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Department: Heart Beats

Non-ST-elevation acute coronary syndromes

Moore, Cathy MSN, APRN, CCRN

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doi: 10.1097/01.CCN.0000461174.92690.60
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Fifty-nine-year-old Mrs. R awoke at 0600 with midsternal chest pain radiating to her left jaw associated with dyspnea, diaphoresis, and nausea. She called 911 and took baby aspirin for chest pain as she had heard you should do. Once the emergency medical services (EMS) crew arrived, Mrs. R was placed on supplemental oxygen at 4 L/min, attached to a cardiac monitor, and peripheral venous access was obtained. Mrs. R's BP was 140/88 with a heart rate of 88. EMS gave her one dose of sublingual (SL) nitroglycerin and transported her to the local hospital within 4 minutes of EMS arrival.

Initial presentation in the ED

Mrs. R arrived in her local ED awake and oriented but anxious, pale, and diaphoretic. She complained of chest pain with radiation to the left jaw. Her BP was 138/90; pulse, 88; respirations, 24; and SpO2, 98% on the supplemental oxygen. Blood specimens, including a fasting lipid panel, cardiac troponin I (cTnI), cardiac troponin T (cTnT), and B-type natriuretic peptide (BNP) were obtained and sent to the lab.1 Creatine kinase myocardial isoenzyme and myoglobin are no longer useful for diagnosis of acute coronary syndromes (ACS).1 A focused health history was obtained. Mrs. R hasn't seen a healthcare provider (HCP) in many years. She has no known allergies and takes no medications. She's a current smoker of one pack per day for 30 years (30 pack years). Her mother died of a myocardial infarction (MI) when she was 64 years old.

ECG interpretation A 12-lead ECG was performed and evaluated for ischemic changes within 10 minutes of arrival to the ED.1 The ECG showed normal sinus rhythm with T wave inversion in leads II, III, aVF (See Admission ECG). These changes most likely represent myocardial ischemia, especially given Mrs. R's history and clinical presentation.

Myocardial ischemia pain management

Mrs. R continued complaining of chest pain (pain intensity rating 7/0-10) with radiation to her left jaw. Mrs. R's BP was 110/74 and heart rate, 86. Her cardiac monitor shows normal sinus rhythm. Due to Mrs. R continued chest pain, the nurses obtained a second peripheral venous access and started an I.V. nitroglycerin infusion after administering two more doses of SL nitroglycerin as ordered. Other physician orders included I.V. morphine and an oral beta-blocker to start after her BNP results came back normal.1

Fifteen minutes later, Mrs. R was pain free (0/0-10) and her skin was warm and dry. Her initial cTnT result was 1.33 μg/L (normal, less than 0.01 μg/L). The cardiologist informed Mrs. R that she had a MI (See Overview of MI.) The cardiologist followed recommended standards of care for non-ST-elevation acute coronary syndromes (NSTE-ACS) and placed Mrs. R on dual antiplatelet therapy (aspirin and clopidogrel) to reduce the risk of recurrent coronary artery thrombosis.1 Now stabilized, she's admitted to the progressive care unit.

New risk factors for MI

Risk factors for ACS continue to be smoking, diabetes, hypertension, aging, low activity lifestyles, dyslipidemia, and obesity. Family history plays a very strong role in the risk of the development of ACS. Several risk factors for ACS have recently been added. The new risk factors include2:

  • HIV treatment with protease inhibitors
  • low levels of 25-hydroxyvitamin D (excluding elevated parathyroid hormone levels)
  • human papillomavirus
  • the illegal herbal stimulant known as Khat pronounced “cot” (causes coronary spasm similar to amphetamines)3
  • psychological stress in spousal caregivers of cancer patients.

Risk scores should be used to assess prognosis in patients with NSTE-ACS.1 The risk assessment scores must be considered in conjunction with patient history. Additional risk factors include history of an MI in a close relative before the age of 55 or a stroke before the age of 65 and moderate-to-severe kidney disease.4 The risk assessment tools calculate risk from the input of age, gender, total serum cholesterol level, serum high-density lipoprotein cholesterol level, smoker status, and systolic BP and if BP is currently being treated with medications.4,5 The tools are ideal for HCPs. Estimated risks need to be discussed with patients, as well as the medical plan of care to decrease risk, if appropriate.

