Myocardial Ischemia

The chest pain associated with myocardial ischemia is attributed to an imbalance between myocardial oxygen (O₂) supply and demand. Most tissues can increase O₂ supply by increasing O₂ delivery, increasing O₂ extraction, or both. O₂ extraction by the myocardium is much greater than that occurring in other tissues, manifested by the O₂ content of coronary venous blood normally being much lower than that of blood coming from other muscles. Because the ability of the myocardium to increase O₂ extraction is limited, the primary mechanism by which the heart increases O₂ delivery in response to increased demands is to increase coronary blood flow.

Coronary blood flow is determined by the driving pressure (i.e., the aortic pressure minus the left ventricular end-diastolic pressure) and the resistance in the coronary arteries. Chest pain can therefore be caused by conditions that increase myocardial O₂ demand (e.g., hypertension, hyperthyroidism, exercise) in the setting of a limited ability to increase O₂ supply, decrease mean aortic pressure (e.g., aortic stenosis), decrease O₂ delivery (e.g., anemia, hypoxemia), or increase the downstream pressure for coronary arterial flow (e.g., aortic and mitral valve disease, left or right ventricular hypertrophy, or dilatation). The importance of coronary arterial diameter is apparent in Poiseuille’s law, which states that resistance is inversely related to the vessel radius taken to the fourth power, explaining why anything that might result in even a small change in coronary arterial diameter (e.g., coronary arterial spasm, thrombosis, atherosclerosis) can result in chest pain.

A wide range of disorders other than angina may be the cause of chest pain. These potential alternative diagnoses are summarized in Box 21-2.

Pericardial Pain

The visceral pericardium has no pain fibers, and the pain fibers in the parietal pericardium are localized to the caudal (i.e., diaphragmatic) region. This sparse, localized distribution of pericardial pain fibers may explain why most noninflammatory causes of pericardial effusions (e.g., myocardial infarction, uremia) are not associated with chest pain and why inflammatory problems may cause pain only when the inflammation spreads to the visceral pleura.

Pulmonary Pain

The lung parenchyma and the visceral pleura are insensitive to most painful stimuli, and interference with stretch fibers tends to cause most intrapulmonary symptoms. Pain can arise from the parietal pleura, the major airways, the chest wall, the diaphragm, and the mediastinal structures. Inflammatory conditions affecting the lung periphery or the peripheral portions of either hemidiaphragm cause chest wall pain when the process extends to the parietal pleura and stimulates the intercostal nerves. Inflammation of the parietal pleura that lines the more central portions of the diaphragm stimulates the phrenic nerves, with the result that the pain is referred to the ipsilateral neck or shoulder. The augmentation of pulmonary pain during inhalation is attributable to the stretching of the inflamed pleura. Airway pain can be described as a burning pain, whereas mediastinal pain is a dull, central type of discomfort. For example, about 50% of patients with mediastinal metastatic disease describe this type of symptom.

Pulmonary Embolus

Most cases of pulmonary embolism do not exhibit chest pain. If the embolism is big, chest tightness can be present, but most of the symptoms are related to circulatory disturbances. If pain is associated with acute pulmonary embolism, it is thought to result from distention of the central pulmonary artery or arteries. Pain occurring later in the illness is attributable to infarction of a peripheral segment of lung and occurs with concomitant inflammation of the adjacent pleura.

Pulmonary Hypertension

The pain of chronic pulmonary hypertension is attributed to the disparity between right ventricular myocardial O₂ supply and demand, although vascular distention also may play a part.

Musculoskeletal Pain

Costochondral and chondrosternal articulations are common sites of anterior and anterolateral chest pain. The articulations of the second, third, and fourth ribs are most commonly involved. When accompanied by swelling, redness, and heat, the condition is referred to as Tietze syndrome. Coughing or trauma can dislocate the costochondral junctions (most commonly those of ribs 10 to 12). The pain resulting from intercostal neuritis most frequently results from cervical osteoarthritis. Intercostal neuritis also is seen with herpes zoster infection, in which the onset of pain may precede the typical rash by 1 or 2 days (Figure 21-1). Thoracic roots most commonly are involved.

Figure 21-1 Herpes zoster infection affecting an intercostal nerve.

