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Specific Causes of Chest Pain
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- Angina
Angina is typically a substernal pressure lasting five to 15 minutes. Most of the time, it will be accompanied by radiation to the jaw, neck, shoulders, or arms. Angina is less likely to have the symptoms often associated with myocardial infarction: sweats, nausea, and shortness of breath. Angina occurs when myocardium becomes ischemic — not enough blood comes through narrowed coronary arteries to meet myocardial needs. This can happen when there is increased demand for oxygen such as during exercise, or decreased supply such as hypotension or anemia. Variant angina occurs due to coronary artery spasm alone.
Anginal pain is not typically affected by respiration or by position, although most patients with angina prefer to sit up. Patients with stable angina will have pain after a predictable amount of exertion, and have identical symptoms with each attack.
Occasionally, symptoms other than pain may occur with transient myocardial ischemia. For example, a profound sense of weakness and breathlessness may be an “angina equivalent.” Atypical symptoms are more likely to occur in the elderly and in diabetics.
The physical exam is usually normal. A new S4 may be heard, suggesting a stiff ventricle due to ischemia. The patient may appear pale and diaphoretic during the attack.
About half of patients with angina will have ECG changes during an attack. Most commonly ST segment depression is seen, but ST elevation is also possible with angina. ST segment elevation occurs in variant angina (Prinzmetal’s angina), where coronary artery spasm (rather than atherosclerosis) is responsible for ischemia.
For individual episodes of angina, give nitroglycerin either as sublingual tablets or spray. Typically, the pain will resolve within three minutes. Long-term management is with long-acting nitrates, beta blockers, or calcium channel blockers, either alone or in combination. Back to Index.
Unstable Angina
Unstable angina may be called “crescendo” or “preinfarction” angina It may herald an impending myocardial infarction. Sudden change in the pattern of angina usually means a physical change within the coronary arteries, such as hemorrhage into an atherosclerotic plaque, rupture of a plaque with intermittent thrombus formation, or spasm. About a third of patients with the clinical syndrome of unstable angina will already have coronary thrombosis on catheterization.
Some experts regard any new-onset angina as unstable. Typically, unstable angina is defined as angina of increasing severity, frequency, duration, or showing increasing resistance to nitrates, or angina occurring at rest.
Untreated, unstable angina progresses to myocardial infarction within three months in half of cases. The patient with new onset or unstable angina should be hospitalized for intensive medical treatment. Back to Index.
Myocardial Infarction
The pain of myocardial infarction is typically substernal, diffuse, with a squeezing or pressure quality. It may radiate to the neck or jaw, shoulders, or arms. Most often, the pain is accompanied by additional symptoms, such as lightheadedness, nausea or vomiting, diaphoresis, or shortness of breath.
The symptoms of myocardial infarction last longer than 15 minutes, and do not respond completely to nitroglycerin. The duration of the pain is variable. Pain may resolve completely after a few hours, or may persist for over 24 hours.
Elderly or diabetic patients are prone to atypical symptoms, such as nausea or dyspnea as the sole symptoms of infarction. As many as one-fourth of myocardial infarctions are “silent” — that is, whatever symptoms were present did not impress the patient enough to seek medical care, or even to remember the incident.
The physical exam usually shows the patient to be pale or grayish. Diaphoresis is often present. The MI victim often has a hard-to-define expression suggesting illness, anxiety, and pain. Pulse rate may be normal, but often bradycardia is present in inferior infarction. Tachycardia is often seen with large infarctions, and may be a bad prognostic sign. Blood pressure is often elevated.
Cardiac exam will usually be normal. Large infarctions may cause signs of ventricular failure or valve dysfunction. S1 may soften as the speed of left ventricular contraction diminishes. In rare cases, the second heart sound may be paradoxically split as the left ventricular contraction time increases due to left bundle branch block and weakened left ventricle. A fourth heart sound (S4) is common due to a stiffened ventricle. Mitral regurgitation may occur if papillary muscles malfunction.
Later in the course of myocardial infarction, other findings may be present: mild fever, pericardial friction rub, VSD murmur due to septal rupture, or severe mitral regurgitation due to papillary muscle rupture.
The ECG may be normal early in myocardial infarction. While only about one percent of patients with a completely normal ECG will have infarction, one-quarter of patients with myocardial infarction will present with a normal ECG.
