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The primary concern for patients with chest pain is whether or not the pain is of cardiac origin. In addition to cardiac disease, chest pain may be due to pulmonary, GI, musculoskeletal, or psychological diseases. Emergent causes of chest pain include MI, aortic dissection, pulmonary embolus (PE), and pneumothorax. Patients with these diagnoses usually present to the emergency room but may on occasion present in the outpatient setting. Chest pain in the office setting is most commonly due to musculoskeletal, GI, and cardiac causes. Approximately 15% of patients with chest pain do not fit into any diagnostic category and remain undiagnosed despite evaluation.
PATHOGENESIS OF CHEST PAIN AND SIGNS AND SYMPTOMS
Chest pain may emanate from inflammation or injury to the structures in and around the thoracic cavity. Muscular chest pain is common and may occur when there is inflammation from overuse or injury to the muscles of the chest wall. The costochondral joints may also become inflamed from overuse or injury or in association with viral illnesses. Rib fractures may produce significant pain and are generally due to trauma, but they may also occur as a result of metastatic cancer.
Gastroesophageal reflux disease (GERD) and esophageal motility disorders are common causes of chest pain. The reflux of acidic gastric contents into the lower esophagus may produce esophagitis and chest pain that is indistinguishable from cardiac chest pain. The symptoms of gastritis and peptic ulcer disease may also be perceived by some patients as a sub-sternal pain. Cholelithiasis and cholecystitis, which usually cause right-upper-quadrant pain, may also produce substernal pain.
Cardiac chest pain results from an insufficient oxygen supply to myocardial tissue, usually from coronary artery disease. The initial step in the development of atherosclerotic heart disease is the fatty streak. Over time, the fatty streak can enlarge into a calcified plaque, eventually narrowing the vessel lumen and impairing blood flow. If the plaque ruptures, lipids and tissue factors are released from the plaque, triggering a series of events that ultimately result in intravascular thrombosis and MI. If the plaque does not rupture, a gradual narrowing of thelumen can cause anginal chest pain. This is typically brought on by exertion as the myocardial oxygen demand exceeds the supply.
Since lung tissue does not have pain fibers, inflammation or irritation of the parietal pleura is responsible for the chest pain from pulmonary diseases such as pneumonia or PE.
Other causes of chest pain include psychological and neurologic diseases, such as herpes zoster and cervical or thoracic radiculopathies. Patients with herpes zoster may experience pain before the rash appears. Disk herniation or osteoarthritic narrowing of the cervical or thoracic foramen may result in nerve compression and chest pain following a radicular pattern. Patients with psychological disease, such as anxiety and panic disorder, may present with a variety of chest symptoms including palpitations, dyspnea, and chest pain as part of their symptom complex.
CLINICAL MANIFESTATIONS OF CHEST PAIN
HISTORY
Patients with chest pain should be asked about its severity, quality, location, and duration; aggravating factors; relieving factors; radiation of pain; and other associated symptoms. Myocardial pain is often described as substernal chest tightness or pressure that radiates to the left arm, shoulders, or jaw. Patients may also complain of diaphoresis, shortness of breath, nausea, and vomiting. Anginal pain is typically brought on by exercise, eating, or emotional excitement. The pain usually lasts from 5 to 15 minutes and disappears with rest or nitroglycerin. Pain that lasts less than 1 minute or longer than 30 minutes should not be considered anginal. Pericardial pain is often persistent, sharp, severe, and relieved by sitting up. Breathing, lying back, or coughing may aggravate the pain. The pain of aortic dissection is anterior and severe; it often has a ripping or tearing quality, with radiation to the back or the abdomen.
Tracheobronchitis may cause a burning pain in the upper sternal area associated with a productive cough. Pain with pneumonia commonly occurs in the overlying chest wall and is aggravated by breathing and coughing. In pneumothorax, the pain is of sudden onset, sharp, unilateral, pleuritic, and associated with shortness of breath. Pleurisy is a sharp pleuritic chest pain, often in association with a preceding viral illness.
GERD causes a burning pain that radiates up the sternum. It is worsened by large meals and lying down. Antacids may relieve the pain. The pain of esophageal spasm, which is usually associated with swallowing, may he indistinguishable from cardiac pain. Since nitroglycerin relaxes smooth muscle, it may relieve the pain.
Musculoskeletal pain from costochondritis can often be reproduced on palpation. Patients are also reluctant to take a deep breath, since this aggravates the pain.
Patients with generalized anxiety will often complain of chest pain. However, this pain is nonspecific. Associated symptoms include overwhelming fear, palpitations, breathlessness, and tachypnea.
PHYSICAL EXAMINATION OF CHEST PAIN
Vital signs help to assess the urgency of the patient's complaints. Hypotension can occur with myocardial ischemia, pericardial tamponade, PE, and GI bleeding. Tachycardia may indicate severe illness, and arrhythmias can occur with cardiac or pulmonary causes of chest pain. The presence of fever suggests an infectious cause, such as pneumonia. Inspection and palpation may reveal ecchymosis from an injury, the rash of shingles, crepitus associated with rib fractures, and the sharply localized tenderness of intercostal muscle pain or costochondritis.
A thorough cardiopulmonary examination is warranted for all patients with chest pain. Patients with myocardial ischemia may have an audible S4 or signs of congestive heart failure, such as an S3 and pulmonary rales. Pericarditis may cause a friction rub and pulsus paradoxus. Beck's triad consisting of jugular venous distention, muffled heart sounds, and decreased blood pressure--suggests cardiac tamponadc, which may he seen in severe cases of pericarditis. In aortic dissection, patients may have hypotension, absence of peripheral pulses, and a murmur of aortic insufficiency. Patients with pneumonia will have crackles on inspiration, dullness to percussion, and egophony, indicating consolidation. Signs of pneumothorax include hyperresonance to percussion, tracheal deviation, decreased breath sounds, and decreased tactile and vocal fremitus. Patients with pulmonary embolism will likely have normal auscultatory findings but may be tachycardic, tachypneic, and have lower extremity edema.
Patients with acute cholecystitis may have rightupper-quadrant abdominal tenderness. GERD and gastritis will often cause epigastric pain on deep palpation. Esophageal spasm and psychogenic chest pain typically do not produce abnormal physical findings.
DIFFERENTIAL DIAGNOSIS
Common causes of chest pain are presented in Box 10-1. In the outpatient setting, musculoskeletal disease is present in over one-third of patients with chest pain. GI disease occurs in approximately 20% of patients seen in the office with chest pain, followed in frequency by cardiac, psychogenic, and pulmonary causes. Cardiac and pulmonary diseases, although not the most common in the outpatient setting, must be considered in any patient presenting with chest pain because of the potentially life-threatening diseases these represent.
DIAGNOSTIC EVALUATION OF CHEST PAIN
The history and physical examination help to classify the chest pain into cardiac, pulmonary, GI, musculoskeletal, or psychogenic causes. An ECG is a critical element for evaluating chest pain.
Although an ECG can be normal in patients with heart disease, ST-segment elevation or depression is indicative of myocardial ischemia. Diffuse ST-segment elevation is consistent with pericarditis, while Q waves can indicate an old or recent MI. Cardiac markers such as creatine phosphokinase (CPK), troponin, and myoglobin are intracellular macromolecules that diffuse from damaged cardiac myocytes into the circulation. These markers are sensitive tests for determining whether myocardial injury or infarction is present. Troponins are the first enzymes to rise and remain elevated for 5 to 14 days. They are the most sensitive and specific for MI. The MB fraction of CPK-MB serves as another sensitive test; it begins to rise within 4 hours and peaks at 24 hours after an MI. It is important to obtain serial cardiac markers, since the first set of cardiac markers is negative in 25% to 50% of patients with an acute MI. However, by 8 hours after the onset of symptoms, up to 95% of patients will have a positive test for CPK-MB or one of the troponins. A negative troponin between 6 and 72 hours after the onset of chest pain is strong evidence against MI and acute coronary syndrome, particularly if the ECG is normal or near normal.
In stable patients with suspected cardiac disease, outpatient exercise stress testing is indicated. Patients should have a baseline ECG to detect abnormalities such as a conduction defect or strain pattern that make interpreting a stress test difficult. Patients with baseline ECG abnormalities or a positive exercise stress test should undergo radionuclide testing, a stress echocardiogram, and/or coronary angiography. If an individual is unable to exercise, then a chemical stress test using either adenosine or dobutamine to achieve a target heart rate may be necessary.
An echocardiogram can detect wall motion abnormalities in areas damaged by ischernic myocardial disease, pericardial effusions, and valvular heart disease. If the cause of pericarditis is not evident, an antinuclear antibody, blood urea nitrogen, creatinine, thyroid-stimulating hormone (TSH), and tuberculosis skin test are indicated.
