Initial evaluation and management of suspected acute coronary syndrome (myocardial infarction, unstable angina) in the emergency department

INTRODUCTION — The clinical presentation of myocardial ischemia is most often acute chest discomfort. The goal of emergency department evaluation is to determine the cause of such discomfort or other related symptoms (eg, dyspnea, weakness) and to initiate appropriate therapy promptly. It is essential that initial assessment and management be rapid but methodical and evidence based.

Diagnostic evaluation emphasizes distinguishing between the following potential, life-threatening causes of chest pain:

●Acute coronary syndrome (ACS; myocardial infarction or unstable angina)

●Nonischemic chest pain, including potentially life-threatening conditions such as aortic dissection, pulmonary embolism, and esophageal rupture (table 1 and table 2A-B)

The diagnosis of acute coronary-related ischemia depends upon the characteristics of the chest pain (if present), specific associated symptoms, abnormalities on electrocardiogram (ECG), and levels of serum markers of cardiac injury. A patient with a possible ACS should be evaluated and treated rapidly. Thus, initial management steps must be undertaken before or during the time the diagnosis is being established.

The initial management of the patient likely to have an ACS will be reviewed here. Discussions of related subjects are found separately:

●(See "Evaluation of the adult with chest pain in the emergency department".)

●(See "Approach to the adult with dyspnea in the emergency department".)

●(See "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

●(See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".)

GUIDANCE AND RESOURCES FOR INSTITUTIONS — The American College of Cardiology (ACC) and the American Heart Association (AHA) recommend that all hospitals establish multidisciplinary teams to develop guideline-based, institution-specific written protocols for triaging and managing patients who present with symptoms suggestive of myocardial ischemia. The management of diagnosed ACS is discussed in detail separately. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes" and "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".)

Immediate cardiology consultation should be available for cases in which the initial diagnosis and treatment plan are unclear or are not addressed directly by available protocols. A number of life-threatening conditions can cause chest pain and dyspnea. It is important to avoid premature diagnostic closure. (See "Evaluation of the adult with chest pain in the emergency department" and "Approach to the adult with dyspnea in the emergency department".)

WHEN TO SUSPECT ACUTE CORONARY SYNDROME — Clinicians should consider the possibility of ACS in any adult who presents to the emergency department complaining of chest discomfort or dyspnea. A personal or family history of ACS or other cardiovascular disease, older age, diabetes, dyslipidemia, cigarette smoking, hypertension, or cocaine use all increase the likelihood. (See "Overview of established risk factors for cardiovascular disease".)

Characteristic presentations (as described below) heighten concern, but clinicians must keep in mind that many patients with ACS present with symptoms such as dyspnea or malaise, either alone or in addition to chest pain. Females are more likely to have associated dyspnea than males, and patients who are older or have diabetes are more likely to present with dyspnea without chest pain. (See 'Clinical presentation' below and 'Atypical presentations' below and "Clinical features and diagnosis of coronary heart disease in women" and "Silent myocardial ischemia: Epidemiology, diagnosis, treatment, and prognosis".)

Pain from coronary-related ischemia is more often characterized as non-focal chest discomfort or pressure rather than pain, is generally gradual in onset, and is exacerbated by activity. Discomfort that radiates, particularly to either or both arms, should increase suspicion for ACS.

IMMEDIATE EMERGENCY DEPARTMENT INTERVENTIONS — In the emergency department, patients presenting with chest pain or other symptoms possibly due to ACS (eg, dyspnea) should be rapidly evaluated to determine if their symptoms are suggestive of acute ischemia or some other potentially life-threatening illness. (See 'Clinical presentation' below and "Evaluation of the adult with chest pain in the emergency department" and "Approach to the adult with dyspnea in the emergency department".)

If ACS is the leading diagnosis, initial assessment and interventions must be performed rapidly. The attached algorithm provides a simple approach to risk stratification while the table provides a concise outline of the immediate interventions needed to manage ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (algorithm 1 and table 3).

During the initial assessment phase, the following steps should be accomplished for any patient at significant risk for ACS:

•Airway, breathing, and circulation assessed

•Preliminary history and examination obtained

•12-lead electrocardiogram (ECG) interpreted

•Resuscitation equipment brought to the bedside

•Cardiac monitor attached to patient

•Oxygen given as necessary

•Intravenous (IV) access and blood work (including high-sensitivity troponin, if available) obtained

•Aspirin 162 to 325 mg given

•Nitrates given (contraindications to nitrates include severe aortic stenosis, hypertrophic cardiomyopathy, suspected right ventricular infarct, hypotension, marked bradycardia or tachycardia, and recent use of phosphodiesterase 5 inhibitor [eg, Viagra])

Caution should be employed in evaluating possible ACS in older adults and patients with diabetes, who are more likely to present with symptoms such as dyspnea or weakness without chest pain even in the presence of acute coronary-related ischemia [1]. (See 'Atypical presentations' below.)

The institution's specific chest pain protocol should be implemented if the history or symptoms are suggestive of acute ischemia. The time for initial assessment, including ECG, and preliminary management of a patient with possible acute coronary-related ischemia is ideally 10 minutes from presentation. Large observational studies report that ECG acquisition is frequently delayed and that females are significantly less likely to be assessed within the recommended 10 minutes or to receive testing with a cardiac biomarker [2-4].

