I. Chest pain: What every physician needs to know.

The evaluation and management of the patient with chest pain syndrome is a diagnostic challenge to all who practice emergency medicine. “Chest pain syndrome” is inclusive of symptoms that may be caused by acute myocardial ischemia and includes such diverse complaints as chest pain, chest pressure, neck pain, jaw pain, shoulder pain, epigastric pain, back pain, palpitations, dyspnea, cough, nausea, weakness and malaise, or dizziness.

In the U.S. alone, over 5 million patients present to the emergency department (ED) with the chief complaint of “chest pain,” the majority of whom are found to have a noncardiac cause for their symptoms (over 55%). The proportion of patients with other complaints who subsequently prove to have an acute coronary syndrome (ACS) is certainly much lower, but knowledge of this may only add to the concerns of the clinician determined not to overlook a case amongst the vast number of candidates

In fact, over 5% of all ED visits are due to chest pain-related complaints. Despite significant investigation into risk stratification scores and a multiplicity of proposed diagnostic algorithms and testing strategies, upwards of 2% of chest pain syndrome patients will be discharged home and be subsequently diagnosed with an acute myocardial infarction within 1 week. For this reason, patients who present to the ED with the complaint of “chest pain” or related complaints should receive triage priority with minimal time delay to evaluation and 12-lead electrocardiography.

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The differential diagnosis of chest pain syndrome is broad and disparate, including disease processes that range from nonurgent to life threatening. Furthermore, within the consideration of life-threatening causes, patients may be suffering from coronary causes, as well as pulmonary embolism, aortic dissection, aortic rupture, pneumothorax, or even esophageal rupture. There are many other diagnoses that are much less time critical, but as diverse as widely as musculoskeletal pain, zoster, pleurisy, pneumonia, or gastroesophageal reflux. Treating all these patients as time critical is necessary until emergent causes of chest pain are excluded.

The common pathophysiology associated with symptoms arising from acute coronary syndrome is decreased myocardial perfusion secondary to occlusive disease of the coronary artery(ies), resulting in reduced oxygen supply to the myocardium. Acute coronary syndrome encompasses ST segment elevation myocardial infarction (STEMI), non-ST segment elevation MI (NSTEMI), and unstable angina (UA).

Unstable angina can include anginal symptoms that occur at rest, are of new onset, or symptoms that are more frequent or longer in duration, but need not include suggestive changes on the electrocardiogram (ECG). Likewise, NSTEMI may present with minimal or no ECG changes, but by definition involves elevated levels of enzymes indicative of myocardial necrosis. STEMI is, as the name implies, an electrocardiographic diagnosis, and the search for it mandates the early ECG (within 10 minutes of ED presentation) now viewed as a universal indicator of quality care.

II. Diagnostic Confirmation: Are you sure your patient has a chest pain?

Symptoms of chest pain syndrome can be quite vague. The practitioner must ask pertinent questions of the patient in order to characterize the pain. How would you describe the pain? Is it dull or aching, sharp or tearing? Where is the pain located? Is it substernal or more specific to one side of the chest? Are there any exacerbating or alleviating factors? Does pain improve when you lean forward, or does it worsen when you take a deep breath?

Chest pain can also be confused with abdominal pain, especially if it is epigastric or higher in the upper abdominal quadrants. The clinician should always keep in mind that presentations may be “classic,” “atypical,” or intermediate between those arbitrary classifications. Patients with chest pain syndrome should be evaluated rapidly to determine the etiology of their pain. Key interventions that should occur in a time-critical fashion are ECG and a focused history and physical examination. Unless the patient is rushed to the cardiac catheterization laboratory on the basis of these three elements, a chest radiograph should also be obtained quickly.

A. History Part I: Pattern Recognition:

ACS is divided into STEMI or non-ST segment elevation-ACS, the latter of which includes NSTEMI and UA.