Subacromial bursitis, biceps or deltoid tendinitis, and arthritis of the shoulder can manifest as chest pain with extension to the shoulder and arm. The brachial plexus and subclavian artery can be compressed by a cervical rib, or by spasm of the scalenus anticus muscle. In the Pancoast syndrome (most commonly but not exclusively caused by bronchogenic carcinoma), invasion of the C8, T1, and T2 nerve roots by tumor may be the cause of considerable pain and other symptoms such as muscular weakness (Figure 21-2).

Figure 21-2 Chest radiograph showing a right apical lesion destroying the posterior parts of the first and second rib, with a soft tissue mass extending into the neck.

Esophageal Reflux or Dysmotility

The chest pain resulting from esophageal reflux or dysmotility (e.g., esophageal spasm, achalasia, hyperactive lower sphincter) results from acid irritation of the esophageal mucosa. Esophageal reflux or dysmotility accounts for the chest pain that occurs in as many as 30% of patients with normal findings on a coronary arteriogram.

Clinical Presentation

If the pain is acute (and therefore generally of short duration) and the patient is hypotensive, myocardial infarction, pulmonary embolism, pericardial tamponade, dissecting aneurysm, and tension pneumothorax should be considered first (see Figure 21-3). Less commonly, this clinical syndrome can result from a ruptured esophagus, which not infrequently is missed because it is rare and the emergency physician may be reassured by normal findings on cardiac evaluation. In other patients, the approach is governed primarily by the findings on history and physical examination, which are interpreted on the basis of actual or estimated previous probabilities for each of the conditions listed in Box 21-1. For example, a middle-aged man with one or more risk factors for coronary artery disease (e.g., hypercholesterolemia, diabetes, hypertension, obesity, smoking) who experiences exertional chest pain typical for coronary artery disease that abates with rest has a greater than 90% probability of having myocardial ischemia as the cause of his symptoms. By contrast, a 20-year-old pregnant woman with a chest infection, cough, and localized chest pain is far more likely to have a spontaneous rib fracture.

History

The onset, duration, location, radiation pattern, character, and intensity of the pain should be ascertained, as should the factors that precipitate or diminish it. Unfortunately, both the sensitivity and specificity of the history are low for many of the conditions that must be considered in the differential diagnosis. For example, most episodes of electrocardiographically documented ischemia in patients with stable angina are asymptomatic. A history of cocaine, crack, or other stimulating drug use should be sought.

Pulmonary Inflammation and Chest Wall Problems

Many adjectives have been used by afflicted persons to describe the pain resulting from conditions that cause pulmonary inflammation or chest wall problems, but the pain is almost always pleuritic in nature in that it increases with forced inhalation or exhalation (e.g., during coughing or sneezing), during spontaneous breathing, and when pressure is applied to the chest wall by bending or lying down. In response to the pleuritic or positional character of the pain, patients frequently limit their depth of inhalation and, accordingly, may complain of dyspnea, rather than or in addition to pain.

An abrupt onset suggests a rib fracture, pneumothorax, or pneumomediastinum (Figure 21-4). A more gradual onset over a few minutes or hours is seen with bacterial pneumonia and pulmonary emboli, and a gradual onset (e.g., days or weeks) is more compatible with chronic infections (e.g., tuberculosis, fungal infections) or tumor.

Figure 21-4 Chest radiograph obtained in patient with retrosternal pain of sudden onset. The image shows a pneumomediastinum, with air at the left heart border and around the aortic knuckle.

Patients with chronic obstructive pulmonary disease who experience an acute exacerbation of bronchitis frequently describe a burning type of chest pain that localizes to the substernal region. A similar symptom can occur in otherwise normal subjects in the setting of tracheobronchitis or during the hyperventilation that accompanies heavy exercise, particularly if the exercise is done in a cold environment.

In many instances, patients with costochondral pain or pain that results from muscle strains describe an episode of chest trauma or unusual upper extremity exercise (e.g., gardening, digging, scraping) that can result in an overuse syndrome. More commonly, no specific inciting event can be determined. The costosternal articulations are common “trigger sites” for the pain of fibromyalgia. Patients with this syndrome also have trigger sites in other locations (Figure 21-5). Musculoskeletal conditions generally are exacerbated by deep breathing and frequently are overlooked as causes of pleuritic or exercise-induced chest pain. The patient often can localize the painful area, where tenderness or muscular spasm may be elicited by palpation.

