January 2019

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Myocardial Infarction
Acute Coronary Syndrome (ACS) is a collection of syndromes associated with acute myocardial
ischemia or infarction usually resulting from abrupt reduction in coronary blood flow (Anderson
et al, 2013). ACS is typically caused by coronary artery obstruction resulting in a sudden
imbalance of myocardial oxygen consumption and demand.

Classification of ACS
ACS is classified based on the presence or absence of ST segment elevation. There are three
major classifications of ACS:

• Non-ST Segment Elevation Acute Coronary Syndrome (NSTE-ACS): Unstable Angina

(UA)
Clinical symptoms suggestive of ACS with the absence of persistent ST elevation and no
elevation in cardiac biomarkers (troponin) [which are elevated with myocardial tissue
damage]; with or without electrocardiogram (ECG) changes indicative of ischemia
(Aroesty, Simons, & Breall, 2017). Diagnosis may be made by clinical history alone.
• Non-ST Segment Elevation Acute Coronary Syndrome (NSTE-ACS): Non-ST Segment
Elevation Myocardial Infarction (NSTEMI)
Clinical symptoms suggestive of ACS with elevated cardiac biomarkers (troponin); with
or without ECG changes indicative of cardiac ischemia (Anderson et al, 2013).
Note: ECG changes suggestive of cardiac ischemia include ST depression, transient ST
elevation or prominent T wave inversions.
• ST-Segment Elevation Myocardial Infarction (STEMI):
ACS symptoms with elevated cardiac biomarkers (troponin); ECG shows persistent ST
elevation or new left bundle branch block (LBBB) (O’Gara et al, 2013). These patients
should be considered for immediate reperfusion therapy (fibrinolysis or percutaneous
coronary intervention [PCI]) (Anderson et al, 2013).

Guidelines for the Identification of Patients with ACS in the Emergency Room (Anderson
et al, 2013)
Clinical History:
Patients with the following signs and symptoms require immediate assessment by the triage
nurse for initiation of the ACS protocol and a STAT ECG:
• Chest pain or severe epigastric pain, nontraumatic in origin, with components typical of
myocardial ischemia or myocardial infarction (MI)
o Central/substernal compression or crushing chest pain
o Pressure, tightness, heaviness, cramping, burning, aching sensation
o Unexplained indigestions, belching, epigastric pain
o Radiating pain in neck, jaw, shoulders, back, or one or both arms
• Severe dyspnea
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• Hypotension
• Syncope

Medical History:
Obtaining a medical history must not delay entry into the ACS protocol. The triage nurse should
take a brief, targeted, initial history with an assessment of current or past history of:
• CABG, PCI, CAD, angina with exertion, or MI
• NTG use to relieve chest discomfort
• Risk factors, including smoking, hyperlipidemia, hypertension, diabetes mellitus, family
history, and cocaine or methamphetamine use
• Regular and recent medication use

Pathogenesis of ACS (Anderson et al, 2013)

• Thrombus or thromboembolism, usually arising on disrupted or eroded plaque:
o Occlusive thrombus, usually with collateral vessels (UA/NSTEMI)
o Subtotal occlusive thrombus on pre-existing plaque
o Distal microvascular thromboembolism from plaque-associated thrombus
• Dynamic obstruction (coronary spasm or vasoconstriction) of epicardial and/or
microvascular vessels
• Progressive mechanical obstruction to coronary flow
• Coronary arterial inflammation
• Secondary UA
• Coronary artery dissection
Clinical Presentations of ACS (Anderson et al, 2013; Aroesty et al, 2017)
• Rest angina (angina commencing when the patient is at rest), usually lasting more than
20 minutes in duration.
• New onset (less than 2 months) severe angina that significantly limits physical activity.
• Increasing angina (increasing in intensity, duration, and/or frequency), or occurs with
less exertion than previous angina.
Carefully assess women, patients with diabetes mellitus, older patients, those with unexplained
dyspnea, history of heart failure or stroke, and patients who complain of chest discomfort but
now have a permanent pacemaker that may conceal 12-lead ECG changes.