Key signs and symptoms of acute coronary syndrome:

1. Chest pain (when present)

  • Usually described as burning, pressure, or tightness
  • Usually located substernal or in the left chest
  • Can be reproducible

2. Pain radiating elsewhere

  • Referred pain to the arm(s), back, neck, or jaw

3. Nausea, vomiting, or unexplained indigestion

4. Vomiting

5. Dyspnea

6. Other symptoms may occur in the absence of chest pain, including these, palpitations, dizziness, and malaise. These “atypical” presentations are more common in females, the elderly, and diabetics.

B. History Part 2: Prevalence:

Traditionally, the most important risk factors for ischemic cardiovascular disease are:

1. Diabetes

2. Hypertension

3. Tobacco use

4. Hypercholesterolemia

5. Family history of cardiovascular disease, especially at a young age (<40 years)

  • Traditional cardiac risk factors are considered poor predictors of clinical outcomes for MI and ACS when recognized in the ED. These factors are poorly predictive of ACS in female patients, and diabetes and family history proved to be weakly predictive in male patients.
  • Traditional risk factors were derived from population-based longitudinal studies, and not a symptomatic ED chest pain cohort. Therefore, the fact that ED patients are symptomatic outweighs the positive predictive value of traditional cardiac risk factors.

Patients who are at high risk for developing complications of NSTE-ACS (non-ST elevated-ACS) can be identified via various risk stratification tests.

The Thrombolysis in Myocardial Infarction (TIMI) risk score is a tool that can be used to determine a patients risk for mortality, ischemia, or need for urgent intervention within 14 days. The score has been tested and validated as a good predictor of adverse outcome. The score is composed of seven elements:

1. Age >= 65 years

2. More than three risk factors for ischemic cardiovascular disease

3. Known ischemic cardiovascular disease

4. Aspirin use in the last 7 days

5. Two episodes of severe angina in the last 24 hours

6. ST segment changes >= 0.5 mm

7. Positive troponin

Score interpretation: risk of 14-day all-cause mortality, new or recurrent MI, severe recurrent ischemia requiring revascularization:

0-1 = 4.7% risk

2 = 8.3% risk

3 = 13.2% risk

4 = 19.9% risk

5 = 26.2% risk

6-7 = 40.9% risk

Other quantitative risk stratification tools for NSTE-ACS that have been validated are the Global Registry of Acute Coronary Events (GRACE) risk score and the Platelet glycoprotein IIb/IIIa in Unstable angina: Receptor Suppression Using Integrilin (PURSUIT) risk score. These two risk scores were compared to the TIMI risk score and neither was found to be a better predictor of death, MI, or 30-day revascularization.

The GRACE score (note these components carry different statistical weights, unlike the components in the TIMI Risk Score; the score can be calculated using an online calculator – www.outcomes-umassmed.org/grace.)

1. Age

2. Heart rate

3. Killip class

4. Creatinine

5. Cardiac arrest at admission

6. ST segment deviation

7. Elevated cardiac enzyme

The PURSUITscore (note these components carry different statistical weights, unlike the components in the TIMI risk score)

1. Age

2. Gender

3. Heart rate

4. Systolic blood pressure

5. Worst Canadian Cardiovascular Society anginal class score

6. Presence of rales

7. ST segment depression

C. History Part 3: Competing diagnoses that can mimic Chest Pain.

Chest pain: differential diagnosis, common presenting symptoms, and physical examination (PEX) findings

Pulmonary embolism – Patients typically present with pleuritic chest pain and shortness of breath, and may have evidence of a concomitant deep vein thrombosis. Hemoptysis is an inconsistent finding.

  • PEX: tachycardia and tachypnea

Aortic dissection – Patients often describe a tearing chest pain that radiates into the back between the scapular spines. Often patients will exhibit a neurologic deficit or complaint at or below the level of the aortic injury.

  • PEX: unequal blood pressure in opposing arms, new cardiac murmur

Pericarditis – Patients often describe an aching, positional chest pain that can be associated with dyspnea

  • PEX: cardiac rub, distended neck veins

Pneumothorax – Patients often describe pleuritic chest pain with associated dyspnea.

