About 8 million patients with chest pain present to a U.S. ED each year.¹ Of these, 50% to 70% are placed into an observation unit or admitted to the hospital, yet only about 10% are eventually diagnosed with an acute coronary syndrome.^2,3,4,5 Still, 2% to 5% of patients with acute myocardial infarctions are missed on initial presentation and discharged from the ED.² We discuss the features and approach that help differentiate acute coronary syndrome from other causes of chest pain. The chapters titled “Acute Coronary Syndromes” and “Low Probability Acute Coronary Syndromes” discuss management of these specific syndromes.

Acute chest pain is the recent onset of pain, pressure, or tightness in the anterior thorax between the xiphoid, suprasternal notch, and both midaxillary lines. Acute coronary syndrome includes acute myocardial infarction and acute ischemia (unstable angina). Acute myocardial infarction is defined by myocardial necrosis with elevation of cardiac biomarkers and is classified by ECG findings as ST-segment elevation myocardial infarction or non-ST-segment elevation myocardial infarction. Unstable angina is a clinical diagnosis defined by chest pain or an equivalent (neck or upper extremity pain) from inadequate myocardial perfusion that is new, occurring with greater frequency, less activity, or at rest. Patients with unstable angina do not have pathologic ST-segment elevation on ECG or cardiac biomarker elevation, but they are at risk of eventual myocardial damage absent recognition and treatment.

The chest wall, from the dermis to the parietal pleura, is innervated by somatic pain fibers. Neurons enter the spinal cord at specific levels corresponding to the skin dermatomes. Visceral pain fibers are found in internal organs, such as the heart, blood vessels, esophagus, and visceral pleura. Visceral pain fibers enter the spinal cord and map to areas on the parietal cortex corresponding to cord levels shared with somatic fibers. Stimulation of visceral or somatic afferent pain fibers results in two distinct pain syndromes. Pain from somatic fibers is usually easily described, precisely located, and often experienced as a sharp sensation. Pain from visceral fibers is generally more difficult to describe and imprecisely localized. Patients with visceral pain are more likely to use terms such as discomfort, heaviness, pressure, tightness, or aching. Visceral pain is often referred to an area of the body corresponding to adjacent somatic nerves, which explains why pain from an acute myocardial infarction may radiate to the neck, jaw, or arms. Factors such as age, sex, comorbid illnesses, medications, drugs, and alcohol may interact with psychological and cultural factors to alter pain perception and communication.

RISK ASSESSMENT

Patients with abnormal vital signs, concerning ECG findings (if available initially), a history of prior coronary artery disease, multiple atherosclerotic risk factors, or any abrupt, new, or severe chest pain or dyspnea should be quickly placed into a treatment bed. Initiate cardiac monitoring and IV access, and obtain an ECG, ideally within 10 minutes of arrival. Identify and treat immediate life needs like supporting the airway, breathing, and circulation. Measure vital signs promptly and at regular intervals. Administer oxygen if ambient saturation is <95%.

Once the patient is stable, focus on history, physical exam, and laboratory findings associated with cardiac (acute coronary syndrome) versus noncardiac chest pain causes. Obtain a focused history that includes symptoms, abridged past medical history, and review of systems, seeking features of life-threatening causes of chest pain, such as acute coronary syndrome, aortic dissection, pulmonary embolism, severe pneumonia, and esophageal rupture. Ask about the onset, timing, severity, radiation, and character of the chest pain; alleviating and exacerbating factors; and presence of associated symptoms, such as diaphoresis, dyspnea, nausea, vomiting, palpitations, and dizziness.

Focus the physical examination on findings pertinent to life-threatening causes of chest pain. Inspect the thorax for prior surgical incisions, chest wall deformities, and symmetric rise and fall with respiration. Palpate the chest wall for tenderness, masses, or crepitus. Auscultate to identify chest consolidation or pneumothorax, murmurs, gallops, or friction rubs, and obtain a chest x-ray immediately to identify immediate life-threatening processes.

HISTORY

Patients with serious and life-threatening intrathoracic disorders, including acute coronary syndrome, may report pain outside the chest, such as in the epigastrium, neck, jaw, shoulders, or arms. Some patients never experience chest pain or have migratory pain that is no longer in the chest at the time of medical evaluation. Patients with acute myocardial infarction who present without chest pain have diagnostic and treatment delays and have an in-hospital mortality rate more than twice that of acute myocardial infarction patients with chest pain.⁶

Classic Chest Pain

Terms such as “typical” and “atypical” symptoms are misleading because symptoms among patients with acute coronary syndrome vary and may not include classic findings. Classic cardiac chest pain is retrosternal left anterior chest crushing, squeezing, tightness, or pressure. Cardiac chest pain is often brought on or exacerbated by exertion and relieved by rest. Traditional teaching is that anginal pain lasts 2 to 10 minutes, unstable angina pain lasts 10 to 30 minutes, and pain from acute myocardial infarction often lasts longer than 30 minutes, but great overlap exists. Other classic features of acute coronary syndrome presentation include radiation of the pain to the arms, neck, or jaw; diaphoresis; dyspnea; and nausea or vomiting.⁷

Nonclassic Chest Pain

Patients with acute coronary syndrome frequently present without a “classic” chest pain story. The absence of classic symptoms contributes to delays in seeking care and in evaluation once they reach the ED.

