A. Introduction. Because chest pain (including “discomfort”) is common and its etiologies range from a life-threatening myocardial infarction to benign musculoskeletal pain, a simple and reliable approach is necessary.
B. Causes of Chest Pain. One way to remember the causes of chest pain is to use an “outside-in” approach. That is, begin with the structures on the exterior of the body and work your way inward when thinking about causes of chest pain.
a. Skin. Varicella-zoster virus infection (shingles) often causes pain before vesicular lesions are noted. The pain usually occurs in a dermatomal distribution.
b. Chest wall. Musculoskeletal pain may result from shoulder arthritis or bursitis, intercostal injury, metastatic disease to the bones or chest wall, or costochondritis. Breast pathology (e.g., tumors, fibrocystic disease) and nerve root compression (from cervical disk herniation) may also lead to chest pain.
c. Lungs. Pleuritis, pneumothorax, pulmonary emboli, infections, malignancies, and connective tissue disorders can all cause chest pain, which is usually pleuritic (i.e., it worsens with inspiration or coughing).
d. Cardiovascular. Pericarditis, myocarditis, myocardial ischemia and infarction, and aortic dissection/acute aortic syndrome can all cause chest pain. Other cardiac causes of chest pain include but are not limited to valve disease, hypertrophic cardiomyopathy, Prinzmetal’s angina (due to coronary vasospasm) and stress cardiomyopathy.
e. Gastrointestinal tract. Esophageal disorders (including esophagitis, spasm, reflux, and rupture) are common causes of chest pain. Other gastrointestinal causes of chest pain include gastric and duodenal ulcers, pancreatitis, and biliary disease.
f. Psychiatric. Anxiety, panic attacks, somatoform disorders.
C. Approach to the Patient. Although the outside-in approach is useful for remembering the differential diagnoses for chest pain, it fails to highlight the four acutely life-threatening causes: myocardial infarction, pulmonary embolism, aortic dissection, and pneumothorax. Because chest pain may represent one of these emergencies, the usual order of evaluation (e.g., history, physical examination, diagnostic tests) may hinder critical early intervention. The first step of the evaluation should therefore include a quick screen for the four “killer” chest pains, followed by a more in-depth evaluation if the etiology of the chest pain is still unclear.
Never forget the four “killer” causes of chest pain:
Myocardial infarction or ischemia
a. Screen for the killer chest pains
i. “Eyeball” the patient. A patient who is clutching his or her chest, is diaphoretic, or is ashen can be presumptively diagnosed as suffering from myocardial infarction from across the room. Even if the presentation is not classic, you can often decide who “looks sick” and may need a more rapid evaluation in a more monitored setting.
ii. Establish intravenous access and cardiac rhythm monitoring immediately in patients who appear ill or who have cardiac risk factors.
iii. Evaluate the patient’s vital signs
Any abnormality of the vital signs should alert you to the possibility that the chest pain has a potentially serious cause.
1. Check blood pressure in both arms. Although a difference in pressure of 10 mm Hg or more may be seen in patients with aortic dissection, local atherosclerosis can also produce blood pressure differences. Therefore, the blood pressure reading is neither sensitive nor specific for aortic dissection.
2. Check respiratory rate and oxygen saturation. Low oxygen saturation may accompany spontaneous pneumothorax, pulmonary embolism, or myocardial infarction (with pulmonary edema).
a. Low oxygen saturation (<92%) is often an indication that an arterial blood gas should be ordered immediately.
b. A normal oxygen saturation may still be accompanied by a significant alveolar-to-arterial (A-a) oxygen gradient during hyperventilation. Therefore, arterial blood gas testing to evaluate for the possibility of pulmonary embolism may still be necessary if the rest of the evaluation is unrevealing.
iv. Look at the electrocardiogram (EKG). The EKG leads are often placed while the vital signs are being checked.
Always obtain a previous EKG when looking for changes suggestive of ischemia or infarction.
1. EKG abnormalities that suggest acute myocardial infarction or ischemia (i.e., acute coronary syndromes) are always grounds for admission. Make sure the patient has intravenous access, a cardiac rhythm monitor, and supplemental oxygen and has been given a full-dose aspirin (usually 325 mg) orally. (The emergent treatment of acute coronary syndromes is discussed in more detail in Chapter 11.)
2. Normal EKG. A normal EKG does not rule out myocardial infarction or ischemia. Nitroglycerin (0.3–0.6 mg sublingually or by aerosol) may be administered and the dose repeated every 3–5 minutes as both a diagnostic challenge and as potential therapy in patients with persistent chest pain.
v. Take a preliminary history
In patients with a history of coronary artery disease or cardiac risk factors and no alternative explanation for chest pain after careful evaluation, admission to rule out myocardial infarction is usually appropriate.
