2.6 HOURS Continuing Education By Kristen J. Overbaugh, MSN, RN, APRN-BC ACUTE CORONARY SYNDROME Even nurses outside the ED should recognize its signs and symptoms. The signs and symptoms of ACS constitute a con- Overview: Acute coronary syndrome (ACS) is the tinuum of intensity from unstable angina to non–ST- segment elevation MI (NSTEMI) to ST-segment umbrella term for the clinical signs and symptoms of elevation MI (STEMI). Unstable angina and NSTEMI myocardial ischemia: unstable angina, non–ST-segment normally result from a partially or intermittently occluded coronary artery, whereas STEMI results elevation myocardial infarction, and ST-segment eleva- from a fully occluded coronary artery. (For more, see tion myocardial infarction. This article further defines Table 1.) ACS and the conditions it includes; reviews its risk fac- According to the American Heart Association (AHA), 785,000 Americans will have an MI this tors; describes its pathophysiology and associated year, and nearly 500,000 of them will experience signs and symptoms; discusses variations in its diag- another.1 In 2006 nearly 1.4 million patients were nostic findings, such as cardiac biomarkers and elec- discharged with a primary or secondary diagnosis of ACS, including 537,000 with unstable angina trocardiographic changes; and outlines treatment and 810,000 with either NSTEMI or STEMI (some approaches, including drug and reperfusion therapies. had both unstable angina and MI).1 The AHA and the American College of Cardiol- ogy (ACC) recently updated practice guidelines and performance measures to help clinicians adhere to a oronary artery disease, in which standard of care for all patients who present with atherosclerotic plaque builds up inside symptoms of any of the three stages of ACS.2-5 the coronary arteries and restricts the Nurses not specializing in the care of patients with flow of blood (and therefore the deliv- cardiovascular disease may not be familiar with cur- ery of oxygen) to the heart, continues rent practice guidelines and nomenclature, but they Cto be the number-one killer of Americans. One nevertheless play significant roles in detecting patients woman or man experiences a coronary artery dis- at risk for ACS, facilitating their diagnosis and treat- ease event about every 25 seconds, despite the time ment, and providing education that can improve out- and resources spent educating clinicians and the comes. Many patients admitted with a diagnosis of public on its risk factors, symptoms, and treatment. NSTEMI or unstable angina are cared for by physi- Coronary artery disease can lead to acute coronary cians other than cardiologists and are therefore less syndrome (ACS), which describes any condition likely to receive evidence-based care. Nurses caring characterized by signs and symptoms of sudden for these patients can be instrumental in promoting myocardial ischemia—a sudden reduction in blood adherence to practice guidelines. flow to the heart. The term ACS was adopted because it was believed to more clearly reflect the WHO’S AT RISK FOR CORONARY ARTERY DISEASE? disease progression associated with myocardial Nonmodifiable factors that influence risk for coro- ischemia. Unstable angina and myocardial infarc- nary artery disease include age, sex, family history, tion (MI) both come under the ACS umbrella. and ethnicity or race. Men have a higher risk than 42 AJN ▼ May 2009 ▼ Vol. 109, No. 5 ajnonline.com Figure 1. The Coronary Arteries and Ischemia Coronary artery disease leads to the interruption of blood flow to cardiac muscle when the arteries are obstructed by plaque. Each artery supplies blood to a specific area of the heart. Depending on the degree to which an artery is blocked, the tissue that receives blood from it is at risk for ischemia, injury, or infarction. • If the left anterior descending artery is occlud- ed (as illustrated here), the anterior wall of the left ventricle, the interventricular septum, the right bundle branch, and the left anterior fasciculus of the left bundle branch may become ischemic, injured, or infarcted. • If the right coronary artery is occluded, the right atrium and ventricle and part of the left ventricle may become ischemic, injured, or infarcted. • If the circumflex artery is blocked, the lateral walls of the left ventricle, the left atrium, and the left posterior fasciculus of the left bundle Illustration by Anne Rains by Illustration branch may become ischemic, injured, or infarcted. Left circumflex artery Left anterior Right coronary descending artery artery Atherosclerotic plaque occluding the artery Area of ischemia, injury, and infarction Posterior descending artery women. Men older than age 45, women older than PATHOPHYSIOLOGY OF ACS age 55, and anyone with a first-degree male