The ECG alone cannot diagnose infarction. A combination of compatible history, ECG, and enzyme changes is required. New Q waves or ST segment elevation is about 75 percent accurate at predicting MI.
Serum creatine kinase (CPK or CK) rises about six to eight hours following infarction, peaking in about 24 hours. Early elevations may be seen with partial or complete reperfusion of ischemic areas.
Patients with possible myocardial infarction (anyone with a compatible chest pain history) should be kept on cardiac monitor. Oxygen therapy, and an IV line, should be established as quickly as possible.
Thrombolytics should be administered to MI patients, if there are no contraindications. Speed of thrombolytic delivery is important, as an intracoronary thrombus becomes “permanent” after several hours. Under most circumstances, thrombolytics should be given in the emergency department by the emergency physician.
Admit all MI patient (and all patients in whom the diagnosis is entertained) to an intensive care environment. Back to Index.
Pneumonia
The pain of lobar pneumonia often begins as a general sense of pressure and aching, usually localized to one side of the chest. The pain begins around the time of the chills or rigors heralding the onset of the infection. Later, pleuritic pain develops as the process affects the pleura. Patients with atypical pneumonia and bronchopneumonia may complain of a central burning sensation provoked by coughing, and also may have pleuritic pain.
The pain of pneumonia is distinguished from cardiac pain by the presence of chills and fever at the onset (the MI victim may develop a slight fever later during the course of infarction), and typical infiltrates on chest x-ray.
Pneumonia may be mistakenly diagnosed in the MI victim because: 1) many cardiac patients will cough because of a sense of breathlessness, or due to pulmonary congestion, 2) rales of pulmonary congestion may be unilateral (most often left-sided), 3) the MI victim may develop a mild fever, 4) the MI victim often has leukocytosis, and 5) atelectasis, commonly seen in older patients, may be interpreted as pneumonia. The physician also must keep in mind that myocardial ischemia can result from the hypoxia and increased metabolic demands of pneumonia. Back to Index.
Pericarditis
The pain of pericarditis is usually substernal, and often radiates to the neck or back. Often the pain is worsened by lying down and improved by leaning forward. While the pain is usually steady, some patients will have accentuation of the pain with each heartbeat. Sharp pain with chest motion or deep breathing is also common.
About three fourths of patients will have some type of pericardial rub. The rub is often described as “the squeak of new leather.” The rub can occur just before systole as the atrial contraction moves the ventricles, during systole as the ventricle lifts against the pericardial sack, or in early diastole as the heart relaxes and moves against the sack again. Sometimes all three components are present.
The ECG shows ST segment elevation over many leads. Typically, the elevations are upwardly rounded from the J point. Later, T wave inversions can be seen.
The greatest danger associated with the diagnosis of pericarditis is not the danger of tamponade; it’s the danger of sending a young myocardial infarction patient home with a diagnosis of pericarditis. Pericarditis patients should be admitted to a monitored bed unless the diagnosis is clear, the severity is mild, and the follow-up is reliable. Back to Index.
Mitral Prolapse
Mitral prolapse is usually asymptomatic. The pain associated with mitral prolapse can be severe, substernal, and crushing, and can radiate to the neck and arms. Additional symptoms such as shortness of breath and nausea may occur, but are unusual.
The typical mitral prolapse patient is young and otherwise healthy. Physical findings of Marfan’s syndrome may be present.
The presence of a mitral murmur does not prove that the chest pain is due to mitral prolapse. An initial episode of cardiac-compatible pain in a patient with mitral prolapse should be treated as possible infarction until proven otherwise. Back to Index.
Aortic Dissection
Aortic dissection is rare compared to myocardial infarction. Almost all patients will be older hypertensive males. Pain typically begins abruptly, with a tearing quality. The pain almost always radiates to the back, or may be felt only in the back, between the shoulder blades.
As the dissection affects the roots of the subclavian and carotid arteries, pulse deficits, neurological signs, or a blood pressure difference between the arms may develop. Most patients will have 20 mm Hg blood pressure difference between the arms. Over half will have an aortic regurgitation murmur. About a third will have neurologic compromise.
Myocardial infarction can occur during dissection as the roots of the coronary arteries are damaged. About 90 percent of patients will have an abnormal ECG, although it will usually not be diagnostic of a localized infarction.
