CHEST PAIN

Chest pain onset, character, location/size, duration,
periodicity, and exacerbators.
Shortness of breath.
Vital signs.
Chest and cardiac examination.
Electrocardiography.
Biomarkers of myocardial necrosis.

General Considerations

Chest pain (or chest discomfort) is a common symptom that can occur as a result of cardiovascular, pulmonary, pleural, or musculoskeletal disease, esophageal or othergastrointestinal disorders, or anxiety states. The frequency and distribution of life-threatening causes of chest pain, such as acute coronary syndrome (ACS), pericarditis, aortic dissection, pulmonary embolism, pneumonia, and esophageal perforation, vary substantially between clinical settings. Systemic lupus erythematosus, rheumatoid arthritis, and HIV are conditions that confer a strong risk for coronary artery disease. Because pulmonary embolism can present with a wide variety of symptoms, consideration of the diagnosis and rigorous risk factor assessment for venous thromboembolism (VTE) is critical. Classic VTE risk factors include cancer, trauma, recent surgery, prolonged immobilization, pregnancy, oral contraceptives, and family history and prior history of VTE. Other conditions associated with increased risk of pulmonary embolism include CHF and COPD. Sickle cell anemia can cause acute chest syndrome. Patients with this syndrome often have chest pain, fever, and cough.

Although uncommon in the office setting, delays in diagnosing life-threatening causes of chest pain can result in serious morbidity and mortality.

Clinical Findings

A. Symptoms

Myocardial ischemia is usually described as dull, aching sensation of “pressure,” “tightness,” “squeezing,” or “gas,” rather than as sharp or spasmodic. Ischemic symptoms usually subside within 5–20 minutes but may last longer. Progressive symptoms or symptoms at rest may represent unstable angina. Prolonged chest pain episodes might represent myocardial infarction, although up to  one-third of patients with acute myocardial infarction do not report chest pain. When present, pain due to myocardial ischemia is commonly accompanied by a sense of anxiety or uneasiness. The location is usually retrosternal or left precordial. Because the heart lacks somatic innervation, precise localization of pain due to cardiac ischemia is difficult; the pain is commonly referred to the throat, lower jaw, shoulders, inner arms, upper abdomen, or back. Ischemic pain may be precipitated or exacerbated by exertion, cold temperature, meals, stress, or combinations of these factors and is usually relieved by rest. However, many episodes do not conform to these patterns; and atypical presentations of ACS are more common in the elderly, women, and persons with diabetes. Other symptoms that are associated with ACS include shortness of breath; dizziness; a feeling of impending doom; and vagal symptoms, such as nausea and diaphoresis. In the elderly, fatigue is a common presenting complaint of ACS. Likelihood ratios for cardinal symptoms considered in the evaluation of acute myocardial infarction are summarized in Table 2–4.

Hypertrophy of either ventricle or aortic stenosis may also give rise to chest pain with less typical features. Pericarditis may produce pain that is greater when supine than upright and may increase with respiration, coughing, or swallowing. Pleuritic chest pain is usually not ischemic, and pain on palpation may indicate a musculoskeletal cause. Aortic dissection classically produces an abrupt onset of tearing pain of great intensity that often radiates to the back; however, this classic presentation occurs in a small proportion of cases. Anterior aortic dissection can also lead to myocardial or cerebrovascular ischemia.

Pulmonary embolism has a wide range of clinical presentations, with chest pain present in only 75% of cases. The chief objective in evaluating patients with suspected pulmonary embolism is to assess the patient’s clinical risk for VTE  zased on medical history and associated signs and symptoms (see above and Chapter 9). Esophageal perforation of the thoracic region is another cause of chest pain, with most cases resulting from medical procedures of the esophagus.

B. Physical Examination

Findings on physical examination can occasionally yield important clues to the underlying cause of chest pain; however, a normal physical examination should never be used as the sole basis for ruling-out most diagnoses, particularly ACS and aortic dissection. Vital sign measurement, including pulse oximetry, is always the first step for assessing the urgency and tempo of the subsequent examination and diagnostic work-up.

Findings that increase the likelihood of ACS include diaphoresis, hypotension, S3 or S4 gallop, pulmonary crackles, or elevated jugular venous pressure (see Table 2–4). Although chest pain that is reproducible or worsened with palpation strongly suggests a musculoskeletal cause, up to 15% of patients with ACS will have reproducible chest wall tenderness. Pointing to the location of the pain with one finger has been shown to be highly correlated with nonischemic chest pain. Aortic dissection can result in differential blood pressures (> 20 mm Hg), pulse amplitude deficits, and new diastolic murmurs. Although hypertension is considered the rule in patients with aortic dissection, systolic blood pressure < 100 mm Hg is present in up to 25% of patients.

A cardiac friction rub represents pericarditis until proven otherwise. It can best be heard with the patient sitting forward at end-expiration. Tamponade should be excluded in all patients with a clinical diagnosis of pericarditis by assessing pulsus paradoxus (a decrease in systolic blood pressure during inspiration > 10 mm Hg) and inspection of jugular venous pulsations. Subcutaneous emphysema is common following cervical esophageal perforation but present in only about one-third of thoracic perforations (ie, those most commonly presenting with chest pain).