  • PEX: Breath sounds will be notably unequal and diminished; tension physiology may result in distended neck veins and hypotension.

Pneumonia – Patients often describe pleuritic chest pain with associated cough, chills, and shortness of breath.

  • PEX: fever, rhonchi, decreased breath sounds

Esophageal rupture – Patients often present with retrosternal or epigastric pain. There is usually an inciting event, such as excessive vomiting, or rarely, blunt chest trauma.

  • PEX: variable and nonspecific

D. Physical Examination Findings.

Physical examination findings can be varied and nonspecific for the symptomatic patient with chest pain.

  • The physical examination can be useful in identifying patients who clearly have noncardiac etiologies to their chest pain.

Patients with ACS may have:

  • Bradycardia, tachycardia, Irregular rhythms
  • Blood pressure may be normal, elevated, or decreased
  • Heart sounds can be diminished
  • An S3 is apparent in 15% to 20% of patients and may predict myocardial failure
  • An S4 may be appreciated in patients with longstanding hypertension
  • Rales may be auscultated on pulmonary examination, indicating left ventricular dysfunction
  • Jugular venous distention, hepatojugular reflex, and pulmonary edema may indicate right-sided dysfunction
  • Findings on examination must be correlated to baseline examinations to determine which are acute and may be due to ACS

E. What diagnostic tests should be performed?

The electrocardiogram (ECG) is critical to making the cardiac diagnosis. The following syndromes have specific ECG findings.

  • ST segment elevation myocardial infarction
  • Dysrhythmia
  • Pulmonary embolism
  • Acute pericarditis
  • Nonspecific findings of ischemia, such as ST segment depression or T-wave inversion, confer higher risk on NSTE-ACS patients but are not necessary for the diagnosis of either UA or NSTEMI.

Chest radiography may help to identify the etiology of symptoms of chest pain syndrome.

  • Mediastinal widening or air (aneurysm, dissection, esophageal injury)
  • Infiltrate (pneumonia)
  • Pneumothorax
  • Pleural or pericardial effusion (infectious, oncologic, etc.)

Complete blood count

Basic metabolic panel

Coagulation studies

Blood type


  • May have utility in certain patients who present with symptoms concerning for PE

Blood cultures

  • Should be obtained in the patient with a suspected infectious etiologies to chest pain

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

Myocardial biomarkers
Creatinine kinase

Intracellular enzyme found in high quantity in skeletal and myocardial muscle.

  • CK-MM is dominant in skeletal muscle cells (although CK-MB is also found here)
  • CK-MB is found more commonly in the myocardium (although CK-MM remains the predominant isoenzyme):
  • CK-MB in the blood elevates 4 to 8 hours after coronary artery occlusion
  • Peaks between 12 to 24 hours after injury
  • Returns to normal between 3 to 4 days after injury

CK-MB can be used as a test for myocardial cell death, but does not turn positive rapidly after onset of symptoms and is also commonly found in other sites so it is not specific to the myocardium.

Myoglobin Protein found in muscle cells, and when muscle is injured this protein is rapidly released into the blood. Myoglobin is not specific to cardiac muscle and can be elevated after physical exertion.

After myocardial infarction serum levels:

  • Rise rapidly, within 3 hours of injury
  • Peak within 4 to 9 hours of injury
  • Degrade within 24 hours of injury

Therefore, myoglobin is sensitive in early MI but will give false negative results if applied as a test at 24 hours after the insult.


  • Main regulatory protein of the thin filament in myofibrils
  • Troponin I not found in skeletal muscle, therefore it is very sensitive to myocardial injury

Troponin I and Troponin T:

  • Become elevated within 6 hours of myocardial injury
  • Peak at 12 hours
  • Remain elevated for 7 to 10 days after injury

Troponins have a high sensitivity and specificity for myocardial injury in the ED, although they may be falsely elevated in patients with renal failure due to bioaccumulation of minute amounts.