Nonclassic presentations include chest pain lasting for seconds, constant pains lasting for 12 to 24 hours or more without waxing and waning intensity, or pain worsened by specific body movements or positions, such as twisting and turning of the thorax. Reports of stabbing, well-localized, positional, or pleuritic chest pain are uncommon with acute coronary syndrome but do not exclude it with certainty. The Multicenter Chest Pain Study reported that 22% of patients with acute myocardial infarction described their chest pain as sharp or stabbing.⁸ Nonclassic presentations of acute coronary syndrome occur more frequently in women, racial minorities, diabetics, the elderly, and patients with psychiatric disease or altered mental status than in other patient groups.^6,9,10 Multiple prescription medications, drugs, alcohol, patient or provider sex, and cultural differences can impact the pain perception or reporting of symptoms.^11,12,13 For example, the term “sharp” in some cultures is interpreted to mean “severe,” rather than knife-like.¹⁴

Premenopausal and early menopausal women with acute coronary syndrome are more likely to present with pain unrelated to exercise, pain not relieved by rest or nitroglycerin, pain relieved by antacids, palpitations without chest pain, or a chief complaint of fatigue.¹⁵ Associated symptoms of nausea, emesis, jaw pain, neck pain, and back pain are more common in women with acute coronary syndrome, while diaphoresis is more common among men.¹⁵

Anginal Equivalents

One large public hospital reported that 47% of 721 consecutive patients with myocardial infarction presented complaining of symptoms other than chest pain.¹⁰ This means ED physicians must consider potential anginal-equivalent symptoms like dyspnea at rest or with exertion, nausea, light-headedness, generalized weakness, acute changes in mental status, diaphoresis, or shoulder, arm, or jaw discomfort. Patients with dyspnea alone have a fourfold increased risk of sudden death from cardiac causes compared with asymptomatic patients, and a twofold increased risk compared with patients with classic angina.¹⁶

Epigastric or upper abdominal discomfort, even when relieved with antacids, should raise suspicion for acute coronary syndrome, especially for patients >50 years old and those with known coronary artery disease. In these two high-risk groups, include an ECG in routine evaluation of abdominal pain. Consider acute coronary syndrome in patients presenting with palpitations, because myocardial ischemia may increase automaticity and irritability, leading to dysrhythmias. Furthermore, tachycardia can cause an increase in myocardial oxygen demand, triggering myocardial ischemia.

Risk Factors

Major risk factors for coronary artery disease include age >40 years old, male or postmenopausal female, hypertension, tobacco use, hypercholesterolemia, diabetes, truncal obesity, family history, and a sedentary lifestyle.^17,18 Cocaine use is associated with acute myocardial infarction even in young people with minimal or no coronary artery disease. Chronic cocaine use may accelerate atherosclerosis and severe coronary artery disease,¹⁹ although some suggest no relationship once controlling for other cardiovascular risk factors.²⁰ Human immunodeficiency virus infection and treatment with highly active antiretroviral therapy can accelerate atherosclerosis.²¹

Although cardiac risk factors are useful in predicting coronary artery disease risk within a given population, they are less useful for diagnosing the presence or absence of acute coronary syndrome in an individual patient.^7,22,23 Patients with known coronary artery disease and prior acute coronary syndrome are at risk for another acute coronary syndrome event. So, identify previous episodes of chest pain, prior echocardiography, stress testing or coronary angiography, or prior revascularization (stent placement or coronary artery bypass graft surgery).

ACUTE MYOCARDIAL INFARCTION SIGNS AND SYMPTOMS: LIKELIHOOD RATIOS

There are no historical features with sufficient sensitivity and specificity to either diagnose or exclude acute coronary syndrome. Radiation to the arms and shoulders, particularly to the right arm or both arms, is the historical feature most strongly associated with acute coronary syndrome (likelihood ratio range of 2.3–4.7).^22,24,25 Chest pain with exertion or associated symptoms of dyspnea, diaphoresis, nausea, or vomiting are associated with twofold likelihood of acute coronary syndrome.^24,25 Pressure-like chest sensation has limited value in the prediction of acute coronary syndrome.²² Sharp, pleuritic, positional chest pain is associated with a decreased likelihood of acute coronary syndrome but cannot eliminate the diagnosis.²² Lack of exertional pain or pain radiation has no diagnostic value for exclusion of acute coronary syndrome.^22,25 Since classic cardiac ischemic pain is not universal and men and women both present with nonclassic symptoms, the diagnostic utility of specific chest pain descriptions does not differ significantly between men and women.²⁶ Tables 48-1 and 48-2 summarize the chest pain characteristics associated with increased or decreased likelihood ratios of acute myocardial infarction.