Diagnosis of Acute Myocardial Infarction

Any one of the following criteria are diagnostic for MI.
• Detection of a rise and/or fall of cardiac biomarker values (preferably cardiac troponin I and
T [cTn]) and at least one of the following:
o Symptoms suggestive of myocardial ischemia
o Development of pathologic Q waves on ECG
o New significant ST-segment-T wave (ST-T) changes or new LBBB
o Identification of intracoronary thrombus by angiography or autopsy
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o Imaging evidence of new loss of viable myocardium or a new regional wall

motion abnormality
• Cardiac death with symptoms suggestive of myocardial ischemia and new ischemia- related
ECG changes or new LBBB, but death occurred before cardiac biomarkers were obtained, or
before cardiac biomarker values would be increased.
• PCI-related MI: defined by elevation of cardiac biomarker values in patients with normal
baseline values or a rise of values > 20% if the baseline values are elevated but stable or
falling. In addition, one of the following:
o Symptoms suggestive of myocardial ischemia
o New ECG changes suggestive of ischemia or new LBBB
o Angiographic loss of patency of a major coronary artery or a side branch, or
persistent slow- or no-flow or embolization
o Imaging that demonstrates new loss of viable myocardium or new regional wall
motion abnormality
• Stent thrombosis associated with MI when detected by coronary angiography or autopsy in
the setting of myocardial ischemia and with a rise and/or fall of cardiac biomarkers
• Coronary artery bypass graft surgery (CABG)-associated MI: elevation of cardiac biomarker
values in patients with normal baseline cTn values. In addition, one of the following:
o New pathologic Q waves or new LBBB
o Angiographic documented new graft or native coronary artery occlusion
o Imaging evidence of new loss of viable myocardium or new regional wall motion
abnormality

Goals of Therapy (Aroesty et al, 2017) and Management Strategies

RECOMMENDATIONS FOR ALL MYOCARDIAL INFARCTIONS
(REGARDLESS OF CLASSIFICATION)
Goals Management
Early identification • Electrocardiogram (ECG) should be performed within 10 minutes
upon arrival to emergency department if not obtained by
Emergency Medical System (EMS) prearrival.
• If initial ECG not diagnostic and patient remains symptomatic,
repeat ECG every 15-30 minutes to detect ischemic changes.
Acute triage • Assess responsiveness, airway, breathing, and circulation.
• Look for evidence of systemic hypoperfusion (hypotension;
tachycardia; impaired cognition; cool, clammy, pale skin);
cardiogenic shock requires aggressive management.
• Left heart failure with hypoxia (dyspnea, hypoxia, pulmonary
edema, and/or impending respiratory compromise) requires
aggressive oxygenation, airway stabilization, diuretic therapy and
afterload reduction.
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• Treat ventricular arrhythmias immediately due to effect on

