Example Case Study Of Acute Coronary Syndrome

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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