Figure 21-5 Tender points in fibromyalgia.

Intercostal neuritis commonly is described as being pleuritic. One potentially distinguishing characteristic is that patients may describe abrupt, electric shock–like sensations occurring in the same distribution as for the pleuritic pain.

Gastrointestinal Disorders

Like angina, the pain of esophageal reflux or dysmotility is located substernally; can radiate to the throat, neck, or left arm; and may be relieved by nitroglycerin. Unlike angina, however, the pain is rarely associated with exertion. Rather, it is exacerbated by bending, stooping, drinking alcohol, or lying supine and frequently is worse in the early morning, in association with acidic gastric secretions. Chest pain from esophageal reflux or spasm typically lasts for 1 hour or longer and may be relieved to a variable degree by sitting upright or by ingesting antacids or food. The history also may be positive for odynophagia, dysphagia, or regurgitation of undigested food.

Esophageal rupture is a life-threatening condition if not recognized rapidly and repaired. It can occur in otherwise healthy persons, in whom it may follow an episode of choking while swallowing, or violent or prolonged vomiting. It usually is accompanied by a distinct acute central episode of chest pain, sweating, and then hypotensive symptoms, with onset of pleuritic pain as gastric fluid leaks into the chest cavity. Dysphagia also may be pronounced. A CT scan with a contrast swallow can be diagnostic, showing air to have leaked into the mediastinum (Figure 21-6).

Figure 21-6 Computed tomography (CT) scan performed with contrast swallow shows the esophagus with air surrounding it in the mediastinum. This appearance is highly suggestive of esophageal rupture.

The pain associated with peptic ulcer disease, biliary colic, or pancreatitis generally begins 1 or 2 hours after eating. Pain associated with peptic ulcer disease may lessen or worsen with eating. The pain associated with biliary colic and pancreatitis frequently is accompanied by nausea and vomiting.

Psychiatric Disorders

Psychiatric disorders should always be considered only if physical explanations have been exhausted. Of note, however, chest pain is a well-recognized manifestation of anxiety, as, for example, in a patient with a near relative of emotional importance (i.e., with whom the patient identifies) who has suffered a heart attack. Depression can produce a myriad of physical symptoms, as can fixative ideology. It often can be most useful to ask the sufferer of chest pain about a particular anxiety regarding the cause of the pain, or if the person knows someone with a similar symptom.

Physical Examination

Although the physical examination may provide a number of clues, the findings may be entirely normal even when the pain results from a life-threatening condition. Shallow, more rapid respirations may suggest pleural inflammation or a musculoskeletal cause of pain. Cyanosis may suggest hypoxemia from a variety of pulmonary or cardiac problems. Xanthelasma and tuberous xanthomas suggest the presence of coronary disease. The onset of clubbing heralds intrapulmonary pathology, as may the finding of significant lymphadenopathy.

In addition to the standard vital signs, blood pressure should be measured in both upper extremities, because a disparity would suggest aortic dissection. Heart rate and rhythm abnormalities suggest acute ischemia or pulmonary embolism. Fever points away from musculoskeletal pain and suggests pneumonia, pulmonary embolus, pancreatitis, or biliary obstruction. Patients with myocardial infarction may be febrile, but the temperature rarely exceeds 38° C.

Elevated jugular venous pressure, abnormalities in the carotid upstroke, crackles, a pleural or pericardial rub, signs of parenchymal consolidation, gallop rhythms, paradoxical or fixed splitting or an increased intensity of the pulmonary component of the second heart sound, and cardiac murmurs have a high specificity for many of the cardiopulmonary disorders associated with chest pain. The sensitivity of these physical findings probably is low, however, because the physical examination may be entirely normal in patients with severe ischemia, pulmonary emboli, and many of the gastrointestinal causes of pain.

Attempts can be made to reproduce or exacerbate the pain by moving the patient’s arms and shoulders and by thoroughly palpating the chest wall, particularly over the peristernal region and the costochondral junctions, as well as the subacromial bursae, the deltoid tendons, the shoulders, and the abdomen. Asking the patient to perform the maneuvers that produce the pain also can be helpful.