ECGs of patients with NSTE-ACS may be normal or have depressed ST segments and/or T wave inversions.6 The defining marker that may indicate a NSTEMI is the elevated serum cardiac biomarker, troponin. Troponin is a very sensitive marker for myocardial necrosis. It's the regulatory protein that controls calcium-mediated interaction of actin and myosin.6 Serum troponin (I or T) is used to diagnose NSTE-ACS.7 A negative serum troponin is useful to rule out MI. Point-of-care troponin is recommended if the lab can't provide results within 60 minutes. The point-of-care troponin is less sensitive, but helpful if results are positive.7 Troponin elevation occurs within 2 to 3 hours after the onset of myocardial necrosis. However, troponin levels can be elevated for reasons other than MI.8 (See Reasons for elevated serum troponin levels other than MI.)9

Figure. Ad
Figure. Ad:
mission ECG

Medical management of NSTE-ACS

Medical management of NSTE-ACS includes early, accurate recognition of possible ECG changes and cardiac-related serum troponin elevation.1 HCPs should do a risk assessment and classify patients as high risk or low risk determining which medical interventions are beneficial.2 Pharmacology is the primary medical management for NSTE-ACS (See Medications associated with NSTE-ACS.)

HCPs may use noninvasive imaging to differentiate between coronary and noncoronary diagnoses especially for low-risk patients. Cardiac magnetic resonance imaging and coronary computed tomography angiography are valuable in recognizing coronary arterial plaques that may be decreasing coronary artery blood flow.10 These diagnostic studies are quicker, less expensive, and less invasive than coronary angiography.10,11 For low-risk patients presenting in the ED, these studies allow earlier discharge thereby improving ED throughput.10

Early interventions improve mortality and morbidity. HCPs must decide what type of reperfusion strategy is appropriate for their patients based on risk factors and clinical presentation.6

Conservative strategies, including noninvasive therapies, are intended for low-risk NSTE-ACS patients.1 The focus of conservative therapy is medications to prevent further coronary artery thrombosis using antiplatelet agents and anticoagulants. It's also important to decrease myocardial oxygen consumption with the negative inotropic effects of beta-blockers. Conservative strategies may be best for patients with serious comorbidities including: active cancer, serious infection, recent stroke, advanced Alzheimer disease, and serious intracranial pathology that prevents the use of antiplatelet therapy.1,6

An early invasive strategy is diagnostic coronary angiography in the cardiac catheterization lab with reperfusion using percutaneous coronary intervention (PCI) if indicated by coronary anatomy.1 An early invasive strategy is indicated in patients with NSTE-ACS who have refractory angina or hemodynamic or electrical instability without serious comorbidities or contraindications.1,6 Not all patients with coronary artery stenosis or occlusion are candidates for PCI. If the cardiac interventionist discovers complex coronary artery stenoses/occlusions, poor left ventricular function, or valvular dysfunction during coronary angiography, the best reperfusion strategy may be coronary artery bypass graft surgery.6

Delayed invasive therapy, also known as ischemia-guided strategy, may be considered for high-risk patients who are stable.1 These patients should have diagnostic coronary angiography with possible reperfusion within 24-72 hours of presentation, as long as the patient remains hemodynamically and electrically stable.1,6 No matter which strategy is implemented to treat the NSTE-ACS, dual antiplatelet therapy should continue for at least one year after the event.1 If the patient is at risk for gastrointestinal bleeding, a proton pump inhibitor should be added.1,9 Fibrinolytic therapy should not be used in NSTE-ACS patients.1

Table
Table:
Medications associated with NSTE-ACS1,8
Table
Table:
Medications associated with NSTE-ACS1,8 (continued)
Table
Table:
Medications associated with NSTE-ACS1,8 (continued)

Nursing management of patients with NSTE-ACS

ST segment monitoring helps detect early electrocardiographic changes that indicate worsening ischemia.6 Ventricular dysrhythmias are associated with increased mortality.6 Patients with active chest pain or dyspnea need bed rest and supplemental oxygen.6 Nurses are responsible for recognizing signs and symptoms of heart failure such as pulmonary crackles, oxygen desaturations, and worsening dyspnea. The goal of therapy is for the patient to be chest pain free without signs and symptoms of heart failure, hemodynamic instability, or electrical instability.6

Patient education

Patients require multifaceted education to decrease the risk factors for a cardiac event.12 Educational information should include:

  • “teach back” principles
  • videos and discussion to improve retention
  • follow-up appointments with their primary care provider, within 7 days of discharge
  • checklists and other online and printed educational material, in the patient's native language and health literacy level12
  • medication adherence is important to decrease mortality and morbidity. Rates of adherence to medications after NSTE-ACS range from 36% to 49%, with cost of medication as a factor.4 Approach the patient's educational needs with a case manager who will assist with hospital transitions and discharge follow-up.1

