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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.
The extensive use of short-term oxygen therapy in acute coronary syndrome (ACS), with rarely reported adverse effects and frequent cases of anecdotal benefit, supports oxygen administration as benign intervention for cardiac patients with pain and subnormal peripheral pulse oximetry. The pain of ACS is effectively decreased by beta-blockers. Though their exact analgesia mechanism is not known, there are several possible routes by which beta-blockers could reduce pain. Nitrates dilate the epicardial coronary arteries, their collaterals, and peripheral vessels, thus improving coronary perfusion and potentiating a favorable ratio of subendocardial-to-epicardial flow. Opioids have long been a part of the ACS treatment armamentarium. Due to its properties as a pulmonary venodilator and anxiolytic, morphine has been the analgesic of choice for ACS pain. Intravenous benzodiazepines should be used for patients with cocaine-associated cardiac chest pain. In this population, the risk of vasospasm from beta-blockers is such that these agents should be avoided.
Abdominal aortic aneurysm (AAA) pain should be considered by the acute care provider as a harbinger of aortic leakage or rupture. Therefore, analgesic selection in AAA is influenced by the high potential for hemodynamic instability. This chapter discusses the role of opioids and NSAIDs in abdominal aortic aneurysm. When treating pain in patients with suspected ruptured AAA, the most important consideration is the effect the analgesic will have on the patient's hemodynamic status. Opioids, in small titrated doses, are the analgesics recommended by experts in AAA pain relief. Most opioids can cause minor reductions in heart rate and blood pressure. Hypotension is much less likely to occur with fentanyl since this agent does not cause histamine release often associated with morphine. In patients with normal renal function, NSAIDs (e.g. ketorolac) have been used perioperatively, without sequelae, in patients undergoing abdominal and retroperitoneal procedures.
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