Case Study About Acute Coronary Syndrome Protocol

I. Acute Coronary Syndrome: What every physician needs to know.

An acute coronary syndrome (ACS) is a constellation of symptoms and signs that result from obstruction of the coronary arteries. Common signs and symptoms include chest pain, dyspnea, and electrocardiographic abnormalities. The most common cause of acute coronary syndrome is blockage of the coronary artery from cholesterol rich plaque and thrombus.

In acute coronary syndrome, a previously quiescent plaque has ruptured, exposing the lipid core, inciting platelet activation and aggregation with subsequent thrombus formation. When the atherothrombotic material is totally occlusive with complete cessation of blood flow through the artery, the acute coronary syndrome is termed ST-Elevation myocardial infarction (STEMI).

If the occlusion is partially obstructive and there is no evidence of myocardial injury (e.g., elevated cardiac troponin), the ACS is termed unstable angina, but if cardiac injury is detected with a partial obstruction, then the term to describe the ACS is non-ST segment myocardial infarction (NSTEMI). ACS unrelated to plaque rupture can infrequently be seen from coronary vasospasm, embolization, or spontaneous coronary dissection.

II. Diagnostic Confirmation: Are you sure your patient has Acute Coronary Syndrome?

The diagnosis of ACS is based on finding a history compatible with active, obstructive coronary disease and supportive evidence based on ST segment deviation on ECG and evaluation of cardiac biomarkers (e.g., cardiac troponin, creatine kinase) suggestive of myocardial infarction.

A. History Part I: Pattern Recognition:

Typical patients with ACS will describe chest pain that is often located at the sternum and can be described as an ache or pressure. The textbook description is "an elephant sitting on my chest' with the patient's fist clenched over the sternum (classically referred to as the Levine's sign).

The chest symptoms classically last more than 20 minutes and may have increased in intensity, frequency, or duration recently. There may be radiation to the neck, jaw, back, or arms. There may be associated dyspnea, diaphoresis, and nausea.

If significant myocardial pump dysfunction is present, the patient may report orthopnea or paroxysmal nocturnal dyspnea. It should be noted that these "typical features" are helpful if present but the absence does not exclude ACS. The symptoms may be localized to the epigastrium or there may be no chest symptoms at all. In fact, some or all of these findings may be absent, especially among elderly patients, women, and those with psychiatric disorders.

The five most important factors from the initial history in the order of importance are (1) the nature of the anginal symptoms, (2) prior history of coronary artery disease (CAD), (3) sex, (4) age, and (5) the number of traditional risk factors present. For those with suspected ACS with prior history of heart disease, advanced age seems to be the most important risk factor (>55 years for males and >65 years for females).

B. History Part 2: Prevalence:

Acute coronary syndromes account for over 2.4 million discharges per year in the U.S. About 500,000 of these are for STEMI and the remainder are for NSTEMI or unstable angina.

The risk factors for coronary artery disease increase the risk for ACS. These include hypertension, hypercholesterolemia, diabetes, smoking, advanced age, and a family history of premature coronary artery disease.

These risk factors increase the risk for underlying atherosclerosis, the substrate for ACS. Several triggers for ACS have been implicated including: anxiety, emotional stress, strenuous exercise, influenza infection, and extreme physiologic stress due to concomitant medical or surgical illness.

C. History Part 3: Competing diagnoses that can mimic Acute Coronary Syndrome.

While the character of symptoms is often different from ACS, aortic dissection, pulmonary embolism, and pericarditis, with or without cardiac tamponade, should be considered. At times, pneumonia, pneumothorax, cholecystitis, peptic ulcer disease, and herpes zoster may be confused with ACS.

D. Physical Examination Findings.

The physical examination related to ACS is often nonspecific, but the complications associated with infarction and cardiac pump dysfunction may be manifest as tachycardia, bradycardia, hypotension, elevated jugular venous pressure, wheezes, crackles, or hepatomegaly. The heart examination may reveal right ventricular heave, sustained LV impulse, the presence of S3 and/or S4 as well as mitral regurgitation.

Aortic regurgitation may suggest an aortic dissection. Diminished heart sounds raise the possibility of a pericardial effusion and/or tamponade physiology. Pulses should be examined as they may be asymmetric or exhibit bruits if there is preexisting vascular disease or if there is an aortic dissection, or if pulses are either diminished and delayed as seen in some cases of severe aortic stenosis.

E. What diagnostic tests should be performed?

A 12-lead ECG should be obtained and interpreted within 10 minutes of hospital triage, if not obtained by emergency medical services (EMS). A chest x-ray should be obtained if pneumonia or aortic dissection is suspected. If STEMI has been diagnosed, chest x-ray and laboratory results should not delay implementation of reperfusion therapy.

