as well as intervention such as percutaneous coronary intervention gives information about dysrhythmias, HR, BP, exercise-­ (PTCI) or surgical intervention such as coronary artery perceived exertion rate, and exercise capacity, myocardial bypass graft (CABG). See specific care of patient under­ oxygen uptake and VO2, oxygen uptake and ventilator going these procedures later in this chapter. threshold (Fletcher et al., 2014). The most common testing is done while the patient is on a treadmill or exercise bicycle. Pharmacological stress agents may be used if a patient COLLABORATIVE CARE is unable to walk a treadmill or perform exercise on the exercise bicycle. Patients with musculoskeletal disorders, The immediate treatment goals for the patient with MI vascular diseases, and chronic pulmonary diseases or the are to restore coronary artery blood flow, limit the infarc- elderly are prime candidates for this type of stress testing. tion size, and balance myocardial oxygen supply and Pharmacological stressing is also used in patients with left demand. bundle branch block and ventricular pacing, which often Pharmacological therapy remains an important inter- interfere with testing and yield false positive results. Phar- vention for patients with ACS. There are many therapies macological stress agents currently in use are dipyridam- involved including those that will decrease ischemia, assist ole, adenosine, and dobutamine. in a decrease in platelet aggregation, and provide pain Single photon emission computed tomography (SPECT) relief. See “Commonly Used Medications” for key infor- myocardial perfusion imaging is widely used in the assess- mation regarding anti-ischemic, antithrombotic, and plate- ment of patients with known or suspected CAD. Comparison let aggregation inhibitor therapies. of images obtained during rest and stress allows diagnosis of the reversibility, severity, and extent of the myocardial perfu- sion defects. This is an important piece in the management Invasive Therapy/ decision-making of the patient with CAD. The timing of the exercise stress test in patients with ACS depends on the spe- Interventions cific risk. The AHA states it is reasonable for patients with Patients who have definitive ischemic ECG changes and/ possible ACS who have normal serial ECGs and cardiac tro- or elevated cardiac markers are typically managed with an ponins to have a treadmill ECG, stress myocardial perfusion early invasive strategy. This strategy involves the use of imaging, or stress echocardiography before discharge or diagnostic catheterization, followed by a PCI or CABG within 72 hours after discharge. It is strongly suggested that surgery as soon as possible. Procedural and nursing care the patient be clinically stable before undergoing any type of for the cardiac catheterization patient are similar to the exercise stress testing (Amsterdam & Wenger, 2014). PCI, so they will be included in the discussion later. 150 Chapter 6 v Commonly Used Medications Anti-Ischemic Therapy: Increase Myocardial Perfusion and Decrease Pain Nitroglycerin Obtaining baseline respiratory rate, depth and rhythm, and size of pupils. Nitroglycerin is an arterial and venous vasodilator. It increases Recording pain level and duration of analgesia. coronary blood flow by dilating the coronary arteries. It is first Continuing to monitor for respiratory depression. given as a 0.4-mg sublingual tablet or spray, and may be fol- lowed with intravenous administration. Desired Effects: Reduces systolic, diastolic, and mean BP Beta Blockers and has antianginal, anti-ischemic, and antihypertensive Blocking beta-1 receptors located primarily in the myocardium effects. When administered sublingually to a patient with and beta-2 receptors in the vasculature and bronchial smooth angina, it usually results in a reduction in pain in 3 to 5 minutes. muscle decreases myocardial contractility, slows heart rate, and decreases systolic BP, thus lowering the cardiac oxygen demand. Nursing Responsibilities: A slower heart rate will also assist in increasing the ventricular fill- Ensuring administration of a therapeutic dose: Sublin- ing time and coronary artery blood flow, so more oxygen will gual: 0.3 to 0.4 mg q 3 to 5 min (maximum dose is three reach the myocardial tissue. Initiate oral beta blockers within the tablets in 15 minutes); Intravenous: Start infusion at first 24 hours of ACS in the absence of HF, low-output state, risk 5 mcg/min and titrate every 3 to 5 minutes until the for cardiogenic shock, or other contraindications to beta blockade desired response is achieved. Receiving beta blockers within 24 hours of hospital arrival after an Ensuring use with extreme caution in patients with hypo- MI reduces mortality in the first week by 14% (Amsterdam & tension; monitoring for unresponsiveness and cardiac Wenger, 2014). dysrhythmias. Beta-blocker