●Initial history and exam – Obtain a brief history and perform a focused physical examination. Important elements of the history include confirmation of the presenting symptoms, characteristics of the pain, exacerbating and alleviating factors, and important associated symptoms, past history of or risk factors for cardiovascular disease, and potential contraindications to thrombolytic therapy (table 4). (See 'Clinical presentation' below.)

The examination should include assessment of hemodynamic status and a screening neurologic examination, especially if thrombolysis is entertained as a potential therapy. (See 'Physical examination' below.)

The history should address other potentially life-threatening, noncardiac causes of chest pain, such as acute aortic dissection, pulmonary embolism, tension pneumothorax, perforating peptic ulcer, and esophageal rupture (table 2A-B). Until the diagnosis of ACS is established, the clinician should keep these diagnoses in mind. (See "Evaluation of the adult with chest pain in the emergency department".)

●Twelve-lead electrocardiogram – A 12-lead ECG should be obtained within 10 minutes of arrival in all patients with possible coronary-related ischemia. (See 'Electrocardiogram assessment' below.)

The 12-lead ECG provides an important basis for initial diagnosis and management and should immediately be shown to an emergency physician for interpretation. If the initial ECG reveals an STEMI, immediate intervention is required. STEMI management is discussed in detail separately. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy" and "Acute ST-elevation myocardial infarction: Management of anticoagulation" and "Acute ST-elevation myocardial infarction: Antiplatelet therapy".)

The initial ECG is often not diagnostic in patients with ACS. Thus, the ECG should be repeated at 15- to 30-minute intervals if the initial study is not diagnostic but the patient remains symptomatic and high clinical suspicion for ACS persists.

●Cardiac monitor – The patient should be placed on a cardiac monitor with emergency resuscitation equipment (including a defibrillator and airway equipment) nearby.

●Supplemental oxygen – Supplemental oxygen should be given as necessary to maintain oxygen saturation above 90 percent. (See "Overview of the acute management of ST-elevation myocardial infarction", section on 'Therapy for specific symptoms and syndromes'.)

●Intravenous access – IV access should be established and blood drawn for initial laboratory work, including cardiac biomarkers (contemporary or high-sensitivity troponin), basic electrolyte concentrations, renal function studies, and a complete blood count with platelets. Indices of coagulation should be obtained in patients at increased risk of coagulopathy due to warfarin or heparin use, a history of liver disease, or a history of excessive or spontaneous bleeding [5]. (See 'Cardiac biomarkers and other laboratory testing' below.)

●Aspirin – All patients with suspected ACS should be given aspirin in a dose of 162 to 325 mg to chew and swallow unless there is a compelling contraindication (eg, history of anaphylactic reaction) or it has been taken prior to presentation. Despite its well-demonstrated benefit, aspirin remains underutilized in the setting of ACS. (See "Aspirin for the secondary prevention of atherosclerotic cardiovascular disease".)

●Sublingual nitrates – In most cases of suspected ACS, sublingual nitroglycerin should be administered at a dose of 0.4 mg every five minutes for a total of three doses, after which an assessment of blood pressure and pain relief should guide the need for IV nitroglycerin.

Before this is done, all patients should be questioned about the use of phosphodiesterase-5 inhibitors, such as sildenafil (Viagra), vardenafil (Levitra), or tadalafil (Cialis); nitrates are contraindicated if these drugs have been used in the last 24 hours (or perhaps as long as 36 hours with tadalafil) because of the propensity to cause potentially severe hypotension. (See "Nitrates in the management of acute coronary syndrome" and "Sexual activity in patients with cardiovascular disease".)

Extreme care should also be taken before giving nitrates in the setting of an inferior myocardial infarction with possible involvement of the right ventricle (waveform 1). In this setting, patients are dependent upon preload to maintain cardiac output, and nitrates can cause severe hypotension. (See "Right ventricular myocardial infarction".)

Pain that responds to sublingual nitroglycerin is frequently thought to have a cardiac etiology or to be due to esophageal spasm. However, pain relief with nitroglycerin in an acute care setting is not helpful in distinguishing cardiac from noncardiac chest pain [6]. In a study of 459 patients who presented to an emergency department with chest pain and were admitted to the hospital, the percentage of patients who had relief of chest pain with nitroglycerin was similar among the 141 patients with ACS and the 275 patients without active coronary disease (35 versus 41 percent experienced relief) [7]. As such, nitroglycerin administration should not be given as a diagnostic test in patients with chest pain or a presentation that is not consistent with ACS, as the response to treatment may cloud the clinical picture. (See "Evaluation of the adult with chest pain in the emergency department".)

●Intravenous morphine sulfate – IV morphine sulfate (initial dose of 2 to 4 mg, with increments of 2 to 8 mg, repeated at 5- to 15-minute intervals) may be given for the relief of severe, persistent chest pain not relieved by other means but should not be given routinely. Morphine can reduce sympathetic stimulation caused by pain and anxiety, thereby decreasing cardiac workload and risks associated with excess catecholamines. However, morphine may worsen outcomes in patients with acute myocardial infarction.