Case presentation continues

Three hours after admission, Mrs. R complained of recurrent chest pain. Her stat ECG was unchanged from her admission ECG. Mrs. R's BP is 136/92 on I.V. nitroglycerin; pulse rate, 98; and respiratory rate, 24. Her pulse oximetry was 98% on 4 L/min of oxygen via nasal cannula. She began having short bursts of ventricular tachycardia. The nurse increased the nitroglycerin infusion, per physician admitting order set, and called a rapid response. In the meantime, a coworker notified Mrs. R's cardiologist of her change in status. The cardiologist prescribed an I.V. beta-blocker, IV heparin, and an IV glycoprotein IIb/IIIa inhibitor in preparation for cardiac catheterization. Mrs. R was emergently sent to the cardiac catheterization lab where she underwent PCI: right coronary artery percutaneous balloon angioplasty and endovascular stent placement and was discharged home on hospital day 4 with a referral to cardiac rehabilitation program.1

Overview of MI

The overall incidence of first-time MI is slowly decreasing over the past two decades. Coronary artery disease remains the leading cause of death worldwide with one in six deaths occurring in the United States.2 Non-ST-elevation myocardial infarction (NSTEMI) has a 50% prehospitalization mortality. Once in the hospital the mortality decreases to 1.9% due to factors such as continued cardiac monitoring and medications reducing myocardial oxygen consumption and decreasing the risk of life-threatening cardiac dysrhythmias.2

NSTEMI is an imbalance between myocardial oxygen supply and demand.7 A NSTEMI involves a partial occlusion of the coronary artery.8 Approximately, 85% of patients diagnosed with NSTEMI have significant coronary artery disease.8 The clinical presentations of an MI include: prolonged chest pain or pressure, nausea and/or vomiting, diaphoresis, pallor, and anxiety. Some patients may exhibit a few of these signs and symptoms or have vague symptoms such as fatigue or pain between the scapulae. Patients may present with anginal equivalents including patients with diabetes, women, and older adults. It's vital that patients experiencing chest pain call 911, chew baby aspirin (unless contraindicated), and not drive to the hospital.

Reasons for elevated serum troponin levels other than MI

  • Sepsis
  • Hypovolemia
  • Atrial fibrillation especially with rapid ventricular response
  • Heart failure
  • Acute neurologic disorder such as stroke or subarachnoid hemorrhage
  • Pulmonary embolism
  • Myocarditis
  • Exertion
  • Aortic valve disease
  • Critically ill patients with diabetes, renal failure, or sepsis
  • Myocardial contusion
  • Renal failure
  • Coronary vasospasm
  • Burns
  • Stress (takotsubo) cardiomyopathy

REFERENCES

1. Amsterdam E, Wenger N, Brindis R, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: executive summary: a report of the American College of Cardiology/American Heart AssociationTask Force on practice guidelines. Circulation. 2014;130(25):2354–2394.
2. Giugliano RP, Braunwald E. The year in non-ST-segment elevation acute coronary syndrome. J Am Coll Cardiol. 2012;60(21):2127–2139.
3. http://www.drugabuse.gov/publications/drugfacts/khat.
4. Assessing Cardiovascular Risk: systematic evidence review from the risk assessment work group. 2013. http://www.nhlbi.nih.gov/guidelines.
5. Risk assessment tool for 10 year risks of developing hard CHD (myocardial infarction and coronary death). National Cholesterol Education Program. http://img.medscape.com/article.
6. Braunwald E. Unstable angina and non-ST elevation myocardial infarction. Am J Respir Crit Care Med. 2012;185(9):924–932.
7. Xu B, MacIsaac AI. What does an elevated troponin mean?—An update on the definition of myocardial infarction. Aust Fam Physician. 2013;42(8):554–559.
8. Up to date. http://www.uptodate.com/contents/antiplatelet-agentsnon-st-elevation-acute-coronary-syndrome.
9. Up to date. http://www.uptodate.com/contents/increase of cardiac troponins in the absence of ACS.
10. Smulders MW, Kietselaer BL, Das M, et al. The role of cardiovascular magnetic resonance imaging and computed tomography angiography in suspected non-ST-elevation myocardial infarction patients: design and rationale of the cardiovascular magnetic resonance imaging and computed tomography angiography (CARMENTA) trial. Am Heart J. 2013;166(6):968–975.
11. Up to date. http://www.uptodate.com/contents/clopidogrel-resistance-and-clopidogrel-treatment-failure.
12. Dechant LM. UA/NSTEMI: Are you following the latest guidelines. Nursing. 2012;42(9):26–33.
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