Myocardial markers in the ED are useful to:

  • Rule patients in for acute myocardial infarction
  • Identify unrecognized acute myocardial infarction in patients with atypical symptoms
  • Risk stratify patients
  • Rule patients out in an observation setting

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


Can identify diagnosis such as pericardial effusion and cardiac tamponade, and can identify wall motion abnormality when the patient is having active ischemia.

Cannot distinguish timeframe of findings

Can be useful in risk stratification and management

Exercise stress testing

Common test applied in many observation units to risk stratify chest pain patients.

Often used on low-risk patients in the “rule out” process after bioenzymes are found not to be elevated.

Coronary computed tomographic angiography (CCTA)

Currently limited to the low-to-intermediate-risk patient who is being evaluated for coronary artery disease

Assess for evidence of coronary artery disease in a noninvasive manner

Can be used to evaluate low-risk patients in the ED and determine safety for discharge to home without further evaluation/observation.

III. Management.

All chest pain patients should have intravenous access obtained, and be placed on a cardiac monitor with supplemental oxygen via nasal cannula.

Treatment of cardiac chest pain

Patient with chest pain syndrome, who do not meet criteria for ACS:

  • Sublingual nitroglycerin may be given in the treatment of painful symptoms; resolution of symptoms does not infer a diagnosis of myocardial ischemia, nor does a lack of relief infer an alternative diagnosis.
  • Oxygen (2 to 4 L via nasal cannula)
  • Aspirin 325 mg PO
  • Pain control (morphine 2 to 5 mg IV q5 to 15 min)

The goal of management in confirmed ACS is to establish reperfusion and limit ischemic injury. Medical management is aimed at decreasing myocardial perfusion demand and preventing the worsening of obstruction.

  • Sublingual nitroglycerin 0.5 mg q5 min × 3 (contraindicated in inferior wall MI)
  • Oxygen (2 to 4 L via nasal cannula)
  • Beta-blocker therapy should be initiated orally within 24 hours; IV beta-blockers are reserved for patients with refractory pain, hypertension, or tachycardia
  • Aspirin 325 mg PO
  • Pain control (morphine 2 to 5 mg IV q5 to 15 min)
  • Heparin (80 units/kg bolus, 18 units/kg/h infusion) or Enoxaparin (1 mg/kg q12 hr subcutaneously)

Patients with STEMI or persistent symptoms of a cardiac origin should be evaluated for emergent mechanical reperfusion or fibrinolytic therapy.

  • Percutaneous cardiac intervention (PCI) with angioplasty vs. stenting
  • Fibrinolytics
  • Clopidogrel (Plavix 600 mg PO)


  • Symptoms compatible with acute myocardial infarction
  • Time to treatment of 6 hours to 12 hours
  • EKG with at least 1 mm ST segment elevations in at least two contiguous leads
  • Interventional management is not available

Contraindications to therapy:


  • Previous hemorrhagic stroke at anytime
  • Cardiovascular accident (CVA or stroke) in the past year
  • Known intracranial neoplasm
  • Active internal bleeding (exclude menses)
  • Suspected aortic dissection
  • Diabetic retinopathy


  • Significantly elevated blood pressure (>180/100 mm Hg)
  • History of prior CVA
  • Current use of anticoagulants (with an INR >2-3)
  • Trauma within the past 2 weeks
  • Known bleeding diathesis
  • Prolonged cardiopulmonary resuscitation (>10 min)
  • Major surgery in past 3 weeks
  • Noncompressible vascular punctures
  • Recent internal bleeding (2 to 4 weeks)
  • Prior allergic reaction to fibrinolytic
  • Pregnancy
  • Active peptic ulcer disease
  • History of chronic severe hypertension


Streptokinase – 1.5 million units over 60 min

Alteplase – >67 kg: 100 mg; 15 mg initial IV bolus, 50 mg infused over next 30 min, 35 mg infused over next 60 min

<67 kg: 15 mg initial IV bolus, 0.75 mg/kg infused over next 30 min, 0.5 mg/kg infused over next 60 min; maximum dose 100 mg

A. Immediate management.

All critical ED patients should be evaluated in the same manner, ensuring that there Airway, Breathing, and Circulation is intact.