DETERMINING WHO NEEDS AN ELECTROCARDIOGRAM — In general, a resting electrocardiogram (ECG) should be obtained in all adults with chest discomfort that does not have an obvious noncardiac cause. An ECG is also obtained routinely in older adults or patients with diabetes with symptoms of unclear etiology, such as dyspnea, nausea, or malaise; patients with syncope; and patients with symptoms or signs consistent with an arrhythmia. However, identifying at triage or early in the emergency department evaluation which younger adult patients should be evaluated with an ECG is occasionally difficult. Keep in mind that a substantial number of patients ultimately diagnosed with an ACS, particularly older patients and those with diabetes, present with complaints other than chest discomfort or do not manifest clear signs of ischemia in their initial ECG. Such presentations are discussed in detail separately. (See 'Atypical presentations' below and 'Importance of serial electrocardiograms' below.)

One research group has proposed the following rule for identifying patients at high risk for ST elevation myocardial infarction (STEMI) who should be evaluated with an ECG [8]:

●Any patient over 30 with chest pain

●Any patient over 50 with any of the following: dyspnea, altered mental status, upper extremity pain, syncope, or weakness

●Any patient over 80 with abdominal pain, nausea, or vomiting

This rule was derived and validated using information from over three million emergency department visits included in a state-wide health surveillance database. Included in the database were 6464 cases of STEMI diagnosed during 2007 to 2008 that provided the dataset for the study. When applied to the validation sample (3294 STEMI cases), the rule had a sensitivity of 91.9 percent (95% CI 90.9-92.8) and a specificity of 76.2 percent (95% CI 76.1-76.2).

This proposed rule should not replace clinical judgement (in fact, the authors encourage clinicians to obtain an ECG based upon such judgement). As an example, a patient in whom a noncardiac diagnosis is likely (eg, younger patient with obvious zoster [shingles] lesions and no other symptoms) may not need an ECG. Nevertheless, this study provides some evidence for clinicians trying to devise appropriate triage protocols for the emergency department or to determine for which patients, including those not presenting with chest pain, an ECG assessment is needed.

Prospective validation of this decision rule in other patient populations is needed before widespread adoption can be recommended. Among the rule's limitations are its relatively low sensitivity and the age cutoffs, which may be too high in some settings. It is worth reiterating the importance of paying close attention to older patients and those with diabetes with symptoms consistent with ACS and using a low threshold for obtaining an ECG in such patients.

ELECTROCARDIOGRAM ASSESSMENT

Initial interpretation and criteria for ischemia — Specific approaches to patients judged to have definite or probable ACS based upon a targeted history and physical examination are initially guided by the accompanying 12-lead electrocardiogram (ECG) [9]. ECG interpretation for this purpose is discussed in detail separately; a focused review is provided below. (See "Electrocardiogram in the diagnosis of myocardial ischemia and infarction" and "Diagnosis of acute myocardial infarction", section on 'ECG'.)

Clinicians must be aware that the initial ECG is often not diagnostic in patients with ACS. Forty-one percent of patients with non-ST elevation myocardial infarction (NSTEMI) do not have the typical ST-depression or T-wave inversion [10]. In patients at intermediate to high risk for ACS without a clear diagnosis, ECGs should be repeated at frequent intervals until the patient's chest pain resolves or a definitive diagnosis is made. (See 'Importance of serial electrocardiograms' below.)

When present, ECG abnormalities are an early sign of myocardial ischemia. Criteria for the two major categories of ECG manifestations of acute myocardial ischemia are listed here:

●Findings consistent with ST elevation myocardial infarction (STEMI):

•New or presumed new ST elevation at the J point in two anatomically contiguous leads using the following diagnostic thresholds:

≥0.1 mV (1 mm) in all leads other than V2 to V3, where the following diagnostic thresholds apply:

-≥0.2 mV (2 mm) in males ≥ 40 years

-≥0.25 mV (2.5 mm) in males <40 years

-≥0.15 mV (1.5 mm) in females

●Findings consistent with NSTEMI:

•New or presumed new horizontal or down-sloping ST depression ≥0.05 mV (0.5 mm) in two anatomically contiguous leads

and/or

•T wave inversion ≥0.1 mV (1 mm) in two anatomically contiguous leads with prominent R wave or R/S ratio >1

Localization of ischemia — The ECG leads are more helpful in localizing regions of transmural than subendocardial ischemia. The anatomic location of a transmural infarct is determined by which ECG leads show ST elevation and/or increased T wave positivity:

●Anterior wall ischemia – Two or more of the precordial leads (V1 to V6) (waveform 2A-B)

●Anteroseptal ischemia – Leads V1 to V3 (waveform 3 and waveform 4)

●Apical or lateral ischemia – Leads aVL and I, and leads V4 to V6 (waveform 5 and waveform 6)

●Inferior wall ischemia – Leads II, III, and aVF (waveform 1)

●Right ventricular ischemia – Right-sided precordial leads (waveform 1)

●Posterior wall ischemia – Septal precordial leads (V1 to V2) (waveform 7) and posterior precordial leads (waveform 8)

The right-sided leads V4R, V5R, and V6R (figure 1) should be obtained if there is evidence of inferior wall ischemia demonstrated by ST elevation in leads II, III, and aVF.

