Complaints of pain localized to the chest pose a diagnostic challenge. Many individuals with chest pain have a benign course due to a self-limiting musculoskeletal process. However, appropriate and dedicated attention must be paid to each individual to approach the most likely clinical etiology. The young active duty population is not immune to atherosclerotic coronary artery disease causing angina pectoris or myocardial infarction.

Sources of Chest Pain

Chest pain may be arbitrarily categorized as arising from:

• The heart, great vessels, and pericardium.
• The gastrointestinal tract.
• The lungs and pleura.
• The chest wall.

Identification of ischemic chest pain requires a high index of suspicion. When the diagnosis of myocardial infarction is overlooked and patients are sent home, the mortality during the next 72 hours is about 25 percent in comparison with about 6 percent for patients with infarction who are hospitalized. We are, therefore, liberal in admissions for evaluation of coronary artery disease. The incidence of acute myocardial infarction in patients hospitalized with acute chest pain is between 25 to 30 percent. Still, identification of those individuals with unstable angina or an acute myocardial infarction may pose considerable uncertainty. Despite conservative admission rates clinicians misdiagnose approximately 5-10 percent of patients with myocardial infarction.

The history dominates decision making. Elements of the history important in discriminating cardiac from noncardiac chest pain are quality, severity, duration and frequency. Knowledge of exacerbating features and maneuvers that tend to ameliorate the discomfort provide insight. Cardiac risk factors should not overly influence clinical thinking. The presence of risk factors simply implies that an individual is more likely to develop overt signs of atherosclerotic heart disease in the years ahead than a person who does not have such markers. They are supportive of an appropriate clinical history, but by no means provide exclusionary criteria.

Pain Character

Chest pain of coronary ischemic origin is classically a dull heavy pressure. Still, an endless list of adjectives has been used to describe the unpleasant feeling of angina pectoris. This discomfort may be confined to the chest or there may be associated aching in one or both arms, more often the left. Neck or mandibular pain or aching confined to the shoulder, wrist, elbow, or forearm may manifest solely or in concert with typical chest pressure. Myocardial ischemia is seldom the cause of discomfort in an area that is no larger than the tip of a finger. Suspect also is the radiation of pain to the digits. Brief bursts of pain lasting seconds or discomfort that persists continuously for days at a time is not due to myocardial ischemia. Effort or emotional stress commonly provokes angina. However, angina may occur at rest if perfusion is significantly compromised. Pain subsides within 1 to 5 minutes if the evoking activity is discontinued. Nitroglycerin hastens this relief.

Role of the Electrocardiogram (ECG)

The 12-lead ECG has limited value in excluding the presence of coronary artery disease. Excluding the diagnosis of angina pectoris or myocardial infarction because of a normal ECG is as great an error as inferring a diagnosis of atherosclerotic coronary artery disease from the incorrect interpretation of nonspecific electrocardiographic abnormalities

Cocaine Use and Chest Pain

Cocaine use is temporally related to the development of acute chest pain and has been associated with acute myocardial infarction. Cocaine causes decreased coronary blood flow through vasoconstriction. There is speculation that rhabdomyolysis, a known complication of cocaine use, may effect thoracic musculature providing another mechanism for the chest pain. All patients presenting for evaluation should be questioned about cocaine use. A urine drug screen is advisable.

Cardiovascular Origin

Aortic dissection is a diagnosis often overlooked when evaluating chest pain. Although uncommon, its consequences are devastating. Pain is typically abrupt and sharp in its onset, with radiation to the infrascapular region. A murmur of aortic insufficiency may be appreciated. The ECG shows no sign of acute myocardial infarction unless dissection involves the coronary ostia. Hypertension may be an antecedent risk. Recognizing this disorder in the differential improves the likelihood of diagnosis and needed emergent treatment. Acute pericarditis is a result of inflammation of the pericardium characterized by chest pain, a pericardial friction rub, an elevated erythrocyte sedimentation rate (ESR), and serial electrocardiographic abnormalities.