1. Cardiac history and risk factors. First, ask about any prior cardiovascular problems.
a. If there is a history of coronary artery disease, the patient has ischemia until proven otherwise.
b. With a negative cardiac history, you can quickly establish the pretest probability of myocardial infarction by assessing cardiac risk factors (i.e., age, male gender, smoking, diabetes, hypertension, high cholesterol, and positive family history) in addition to pain characteristics.
2. Other risk factors. The preliminary history can also help elucidate any predisposing factors to the other “killer” chest pains. For example, a history of cancer or inactivity may contribute to pulmonary embolism. On the other hand, the risk factors of uncontrolled hypertension, a history of Marfan’s syndrome/connective tissue disorder, known aortic aneurysm, known aortic valve disease, recent aortic manipulation, or a family history of aortic disease may increase the likelihood of aortic dissection.
vi. Perform a preliminary physical examination. Frequently, you will have time between tests to look at the neck veins, listen to the heart and lungs, palpate the upper abdomen for tenderness, and evaluate the pulses in the arms and legs. This quick examination can help identify important diagnoses.
vii. Evaluate the chest radiographs. Always compare new images to old images, if they are available.
1. Spontaneous pneumothorax can be subtle, and you need to look carefully, especially in the apices.
2. Esophageal rupture may lead to air in the mediastinum (pneumomediastinum).
3. Myocardial infarction or aortic dissection may be accompanied by enlargement of the heart or mediastinum, respectively; however, these structures are often exaggerated on anteroposterior films. The presence of pulmonary edema may also be suggestive of myocardial infarction.
viii. Order an arterial blood gas analysis. If not performed earlier, an arterial blood gas analysis with the patient breathing room air is usually necessary. Always perform an arterial blood gas when considering a diagnosis of pulmonary embolism.
b. Further define the cause of the chest pain
i. Take a more detailed patient history
1. Type of chest pain. Pulmonary embolism frequently presents with pleuritic chest pain; myocardial infarction may present with “crushing” chest pain or only a mild “discomfort”; and aortic dissection is often characterized by the sudden onset of severe pain that radiates to the back.
2. Radiation of chest pain. Pain that radiates to the neck or left arm should be considered cardiac until proven otherwise.
a. Atypical patterns may still indicate ischemia and include pain, tingling, or numbness in the left fingertips unaccompanied by arm pain and pain in the outer left shoulder.
b. It is wise to consider any neck, upper abdominal, or upper back pain as cardiac in origin until proven otherwise.
3. Onset of chest pain. Spontaneous pneumothorax, aortic dissection, and pulmonary embolism usually present with abrupt pain, whereas pain from myocardial infarction or ischemia may build more gradually. Spontaneous pneumothorax and pulmonary embolism often occur while the patient is at rest, whereas aortic dissection and myocardial infarction may occur with rest or exertion.
4. Duration of chest pain. Pain that only lasts seconds or that has been constant for a long period of time without requiring medical attention (more than 24 hours) is less likely to be caused by one of the four killer chest pains. A myocardial infarction is almost always associated with more than 20 minutes of chest pain.
5. Associated symptoms. Dyspnea, diaphoresis, or lightheadedness should alert you to the possibility of a serious cause of chest pain.
6. Aggravating and mitigating factors
a. Deep inspiration often aggravates pain from the pleura or pericardium (e.g., pleurisy from a pulmonary embolism or pericarditis).
b. Exertion may worsen the pain from myocardial infarction or aortic dissection. Rest may ease the pain from cardiac ischemia, often gradually.
c. Position. Patients with pericarditis often feel worse when supine and better when sitting up. Patients with musculoskeletal pain may feel worse in certain positions. The pain of myocardial infarction is usually unaffected by changes in position, but this is not always the case.
d. Food intake. Pain on swallowing may help localize the problem to the gastrointestinal tract. Chest pain after a meal may indicate gastrointestinal pathology but can also occur with myocardial infarction or ischemia.
e. Nitroglycerin. If chest pain decreases with nitrates (e.g., sublingual nitroglycerin), a cardiac etiology should be suspected; however, esophageal spasm may also respond to this therapy.
ii. Perform a complete physical examination. Pay extra attention to the following parts of the exam.
1. Jugular venous pressure. An elevated jugular venous pressure should alert you to the possibility of a serious disorder (e.g., myocardial infarction, pulmonary embolism, tension pneumothorax), but a normal jugular venous pressure does not exclude these disorders.