The posterior leads V7, V8, and V9 (figure 2) may also be helpful if there is evidence of posterior wall ischemia as suggested by prominent R waves and ST depressions in leads V1 and V2.

Importance of serial electrocardiograms — If the initial ECG is not diagnostic but the patient remains symptomatic and clinical suspicion for ACS remains high, the ECG should be repeated at least every 15 to 30 minutes. Patients whose repeat ECGs are diagnostic for or strongly suggestive of either STEMI or NSTEMI should be managed for those diagnoses. (See "Overview of the acute management of ST-elevation myocardial infarction" and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

The initial ECG is often not diagnostic in patients with ACS. In two series, the initial ECG was nondiagnostic in 45 percent and normal in 20 percent of patients subsequently shown to have an acute myocardial infarction [1,11]. In the early hours of infarction, peaked, hyperacute T waves may be the only abnormality. In addition to evolution of the ECG, an uncommon source of error is pseudonormalization of baseline T wave inversion [12].

Some clinicians assume that an ECG obtained while the patient is experiencing chest pain that fails to show evidence of ischemia rules out the possibility of ACS. This assumption is false, as demonstrated by two prospective observational studies [13,14].

Left bundle branch block or pacemaker — Both left bundle branch block (LBBB) (waveform 9 and waveform 10), which is present in approximately 7 percent of patients with an acute myocardial infarction, and pacing can interfere with the ECG diagnosis of coronary-related ischemia [15]. Another problem is that approximately one-half of patients with LBBB and an acute myocardial infarction do not have chest pain as a symptom of their ischemia [16]. As a result, patients with LBBB are much less likely to receive aspirin, beta blockers, and reperfusion therapy [17], particularly if they present without chest pain [16]. Similar observations have been made in patients with a paced rhythm [18].

Careful evaluation of the ECG may show some evidence of ACS in patients with these abnormalities (see "Electrocardiographic diagnosis of myocardial infarction in the presence of bundle branch block or a paced rhythm"). However, the clinical history and cardiac biomarkers are of primary importance in diagnosing an ACS in this setting.

CLINICAL PRESENTATION — Certain characteristics of the patient's chest discomfort and associated symptoms increase the likelihood of ACS, while others make the diagnosis unlikely. Important characteristics are highlighted below. A more detailed discussion is found separately. (See "Approach to the patient with suspected angina pectoris".)

Of note, patients who are older or have diabetes are more likely to present with symptoms such as dyspnea, weakness, nausea and vomiting, palpitations, and syncope, and may not manifest chest discomfort. (See 'Atypical presentations' below.)

Ischemic chest pain — Ischemic pain has a number of features that tend to distinguish it from noncardiac pain. These characteristics are described below using the OPQRST mnemonic. Symptoms associated with the highest relative risk of myocardial infarction include radiation to an upper extremity, particularly when there is radiation to both arms, and pain associated with diaphoresis or with nausea and vomiting [19-21]. An important question is whether current pain is reminiscent of prior myocardial infarction. Of note, no one pain characteristic has sufficient positive or negative predictive value to definitively diagnose or exclude ACS.

●Onset – Ischemic pain is typically gradual in onset, although the intensity of the discomfort may wax and wane.

●Provocation and palliation – Ischemic pain is generally provoked by an activity, such as exercise, that increases cardiac oxygen demand [20,22]. Ischemic pain does not change with respiration or position. It may or may not respond to nitroglycerin and, if there is improvement, this may only be temporary. Relief of pain following the administration of therapeutic interventions (eg, nitroglycerin, "gastrointestinal cocktail" of viscous lidocaine and antacid) does not reliably distinguish nonischemic from ischemic chest pain [23-25].

●Quality – Ischemic pain is often characterized more as a discomfort than pain, and it may be difficult for the patient to describe. Terms frequently used by patients include squeezing, tightness, pressure, constriction, crushing, strangling, burning, heartburn, fullness in the chest, band-like sensation, knot in the center of the chest, lump in throat, ache, heavy weight on chest (elephant sitting on chest), like a bra too tight, and toothache (when there is radiation to the lower jaw). It is generally not described as sharp, fleeting, knife-like, stabbing, or like "pins and needles" [20].

Increased pain severity does not appear to correlate with an increased likelihood of acute myocardial infarction [26].

In some cases, the patient cannot qualify the nature of the discomfort but places his or her clenched fist in the center of the chest, known as the "Levine sign."

●Radiation – Ischemic pain often radiates to other parts of the body including the upper abdomen (epigastrium), shoulders, arms (upper and forearm), wrist, fingers, neck and throat, lower jaw and teeth (but not upper jaw), and not infrequently to the back (specifically the interscapular region). The old dictum that "pain above the nose or below the navel is rarely cardiac in origin" still holds. Pain radiating to the upper extremities is highly suggestive of ischemic pain [19,20,22,27].