1. What laboratory studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

Cardiac specific troponin is the preferred biomarker to diagnose myocardial injury; however, these may be initially negative in STEMI patients presenting early and some NSTEMI patients.

2. What imaging studies (if any) should be ordered to help establish the diagnosis? How should the results be interpreted?

A 12-lead electrocardiogram should be obtained and interpreted within 10 minutes of presentation. While imaging studies, such as stress testing with echocardiographic or nuclear imaging and coronary angiography, are used to assess risk during ACS, these studies are not used to make a diagnosis of ACS.

III. Management.

Management of ACS is determined by the patient's risk. In the case of ACS, to complete coronary occlusion, STEMI, the goal is for immediate revascularization to salvage myocardium. For NSTEMI and unstable angina (UA), treatment is to mitigate the changes of recurrent infarction and/or to reduce the size of infarction.

Medical therapy is guided by the degree of patient risk for ischemic complications and balanced against the risk for bleeding or other complications from these treatments. If the patient is diagnosed with STEMI, the decision must be made as to whether fibrinolysis will be administered, primary percutaneous coronary intervention (PPCI) will be performed, or whether the patient will be transferred for primary PCI.

Determination of PPCI vs. fibrinolysis for STEMI

If PCI can be performed by skilled personnel in a timely fashion, door to balloon time <90 minutes, this is the preferable strategy for STEMI. If the patient is at a hospital where PCI is not performed, it is advisable to administer fibrinolysis if the delay related for transfer for PCI will exceed 60 minutes or if the total door to balloon time will exceed 120 minutes.

If transfer can be arranged rapidly and PCI can be performed within 120 minutes from initial presentation, the patient can be transferred to the PCI capable hospital. It is advisable to transfer the patient to a PCI capable hospital routinely after administration of fibrinolysis in case the medication does not work or if there is recurrent infarction.

A. Immediate management.

As mentioned previously, the management of STEMI is emergent revascularization with fibrinolysis or preferably PPCI. Aspirin and unfractionated heparin or bivalirudin should be administered. Clopidogrel, ticagrelor, or prasugrel can be administered in addition to aspirin for STEMI.

Early risk stratification is of paramount importance for patients presenting with NSTEMI/UA. Risk stratification tools, including the TIMI Risk Score for UA/NSTEMI and the GRACE risk score to help divide patients into low- or high-risk categories.

Immediate management involves administration of oxygen and placement of IV access. Aspirin (162 to 325 mg) is administered orally or rectally. Analgesia with morphine may be administered while blood pressure and oxygenation are monitored. If possible, the patient should chew the aspirin to enhance absorption.

An antithrombin should be selected for patients who are not low risk. Unfractionated heparin may be administered (50 units/kg up to maximum of 4000 units). Low molecular weight heparins (LMWH) have the advantage of fixed dosing that does not require monitoring, but should be avoided in patients who will be going on to coronary artery bypass grafting (CABG) surgery and in those with renal failure. Fondaparinux can be administered to patients who will be managed medically. Bivalirudin can be administered instead of UFH or LMWH.

Additional antiplatelet therapy should be administered to high-risk individuals with NSTEMI. A loading dose of clopidogrel or ticagrelor can be administered in the emergency department for NSTEMI. Prasugrel should be administered in the catheterization laboratory if the patient requires PCI and clopidogrel or ticagrelor have not already been administered.

Glycoprotein IIb/IIIa receptor antagonists are administered for high-risk individuals.

Oral beta-blocker therapy should be administered within 24 hours of presentation unless there are signs of heart failure, there is evidence of a low output state, increased risk for cardiogenic shock, or other contraindications to therapy.

An oral angiotensin converting-enzyme inhibitor (ACE-I) should be administered to those with left ventricular ejection fraction of ≤ 40%, without hypotension as defined by SBP <100 mm Hg or SBP >30 mm Hg below baseline, or shock, history of bilateral renal artery stenosis, or prior known allergy to ACEI. An angiotensin receptor blocker (ARB) may be used instead of an ACE-I if the patient is intolerant due to allergy or cough.

Invasive therapy, cardiac catheterization, should be performed in patients whose procedural risk is not prohibitive, if that patient's risk is not low. The angiogram allows for determination of whether medical therapy, CABG surgery, or PCI is the preferred management.

For patients initially selected for conservative therapy, recurrent symptoms, hemodynamic instability, or the development of heart failure, should prompt coronary angiography. Angiography is usually performed on an urgent basis (within 48 to 72 hours) but should be performed sooner for those with symptoms refractory to medical therapy or in those who develop hemodynamic instability.