cardiac output and exacerbation of myocardial ischemia.
Initial therapy • Continuous cardiac monitoring.
• Administer oxygen to patients with arterial saturation <90%,
patients in respiratory distress including those with heart failure,
or those with other high-risk factors for hypoxia.
NOTE: Supplemental oxygen shows no benefit to patients with
oxygen saturation ≥ 90%.
• Establish intravenous (IV) access.
• Obtain serial cardiac troponin I or T levels at presentation and 3-6
hours after symptom onset.
Relief of ischemic • Administer sublingual NTG every 5 minutes up to 3 times for
pain continuing ischemic pain; administer IV NTG for persistent
ischemia, heart failure, or hypertension. Use caution if risk of
hypotension, suspicion/confirmed right ventricular failure, or
severe aortic stenosis. Contraindicated if phosphodiesterase
inhibitor (i.e. Viagra) taken within the previous 24 hours.
• IV morphine should be avoided unless patient has an
unacceptable level of pain. Initial dose is 2-4 mg, with increments
of 2-8 mg at 5- to 15-minute intervals.
• Discontinue nonsteroidal anti-inflammatory drugs (NSAIDs),
except aspirin, because of increased risk of adverse cardiac
events.
Stabilize • Atrial fibrillation and flutter can cause symptomatic
hemodynamics/pr hypoperfusion; ventricular tachycardia and fibrillation are life-
event and manage threatening.
arrhythmias • Treat with prophylactic IV β-blocker and maintain serum
potassium between 3.5 and < 4.5 meq/L and serum magnesium
above 2.0 meq/L.
• Avoid prophylactic lidocaine.
• Treat symptomatic bradycardia and heart block with atropine or
temporary pacing.
Estimation of risk High risk patients require aggressive management. This includes those of
advanced age, or those with low blood pressure, tachycardia, heart
failure, and an anterior MI. (See TIMI score later).
β-Blocker therapy • To prevent recurrent ischemia and life-threatening ventricular
arrhythmias.
• Start IV β-blocker (metoprolol or atenolol) in all patients without
contraindications within 24 hours; defer in patients that are
hemodynamically unstable.
• Contraindications are heart failure, low output state, risk for
cardiogenic shock, bradycardia, PR interval > 0.24 seconds,
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second- or third- degree heart block without permanent

pacemaker, reactive airway disease/active bronchospasm.
Dual antiplatelet • Aspirin: loading dose 162-325 mg uncoated aspirin; maintenance
therapy (O’Gara et dose 81-325 mg/day (81 mg/day is preferred dose and is the only
al., 2013) dose option when used concomitantly with ticagelor.)
• P2Y12 inhibitors for 12 months, regardless if treated with primary-
PCI or ischemia-guided strategy. Loading and maintenance doses
are the same for both indications, however prasugrel is an option
only in primary PCI, not in ischemia-guided strategy.
• Clopidogrel: Loading dose 300-600 mg; maintenance dose
75 mg/day
• Ticagelor: Loading dose 180 mg; maintenance 90 mg
every 12 hours (must only be given with aspirin 81
mg/day)
• Prasugrel (primary PCI only): Loading dose 60 mg; maintenance
10 mg/day (contraindicated with history of stroke or TIA, age ≥
75 years, and weight < 60 kg.)
Cholesterol • High-intensity statin therapy should be initiated as early as
therapy possible; obtain fasting lipid panel within 24 hours.
• Atorvastatin 80 mg daily or rosuvastatin 20 or 40 mg daily
Long-term • Antiplatelet therapy to reduce the risk of recurrent coronary
management artery thrombosis or, with PCI, coronary artery stent thrombosis
• Statins
• Oral anticoagulation in the presence of left ventricular thrombus
or chronic atrial fibrillation to prevent embolization
• Possible use of angiotensin converting enzyme (ACE) inhibitor in
patients at increased risk
• β-blockers, if no contraindications

RECOMMENDATIONS BASED ON CLASSIFICATION

Goals Unstable Angina/NSTEMI STEMI
Invasive Urgent/immediate diagnostic Reperfusion therapy should be
interventions angiography with intent to re- administered to all eligible
(O’Gara et al, vascularize (within 2 hours) in patients with STEMI with symptom
2013) NSTE-ACS patients with: onset within the prior 12 hours:
• Hemodynamic instability • PCI-capable hospitals –
or cardiogenic shock door-to-balloon time
• Severe left ventricular within 90 minutes upon
dysfunction or heart arrival.
failure • Non-PCI-capable hospitals
• Recurrent or persistent – transfer to PCI hospital
rest angina despite for door-to-balloon time of
intensive medical therapy 120 minutes. If arrive
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• New or worsening mitral within 2 hours of onset of

regurgitation or new symptoms, administer lytic
ventricular septal defect therapy then transfer.
• Sustained ventricular Fibrinolysis is recommended for
arrhythmias patients with symptom onset
Within 24 hours of admission for within 12 hours who cannot
initially stabilized high-risk receive primary PCI within 120
patients. minutes of first medical contact.
Time from hospital arrival to
Not recommended in those with initiation of fibrinolytic drug
extensive co-morbidities, for infusion (door-to-needle time)
whom the risks are likely to should <30 minutes. High risk of
outweigh the benefits of bleeding with fibrinolysis.
revascularization OR in those with
acute chest pain and low
likelihood of ACS who are
troponin negative (especially
women).

