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ACS: A triad of troubles sets the stage for MI

Bermudez, Natalie MSN, RN

doi: 10.1097/01.NME.0000421577.99021.b3
Department: Heart Matters

Clinical Educator for Telemetry • Bethesda Memorial Hospital • Boynton Beach, Fla.

The author has disclosed that she has no financial relationships related to this article.

Mr. O, 55, presents to the ED complaining of intermittent sharp chest pain and “heaviness,” with discomfort radiating to his jaw and shortness of breath. He says he has been feeling this way for the past few hours and was sitting in his recliner watching TV at the time of onset. He has a history of hyperlipidemia, but he isn't taking any medications to treat it. He has been smoking since he was 18 and estimates smoking about 2 packs a day. He reports that his father died of a myocardial infarction (MI) at age 63. He doesn't visit a primary healthcare provider regularly.

His 12-lead ECG is negative for ST-segment elevation, but his cardiac biomarkers are positive. Administration of I.V. nitroglycerin at 20 mcg/minute and morphine sulfate 2 mg relieves his chest pain. He also receives a baby aspirin. Mr. O is admitted to the coronary care step-down unit with a diagnosis of non-ST elevation myocardial infarction (NSTEMI) for further evaluation and treatment.



Although Mr. O is stable now, the stage may be set for an MI. His condition is associated with a coronary occlusion triad—plaque rupture, thrombus formation, and vasoconstriction—that could be fatal without intervention. Here's how to bring down the curtain on this dangerous situation before his condition worsens.

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Presenting the main characters

Acute coronary syndrome (ACS) is an umbrella term used to describe occlusive or partially occlusive coronary vascular events known as unstable angina (UA), NSTEMI, and ST-segment elevation myocardial infarction (STEMI). These terms describe three severe stages of coronary occlusion that result in insufficient or complete lack of perfusion to myocardial tissue (see ACS tissue destruction).

The type of ACS is diagnosed based on partial, intermittent, or complete occlusion of coronary vessels, which can be rapidly determined through a 12-lead ECG and serum cardiac biomarkers. Troponin (I or T) levels are the preferred cardiac biomarker for evaluation of ACS because they're the most specific indicator of myocardial tissue death.

The following is an outline of 12-lead ECG changes and cardiac biomarkers in relation to UA, NSTEMI, and STEMI. The severity, onset, duration, and treatment differ depending on the specific type of ACS.

UA is described as chest pain that occurs while at rest or chest pain that persists following treatment with sublingual nitroglycerin. The 12-lead ECG is negative for ST-segment elevation. However, ST-segment depression and/or T-wave inversion are usually present. Cardiac biomarkers are negative. UA indicates that plaque disruption has occurred with partial or intermittent occlusion of a coronary vessel without any permanent myocardial damage.

Figure. AC

Figure. AC

Anticipate that the patient will undergo cardiac stress testing to localize areas of ischemia and/or diagnostic cardiac catheterization to measure the degree of coronary artery stenosis.

ECG changes with NSTEMI are the same as with UA; however, cardiac biomarkers are positive. Elevated cardiac biomarkers indicate that plaque disruption has occurred with significant myocardial injury or infarct (necrosis).

The patient will likely undergo nonemergent diagnostic cardiac catheterization with possible percutaneous coronary intervention (PCI), such as angioplasty and/or stent placement. According to the American College of Cardiology (ACC) Foundation/American Heart Association (AHA) Taskforce on Practice Guidelines/Society for Cardiovascular Angiography and Interventions 2011 Guideline for Percutaneous Coronary Intervention, PCI to improve survival is reasonable in patients with UA/NSTEMI when an unprotected left main coronary artery is the culprit lesion and the patient isn't a candidate for coronary artery bypass grafting (CABG).

STEMI is confirmed when chest pain and associated symptoms occur with the presence of ST-segment elevation. STEMI indicates that plaque disruption has resulted in a complete occlusion of a coronary vessel. STEMI is accompanied by elevated cardiac biomarkers.

The most effective treatment for a complete occlusion is reperfusion therapy at the site of blockage. This can be accomplished by either administration of I.V. fibrinolytic therapy, such as tissue plasminogen activator, or PCI with angioplasty and/or stent placement. The ACC/AHA Task Force on Performance Measures 2008 Performance Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction recommends that patients identified with STEMI be treated with PCI within 90 minutes (from time of arrival or symptom onset) or fibrinolytic therapy within 30 minutes, if not meeting exclusion criteria. (For details on exclusion criteria, visit

CABG is the treatment if stenosis of coronary vessels is severe or if percutaneous transluminal coronary angioplasty (PTCA) and/or stenting are unsuccessful.

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Treatments take center stage

Your patient, Mr. O, undergoes cardiac catheterization with PTCA and placement of a drug-eluting stent to treat an 85% occlusion of the left anterior descending artery. He returns to the coronary care step-down unit where he's monitored for complications such as bleeding and signs and symptoms of reocclusion.

An echocardiogram reveals an ejection fraction of 65%, with normal left ventricular wall motion. Results of a cholesterol panel show a total cholesterol level of 280, with a low-density lipoprotein cholesterol level of 150.

He's discharged home on the following medications: aspirin, 325 mg daily; clopidogrel, 75 mg daily; metoprolol, 50 mg daily; and simvastatin, 20 mg at bedtime. He's instructed to follow up with a primary care physician and cardiologist in 1 week.

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Curtain call: Award-winning nursing care

It's imperative that you know what to do when treating patients during a cardiac emergency. Many hospitals have developed specific chest pain protocols (see The Joint Commission core measures for acute MI). Familiarize yourself with your healthcare organization's protocols for responding to emergency situations such as chest pain, carrying out preapproved medical interventions, and following the appropriate procedure for notifying healthcare providers of such events.

Your priorities are to quickly assess the patient, provide appropriate emergent care, obtain a 12-lead ECG for rapid evaluation, and obtain specimens for serum cardiac biomarkers to identify the stage of ACS and provide the appropriate treatment and/or interventions. Your role in responding rapidly to patients experiencing chest pain is vital to achieve positive patient outcomes.

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The Joint Commission core measures for acute MI

  • Aspirin upon arrival
  • Aspirin prescribed at discharge
  • Angiotensin-converting enzyme inhibitor or angiotensin II receptor blocker for left ventricular systolic dysfunction
  • Beta-adrenergic blocker prescribed at discharge
  • Fibrinolytic therapy received within 30 minutes of hospital arrival or primary PCI therapy received within 90 minutes of hospital arrival
  • Statin prescribed at discharge
  • Adult smoking cessation/advice counseling

Source: The Joint Commission. Acute Myocardial Infarction Measure Set.

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Learn more about it

American College of Cardiology/American Heart Association Task Force on Performance Measures. ACC AHA 2008 Performance Measures for Adults With ST-Elevation and Non-ST-Elevation Myocardial Infarction.
    American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines/Society for Cardiovascular Angiography and Interventions. 2011 ACCF/AHA/SCAI Guideline for Percutaneous Coronary Intervention.
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                        © 2012 Lippincott Williams & Wilkins, Inc.