therapy is contraindicated when the patient Monitor blood pressure every 3 to 5 minutes if on intrave- has a heart rate less than 60 beats per minute, systolic blood nous dose to maintain SBP > to 90 mmHg. pressure less than 100 mmHg, moderate or severe left ventricular If the patient’s blood pressure does decrease, lowering failure, shock, PR interval on the electrocardiogram greater than the head of the bed, increasing the rate of IV fluids, or 0.24 second, second or third-degree heart block, and active decreasing the dose of nitroglycerin temporarily should asthma and/or reactive airway disease. resolve the problem. Assess patient for a headache (50% of patients develop Desired Effects: Beta blockers block the cardiac effects of this effect). beta-adrenergic stimulation; as a result, heart rate, myocar- Side and/or Toxic Effects: Symptoms of overdose include dial irritability, and force of contraction decrease. They have hypotension; tachycardia; warm, flushed skin; headache; also been associated with a decrease in platelet ­aggregability. confusion, nausea; convulsions; and cardiovascular col- When administered intravenously the effects occur within 1 lapse. These symptoms may occur because ethanol is the to 2 minutes. diluent in IV nitroglycerin. When high doses of IV nitroglyc- Nursing Responsibilities: erin are administered, the patient may experience ethanol Administering a therapeutic dose once the patient’s intoxication (Wilson, Shannon, & Shields, 2016). hemodynamic condition has stabilized following an MI. AHA recommends an initial intravenous dose of 5 mg of Morphine Sulfate metoprolol followed by two additional doses at 5-minute intervals for a total of 15 mg. The patient is converted to Morphine sulfate, an opioid analgesic, is used when chest dis- oral dosing if IV is tolerated. comfort is not relieved with nitroglycerin, when the patient Observing monitor pattern, heart rate, respiration, blood becomes agitated, or when he or she is experiencing the compli- pressure, and circulation closely during administration. cation of pulmonary congestion. Administration is stopped if bradycardia, heart block, or Desired Effects: Morphine helps to increase the coronary hypotension develop. blood flow by dilating arteries and veins while it controls Monitoring for signs and symptoms of heart failure. severe pain and anxiety. It also reduces preload, which, in Side and/or Toxic Effects: Bradycardia, hypotension, and effect, decreases the workload of the myocardial tissue. heart blocks are serious side effects. Bronchospasm and Nursing Responsibilities: dyspnea may also occur as may indications of poor perfu- Providing a therapeutic dose, usually 2 to 10 mg IV in sion such as syncope, confusion, or dizziness. divided doses.  Care of the Patient with Acute Coronary Syndrome 151 Commonly Used Medications Antithrombotic Therapy Prevention of Thrombin-Mediated Fibrin Deposition and Stabilization of Platelet-Rich Thrombi Aspirin Unfractionated Heparin (UFH) Giving aspirin as soon as possible inhibits platelet activity and interrupts platelet aggregation at the site of plaque rupture. Desired Effects: UHF inhibits formation of new clots but does not lyse already existing thrombi. It prevents throm- Desired Effects: It inhibits platelet aggregation, reducing boembolic complications during the acute stage of an the ability of blood to clot. It is used to prevent recurrence of MI. MI, and in prophylaxis against MI in patients with unstable angina. Nursing Responsibilities: Initial loading dose of 60 IU/kg (maximum 4000 IU) with Nursing Responsibilities: initial infusion of 12 IU/kg per hour (maximum 1000 IU/h) Administration of a therapeutic dose. If a patient does adjusted per activated partial thromboplastin time (aPTT) not take aspirin regularly the initial dose should be 160 to to maintain therapeutic anticoagulation. 325 mg. The patient should chew the dose in the acute Continued for 48 hours or until PCI or CABG is phase to increase absorption. If a patient regularly takes p ­ erformed. an aspirin daily, check with the physician for orders on Monitor aPTT levels closely. appropriate dosage. Checking platelet count for heparin induced thrombocy- Monitoring platelet count, prothrombin time and interna- topenia (HIT). tional ratio unit in patients with concurrent anticoagulant Observing for signs and symptoms of internal and exter- therapy. nal bleeding. Using enteric-coated tablets to reduce gastrointestinal disturbances. Side and/or Toxic Effects: The most common problem- atic adverse effect is bleeding. Side and/or Toxic Effects: The most common side effects are bleeding, GI discomfort, and tinnitus. Low Molecular Weight Heparins P2Y12 Inhibitor: Clopidogrel Low molecular weight heparins (LMWH) have a relatively low or Ticagrelor degree of binding to plasma proteins and cells; they also have a more