●Site – Ischemic pain is not felt in one specific spot; rather, it is a diffuse discomfort that may be difficult to localize. The patient often indicates the entire chest, rather than localizing it to a specific area by pointing a single finger.

●Time course – Angina is usually brief (two to five minutes) and is relieved by rest or with nitroglycerin. In comparison, patients with an ACS may have chest pain at rest, and the duration is variable but generally lasts longer than 30 minutes. Classic anginal pain lasting more than 20 minutes suggests ACS. Continuous pain that does not wax and wane and persists for over 24 hours is unlikely to be due to ACS [28].

Historical features increasing likelihood of ACS — Historical features that increase the likelihood of ACS include the following:

●Patients with a prior history of ACS have a significantly increased risk of recurrent ischemic events.

●A prior history of other vascular disease is associated with a risk of cardiac ischemic events comparable to that seen with a prior history of ACS.

●Risk factors for ACS, particularly age, male sex, diabetes, hypertension, dyslipidemia, and cigarette smoking [29]. (See "Overview of established risk factors for cardiovascular disease".)

●Recent use of cocaine or other sympathomimetic drugs (eg, methamphetamine, cathinones) [30]. (See "Clinical manifestations, diagnosis, and management of the cardiovascular complications of cocaine abuse" and "Methamphetamine: Acute intoxication" and "Acute amphetamine and synthetic cathinone ("bath salt") intoxication".)

Associated symptoms — Ischemic pain is often associated with other symptoms. The most common is shortness of breath, which may reflect mild pulmonary congestion resulting from ischemia-mediated diastolic dysfunction. Other symptoms may include belching, nausea, indigestion, vomiting, diaphoresis, dizziness, lightheadedness, clamminess, and fatigue.

Noncardiac chest pain — Specific chest pain characteristics can be used to help differentiate cardiac from noncardiac causes. (See "Evaluation of the adult with chest pain in the emergency department".)

Systematic reviews have identified the following characteristics as more typical of nonischemic chest discomfort [19]:

●Pleuritic pain, sharp or knife-like pain related to respiratory movements or cough

●Primary or sole location in the mid or lower abdominal region

●Any discomfort localized with one finger

●Any discomfort reproduced by movement or palpation

●Constant pain lasting for days

●Fleeting pains lasting for a few seconds or less

●Pain radiating into the lower extremities or above the mandible

However, some patients with ACS present with so-called "atypical" chest pain. This was illustrated in the Multicenter Chest Pain Study in which acute ischemia was diagnosed in 22 percent of patients who presented with sharp or stabbing pain and 13 percent who presented with pleuritic-type pain [31]. (See 'Atypical presentations' below.)

In addition, some patients who appear to have a noncardiac cause of chest pain have other serious conditions including acute aortic dissection, pulmonary embolism, tension pneumothorax, myocarditis, perforating peptic ulcer, and esophageal rupture (table 5). It is essential to consider these alternate diagnoses to avoid potentially dangerous errors in management, such as the administration of antiplatelet, anticoagulant, or thrombolytic therapy to a patient with an aortic dissection.

ATYPICAL PRESENTATIONS — Some patients with ACS present with symptoms other than chest pain. In a review of over 430,000 patients with confirmed acute myocardial infarction from the National Registry of Myocardial Infarction II, one-third had no chest pain on presentation to the hospital [32]. These patients often present with symptoms such as dyspnea alone, weakness, nausea and/or vomiting, epigastric pain or discomfort, palpitations, syncope, or cardiac arrest. They are more likely to be older or have diabetes [20,32-34]. (See "Clinical features and diagnosis of coronary heart disease in women", section on 'Clinical presentation' and "Prevalence of and risk factors for coronary heart disease in patients with diabetes mellitus", section on 'Silent ischemia and infarction'.)

The absence of chest pain has important implications for therapy and prognosis. In the Registry report, patients without chest pain were much less likely to be diagnosed with a confirmed myocardial infarction on admission (22 versus 50 percent in those with chest pain) and were less likely to be treated with appropriate medical therapy and to receive thrombolytic therapy or primary percutaneous coronary intervention (PCI; 25 versus 74 percent) [32]. Not surprisingly, these differences were associated with an increase in in-hospital mortality (23.3 versus 9.3 percent, adjusted odds ratio [aOR] 2.21, 95% CI 2.17-2.26).

PHYSICAL EXAMINATION — The initial physical examination should focus on findings that permit rapid triage and aid in immediate diagnosis and management and should include the following:

●Responsiveness, airway, breathing, and circulation – In patients in respiratory or cardiorespiratory arrest, the appropriate resuscitation algorithms should be followed (algorithm 2 and algorithm 3 and algorithm 4). (See "Advanced cardiac life support (ACLS) in adults" and "Overview of advanced airway management in adults for emergency medicine and critical care" and "Basic airway management in adults" and "Rapid sequence intubation in adults for emergency medicine and critical care".)