The absence of physical examination findings in patients with suspected pulmonary embolism usually serves to ncrease the likelihood of pulmonary embolism, although a normal physical examination is also compatible with the much more common conditions of panic/anxiety disorder and musculoskeletal disease.

C. Diagnostic Studies

Unless a competing diagnosis can be confirmed, an ECG is warranted in the initial evaluation of most patients with acute chest pain to help exclude ACS. ST segment elevation is the ECG finding that is the strongest predictor of acute myocardial infarction (see Table 2–4); however, up to 20% of patients with ACS can have a normal ECG. A 2007 study concluded that patients with suspected ACS can be safely removed from cardiac monitoring in the emergency department if they are pain-free at initial physician assessment and have a normal or nonspecific ECG. This decision rule had 100% sensitivity for serious arrhythmia (95% confidence interval, 80–100%), but deserves further validation. Clinically stable patients with cardiovascular disease risk factors, normal ECG, normal cardiac biomarkers, and no alternative diagnoses (such as typical GERD or costochondritis) should be followed-up with a timely exercise stress test that includes perfusion imaging. The ECG can also provide evidence for alternative diagnoses, such as pericarditis and pulmonary embolism. Chest radiography is often useful in the evaluation of chest pain, and is always indicated when cough or shortness of breath accompanies chest pain. Findings of pneumomediastinum or new pleural effusion are consistent with esophageal perforation. Sixty-four–slice CT coronary angiography has been studied for diagnosing acute coronary syndromes and predicting outcomes in the emergency department. One study of 58 patients found a high positive predictive value for diagnosing acute coronary syndromes, and a negative predictive value of 97%. Another study found that it compared favorably with stress nuclear imaging in the detection and exclusion of ACS in low-risk chest pain patients. CT is the study of choice at most centers for the diagnosis of esophageal perforation as well as for aortic dissection (helical CT). Current generation highly-sensitive assays for cardiac troponin I have been studied in an effort to more rapidly prognosticate outcomes in patients presenting with suspected ACS. Patients presenting to the emergency department with chest pain of intermediate or high probability for ACS without electrocardiographic or biomarker evidence of a myocardial infarction can be safely discharged from an observation unit after stress cardiac magnetic imaging.

The role of CT coronary calcium assessment in the evaluation of chest pain in the emergency department is still being defined. A study suggests that the coronary artery calcium score appears to be an effective initial tool for risk stratification of low- to intermediate-risk patients with possible acute coronary syndromes, on the basis of its high negative predictive value and additive diagnostic value.

In the evaluation of pulmonary embolism, diagnostic test decisions and results must be interpreted in the context f the clinical likelihood of VTE. A negative D-dimer test is helpful for excluding pulmonary embolism in patients with low clinical probability of VTE (3 month incidence = 0.5%); however, the 3-month risk of VTE among patients with intermediate and high risk of VTE is sufficiently high in the setting of a negative D-dimer test (3.5% and 21.4%, respectively) to warrant further imaging given the lifethreatening nature of this condition if left untreated. CT angiography (with helical or multidetector CT imaging) has replaced ventilation-perfusion scanning as the preferred diagnostic test for pulmonary embolism, having approximately 90–95% sensitivity and 95% specificity for detecting pulmonary embolism (compared with pulmonary angiography). However, according to guidelines published by the American Academy of Family Physicians
and the American College of Physicians (AAFP/ACP), the sensitivity of helical CT is probably not sufficiently high to exclude pulmonary embolism among patients with high clinical probability of VTE, in whom lower extremity ultrasound or pulmonary angiogram may be appropriate. When ventilation-perfusion scanning is performed, only results that are normal or high probability are useful for improving one’s clinical assessment of pulmonary embolism. Panic disorder is a common cause of chest pain, accounting for up to 25% of cases that present to emergency departments and a higher proportion of cases presenting in primary care office practices. Features that correlate with an increased likelihood of panic disorder include absence of coronary artery disease, atypical quality of chest pain, female sex, younger age, and a high level of self-reported anxiety.

Treatment

Treatment of chest pain should be guided by the underlying etiology. The term “noncardiac chest pain” is used to describe patients who evade diagnosis after receiving extensive work-up. Although under-studied, one small trial of patients with noncardiac chest pain found that about half fulfilled criteria for anxiety or depression and almost half reported symptom improvement with high-dose
proton-pump inhibitor therapy.

When to Refer

• Refer patients with poorly controlled, noncardiac chest pain to a pain specialist.
• Refer patients with sickle cell anemia to a hematologist.

When to Admit

• Failure to adequately exclude (to a sufficient degree) life-threatening causes of chest pain, particularly myocardial infarction, dissecting aortic aneurysm, pulmonary embolism, and esophageal rupture.
• Pain control for rib fracture that impairs gas exchange.