After resuscitation, if indicated, IV access, oxygen supplementation, and telemetry monitoring should be initiated.

All patients with a complaint of “chest pain” should have an ECG in a time critical fashion (initiated triage).

Initial management should be geared towards identifying the etiology of the chest pain complaint.

B. Physical Examination Tips to Guide Management.

All patients who present to the ED with a complaint of chest pain syndrome should be monitored on telemetry until a diagnosis is confirmed.

Myocardial ischemia can be associated with adverse events such as dysrhythmia and/or rupture of the papillary muscle, ventricular wall, or septum. It is very important for these patients to be continuously monitored, with frequent repeat focused physical examinations to ensure that they are not exhibiting signs of cardiac failure.

Hypotension may be indicative of rupture or cardiogenic shock. This alteration in a vital sign would need immediate attention by the ED physician or consultant cardiologist as these patients may require instrumentation in order to maintain their mean arterial pressure. In the setting of myocardial rupture, emergent cardiothoracic surgical consultation is warranted. A papillary muscle rupture may be noted by a new onset murmur with accompanied signs of pulmonary edema.

Hypertension should be managed to reduce pump and myocardial oxygen demand. For example, patients who continue to have pain symptoms or anxiety will remain hypertensive.

Tachycardia, like hypertension, may be due to catecholamine surge secondary to pain or anxiety. However, patients who suffer myocardial injury are prone to dysrhythmias, so it is imperative for the ED physician to evaluate any significant changes in rhythm to ensure that the patient does not require further intervention.

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

  • Cardiac markers should be evaluated in a serial fashion. There are a number of published pathways for determining the frequency of enzyme assays, but regardless, the time of symptom onset should be a factor, given that even with ultra-high-sensitivity troponin assays, levels may not be abnormal until at least 4 to 6 hours after cell death.
  • Patients initiated on anticoagulation (heparin) should have PTT levels monitored every 4 hours, as well as a complete blood count for hemoglobin levels

D. Long-term management.

Patients with chest pain require varying levels of care dependent upon their ED evaluation.

Low-risk chest pain: Patient without known coronary artery disease, and does not have an obvious acute myocardial injury

  • These patients should undergo further evaluation in an observation unit.
  • This evaluation should include repeat cardiac markers, repeat ECG, definitive testing to establish cardiac risk such as exercise or chemical stress test.

Moderate-risk chest pain:

  • These patients should be admitted to a non-ICU monitored setting, either a “step-down” unit or a telemetry unit.

High-risk chest pain:

  • These patients may require ICU level care.

E. Common Pitfalls and Side-Effects of Management

It is often difficult to identify patients who are sufficiently low risk for a cardiac event to be discharged to home. This is still a topic that is highly investigated and debated among experts in this field of medicine.

Anticoagulation: Patients should always be reassessed for bleeding events when maintained on these medications.

IV. Management with Co-Morbidities

Cocaine induced chest pain:

Management focuses on the reversal of coronary vasoconstriction, hypertension, and tachycardia. Initial management should be identical to the common complaint of chest pain with the following exceptions:

  • Benzodiazepine (diazepam 1 mg IV) – reduces the catecholamine surge associated with cocaine intoxication.
  • Beta-blocker use should be avoided; verapamil (calcium channel blocker) would be better suited in this situation.

Aspirin allergy:

Initial management should be identical to the common complaint of chest pain with the following exceptions:

  • Clopidogrel (Plavix 75 mg PO) can be used instead of aspirin in patients with a significant allergy.