●Evidence of systemic hypoperfusion (hypotension; tachycardia; impaired cognition; cool, clammy, pale, ashen skin) – Cardiogenic shock complicating acute myocardial infarction requires aggressive evaluation and management (table 6). (See "Clinical manifestations and diagnosis of cardiogenic shock in acute myocardial infarction" and "Prognosis and treatment of cardiogenic shock complicating acute myocardial infarction".)

●Evidence of heart failure (jugular venous distention, new or worsening pulmonary crackles, hypotension, tachycardia, new S3 gallop, new or worsening mitral regurgitation murmur) – Aggressive management is needed for patients with heart failure complicating an acute myocardial infarction, depending upon the severity of the heart failure and the presence of other risk factors (table 7 and table 6) [35]. (See "Treatment of acute decompensated heart failure in acute coronary syndromes".)

●Focused neurologic examination – A screening neurologic examination should be performed to assess for focal lesions or cognitive deficits that might preclude safe use of thrombolytic therapy (table 4). (See "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy".)

The cardiac and general physical examinations of patients with possible ACS are reviewed in greater detail separately. (See "Auscultation of heart sounds" and "Auscultation of cardiac murmurs in adults" and "Evaluation of the adult with chest pain in the emergency department", section on 'Physical examination' and "Approach to the adult with dyspnea in the emergency department", section on 'Physical examination'.)

CARDIAC BIOMARKERS AND OTHER LABORATORY TESTING — Serial serum cardiac biomarkers (sometimes referred to as cardiac enzymes) of acute myocardial damage are essential in the evaluation of patients with suspected ACS. They should be obtained in any patient at significant risk of ACS. High-sensitivity troponin is the preferred test whenever available. The use and test characteristics of troponin are discussed separately. (See "Troponin testing: Clinical use" and "Elevated cardiac troponin concentration in the absence of an acute coronary syndrome".)

Basic electrolyte concentrations, kidney function studies, and a complete blood count with platelets should be obtained in patients with suspected ACS. Anemia can exacerbate myocardial ischemia, and patients with a low hemoglobin may require blood transfusion. Transfusion thresholds and implementation are reviewed separately. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Acute MI'.)

Indices of coagulation should be obtained in patients at increased risk of coagulopathy due to warfarin or heparin use, a history of liver disease, or a history of excessive or spontaneous bleeding. Additional laboratory testing is obtained depending on clinical circumstances, including patient comorbidities.  

MANAGEMENT

ST elevation — The management of patients who meet the criteria for ST elevation myocardial infarction (STEMI) is discussed separately. The accompanying table provides a concise summary of the immediate treatment interventions needed in these patients (table 3). (See 'Electrocardiogram assessment' above and "Overview of the acute management of ST-elevation myocardial infarction".)

Selection and implementation of the optimal reperfusion strategy is the most important step in the management of STEMI and is discussed separately. Reperfusion therapy, whether percutaneous coronary intervention (PCI) or thrombolytics, should not await the result of cardiac biomarker measurement. (See "Acute ST-elevation myocardial infarction: Selecting a reperfusion strategy" and "Primary percutaneous coronary intervention in acute ST elevation myocardial infarction: Determinants of outcome" and "Acute ST-elevation myocardial infarction: The use of fibrinolytic therapy".)

Rapid implementation of primary PCI is more likely to be achieved if the hospital protocol involves immediate activation of the PCI team by the emergency clinician and immediate transfer of the patient to the catheterization laboratory [36].

Anemic patients may require blood transfusion. Transfusion thresholds and implementation are reviewed separately. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Acute MI'.)

Non-ST elevation

Diagnosis and treatment — A patient whose presentation raises concern for coronary-related ischemia but who does not manifest ST elevations on electrocardiogram (ECG) is suspected of having a non-ST elevation myocardial infarction (NSTEMI) or possibly unstable angina. The management of patients with NSTEMI is discussed separately. The accompanying table provides a concise summary of the immediate treatment interventions needed in these patients (table 3). (See 'Electrocardiogram assessment' above and "Overview of the acute management of non-ST-elevation acute coronary syndromes".)

Unstable angina and NSTEMI comprise part of the spectrum of ACS. Angina is considered unstable if it presents in any of the following three ways:

●Rest angina, generally lasting longer than 20 minutes

●New-onset angina that markedly limits physical activity

●Increasing angina that is more frequent, lasts longer, or occurs with less exertion than previous angina

NSTEMI is distinguished from unstable angina by the presence of elevated serum biomarkers. ST segment elevations and Q waves are absent in both unstable angina and NSTEMI. As a result, unstable angina and NSTEMI can be indistinguishable at initial evaluation since an elevation in serum biomarkers may not be detectable for two to four hours after a myocardial infarction with contemporary troponin assays and one to three hours with high-sensitivity assays, and at least 12 hours are required to detect elevations in all patients. (See 'Cardiac biomarkers and other laboratory testing' above and "Acute coronary syndrome: Terminology and classification".)

Thrombolytic therapy should not be administered to patients with unstable angina or NSTEMI unless subsequent ECG monitoring documents ST segment elevations that persist. Repeat ECGs are an essential part of management in these patients. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes" and 'Importance of serial electrocardiograms' above.)

