Chapter 21 Chest Pain
Chest pain is a very common symptom, and its severity and etiology will depend, to a large extent, on the clinical circumstances in which it occurs. Chest pain is the most frequent new symptom reported by patients seen in outpatient clinics. Although it is an extremely nonspecific symptom (Box 21-1), it may be the presenting manifestation of a number of conditions, most of which will be relatively benign. Also, in many patients with such pain, a firm diagnosis may never be established. When chest pain is a presenting symptom in the emergency department setting, however, more serious, acute, and potentially life-threatening causes need to be considered. Accordingly, a complaint of chest pain requires thorough and careful investigation.
Causes of Chest Pain
Pericarditis (infections, Dressler syndrome)
Biceps, supraspinatus, or deltoid tendinitis
Hyperabduction or strain of the anterior scalene or rectus abdominis muscles
Slipping rib syndrome (pain at the costochondral junction, generally affecting the eighth, ninth, or tenth rib; may be posttraumatic)
The pathophysiology of chest pain is understood for many but not all of the conditions with which it is associated. The most common form of chest pain is musculoskeletal pain. The causes of this form of chest pain are legion—in some instances involving an organic process, often due just to excessive coughing, as discussed later on. Of note, however, possible psychiatric or psychogenic reasons for chest pain need to be kept in mind. Cardiac disease is the most important cause of chest pain overall, so this entity is first in the overview of potential causes.
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.
Potential Causes of Chest Pain Other Than Angina
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.
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.
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.
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.
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.