predictable anticoagulant effect, a longer half-life, and a Both clopidogrel (Plavix) and ticagrelor (Ticlid) are drugs that lower incidence of thrombocytopenia than UHF. The inhibit platelet aggregation. This therapy is used to prevent thrombotic low molecular weight heparin enoxaparin (Lovenox), given sub- events in patients who have had a myocardial infarction with cutaneously, is preferred. Enoxaparin has a longer half-life acute ST-segment elevation. Either clopidogrel or ticagrelor, in than heparin and provides more sustained and predictable addition to aspirin, should be administered for up to 12 months to anticoagulation. all patients with NSTE-ACS without contraindications who are Contraindications for both forms include hypersensitivity treated with either an early invasive§ or ischemia-guided strategy to heparin, previous heparin-induced thrombocytopenia, (Amsterdam & Wenger, 2014). uncontrollable active bleeding, and the inability to monitor Desired Effect: The desired effect is a prolongation of bleed- platelet counts. ing time and prevention of MI in patients with recent MI or Desired Effects: As with UHF, enoxaparin inhibits the for- unstable angina. mation of new clots but does not lyse existing clots. Anti- Nursing Responsibilities: thrombotic properties are due to its anti-factor Xa and Administration of a therapeutic dose: clopidogrel: 300– antithrombin (antifactor IIa) in coagulation activity. 600 mg, followed by 75 mg daily. Ticagrelor: 180-mg Nursing Responsibilities: loading dose, then 90 mg twice daily. Administration of a therapeutic dose: usually 1 mg/kg Observing for bleeding episodes, especially GI bleeding. every 12 hours for 2 to 8 days; given concurrently with Reviewing periodic platelet count, bleeding time, and aspirin 100 to 325 mg per day. lipid profile. Monitoring baseline coagulation studies. Should hold clopidogrel or ticagrelor for at least 5 days Watching platelet count closely and withholding the drug before CABG. if the level of platelet count is less than 100,000 mm3. Side and/or Toxic Effects: The most serious adverse Assessing for signs of unexplained bleeding. effects include bleeding and purpura. 152 Chapter 6 Reperfusion Therapy Artery Cross Section Percutaneous Transluminal Coronary artery Plaque Coronary Intervention located on the surface of the heart Percutaneous Transluminal Coronary Intervention (PTCI) Narrowed artery is recommended method of reperfusion when it can be per- Heart Closed stent formed in a timely manner. An ideal first medical contact to Coronary around balloon device time should be 90 minutes or less (O’Gara et al., catheter A artery Plaque 2013). PTCI is the placement of a small mesh tube called a stent into an infarcted or narrowed coronary artery. The procedure consists of cardiac catheterization and insertion of a catheter with a balloon tip that is inflated to open the artery, called percutaneous transluminal coronary angio- Catheters Closed stent plasty (PTCA), followed by a stent placement. Drug-eluting Expanded stent Balloon stents are coated with medications that prevent restenosis B by reducing inflammation and the formation of thrombin. Other PCTI procedures include percutaneous arthrec- tomy and thrombus aspiration. To be most effective, these procedures should be performed within 90 minutes of the patient’s arrival in the ED and medical evaluation. The Stent-widened artery Compressed plaque Increased goal of treatment is to open the blockage in the coronary C blood flow artery and reperfuse the myocardium, limiting the amount of damage. PCI is indicated in coronary arteries that have at least 70% narrowing. During a PTCI, a catheter with a balloon is inserted into an arterial access (femoral, brachial, or radial artery) and guided to the desired site. The balloon is inflated, Compressed plaque expanding the stent, which in turn squeezes the atheroscle- rotic plaque against the vessel wall and widens the arterial lumen. After the stent is in place, the balloon is deflated Widened Stent artery and removed. The stent remains in place, holding the plaque against the arterial walls and providing structural support (2 Figure 6-6). Figure 6-6 Stent placement following angioplasty. Patients with stent placement usually require dual antiplatelet therapy (DAPT) with aspirin and clopidogrel treat acute coronary syndromes. The most commonly used for one year. During this time, the endothelium grows over thrombolytic drugs include alteplase (Activase), reteplase the stent, incorporating the device into the artery and (Retavase), and tenecteplase (TNK-tPA). reducing the tendency to clot. DAPT is maintained after The physician may also give the patient platelet GP IIb- stenting to reduce the risk of vessel thrombosis (Amster- IIIa inhibitors. These inhibitors may be used for patients dam & Wenger, 2014). (2 Figure 6-7). with unstable