2. Cardiac examination
a. Heart sounds. Listen carefully for a third (S3) or fourth (S4) heart sound, which may indicate impaired ventricular contractility or ventricular relaxation, respectively. Both impaired ventricular contractility and impaired relaxation can accompany cardiac ischemia.
b. Murmurs may also increase the likelihood of a cardiac etiology of chest pain. A mitral regurgitation murmur may accompany a myocardial infarction with papillary muscle dysfunction, whereas a systolic ejection murmur may indicate aortic stenosis or hypertrophic cardiomyopathy (both of these conditions can predispose the patient to ischemia). A diastolic murmur resulting from aortic valve insufficiency may develop with ascending (proximal) aortic dissection.
3. Lung examination. Listen carefully for rales (e.g., from myocardial infarction with pulmonary edema) and pleural friction rubs (e.g., from pulmonary embolism, infection, or other pleural processes).
4. Chest wall examination. Minimal tenderness to palpation is nonspecific, but if the chest pain is exactly and reliably reproduced (especially in a well-localized area such as a costochondral junction), a musculoskeletal etiology is likely. Briefly inspect the skin for lesions or trauma. Consider radiographs if bony crepitus is elicited or rib fracture is considered.
5. Abdominal examination. Palpate for any upper abdominal tenderness that may indicate a gastrointestinal or aortic cause of the chest pain.
6. Pulses. Check pulses in the arms and legs bilaterally.
1. Myocardial infarction
a. Because coronary artery disease is such a common disease, it is always better to admit patients for “rule out myocardial infarction (ROMI)” if there is any doubt as to the diagnosis, even in young patients.
b. More than 20 minutes of unexplained chest pain may represent a myocardial infarction, whereas chest pain that lasts less than 20 minutes but increases in frequency or duration or occurs with minimal exertion often represents unstable angina; both patterns are indications for admission.
c. Frequently, patients with chest pain are given an antacid and lidocaine swish and swallow (“GI cocktail”) to evaluate possible reflux esophagitis. Many patients who “benefit” from this “diagnostic test” may actually have ischemic pain that is improving spontaneously or from bed rest and oxygen therapy.
2. Pulmonary embolism. Clinical suspicion is critical. There is often no clinical evidence to suggest deep vein thrombosis, and subtle symptoms and signs may be inappropriately rationalized away. If you have a high clinical index of suspicion, consider empiric anticoagulation before sending the patient for diagnostic tests if there are no contraindications.
3. Aortic dissection
a. Most dissections occur either within several centimeters of the aortic valve (type A or ascending aortic dissection) or just distal to the left subclavian artery takeoff (type B or descending aortic dissection). If the patient has abrupt onset of symptoms, pain that radiates to the back, unequal blood pressures, or other suspicious findings (such as acute aortic valve insufficiency or end-organ hypoperfusion due to dissection into a branch such as a stroke), aortic dissection should be ruled out immediately.
b. Computed tomography (CT) and transesophageal echocardiography (TEE) are equally effective in diagnosing ascending aortic dissection. TEE can be less sensitive for distal descending aortic dissection or for the visualization of the distal ascending aorta and proximal aortic arch. The choice of test to use depends on the patient (e.g., poor renal function may weigh against a CT scan), institutional preferences, and test availability. If clinical suspicion is high, a surgeon should be consulted immediately regarding subsequent evaluation because the mortality rate may be as high as 1% per hour during the first 48 hours. Transthoracic echocardiography is not sensitive enough to rule out dissection, especially in the descending aorta.
c. If dissection is strongly suspected, blood pressure control and avoidance of anticoagulants become essential.
d. Increasingly, patients with symptoms of dissection may be identified as having “intramural” aortic hematoma due to rupture of vasa vasorum within the thoracic aorta. Prognosis and therapy appear to be similar to those with true aortic dissection.
Suggested Further Readings
Amsterdam EA, Wenger NK, Brindis RG, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes. Executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. Circulation 2014;130:2354–94.Find this resource:
Chest pain of recent onset: assessment and diagnosis. National Institute for Health and Care Excellence (NICE), 2016. (Accessed October 25, 2017, 2017, at https://www.nice.org.uk/guidance/cg95.)
Fanaroff AC, Rymer JA, Goldstein SA, Simel DL, Newby LK. Does this patient with chest pain have acute coronary syndrome? The Rational Clinical Examination Systematic Review. JAMA 2015;314:1955–65.Find this resource:
Lee TH, Goldman L. Evaluation of the patient with acute chest pain. N Engl J Med 2000;342:1187–95. (Classic Article.)Find this resource: