Opioids are utilized frequently for the treatment of moderate to severe acute pain in the perioperative setting, as well as in the treatment of cancer-related pain. When prescribing chronic opioid therapy to patients with chronic pain, it is crucial for the practitioner to be aware not only of the issues of tolerance and withdrawal, but also to have knowledge of the possibility for opioid-induced hyperalgesia (OIH). An understanding of the differences between tolerance and OIH when escalating opioid therapy allows the titration of opioid as well as nonopioid analgesics in order to obtain maximum control of both chronic and acute pain. A case study is described to highlight the importance of judicious utilization of opioids in the treatment of cancer-related pain. In this case, high-dose opioid therapy did not improve chronic pain and contributed to a hyperalgesic state in which a young man experienced severe intractable pain postoperatively after two routine thoracotomies, despite aggressive pharmacologic measures to manage his perioperative pain. Furthermore, it illustrates the potential advantages of opioid rotation to methadone when OIH is suspected.

This study was designed to examine the effect of increases in the partial pressure of carbon dioxide (PCO2) in coronary artery blood on coronary blood flow, coronary reactive hyperemia and the coronary response to intracoronary adenosine administration. The left anterior descending coronary artery was cannulated and perfused over a wide range of perfusion pressure (P) and flow (F) with blood equilibrated with 0 to 40% carbon dioxide in 16 open chest dogs. Increases in coronary artery PCO2 from 20 +/- 2 to 93 +/- 8 to 211 +/- 22 mm Hg (mean +/- SEM) increased the coronary flow from 28 +/- 3 to 68 +/- 16 to 87 +/- 22 ml/min, respectively, at a perfusion pressure of 60 mm Hg and from 49 +/- 6 to 139 +/- 30 to 206 +/- 48 ml/min, respectively, at a perfusion pressure of 100 mm Hg. Coronary reactive hyperemia following a 30 second coronary perfusion line occlusion and the response to an intracoronary bolus of adenosine (60 micrograms) were prominent at a low PCO2 but absent at a high PCO2. Beta-adrenergic blockade did not abolish the increase in coronary flow that occurred at increased PCO2. Thus, progressive elevations of regional coronary PCO2 produced substantial increases in coronary blood flow and maximal or near maximal coronary vasodilation.

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