Low-risk individuals should have a serial biomarker measurement. If these become elevated, an coronary angiography should be considered. For low-risk individuals whose biomarkers remain normal, further risk stratification can occur with stress testing.

Pharmacologic testing can be used for those who cannot exercise. Imaging (echocardiography or nuclear imaging) should be added to the exercise ECG testing if the 12-Lead ECG exhibits ST segment abnormality or left bundle branch block.

B. Physical Examination Tips to Guide Management.

The patient should be monitored for the development of mechanical complications of infarction. The development of signs of congestion (S3, crackles, elevated JVP) or a new murmur should prompt further work-up and aggressive therapy. Patients with signs of confusion and lethargy may be developing cardiac insufficiency and this should be considered even if narcotics for pain have been administered.

C. Laboratory Tests to Monitor Response To, and Adjustments in, Management.

Complete blood count evaluating for anemia, leukocytosis, thrombocytosis, or thrombocytopenia should be obtained at baseline. Serum chemistries evaluating glucose, potassium, magnesium, bicarbonate, and renal function should be obtained at baseline for management of ACS.

A lipid profile should be obtained, and for those with elevated blood glucose, glycated hemoglobin should be measured. Stool guaiac is often obtained to screen for occult blood. Serum creatinine, platelet count, and hemoglobin are monitored to assess for contrast-induced nephropathy, or bleeding complications or thrombocytopenia associated with anticoagulant, antiplatelet therapy, or procedures.

D. Long-term management.

Long-term management includes use of medications shown to be beneficial in the secondary prevention of atherosclerotic disease and congestive heart failure. These include reduction of blood pressure with a goal of 130/80 mm Hg and cholesterol reduction with an LDL cholesterol goal of <70 mg/dl.

Patients should receive dual antiplatelet therapy with aspirin (75 mg to 100 mg QD) and either clopidogrel, ticagrelor, or prasugrel. The choice of the agent added to aspirin is somewhat dependent on the management strategy pursued in hospital and the optimal agent is a matter of debate.

The duration of dual antiplatelet therapy is suggested by societal guidelines to be 12 months regardless of whether the patient was managed with medical therapy alone or revascularization using PCI or CABG surgery for ACS. Beta-blockers and ACE inhibitors are used particularly in those patients who are hypertensive or whose ejection fraction is reduced. The goal for glycated hemoglobin for diabetic patients is <7.0%. Patients should receive smoking cessation counseling and referral to cardiac rehabilitation.

E. Common Pitfalls and Side-Effects of Management

Cardiac specific troponin elevation may occur in situations besides ACS. Elevated cardiac biomarkers can occur in the setting of profound demand ischemia during noncardiac illness, and ACS should be diagnosed, and anticoagulant and invasive therapies implemented with caution in these settings.

Nitrates should be avoided in those who have received phosphodiesterase III inhibitors for erectile dysfunction within 48 hours or those with SBP <90 mM Hg or >30 mm Hg below baseline and in those with a heart rate (HR) <50 beats/min or >100 beats/min in the absence of heart failure or right ventricular infarction.

Prasugrel should not be administered to patients with prior transient ischemic attack (TIA) or stroke, and a lower dose should be considered for those <60 Kg or >75 years of age. Prasugrel should be held for 7 days prior to CABG; ticagrelor and clopidogrel should be held for 5 days prior to CABG, if possible.

Abciximab should not be used for those who will not be undergoing PCI. Glycoprotein IIb/IIIa receptor antagonists can cause thrombocytopenia and unfractionated heparin can cause the heparin induced thrombocytopenic (HIT) syndrome. Eptifibatide, tirofiban, and enoxaparin should be dose adjusted for renal insufficiency.

Intravenous beta-blockers given during the first 24 hours of ACS may be associated with adverse outcomes and should be reserved for those who are hypertensive and with ongoing symptoms. NSAIDS apart from aspirin and steroids should be avoided in ACS.

Nitroglycerine 0.4 mg sublingually every 5 minutes up to 3 times. If chest pain persists, then 5 to 10 mcg/min titrating up 10 mcg/min every 10 minutes until chest pain free or SBP <100 mm Hg.

  • Morphine 1 to 5 mg IV, repeat as tolerated

  • Aspirin 162 to 325 mg orally or rectally initially, then 75 to 100 mg orally daily

  • Clopidogrel 300 to 600 mg orally once, then 75 mg daily; may consider 150 mg orally daily for first 7 days of ACS.

  • Prasugrel 60 mg orally once, then 10 mg orally daily; may use 5 mg orally daily for those <60 Kg or >75 years.