PHYSICAL EXAMINATION

The examination of patients with acute coronary syndrome is often normal, and there are no exam findings that are sensitive or specific enough to exclude or diagnose acute coronary syndrome. Use the exam in conjunction with history to identify or exclude other causes of chest pain and to guide therapy.

Vital sign abnormalities from acute coronary syndrome may include hyper- or hypotension, tachycardia, or bradycardia. Tachycardia may result from increased sympathetic tone and decreased left ventricular stroke volume. Bradycardia may occur due to ischemia or infarction involving the conduction system or alterations in sympathetic and parasympathetic activation of the sinoatrial or atrioventricular nodes. Patients with acute myocardial ischemia or infarction may have abnormal heart sounds due to changes in ventricular function or compliance, such as an S₃ or S₄ gallop, diminished S₁, or a paradoxically split S₂. New murmurs in patients with chest pain may be associated with acute myocardial infarction with chordae tendineae rupture or aortic root dissection. Ischemia-induced congestive heart failure may produce crackles on auscultation of the lungs.

Physical examination findings most strongly associated with acute myocardial infarction in patients presenting with acute chest pain are hypotension, S₃ gallop, and diaphoresis, although the frequency, interrater reliability, and added diagnostic value are limited.²² Reproducible chest wall tenderness is suggestive of a musculoskeletal etiology but is reported in up to 15% of patients with confirmed acute myocardial infarction and cannot alone exclude the diagnosis of acute coronary syndrome.²⁸

RESPONSE TO THERAPY

Response to medications poorly discriminates between cardiac and noncardiac chest pain. While nitroglycerin reduces anginal pain, it may also relieve the pain from noncardiac conditions such as esophageal spasm.^22,29,30,31 Similarly, relief from antacid or combination “GI cocktail” therapy does not represent a noncardiac cause of chest pain.^32,33 Combine the above responses with other features to best assess the likely presence or absence of acute coronary syndrome.

Life-threatening concerns in acute chest pain are acute coronary syndrome, aortic dissection, pulmonary embolism, pneumonia, tension pneumothorax, and esophageal rupture. Other diagnoses with the potential for morbidity and mortality include simple pneumothorax, myocarditis, pericarditis, aortic stenosis, perforated ulcer, and cholecystitis. Benign causes of chest pain include anxiety, musculoskeletal pain, esophagitis, and gastritis. Common causes of chest pain are listed in Table 48-3. Table 48-4 summarizes the classic symptoms of the life-threatening causes of acute chest pain.

PULMONARY EMBOLISM

Symptoms of pulmonary embolism include sharp chest pain (may worsen with inspiration, called “pleuritic”), dyspnea, hypoxemia, syncope, or shock. There may be associated cough or hemoptysis. Patients with pulmonary embolism may be febrile and have leg swelling or pain, and some patients will report chest wall tenderness. Common physical examination findings include tachypnea, tachycardia, and hypoxemia. Pulmonary embolism risk factors include recent surgery, trauma, prolonged immobility, active cancer, estrogens from birth control pills or hormone replacement therapy (particularly when combined with smoking), procoagulant syndromes, or a history of prior pulmonary embolism or deep venous thrombosis.^34,35

Clinical decision aids, such as the Wells and Revised Geneva Scores, can risk stratify patients with possible pulmonary embolism.^36,37 The Pulmonary Embolism Rule-Out Criteria exclude pulmonary embolism in patients with a low pretest probability without further diagnostic testing.³⁸ Normal D-dimer testing, measured by a sensitive enzyme-linked immunosorbent assay, in a hemodynamically stable low- to intermediate-risk patient (with a Revised Geneva Criteria Score of 0 to 10) makes pulmonary embolism exceptionally unlikely; in those with higher risk assessment, a negative D-dimer has limited value.^39,40 In patients with pulmonary embolism, elevated cardiac troponin (cTn) indicates ventricular dysfunction and identifies patients with an elevated risk of death and complications.⁴¹

In pulmonary embolism, ECG findings are nonspecific, with the most common finding being sinus tachycardia. Chest radiographs are usually normal, but in rare cases may show signs of pulmonary infarction. CT pulmonary angiography is the test of choice and is highly sensitive for the detection of large to medium-sized pulmonary emboli. See more details on pulmonary embolism in the chapter 46, “Venous Thromboembolism.”

AORTIC DISSECTION

Pain from aortic dissection is classically described as a ripping or tearing sensation radiating to the interscapular area of the back. The pain is often sudden in onset, maximal at the time of symptom onset, and may migrate or be noted above and below the diaphragm. Lack of sudden-onset pain decreases the probability of aortic dissection but cannot exclude it.⁴²

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