Anticoagulant Choice of agent (enoxaparin, • UFH to maintain

therapy bivalirudin, fondaparinux or therapeutic activated
unfractionated heparin [UFH]) clotting time (ACT). If given
depends on intervention strategy with GP IIb/IIIa receptor
planned. antagonist planned: 50-70
U/kg IV bolus; if no GP
IIb/IIIa receptor antagonist
planned: 70-100 U/kg bolus
• Bivalirudin 0.75 mg/kg IV
bolus, then 1.75 mg/kg/h
infusion with or without
prior treatment with UFH.
(Preferred if high risk of
bleeding).
• Fondaparinux: not
recommended as sole
anticoagulant for primary
PCI.

Risk Assessment
• Early Risk Stratification (UA/NSTEMI): identify patients at highest risk for future cardiac
events.
o Presence and extent of ST segment depression
o Elevated cardiac biomarkers
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o Evidence of hemodynamic instability

o Persistent chest pain despite appropriate medical therapy

• Thrombolysis in Myocardial Infarction (TIMI) Risk Score (Antman, Cohen, & Bernink, 2000)
Seven variables at presentation were independently predictive of outcome in patients with
unstable angina or an acute non-ST elevation MI (1 = present, 0 = absent)
o Age ≥ 65 years
o Presence of at least 3 risk factors for coronary heart disease (hypertension, diabetes,
dyslipidemia, smoking, or positive family history of early MI)
o Prior coronary stenosis ≥ 50%
o Presence of ST segment deviation on admission electrocardiogram
o At least 2 anginal episodes in prior 24 hours
o Elevated serum cardiac biomarkers
o Use of aspirin in prior 7 days (possible marker of more severe coronary disease)
o TIMI Scoring:
▪ Low risk score = 0 to 2
▪ Intermediate risk score = 3 to 4
▪ High risk score = 5 to 7

References:
Anderson, J. L., Adams, C. D., Antman, E. M., Bridges, C. R., Califf, R. M., Casey, D. E., Chavey, W. E.,…Wright, R. S. (2013). 2012
ACCF/AHA Focused Update Incorporated Into the ACCF/AHA 2007 Guidelines for the Management of Patients With Unstable
Angina/Non–ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology Foundation/American Heart
Association Task Force on Practice Guidelines. Circulation, 127, e663-e828. doi.org/10.1161/CIR.0b013e31828478ac

Antman, E. M., Cohen, M., Bernink, J. L. (2000). The TIMI Risk Score for Unstable Angina/Non–ST Elevation MI: A Method for
Prognostication and Therapeutic Decision Making. The Journal of the American Medical Association, 284(7), 835-842.
doi:10.1001/jama.284.7.835

Aroesty, J., Simons, M., & Breall, J. (2017). Overview of the acute management of non-ST elevation acute coronary syndromes.
UpToDate. Retrieved from https://www.uptodate.com/contents/overview-of-the-acute-management-of-non-st-elevation-acute-
coronary-syndromes

O’Gara, P. T., Kushner, F. G., Ascheim, D. D., Casey, D. E., Chung, M. K., de Lemos, J. A.,…Zhao, D. X. (2013). 2013 ACCF/AHA
Guideline for the Management of ST-Elevation Myocardial Infarction: A Report of the American College of Cardiology
Foundation/American Heart Association Task Force on Practice Guidelines. Circulation, 127, e362-e425.
doi.org/10.1161/CIR.0b013e3182742cf6