Page 535 - Cardiac Nursing

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P P P Pathophysiology and Management
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A A A Acute Coronary Syndromes
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Jean Marie Blue Verrier /
Michaelene Hargrove Deelstra
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In 2005, there were an estimated 16 million people in the United I In the lastt several years, there has been an unprecedented focus
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States withh coronary heart disease (CHD), tran lating to approx- on quantifying and improving health care delivery. The American
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Collegee of Cardi lology (ACC) and the American Heart Associa-
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imatelyy 1 in every 15 Americans. Of thesee cases, 1 2.2 million were e Co ll eg of C ar di
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new or recurrent CHD. There were 451,300 CHD-related deaths tion (AHA) jointly have developed a long-term strategy to im-
in 2004. 1 prove clinical care. The initial phase created practice guidelines
Acute coronary syndromes (ACS) have evolved over the last that synthesized available evidence to guide care. The second
10 years into an operational term referring to a constellation of clin- phase developed performance measures to assess and improve the
ical symptoms that equate to myocardial ischemia. Ischemic heart quality of cardiovascular care. Table 22-1 presents the ACC/AHA
disease is one type of CHD. ACS encompasses ST-elevation my- STEMI/NSTEMI performance measurement set developed in
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ocardial infarction (STEMI), non-ST-elevation myocardial infarc- January 2006. The measures include aspirin therapy at arrival
tion (NSTEMI), and unstable angina (UA). Identification of ACS and at discharge; -blocker therapy at arrival and at discharge;
at the earliest point in the health care continuum allows paramedics low-density lipoprotein cholesterol (LDL-C) assessment; lipid-
to initiate immediate cardiac medications and route patients to the lowering therapy at discharge; angiotensin-converting enzyme in-
most appropriate facilities for care. The shortest time to reperfusion hibitor (ACEI) and/or angiotensin II receptor blocker (ARB) ther-
is the most desirable goal of treatment and management of the pa- apy for left ventricular (LV) systolic dysfunction; time-to-fibrinolytic
tient population with ACS. 2,3 therapy; time-to-percutaneous coronary intervention (PCI);
UA/NSTEMI constitutes a clinical syndrome that is a subset of reperfusion therapy; and adult smoking cessation advice/counsel-
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ACS. UA/NSTEMI is usually, but not always, caused by atheroscle- ing. Pathogenesis of ACS is presented in Chapter 5. PCI is pre-
rotic coronary artery disease (CAD, a type of CHD) and is associ- sented in Chapter 23. ACS risk factors are presented in Chapter
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ated with an increased risk of cardiac mortality. CAD is also associ- 32. For a complete presentation of the care of patients with
ated with an increased incidence of myocardial infarction (MI). As a STEMI and UA/NSTEMI, refer to the original sources for the
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subset of ACS, UA/NSTEMI is defined by electrocardiographic ST- ACC/AHA STEMI 2,3 and NSTEMI Guidelines, which simply
segment depression or prominent T-wave inversion. Biomarkers of are abstracted here for purposes of this chapter.
myocardial necrosis, such as troponin, may or may not be present.
No ST-segment elevation is present on electrocardiogram (ECG).
The patient typically has chest discomfort or an anginal equivalent. 4 PRESENTATION OF ACS
Variant (Prinzmetal’s) angina is an unusual form of UA that
occurs spontaneously and frequently is not related to exertion. Morbidity and mortality from ACS can be reduced significantly if
The chest discomfort tends to be prolonged and severe. It is symptoms are recognized early. The symptoms of UA/NSTEMI
caused by spasm of the epicardial coronary artery/arteries and and STEMI include midsternal or substernal compression or
classically is characterized by transient ST-segment elevation that crushing chest discomfort. The patient may describe it as a cramp-
resolves with nitroglycerin (NTG) use. ing, burning, or an aching sensation in the midsternal area. The
Patients presenting with STEMI have a high likelihood of discomfort may also be described as pressure, tightness, or heavi-
coronary thrombus causing a complete occlusion of the artery. ness in the chest. Unexplained indigestion or belching with or
Angiographic evidence of coronary thrombus formation is seen in without epigastric pain is also a common subjective complaint.
more than 90% of patients with STEMI but in only 35% to 75% The pain may radiate to the neck, jaw, shoulders, back, or one or
of patients presenting with UA/NSTEMI. There is ST-segment both arms. Commonly there is associated dyspnea, nausea and/or
elevation evident on ECG. Biomarkers of myocardial necrosis vomiting, and diaphoresis. Women more often than men present
such as troponin are typically elevated. The patient generally has with atypical chest pain. Patients with diabetes also may present
chest discomfort or an anginal equivalent. 2 atypically due to diabetes-associated autonomic dysfunction.
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