Intercostal neuritis frequently is associated with hyperalgesia or anesthesia over the distribution of affected intercostal nerves. Biliary colic and pancreatitis frequently are associated with right upper quadrant and midline abdominal tenderness, respectively. Clearly, it is vital not to miss important physical disease in the chest wall. Careful, gentle palpation with both hands over the skin, musculature, ribs, and vertebrae may identify tender areas that signify a serious problem (Figure 21-7, A and B).

Figure 21-7 A, Chest radiography showing two soft tissue masses originating from bone. Clinical findings included tenderness on the left side of the chest and over the upper thoracic spine. B, Coronal computed tomography (CT) image showing the soft tissue mass invading and destroying a thoracic vertebra.

Diagnostic Tests

Patients without a previous diagnosis of coronary artery disease are not likely to have an acute myocardial infarction as the explanation for the acute onset of chest pain if the pain does not radiate to the neck, left shoulder, or arm and if the electrocardiogram and serial serum troponin levels are normal. Although the finding of flat or downsloping ST segment depression greater than 0.1 mV increases the likelihood that an episode of chest pain is caused by myocardial ischemia, the tracing may be normal at rest, between attacks, or even in the presence of active ischemia. Up to 80% of patients with coronary disease exhibit these ST segment changes during exercise, but such changes also may be found in up to 15% of patients with no evidence of disease at cardiac catheterization. Nonspecific ST-T wave changes have been documented in the setting of acute cholecystitis and esophageal spasm, as well as in other conditions for which chest pain is a presenting symptom (Table 21-1).

Table 21-1 Electrocardiographic Findings in Conditions Manifesting with Chest Pain

Chest radiographs should be obtained in all patients with chest pain unless a clear-cut musculoskeletal cause of the pain is evident on clinical evaluation. With myocardial ischemia or infarction, the chest radiograph may be entirely normal in appearance. Alternatively, it may reveal pulmonary edema, upper lobe vascular redistribution, valvular disease, or pericardial disease.

Chest radiographs may be normal-appearing in the setting of acute pulmonary emboli, although minor degrees of atelectasis, small effusions, or distention of the central pulmonary vessels may be seen. A small or an apical pneumothorax can be difficult to see, but if this lesion is suspected, a film exposed with the patient in full expiration will make it much larger and obvious. Careful radiographic review of all ribs should identify a fracture, most commonly located in the lower ribs if due to coughing. Local rib tenderness always warrants a chest radiograph (Figure 21-8). Anatomic anomalies such as a cervical rib, which may be the cause of root pain, should be looked for as appropriate. If pleuritic pain is associated with minor change, such as the obliteration of a costophrenic angle, obtaining a follow-up radiograph 24 hours later may show obvious development of the cause of chest pain. Pericardial causes of pain will become evident only if an effusion is gathering by causing the cardiac outline to enlarge; an effusion also may be a sign of malignant disease elsewhere within the chest, or of joint disease in connective tissue disorders.

Figure 21-8 Splaying of the left sixth rib by a metastasis from a Ewing sarcoma manifesting as a soft tissue mass. The patient was a young man who presented with vague chest pain.

A widened mediastinum or an apical effusion on films exposed with the patient in the supine position (Figure 21-9) suggests the possibility of a ruptured aortic aneurysm.

Figure 21-9 Aortic aneurysm. Chest computed tomography (CT) scan showing a dissecting aortic aneurysm.

A set of routine blood tests should be performed to identify abnormality of white cell count or renal or liver function an abnormality here may focus further investigations as appropriate. In addition, troponin T increases 4 to 12 hours after myocardial infarction and is a better predictor of acute infarction than creatine kinase–MB, because the latter increases in both infarction and ischemia. Troponin T can increase as a result of rhabdomyolysis in absence of ischemia, however. A normal result on D-dimer assay excludes pulmonary embolism for all practical purposes in all patients except those believed to be at high risk for this condition.

Computed tomography can be diagnostic for pulmonary embolism (especially when performed as a CT pulmonary angiogram), as well as for pneumothorax, esophageal rupture, pericardial disease, small pleural effusions, superior sulcus tumors, and mediastinal disease.