Pain arising from the gastrointestinal tract, especially the esophagus, may give rise to chest discomfort that is similar to angina pectoris. Gastroesophageal reflux disease is the most common esophageal cause of noncardiac chest pain. Patients describe the discomfort as a burning sensation or squeezing pain located in the retrosternal area between the xyphoid and the suprasternal notch. Clues to the diagnosis include an association of symptoms with meals, posture, and relief by belching or antacids. Medical management involves dietary modifications, smoking cessation, and histamine type 2 (H2) antagonists or antacids. GI referral is warranted when these interventions are unsuccessful in alleviating symptoms. The pain of peptic ulcer disease may also be appreciated high in the epigastrium or lower chest. The relationship to meals and relative lack of response to nitroglycerine should help distinguish this pain from angina pectoris.

Diffuse esophageal spasm is a neuromuscular disorder of the esophagus characterized by chest pain and difficulty in swallowing. Note that nitroglycerin promptly relieves esophageal spasm causing confusion in the diagnosis. Vigorous disordered contractions in the body of the esophagus are induced by ingestion of cold liquids or normal swallowing during a meal. Anxiety and stress are also common precipitating factors. There is usually no exertional component but increased abdominal pressure from lifting, sit-ups, or running can cause reflux. Diagnosis rests on history and verification of esophageal spasm by manometric studies.

Pain of pulmonary origin characteristically has a distinct pleuritic quality varying with the respiratory cycle. Intercostal nerves supply sensory afferents to the costar parietal pleura. Inflammation arising from this region is appreciated in the adjacent chest wall. Referred pain originating in the diaphragm is appreciated in the ipsilateral shoulder. Differentiating features of pulmonic from musculoskeletal pain are the more intense nature of pleuritic pain and the worsening of musculoskeletal pain by extension, abduction, or adduction of the arm and shoulder. Pain centered around involved muscle groups may also distinguish musculoskeletal from pleuritic chest pain.

1. Spontaneous pneumothorax tends to occur in young adult males producing sharp pleuritic chest discomfort and dyspnea.

2. Pulmonary embolus may produce pleuritic pain, however, dyspnea, and tachypnea are most frequent. Inciting factors for pulmonary embolus include the post-operative period after long recumbent or inactive periods and following trauma where the same immobility may result in venous stasis and thrombosis.

Tietze's syndrome or costochondritis is a self-limiting discomfort. Its quality is sharp or burning and is exacerbated by mechanical activity of the chest wall, specifically respiration. The second or third costal cartilages on either side are the most common area of involvement, but any of the costochondral articulations can be involved. Nonsteroidal anti-inflammatory agents or aspirin may offer temporary relief but reassurance tends to be as useful.

Rarely, no etiology is found on standard evaluation of chest pain from the cardiology or gastrointestinal consultation. Consideration of panic disorder should also be included in the differential. Recent studies of some individuals with unexplained chest pain and normal coronary arteries reveal abnormalities of flow in the cardiac microcirculation and/or esophageal causes of chest pain. Visceral hypersensitivity may also link non-chest pain and irritable bowel syndrome.

No individual variable separates patients with coronary chest pain from other likely etiologies. Additive information gathered from a carefully directed history is necessary. A combination of variables (sharp or stabbing pain, no history of angina or myocardial infarction, and pain with pleuritic or positional components or pain reproduced by palpation) define a very low risk group for having unstable angina or a myocardial infarction. A cautious, yet practical, approach to the evaluation of chest pain with close attention to symptoms and physical examination with further targeted testing and referral leads to appropriate management.

1. Hurst JW, Atherosclerotic coronary heart disease: historical benchmarks, methods of study and clinical features, differential diagnosis and clinical spectrum. In the Heart Arteries and Veins. New York, NY. McGraw Hill Inc 1990, pp. 961-1028.