An aggressive approach to reperfusion using PCI is best suited for patients with an elevated troponin level or possibly for patients with unstable angina and other high-risk features (see 'High-risk patient' below). For patients at lower risk, approaches vary based upon hospital protocol.

Anemic patients may require blood transfusion. Transfusion thresholds and implementation are reviewed separately. (See "Indications and hemoglobin thresholds for RBC transfusion in adults", section on 'Acute MI'.)

Risk stratification — Both patient outcomes and the effectiveness of specific treatments for patients with unstable angina and NSTEMI vary according to the presence or absence of high-risk features in their presentation. This fact underscores the importance of accurate risk stratification in the emergency department. Risk stratification is discussed in detail separately. (See "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Very high-risk patients' and "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Early risk stratification tools'.)

Cardiac arrhythmias during ACS — Disturbances of cardiac rhythm during a myocardial infarction are usually detected by cardiac monitor rather than by physical examination or 12-lead ECG:

●Sustained ventricular tachyarrhythmias in the peri-infarction period must be treated immediately because of their deleterious effect on cardiac output, possible exacerbation of myocardial ischemia, and the risk of deterioration into ventricular fibrillation (algorithm 2). (See "Ventricular arrhythmias during acute myocardial infarction: Incidence, mechanisms, and clinical features".)

●While supraventricular tachyarrhythmias in the peri-infarction period may pose less immediate risk of cardiac arrest, the management of such arrhythmias is important because any tachycardia can increase myocardial oxygen demand, thereby exacerbating ischemia and possibly decreasing cardiac output (algorithm 4). (See "Supraventricular arrhythmias after myocardial infarction".)

●Bradyarrhythmias occurring early in the setting of an inferior wall myocardial infarction (within the first 24 hours) may respond to treatment with atropine (algorithm 3). Later bradyarrhythmias, wide QRS-complex bradyarrhythmias, and those occurring in the setting of an anterior wall myocardial infarction may require temporary pacemaker placement. (See "Conduction abnormalities after myocardial infarction".)

Disposition of patient without STEMI — For patients without STEMI, the ECG remains a critical component in determining risk for adverse outcomes in ACS. The patient's hemodynamic status, serum biomarkers, and historical risk factors, as well as available hospital resources, should also be used to determine appropriate disposition. Cardiology consultation is useful generally and for any case in which the diagnosis or treatment plan are unclear. The utility of epidemiologic risk factors in determining acute, individual risk has been questioned [37].

High-risk patient — The patient is at high risk for ACS if ST segment depression (≥0.05 mV [0.5 mm]) is present in two or more contiguous leads or serum biomarkers are elevated. A high score on a validated ACS risk stratification tool suggests the patient is at high risk. Such scores include the HEART Score (table 8) and EDACS Score [38]. (See "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Very high-risk patients' and "Risk stratification after non-ST elevation acute coronary syndrome", section on 'Early risk stratification tools'.)

This patient is typically admitted to an intensive care unit, coronary care unit, or monitored cardiac unit depending upon the persistence of symptoms and evidence of hemodynamic compromise. Those with persistent pain or hemodynamic compromise generally undergo urgent angiography and revascularization. Others with resolution of symptoms and stable hemodynamics are typically referred for early elective angiography and revascularization if appropriate.

If there is no ST segment elevation or depression, regardless of the presence or absence of Q waves, the patient with definite or probable ACS should still be admitted to a monitored care unit for further evaluation. Those patients manifesting high-risk features either on presentation or during their emergency department course should be admitted and considered for early PCI. (See "Overview of the acute management of non-ST-elevation acute coronary syndromes", section on 'Choosing a revascularization strategy'.)

Low- and moderate-risk patient — The management, including methods for risk assessment, of patients who have no ECG changes and normal serum biomarkers but are still considered to be at low or moderate risk for ACS is discussed separately. (See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".)

IMPACT OF MISSED DIAGNOSIS — With careful evaluation using effective risk scores, serial electrocardiograms (ECGs), and appropriate diagnostic testing, only a very small percentage of patients with an ACS are mistakenly discharged from the emergency department [39,40]. However, patients whose diagnosis is missed initially have an increase in short-term mortality [33,39,41,42]. This issue was evaluated in a review of 10,689 Black, White, and Hispanic American patients who presented to the emergency department with symptoms suggesting acute coronary-related ischemia: 8 percent had an acute myocardial infarction, and 9 percent had unstable angina [33]. Among the patients with an ACS, 2.2 percent were mistakenly discharged from the emergency department. Atypical presentation most frequently led to missed diagnosis. The patients with missed myocardial infarction had the following characteristics:

●Females less than 55 years of age

●Not White Americans

●Shortness of breath as the major presenting symptom

●Normal or nondiagnostic ECG

Misreading of the ECG was an infrequent problem. There was a nonsignificant trend toward an increased risk-adjusted 30-day mortality ratio for patients who were not hospitalized (1.9 and 1.7 in the patients with myocardial infarction and unstable angina, respectively). While improvements in care since the publication of this study have reduced the rate of missed ACS in the emergency department, lessons about which patient groups are most at risk bear remembering.