The chest x-ray may show an ascending aorta that extends beyond the rim of calcification, or may show a widened mediastinum. Aortography will demonstrate the dissection. Back to Index.
Pulmonary Embolism
Most pulmonary embolism patients will have obvious predisposing factors: either CHF, a history of previous PE or DVT, or major risk factors such as cancer, immobilization, recent surgery, or oral contraceptives.
The pain of pulmonary embolism is usually pleuritic with smaller peripheral emboli, or generalized and substernal with a large central embolism. Often the pain begins as a generalized discomfort, progressing to pleuritic pain as infarction of lung occurs or as the embolus breaks up and moves peripherally. At presentation to the ER, 75 percent of patients will have pleuritic pain. Most patients complain of shortness of breath.
The typical findings of pulmonary embolism are tachycardia and tachypnea. Lung exam is usually normal, but rales or wheezes may occur. About a third of the time, the pulmonary component of the second heart sound is increased.
Most patients will have some abnormality of the chest x-ray. About half will have an elevated diaphragm on the side of the embolism. Atelectasis or infiltrates are common. X-ray findings diagnostic of pulmonary embolism include a pleural-based infiltrate with a round inner border, vessel cutoff, or a unilaterally dilated outflow tract with decreased vascularity distal to it.
The ECG is usually abnormal in pulmonary embolism. The most common abnormality is T-wave inversion, usually in the right heart leads, occurring in about 40 percent of patients. About 20 percent will have ST segment depression, and another 20 percent will have the “typical” S1-Q3-T3 pattern.
Arterial blood gases can be helpful in ruling out PE in patients who, by history, would be expected to have normal lungs. An elevation of the arterial-alveolar gradient on room-air blood gases can increase the suspicion of pulmonary embolism:
A-a = (Bar.Press.-47) x .21 - 1.25 x PaCO2 - PaO2.
Normal gradient is 10 mm plus 2 mm per decade over age 30.
Order a lung perfusion scan when pulmonary embolism is suspected. Some patients may require angiography, or doppler studies of the legs to confirm the diagnosis. Back to Index.
Esophageal Rupture
Esophageal rupture usually follows an episode of violent emesis. Often the patient will complain that something “tore” in the chest. Pain is usually constant and severe, but worsened with change of position or deep breathing. It often radiates to the back.
Mediastinitis develops rapidly, with fever and toxicity. As gas forms within the tissues, a “cardiac crunch” may occur due to mediastinal emphysema.
The chest x-ray will usually show a widened mediastinum, often with mediastinal air. Back to Index.
Esophagitis
Esophageal pain may be due to esophageal mucosal irritation or spasm of the esophageal muscles. It usually occurs in a patient with a history of heartburn, reflux, dysphagia, or symptomatic hiatal hernia.
Pain due to mucosal irritation (reflux esophagitis) is usually steady for hours. It’s usually well-localized to the lower substernal area and radiates to the upper stomach. It may radiate into the neck, but rarely radiates to the arms. When radiation occurs, it’s usually symmetrical.
The pain of esophageal spasm is poorly localized, and may mimic angina in nature and severity. The pain usually follows a meal, or may be provoked by the act of swallowing.
There are no physical, lab, or x-ray findings that are typical for esophageal pain. The presence of an air-fluid level in a hiatal hernia on chest x-ray isn’t helpful in proving the cause of pain — it occurs in many older individuals with chest pain due to other causes.
Therapeutic trials may only confuse the physician who is considering an esophageal cause for chest pain. Most patients with esophageal spasm will have relief with nitroglycerin. Only 20 percent of patients with esophagitis will have relief with a “GI cocktail” in the emergency department. But the same number of cardiac patients will claim pain relief, probably due to placebo effect or due to the natural course of the pain.
Some patients present with a clear history of past attacks proven due to esophageal disease. However, the diagnosis of new-onset esophageal pain should be entertained only after angina and infarction are ruled out. No tests are available in the acute setting that can reliably prove esophageal pain. Back to Index.
Back to Chest Pain Manual Index
Copyright 1996 Mad Scientist Software
Citation:
Argyle, B., Blood Gases Computer Program Manual.
Mad Scientist Software, Alpine UT, 1996.
Back to Main Text Resource Index Go to Mad Scientist Software's main index page