or ACS begins when a disrupted atherosclerotic plaque female relative who developed coronary artery dis- in a coronary artery stimulates platelet aggregation ease before age 55 or 65, respectively, are also at and thrombus formation. It’s the thrombus occlud- increased risk. Modifiable risk factors include ele- ing the vessel that prevents myocardial perfusion vated levels of serum cholesterol, low-density (see figure 1). In the past, researchers supposed that lipoprotein cholesterol, and triglycerides; lower lev- the narrowing of the coronary artery in response to els of high-density lipoprotein cholesterol; and the thickening plaque was primarily responsible for the presence of type 2 diabetes, cigarette smoking, obe- decreased blood flow that leads to ischemia, but sity, a sedentary lifestyle, hypertension, and stress. more recent data suggest that it’s the rupture of an [email protected] AJN ▼ May 2009 ▼ Vol. 109, No. 5 43 unstable, vulnerable plaque with its associated afterload, ultimately increasing myocardial demand inflammatory changes—or as Hansson puts it in a for oxygen. As oxygen demand increases at the same review article in the New England Journal of time that its supply to the heart muscle decreases, Medicine, “most cases of infarction are due to the ischemic tissue can become necrotic. Low cardiac formation of an occluding thrombus on the surface output also leads to decreased renal perfusion, which of the plaque.”6 in turn stimulates the release of renin and Myocardial cells require oxygen and adenosine angiotensin, resulting in further vasoconstriction. 5␤-triphosphate (ATP) to maintain the contractility Additionally, the release of aldosterone and antidi- and electrical stability needed for normal conduc- uretic hormone promotes sodium and water reab- tion. As myocardial cells are deprived of oxygen sorption, increasing preload and ultimately the and anaerobic metabolism of glycogen takes workload of the myocardium.8 Mastering the concepts of preload and afterload will guide the nurse in understanding the pharmaco- logic management of ACS. Preload, the blood vol- Angina continues to be recognized as ume or pressure in the ventricle at the end of diastole, increases the amount of blood that’s pumped from the classic symptom of ACS. Chest the left ventricle (the stroke volume). Ischemia decreases the ability of the myocardium to contract pain associated with NSTEMI is efficiently; therefore, in a patient with ACS an increase in preload hastens the strain on an already normally longer induration and more oxygen-deprived myocardium, further decreasing cardiac output and predisposing the patient to heart severe than chest pain associated with failure. As I’ll describe in further detail below, medica- tions such as nitroglycerin, morphine, and β-blockers act to decrease preload. These medications, along with unstable angina. angiotensin-converting enzyme (ACE) inhibitors, also decrease afterload, which is the force the left ventricle has to work against to eject blood.9 In myocardial over, less ATP is produced, leading to failure of the ischemia, the weakened myocardium cannot keep up sodium–potassium and calcium pumps and an with the additional pressure exerted by an increase in accumulation of hydrogen ions and lactate, result- afterload. ing in acidosis. At this point, infarction—cell death—will occur unless interventions are begun SIGNS AND SYMPTOMS that limit or reverse the ischemia and injury. During The degree to which a coronary artery is occluded the ischemic phase, cells exhibit both aerobic and typically correlates with presenting symptoms and anaerobic metabolism. If myocardial perfusion with variations in cardiac markers and electrocar- continues to decrease, aerobic metabolism ceases diographic findings. Angina, or chest pain, contin- and eventually anaerobic metabolism will be signif- ues to be recognized as the classic symptom of ACS. icantly reduced. This period is known as the injury In unstable angina, chest pain normally occurs phase. If perfusion is not restored within about 20 either at rest or with exertion and results in limited minutes, myocardial necrosis results and the dam- activity. Chest pain associated with NSTEMI is nor- age is irreversible. Impaired myocardial contractil- mally longer in duration and more severe than chest ity, the result of scar tissue replacing healthy tissue pain associated with unstable angina. In both condi- in the damaged area, decreases cardiac output, lim- tions, the frequency and intensity of pain can iting perfusion to vital organs and peripheral tissue increase if not resolved with rest, nitroglycerin, or and ultimately contributing to signs and symptoms both and may last longer than 15 minutes. Pain may of shock. Clinical manifestations