OBSERVATION — Some patients without clear evidence of ACS by clinical history, electrocardiogram (ECG), or biomarker measurement ultimately sustain a myocardial infarction or develop unstable angina. Therefore, patients with an uncertain diagnosis after initial assessment require further observation and evaluation. The management of such patients, including the use of chest pain observation units, is discussed separately. (See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome".)

REST AND STRESS IMAGING STUDIES — Rest imaging tests, including radionuclide myocardial perfusion imaging (rMPI) and echocardiography, may be of value in the evaluation of patients who have persistent chest pain suggestive of an ACS, a nondiagnostic electrocardiogram (ECG), and initially or serially negative cardiac biomarkers. Some patients in whom the chest pain has resolved may undergo stress testing with or without imaging. Use of these diagnostic tests is discussed separately. (See "Evaluation of emergency department patients with chest pain at low or intermediate risk for acute coronary syndrome", section on 'Noninvasive evaluation' and "Noninvasive testing and imaging for diagnosis in patients at low to intermediate risk for acute coronary syndrome".)

In addition to detecting myocardial dysfunction or ischemia consistent with the diagnosis of a myocardial infarction, imaging studies such as a contrast-enhanced chest computed tomography (CT) or cardiovascular magnetic resonance imaging (MRI) can be used to differentiate a myocardial infarction from an aortic dissection in patients for whom this distinction is initially unclear. (See "Clinical features and diagnosis of acute aortic dissection", section on 'Diagnosis'.)

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Non-ST-elevation acute coronary syndromes (non-ST-elevation myocardial infarction)" and "Society guideline links: ST-elevation myocardial infarction (STEMI)" and "Society guideline links: Adult with chest pain in the emergency department".)

SUMMARY AND RECOMMENDATIONS

●Differential diagnosis of chest pain – Chest discomfort can be caused by a number of life-threatening conditions, including pulmonary embolism, aortic dissection, and pneumothorax. Emergency clinicians must avoid premature diagnosis of acute coronary syndrome (ACS). The evaluation of chest pain in the emergency department is discussed separately. (See "Evaluation of the adult with chest pain in the emergency department".)

●Immediate interventions – If ACS is the leading diagnosis, initial assessment and interventions must be performed rapidly to minimize potential injury to the myocardium. During the initial assessment phase, the following steps should be accomplished for any patient at significant risk for ACS:

•Airway, breathing, and circulation assessed

•Preliminary history and examination obtained (See 'Clinical presentation' above.)

•12-lead electrocardiogram (ECG) interpreted

•Resuscitation equipment brought to the bedside

•Cardiac monitor attached to patient

•Oxygen given as necessary

•Intravenous (IV) access and blood work obtained (including contemporary or high-sensitivity troponin; hemoglobin to assess for anemia) (See 'Cardiac biomarkers and other laboratory testing' above.)

•Aspirin 162 to 325 mg given

•Nitrates given (unless contraindicated) (see 'Immediate emergency department interventions' above)

●Electrocardiogram – The initial ECG is often not diagnostic in patients with ACS. In patients without a clear diagnosis but at risk for ACS, ECGs should be repeated at frequent intervals (every 15 to 30 minutes) until the patient's chest pain resolves or a definitive diagnosis is made. ECG assessment is described in the text. (See 'Electrocardiogram assessment' above.)

●Risk factors – Important risk factors for acute myocardial infarction include a personal or family history of ACS or other cardiovascular disease, older age, diabetes, dyslipidemia, cigarette smoking, hypertension, and abuse of cocaine or other sympathomimetic drugs. (See "Overview of established risk factors for cardiovascular disease" and 'When to suspect acute coronary syndrome' above.)

●Clinical presentation – Characteristics of the patient's chest discomfort and associated symptoms that increase or decrease the likelihood of ACS are described in the text. Many patients with ACS present with symptoms such as dyspnea or malaise, either alone or in addition to chest pain. Females are more likely to have associated dyspnea than males, and patients who are older or have diabetes are more likely to present with dyspnea without chest pain. Relief of symptoms following the administration of therapeutic interventions (eg, nitroglycerin, "gastrointestinal cocktail" of viscous lidocaine and antacid) does not reliably distinguish nonischemic from ischemic chest pain. (See 'Clinical presentation' above and 'Atypical presentations' above.)

●Physical examination – The initial physical examination should focus on findings that permit rapid triage and aid in immediate diagnosis and management. (See 'Physical examination' above.)

●Algorithm and rapid overview table for management – The attached algorithm provides a simple approach to risk stratification while the table provides a concise outline of the immediate interventions needed to manage ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina (algorithm 1 and table 3). Management and risk stratification are discussed further in the text. (See 'Management' above.)

●Missed diagnosis – With careful evaluation using appropriate risk scores and diagnostic testing, only a very small percentage of patients with an ACS are mistakenly discharged from the emergency department. However, these patients have an increase in short-term mortality. American patients whose ACS was missed are more likely to be females less than 55 years of age, not White Americans, patients with shortness of breath as the major presenting symptom, and patients with a normal or nondiagnostic initial ECG. (See 'Impact of missed diagnosis' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Thomas Ryan, MD, who contributed to earlier versions of this topic review.