Renal failure:

Patients with renal failure often have elevated troponin levels. Despite this finding, elevated troponin is a harbinger for adverse outcomes in end-stage renal disease patients.

V. Patient Safety and Quality Measures

A. Appropriate Prophylaxis and Other Measures to Prevent Readmission.

Patients with coronary artery disease should be counseled in the following treatments and lifestyle modifications:

Aspirin use – under the guidance of a primary care physician patients should be instructed to take daily aspirin

Blood pressure control – via various mechanisms such as medication, diet, and weight loss

Cholesterol control, cigarette smoking cessation

Diet – the American Heart Association issues dietary guidelines that are heart healthy.

Exercise – patients should be cleared by a primary physician before initiating an aggressive weight loss plan.

Patients discharged from the ED should be encouraged to follow up with their primary care physician in a timely manner. They should also be given strict return precautions should their symptoms return or worsen.

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

Most of the evidence for the initial management of STEMI comes from the most recent set of guidelines by the American Heart Association:

Antman, EM, Anbe, DT, Armstrong, PW. “ACC/AHA Guidelines for the management of patients with ST-elevation myocardial infarction—executive summary”. Circulation. vol. 110. 2004. pp. 588-636.

Aspirin therapy should be given to STEMI patients in the dose of 162 mg PO (Class I, LOE: A) to 325 mg PO (Class I, LOE: C). Oral beta-blocker should be administered to patients without contraindications (Class I, LOE:A)

Initial STEMI treatment should be initiated and selected by the emergency physician. Initiation of fibrinolytics should occur within 30 minutes of arrival; however, if PCI is selected the balloon should be up by 90 minutes after arrival at the hospital (Class I, LOE: B).

A 12-lead ECG should be performed and provided to a physician within 10 minutes of ED arrival (Class I, LOE: C). For patients with diagnostic ECG, reperfusion therapy should be initiated as soon as possible and is not contingent on biomarkers (Class I, LOE: C).

Most of the evidence for the initial management and treatment of UA/NSTEMI comes from the most recent set of guidelines by the American Heart Association:

Wright, RS, Anderson, JL, Adams, CD. “2011 ACCF/AHA focused update of the guidelines for the management of patients with unstable angina/non-ST-elevation myocardial infarction (updating the 2007 guideline)”. Circulation. vol. 123. 2011. pp. 2022-60.

If the diagnosis of NSTEM/UA is likely or definite:

Aspirin should be administered to UA/NSTEMI patients as soon as possible upon presentation to the ED (Class I, LOE: A).

Clopidogrel should be administered to UA/NSTEMI patients who have a severe GI intolerance to Aspirin (Class I, LOE: B).

Select management strategy:

Initial conservative strategy

Initiate anticoagulation therapy (Class I, LOE: A)

Enoxaparin or UFH (Class I, LOE: A), Fondaparinux (Class I, LOE: B)

Initiate clopidogrel (Class I, LOE: B)

Invasive strategy

Initiate anticoagulation therapy (Class I, LOE: A)

Enoxaparin or UFH (Class I, LOE: A), bivalirudin (Class I, LOE: B)

Add second antiplatelet agent (Class I, LOE: A)

Clopidogrel (Class I, LOE: B) or GP IIB/IIIa inhibitor (Class I, LOE: A)

After angiography: CABG, PCI, or medical therapy alone

Most of the evidence for the initial management of STEMI comes from the most recent set of guidelines by the American Heart Association:

ACC/AHA Guidelines for the Management

O’Gara, PT, Kushner, FG, Ascheim, DD. “2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines”. Circulation.. vol. 127. 2013. pp. 529-555.

Aspirin therapy should be given to STEMI patients in the dose of 162 mg PO (Class I, LOE: A) to 325 mg PO (Class I, LOE: C). Oral beta-blocker should be administered to patients without contraindication (Class I, LOE: A).

C. DRG Codes and Expected Length of Stay.

ICD-9 Codes: 410-414.99