  • Ticagrelor 90 mg orally once, then 180 mg orally twice daily

  • Unfractionated heparin 50 U/kg IV up to 4,000 U, then 12 U/hr up to 1,000 U/hr IV

  • Fondaparinux 2.5 mg subcutaneously daily up to 8 days

Lovenox (UA/NSTEMI 1 mg/kg subcutaneously twice daily, dose adjust for GFR <30 cc/hr; STEMI 30 mg IV and 1 mg/kg subcutaneously twice daily if <75 years, if >=75 years, no bolus and 0.75 mg/kg subcutaneously twice daily if GFR <30 cc/min and <75 years then 30 mg IV and 1 mg/kg subcutaneously daily and if >=75 years no bolus and 1 mg/kg subcutaneously daily.

Bivalirudin 0.1 mg/kg IV bolus then 0.25 mg/kg/hr IV for NSTEMI/UA and for PCI 0.75 mg/kg IV bolus (0.5 mg/kg IV if already on therapy) then 1.75 mg/kg/hr for duration of procedure or 4 hours thereafter. Reduce infusion rate to 1 mg/kg/hr if GFR <30 cc/min.

  • Eptifibatide 180 mcg/kg IV twice followed by 2 mcg/kg/min IV; reduce to 1 mcg/kg/min if GFR is <50 cc/min

  • Tirofiban 0.4 mcg/kg/min for 30 minutes then 0.1 mcg/kg/min; 0.2 mcg/kg IV bolus and 0.05 mcg/kg/min for patients with GFR <30 cc/min

  • Abciximab 0.25 mg/kg IV bolus then 0.125 mcg/kg/min (up to 10 mg/min)

IV. Management with Co-Morbidities

Patients with impaired renal function, elderly patients, and women are at increased risk of bleeding complications from overdosing of medications and from invasive procedures. These patients should have close attention to dose adjustment, appropriate use of medications, and the appropriate use of invasive therapies.

Patients should also be counseled on the importance of dual antiplatelet therapy to prevent recurrent MI and to prevent stent thrombosis if a stent was implanted during PCI. Patients should be counseled regarding the the importance of lifestyle modification of risk factors as well as medical therapy for secondary prevention. In particular, patients with ACS should be counseled on smoking cessation and the importance of exercise in addition to compliance with diet and prescribed medical therapy to improve secondary prevention.

V. Patient Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Patients with ACS are often started on multiple medications. Appropriate patient education regarding the utility of each of these medications, anticipated side effects, and dangers of discontinuation should be emphasized. Patients should be counseled regarding what types of symptoms require reevaluation and follow-up with a cardiologist. The patient should be referred for cardiac rehabilitation.

B. What's the Evidence for specific management and treatment recommendations?

"2011 ACCF/AHA Focused Update incorporated into the ACC/AHA 2007 guidelines for management of unstable angina/non-ST-elevation myocardial infarction". Circulation. vol. 123. 2011. pp. e426-e579.

"Primary and secondary prevention of cardiovascular disease: Antithrombotic therapy and management". Chest. vol. 41. 2012. pp. e637S-e668S.

Bavry, AA, Kumbhani, DJ, Rassi, AN. " Benefit of early invasive therapy in acute coronary syndromes: A meta-analysis of contemporary randomized clinical trials". J Am Coll Cardiol. vol. 48. 2006. pp. 1319-25.

C. DRG Codes and Expected Length of Stay.

DRG 303 Coronary Artery Disease with Unstable Angina

DRG 280 Acute MI discharged alive with major CC

DRG 281 Acute MI discharged alive with CC

DRG 282 Acute MI discharged alive without MCC/CC

DRG 283 Acute MI expired with major CC

DRG 284 Acute MI expired with CC

DRG 285 Acute MI expired without MCC/CC

Expected length of stay for uncomplicated ACS ranges from 1 day or longer depending upon the presence or absence of complications of therapy or the disorder.

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I. Problem/Condition

Overview, presentation, and pathophysiology

Acute coronary syndrome (ACS) is the term applied in the setting of suspected myocardial ischemia based on symptoms, abnormalities on the EKG (electrocardiogram), and levels of serum markers of cardiac injury. There are three types of ACS which are classfied by electrocardiogram (EKG) and biomarkers of myocardial injury. The three types of ACS includes ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI) and unstable angina (UA).

