Proton pump inhibitors (PPIs) are recommended as a first-line therapy when chest pain is thought to be caused by esophageal spasm. Both long- and short-acting nitrates have been shown to provide some relief of pain caused by esophageal spasm. Calcium channel blockers decrease the amplitude and duration of esophageal spasms, but their use does not consistently result in better analgesia than achieved with placebo. This chapter discusses the use of anticholinergic agents such as atropine, hyoscyamine, or propantheline bromide decrease peristaltic contractions and reduce esophageal sphincter tone. There is evidence supporting the use of antidepressants such as tricyclics, trazodone, and SSRIs for treating chest pain caused by esophageal spasm. Regardless of their possible utility in the long term, antidepressants are not likely to be of help in the acute management of esophageal spasm pain in the ED.

Sophisticated studies of the pathophysiology of chest pain in patients without serious heart disease began with Likoff's report of 15 women with recurrent chest pain, abnormal electrocardiograms (ECGs), and normal coronary angiograms. The most promising current hypothesis on the mechanism of chest pain syndromes postulates that the essential common feature in these patients is abnormal visceral pain perception. Research into the factors which contribute to chest pain syndromes has led to the development of at least four major hypotheses: esophageal spasm, esophageal irritation, smooth muscle dysfunction, and microvascular angina. An understanding of the history and the current pathogenetic mechanisms of chest pain syndromes provides a roadmap for efficiently evaluating chest pain patients. A systematic approach to each of the factors contributing to the patient's recurrent chest pain is best coordinated by a primary care physician over the course of the syndrome.