A chest x-ray can detect pneumonia, pneumothorax, or other lung pathology. If PE is suspected, a ventilation/perfusion scan or a spiral computed tomography scan (CT scan) is generally indicated. Spiral CT scanning is the preferred test in those with abnormal chest x-ray findings due to underlying diseases such as COPD. Newer algorithms for assessing patients with possible pulmonary embolism utilize testing blood levels of D-dimer. A totally normal D-dimes level in a low-risk patient is strong evidence against a pulmonary ~mholism. Patients with suspected PE should also iave a venous Doppler to rule out DVT.
Patients suspected of having musculoskeletal chest pain might not require any diagnostic testing.
TREATMENT OF CHEST PAIN
Any patient with suspected. MI, unstable angina, or PE should be hospitalized for evaluation. Patients who present with MI should be stabilized initially with oxygen, nitroglycerin, and morphine for pain control. Aspirin alone has been shown to reduce the mortality from acute MI by more than 20%, and all patients with suspected MI should receive aspirin as soon as possible. In patients allergic to aspirin, clopidogrel may be used. Other drugs used to treat an acute MI include beta blockers, heparin, nitrates, angiotensin-converting enzyme (ACE) inhibitors, and thrombolytics. Ideally, the systolic blood pressure should be maintained at 100 to 120 mmHg (except in patients with previously severe hypertension) and the heart rate kept at about 60 beats per minute. Thrombolytics should be considered in patients below 75 years of age with ST-segment elevation and a history consistent with an acute MI who present within 6 hours of the onset of chest pain. Recent studies suggest that treatment within 12 hours after the onset of pain may still be beneficial for older patients. Contraindications for thrombolytics include active internal bleeding, history of cerebrovascular disease, recent surgery, intracranial neoplasm, arteriovenous malformation, aneurysm, bleeding diathesis, or severe uncontrolled hypertension. Percutaneous transluminal coronary angioplasty (PTCA) is emerging as an alternative to thrombolytic therapy in institutions that can provide emergent catheterization. Glycoprotein inhibitors are useful when added to heparin in patients with unstable angina and non-Q-wave infarctions.
Patients with stable angina may he treated in the outpatient setting and started on aspirin and sublingual nitroglycerin for anginal episodes. Beta blockers reduce the frequency of symptoms, increase anginal threshold, and reduce the risk of a subsequent MI in patients with a previous MI. Long-acting nitrates reduce anginal pain but do not increase longevity and require a daily nitrate-free period to avoid tolerance. For patients who continue to have angina despite maximal therapy with beta blockers and nitrates, calcium channel blockers may aid in controlling symptoms. Aggressive treatment of risk factors such as hypertension, inactivity, and lipids is also an important component of long-term management. Evidence-based guidelines from the Adult Treatment Panel III (ATP I11) of the National Cholesterol Education Program recommend lowering the low-density-lipoprotein cholesterol (LDL-C) to <100 mg/dl, in individuals with coronary artery disease. Newer evidence suggests that an LDL-C <75 mg/dL may even he a more appropriate target in patients with coronary artery disease.
Aortic dissection is an emergency and requires hospitalization and surgical consultation. Pericarditis may improve with aspirin or other NSAIDs. Steroids should be considered in severe cases. PE requires anticoagulation. Warfarin is started concomitantly with heparin; once the international normalized ratio (INR) reaches the therapeutic level, heparin may be discontinued. A smaller pneumothorax (<30%) in astable individual can be managed conservatively; a larger pneumothorax requires chest tube insertion. Treatment for patients with pneumonia or bronchitis is outlined in Chapter 29. Costochondritis is treated with NSAIDs.
KEY POINTS OF CHEST PAIN
- Chest pain can be due to pulmonary, GI, cardiac, musculoskeletal, or psychological causes.
- The most common emergent causes of chest pain include Ml, unstable angina, aortic dissection, PE, and pneumothorax.
Cardiac chest pain that lasts more than 30 minutes is most probably secondary to infarction.
- Beck's triad jugular venous distention, muffled heart sounds, and decreased blood pressure indicates cardiac tamponade.
- Signs of pneumothorax include hyperresonance to percussion, tracheal deviation,decreased breath sounds, and decreased tactile and vocal fremitus.
- A patient who presents with MI should be stabilized initially with oxygen, nitroglycerin, and morphine for pain control.
- Contraindications to thrombolytics include active internal bleeding, history of cerebrovascular disease, recent surgery, intracranial neoplasm, arteriovenous malformation, aneurysm, bleeding diathesis, and severe uncontrolled hypertension.
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