NSTEMI and UA are frequently indistinguishable on initial evaluation, however, they are differentiated by the presence or absence of biomarker elevation. Unstable angina (UA) is considered in patients with symptoms suggestive of ACS without elevated in biomarkers with or without EKG changes. Non-ST elevation MI (NSTEMI) by definition has elevation of biomarkers suggesting myocardial injury along with ST depressions and/or T wave inversions without ST segment elevations or pathologic Q waves. ST-elevation MI (STEMI) is distinguished by new ST elevation in contiguous leads or new left bundle branch block (LBBB) and those with a true posterior MI. These three entities encompasses the term acute coronary syndrome. Nondiagnostic initial EKG is frequently seen and repeated EKG is recommended in patients suspected of having ACS. Of note, certain clinical conditions such as LBBB or paced rhythm will interfere with interpretation of EKG. Troponin is the preferred marker for the diagnosis of myocardial injury for diagnostic categories discussed because of its increased specificity and sensitivity over CK-MB. Keep in mind negative troponin assay at the time of presentation does not exclude the possibility of myocardial injury. Most patients will become positive within 8 hours.

The clinical presentation of STEMI, NSTEMI and UA can be similar. Classically, the chest discomfort is described as a pressure-like or squeezing sensation with radiation to the shoulder, neck, jaw, or arms. The discomfort may be associated with nausea, vomiting, dyspnea, and diaphoresis. Unstable angina does have additional characterization described as angina of new onset, rest angina lasting longer than 20 minutes, or increased frequency of angina (crescendo angina). Certain subgroups - females, diabetics and the elderly - may have atypical clinical symptoms of ACS. Rather than chest discomfort, they may describe dyspnea, syncope, weakness, fatigue, or epigastric discomfort that are angina equivalents in retrospect.

Pathophysiology: ACS generally involves rupture of an atherosclerotic plaque in a coronary artery and subsequent thrombus formation. The thrombus occludes or partially occludes the artery. The degree and duration of obstruction, amount of myocardium involved and compensatory mechanisms all affect the final outcome. In some situations, other mechanisms, such as increased physiologic demands (e.g., anemia, tachyarrhythmia, hemorrhage, cocaine) on the myocardium, rather than plaque rupture, can lead to ACS.

II. Diagnostic Approach

A. What should be in the differential diagnosis?

There are a number of differential diagnoses to be considered when a clinician is evaluating a patient with a suspected ACS. These can be classified by organ systems.


With respect to other cardiac disease diagnoses, aortic dissection, pericarditis, left ventricular aneurysm, and early repolarization are all diagnoses that should be considered.


Gastrointestinal diseases often present with symptoms that can mimic ACS. Disorders involving the esophagus, stomach, biliary system, and pancreas such as esophageal spasm, esophageal rupture, penetrating peptic ulcer, gastrointestinal reflux disease (GERD), cholelithiasis, cholecystitis, and pancreatitis can manifest as with symptoms resembling ACS.


Pulmonary diseases such as a pulmonary embolism or pneumothorax can present with symptoms that can be mistaken for ACS. In particular, it is critical not to overlook these two diseases in the diagnostic process given the potential for life-threatening consequences.


While musculoskeletal disorders characteristically have reproducible pain with palpation or movement, which allows for some differentiation from ischemic pain, it is important to still consider ACS even if the initial assumption is a musculoskeletal etiology. Common musculoskeletal disorders in the differential diagnosis include costochondritis, rib fracture, toothache, and arthritis.


Neuropathic pain, cervical disc diseases and herpetic neuralgia related to zoster are neurologic etiology to consider in the differential diagnosis of ACS.

B. Describe a diagnostic approach/method for ACS.

Initial diagnostic and management approach to acute coronary syndrome

The main goals in the initial approach to a patient with chest discomfort and potential ACS should be to:

  1. Assess the likelihood of ACS versus other diagnoses (see questions below).

  2. Do a risk stratification if ACS is still suspected (use thrombolysis in myocardial infarction (TIMI) risk score).

  3. Choose the pathway of either STEMI versus UA/NSTEMI (use institutional protocols and pathways).

  4. Initiate appropriate treatment (even before biomarker results).

These steps should be performed quickly and thoroughly, utilizing established institutional protocols and order sets.

1. Historical information important in the diagnosis of this problem

When evaluating a patient with suspected ACS it is important to perform quick and focused history and physical. Following are questions which are important in initial evaluation of patients suspected of having ACS.

General symptom characteristics questions including onset, location, duration, characteristic, exacerbating and relieving factors as well as any associated symptoms of the complaint.

Risk factor assessment particularly cardiac risk factors which include history of tobacco use, cocaine use, hypertension, hyperlipidemia, diabetes and family history of pre-mature heart disease (Male before 55 years old (yo), Female before 65 yo).

Physical Examination should first evaluate airway, breathing, and circulation. Assessment of hemodynamic status, screening neurologic exam should be done especially if thrombolytic therapy is needed.