angina, NSTEMI or in conjunction with PCTI. Fibrinolytic Therapy GP IIb-IIIA medications prevent platelet aggregation by keeping fibrinogen from binding to the GP IIb-IIIA receptors If fibrinolytic therapy is used as the primary reperfusion on the platelet surface. See “Commonly Used Medications” strategy, administration should occur within 30 minutes for more information regarding these medications. Contra- of arrival. This may occur if the patient is at a non- indications to fibrinolytic therapy are displayed in Box 6-8. PCI-capable facility, or if the time to intervention is greater than 120 minutes. Individuals who receive primary fibri- nolytic therapy should also receive adjunctive antiplatelet and anticoagulant therapy (O’Gara et al., 2013). NURSING CARE Fibrinolysis is achieved with the use of tissue plasmin- The nurse prepares the patient for the procedure. The first ogen activators (tPA) to quickly lyse the thrombus. step is to ascertain that the patient understands the proce- These thrombolytic drugs are the most common used to dure and that the consent form is signed. A m ­ edication  Care of the Patient with Acute Coronary Syndrome 153 Box 6-8 Contraindications for the Use of Fibrinolytic Therapy Absolute Contraindications Active internal bleeding Known history of cerebral aneurysm or arteriovenous malformation (AVM) Previous cerebral hemorrhage Figure 6-7 Coronary artery before angioplasty with Pregnancy stent insertion. Recent ischemic stroke Severe uncontrolled hypertension Suspected aortic dissection Traumatic CPR history, and any allergic reactions, especially to radio- graphic contrast media, aspirin, or clopidogrel, must Relative Contraindications be obtained. Routine pre-procedure laboratory work Active peptic ulcer disease should be reviewed and abnormal values reported to the Current use of anticoagulants physician. Hydration should be considered an impor- Prior ischemic stroke tant component prior to contrast administration which Dementia Recent surgery may have a nephrotoxic impact on the kidneys (Box 6-9). Recent internal bleeding Intravenous access must then be established with fluid at a keep-vein-open rate. The nurse should document peripheral pulses using a 0 to 4 scale regardless of access site, which may include radial, brachial or femoral but will receive analgesics and sedatives to keep her ­arteries. relaxed and comfortable. The patient should be notified The nurse should explain to the patient what to that she might experience mild chest pain during balloon expect during the procedure. The patient will be awake inflation. Commonly Used Medications GP IIB-IIIA Inhibitors Introduction 0.125 mcg/kg/min for the next 12 hours; eptifibatide ­(Integrilin)—Intravenous infusion of 180 mcg/kg initial bolus Three different agents fall into this category: eptifibatide (Integrilin) followed by a 2 mcg/kg/min drip for up to 72 hours; tirofiban and tirofiban (Aggrastat), which are small molecular agents, and (Aggrastat)—Intravenous loading dose of 0.4 mcg/kg/min abciximab (ReoPro), which is a monoclonal antibody fragment. for 30 minutes followed by 0.1 mcg/kg/min for 12 to These drugs should be given as soon as possible and can be given 24 hours. prior to catheterization or PCI. The GP IIb-IIIa inhibitors are contra- Monitoring platelet count, hemoglobin, and hematocrit indicated for patients with bleeding diathesis, acute abnormal prior to initiation of therapy and throughout treatment. bleeding, or history of stroke within the last month. Renal dialysis, a Monitoring partial thromboplastin time (PTT) and interna- history of major surgery within 6 weeks, or a platelet count of less tional ratio (INR). than 100,000 mm3 are also contraindications (Wilson et al., 2016). Withholding the medication if thrombocytopenia is Desired Effects: The desired effect is inhibition of platelet confirmed. aggregation, and effectiveness is indicated by minimizing Monitoring for signs and symptoms of internal and exter- thrombotic events during treatment of ACS. nal bleeding at all invasive sites but especially at the Nursing Responsibilities: sheath insertion site by observing the site and palpating Administering the appropriate doses as prescribed: the site and pulses distal to it. ­Abciximab (ReoPro)—Intravenous dose of 0.25 mg/kg Side and/or Toxic Effects: The most significant adverse bolus over 5 minutes followed by a continuous infusion of effect is bleeding. 154 Chapter 6 monitored. The platelet count may indicate the patient’s Box 6-9 Risk Factors for tendency to bleed, especially if the patient has been given glycoprotein IIb/IIIa receptor inhibitors and/or tPA Contrast-Induced Acute because these can cause thrombocytopenia. If the patient Kidney Injury should start to bleed from the insertion site, the nurse can either apply manual pressure to the site, or use a special Creatinine level ≥1.5 mg/dL