During this part of the evaluation it is necessary to address other potential life threatening conditions such as acute aortic dissection, pulmonary embolism, tension pneumothorax, perforating peptic ulcer, or esophageal rupture.

Next, obtain EKG, place resuscitation equipment at bedside, attach patient to cardiac monitor, oxygen as necessary, obtain blood work and intravenous (IV) access. Administer aspirin, nitrate, and morphine (unless contraindicated).

All patients with suspected ACS should undergo evaluation with an EKG, cardiac biomarkers such as troponin I/T and/or creatine kinase, muscle, brain (CKMB), a chest radiograph, as well as routine labs such as a complete blood count (CBC), a chemistry panel, coagulation studies, and a fasting lipid panel.


An EKG should be obtained within 10 minutes of symptom presentation. With ACS, the EKG can have a variety of presentations ranging from normal to dramatic ST segment elevation. The diagnostic criteria for a STEMI are gender specific and listed below.

New ST segment elevation at the J point in two contiguous leads:

  • >0.1 millivolts (mV) in all leads other than leads V2-V3.

  • For leads V2-V3

    • ≥ 0.25 mV in men <40 years old

    • ≥ 0.20 mV in men >40 years old

    • ≥ 0.15 mV in women

In addition two other groups of patients with an ACS are considered to have an STEMI: those with new or presumably new LBBB and those with true posterior MI.


Troponin I or T are the preferred biomarkers in the diagnostic process of ACS due to their high specificity and sensitivity. Serial measurements of these biomarkers should be done after the first sample is obtained. The International Joint Task Force recommends a repeat draw within 6-9 hours with a third draw between 12 and 24 hours if suspicion remains high. However, if a myocardial infarction is occurring, most often the troponin level will be elevated in the first 2-3 hours.

The biomarkers should demonstrate the typical rise and fall pattern and at least one value should be above the 99th percentile of the upper range limit for a diagnosis of STEMI or NSTEMI. It should be noted that troponin values could remain elevated for 1-2 weeks after a myocardial infarction.

The other biomarker option is the CKMB. Like the troponins, serial measurements along with a rise and fall pattern plus a value above the 99th percentile of the upper range limit are necessary for the diagnosis of STEMI or NSTEMI.

Chest radiograph

A chest radiograph should also be performed to look for pulmonary edema accompanying ACS. The chest x-ray is also valuable in evaluating other critical differential diagnoses such as aortic dissection - which may show a widened mediastinum - or a pneumothorax.


While the history, EKG and biomarkers are the pillars of diagnosis of ACS, echocardiography may play a role in select situations. If there is a high suspicion for a myocardial infarction but the EKG is without acute changes, and biomarkers are still pending, an echocardiogram performed at this juncture can be used to look for new wall motion abnormalities, which would indicate an acute myocardial infarction (AMI) by the new universal definition.

However, if biomarkers are not elevated, they take precedence over the imaging findings. The American College of Cardiology has given a class I recommendation for the use of an echocardiogram to diagnose AMI when not obvious by standard tests but it does NOT recommend echocardiograms for diagnosis when diagnosis is clear by usual tests.

C. Criteria for classifying diagnosis:

Criteria for diagnosis of ST elevation myocardial infarction

  • Clinical context compatible with ACS

  • EKG

    • ST segment elevation or

    • New left bundle branch block (LBBB)

  • Elevated biomarkers that rise and fall in typical pattern

Criteria for diagnosis of non-ST elevation myocardial infarction

  • Clinical context compatible with ACS

  • EKG:

    • Normal or

    • ST segment depression or T wave inversions or non-specific changes

  • Elevated biomarkers that rise and fall in typical pattern

Criteria for diagnosis of unstable angina

  • Clinical context compatible with ACS

  • EKG:

    • Normal or

    • ST depression, T wave inversions or non-specific changes

  • Negative biomarkers

D. Over-utilized or “wasted” diagnostic tests associated with the evaluation of this problem.

With the new troponin assays, serum markers, such as myoglobin and lactate dehydrogenase (LDH), which were previously used in the diagnosis of ACS/AMI, are usually unnecessary. They are neither specific nor sensitive compared to the troponins. However, because myoglobin rises very rapidly and returns to normal rapidly, they could be useful in evaluating recurrent chest pain after an AMI when troponin and CKMB levels are still elevated.

Other markers such as C-reactive protein (CRP), lipoprotein A and homocysteine have a relationship to coronary artery disease but are not part of the standard set of tests recommended in clinical guidelines.

III. Management:

A. Management of acute coronary syndrome

In evaluating a patient with a suspected ACS, there are a number of steps that should be undertaken immediately and simultaneously.

  • Obtain a focused history to gain key and relevant information. Use the questions listed in section II.B to query the patient on general symptoms, risk factors, contraindications to thrombolysis, TIMI, and other miscellaneous but relevant questions.

  • Complete an urgent EKG within 10 minutes of symptoms and while you are eliciting responses to the above questions.

  • Place the patient on continuous cardiac and oxygen monitoring.

  • Do a brief physical exam and obtain blood pressure in both arms to screen for a dissecting aortic aneurysm.

  • Obtain or ensure adequate intravenous (IV) access is available.

  • Order labs including troponin I or T, CKMB, a lipid profile, CBC, chemistry panel, coagulation profile, and a chest X-ray.

  • Repeat the EKG in 10 minutes if the first EKG is non-diagnostic and suspicion is still high for a ACS.

    • Do a right-sided EKG if an inferior myocardial infarction is suspected.

  • If the EKG shows ST segment elevation and suspicion for ACS is still high activate cath lab:

    • Give aspirin 162-325 milligrams (mg) orally or rectally, oxygen and nitroglycerin (NTG) - if no contraindication exists for NTG (e.g., aortic dissection, right ventricular infarction or recent use of phosphodiesterase inhibitors such as sildenafil).

    • Give morphine as needed for pain.

    • Beta blocker should be started within 24 hours if no contraindication exists.

    • Statin therapy (atorvastatin 80 mg) should be initiated.

    • Start P2Y12 receptor blocker.

    • Anticoagulation should be started.

    • Consider percutaneous coronary intervention (PCI) within 90 minutes of arrival Or a thrombolytic therapy within 30 minutes of arrival if symptom onset within 12 hours for patients who cannot receive PCI within 120 minutes.

    • Consult cardiology immediately.

    • If the troponins are elevated, this is a STEMI.

    • Coronary artery bypass graft (CABG) if failure of fibrinolysis and PCI.

  • If there is no ST segment elevation on EKG and suspicion is still high for ACS:

    • Give aspirin 162-325 mg orally or rectally, oxygen and NTG - if no contraindication exists for NTG (e.g., aortic dissection, right ventricular infarction or recent use of phosphodiesterase inhibitors such as sildenafil).

    • Start P2Y12 receptor blocker.

    • Give morphine as needed for pain.

    • Beta blocker should be started with in 24 hours if no contraindication exists.

    • Statin therapy (atorvastatin 80 mg) should be initiated.

    • Anticoagulation should be started.

    • If the cardiac biomarkers are elevated, this is an NSTEMI.

      • Consult cardiology for possible early invasive strategy in moderate to high-risk patients.

    • If the troponins are NOT elevated, then diagnosis is possibly unstable angina (UA).

      • Consider a cardiology consult for possible early invasive strategy in moderate to high-risk patients.

Of note; cocaine associated chest pain and MI should be managed in a manner similar to other ACS with two caveats; benzodiazepine should be administered early, beta blocker should not be used in acute cocaine intoxication as this can exacerbate coronary artery vasoconstriction.

See the "ST elevation myocardial infarction" and "Non-ST elevation myocardial infarction" chapters for further management steps.

B. Common Pitfalls and Side-Effects of Management of this Clinical Problem

Pitfalls in the diagnosis of ACS can occur anywhere in the process but often occur in several key places - namely the clinical context or presentation, the EKG interpretation and the troponin interpretation.


An acute coronary syndrome can present in a variety of ways, which can lead to uncertainty and delay in appropriate care. The classic symptoms of pressure-like chest discomfort with radiation down the left arm along with nausea, diaphoresis and dyspnea may not be present. Some patients may have no chest pain at all.

Others may have symptoms that suggest a gastrointestinal or musculoskeletal etiology. Therefore a high degree of suspicion should be maintained in all patients with chest pain or potential anginal equivalents. Additionally, certain subgroups - females, the elderly, diabetics, and even the young - can present in an atypical manner leading to mistriage and misdiagnosis.

It is critical to consider life-threatening diagnoses such as aortic dissection in any patient with chest discomfort. Using thrombolytic therapy in this situation could lead to fatal outcomes.

Response to medications - a GI cocktail or nitroglycerin - does not differentiate between cardiac versus non-cardiac etiology and should not be used to triage patients.


The EKG may be misinterpreted especially when there is ST segment elevation. The misread can be either a false positive or false negative EKG for STEMI. Clinical conditions that can lead to misinterpretation are listed below.

  • Acute pericarditis or myocarditis

  • Left ventricular hypertrophy (LVH)

  • Early repolarization

  • Hyperkalemia

  • LBBB

  • Wolf Parkinson White (WPW) syndrome

  • Brugada syndrome

  • Subarachnoid hemorrhage

  • Cholecystitis

  • Transposition of leads

  • Misinterpretation of the J point displacement

  • Left bundle branch block

  • Paced rhythm

  • Chronic ST elevation

  • Old myocardial infarction with Q waves


Troponins are easily misinterpreted as they can occur in other cardiac and non-cardiac conditions.

Troponin elevation in other cardiac conditions (besides ST elevation myocardial infarction and non-ST elevation myocardial infarction)

  • Congestive heart failure

  • Aortic dissection

  • Ventricular aneurysm

  • Pericarditis/myocarditis

  • LVH

  • Cardiac trauma

  • Cardioversion and defibrillation

  • Hypertrophic cardiomyopathy (HCM)

  • Arrhythmias (tachycardia and bradycardia)

  • Heart block

  • Takotsubo

  • Infiltrative diseases

  • Inflammatory diseases

  • Drugs and toxins

Troponin elevation in non-cardiac conditions

  • Pulmonary diseases

    • Pulmonary embolism

    • Pulmonary hypertension (HTN)

  • Renal failure

  • Sepsis

  • Neurological diseases:

    • Cerebrovascular accident

    • Subarachnoid hemorrhage

  • Burns

  • Extreme exertion

Drugs and dosages used in the management of acute coronary syndrome

The purposes of the medications used in the initial treatment of ACS are to relieve pain and to restore blood flow to the coronary artery. The ultimate intent is to save as much myocardium as possible by halting thrombus formation via inhibition of platelet activation and aggregation.

See for an overview of the options for medication classes and drugs commonly used in ACS. Other medication classes/drugs may be available and all options and contraindications must be taken into consideration before prescribing medications in ACS.

Table I.

Medications commonly used in acute coronary syndrome
Drug Name ClassRouteDose Comments
Aspirin (ASA)AntiplateletPO or rectal162-325mgReduces mortality
Clopidogrel AntiplateletPO75mgUse if ASA allergy
Oxygen OxygenNC or face mask2-4 L NCKeep pulse oximetry ≥90%
NTG NitratesSL, topical, or IV0.4mg SL every 5 minutes x 3 PRN chest pain; 0.5-2 inch topical; start 5mcg/min IV and titrate to pain reliefContraindicated in systolic BP <90mmHG, right ventricular infarction or use of phosphodiesterase inhibitor in past 24 - 48 hours.
MorphinePain medicationIV1-4mg IV
MetoprololBeta-blockerPO or IV5mg IV25mg POReduces mortality;avoid in cocaine-related ACS, hypotension
HeparinAnticoagulant;unfractionated heparinIVSTEMI: 12 units/kg/hour IV; start 60 units/kg IV x1; max: 4000 units/bolus; 1000 units/hourNSTEMI: 12-15 units/kg/hour IV: 60-70 units/kg IV x1; max 5000 unit bolus;1000 units/hourGoal PTT 50-70 seconds
EnoxaparinAnticoagulant;LMWHIV orSC1mg/kg SC every 12 hoursAdjust dose further for weight and creatinine clearance less than 30ml/min.
TNKaseThrombolyticagentIV30-50mg IV x 1 based on weightUse in STEMI if unable to do PCI.Goal door to drug time is 30 minutes.Improves mortality. Review inclusion criteria and contraindications.
LisinoprilACE-inhibitorPO5mg PO dailyTitrate and start within 24 hours, especially if EF <40%
ValsartanARBPO80-320mg PO daily For ACE-inhibitor intolerant
Eptifibatide Glycoprotein IIb/IIa receptor antagonistIVACS: Start: 180mcg/kg IV bolus, then begin infusion, 2mcg/kg/min IV. Max: 22.6mg/bolus; 15mg/hour infusionFor PCI patients:Infuse up to 96 hours. Infuse 18-24 hours post-procedure.Non PCI patients:Infuse up to 72 hours. May use with ASA and heparin.
Atorvastatin StatinPO80mg daily

Antman, EM, Cohen, M, Bernink, PJLM. "The TIMI Risk Score for Unstable Angina/Non-STEMI". JAMA. vol. 284. 2000. pp. 835-842.

Hillis, LD, Lange, RA. "Optimal Management of Acute Coronary Syndromes". NEJM. vol. 360. 2009. pp. 2237-2240.

Kumar, A, Cannon, CP. "Acute Coronary Syndromes: Diagnosis and Management, Part I". Mayo Clin Proc. vol. 84. 2009. pp. 917-938.

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