10 These findings were somewhat serendipitous given that co-oximetry measurement was performed on all blood gas samples as a standard and the anesthesiology care providers did not intend to assess such values as part of routine clinical care. 10 An arterial blood gas measured 25 minutes following anesthesia induction and 1 hour later demonstrated COHb levels of 9.1% and 28%, respectively. 9– 11 The earliest case report of such toxicity described a rise in COHb in a 76 year old, non-smoking woman undergoing general endotracheal anesthesia for thyroid resection. 8 Several studies and anecdotal case reports during that period described high CO concentrations within the anesthesia circuit along with clinical signs of CO toxicity and elevated carboxyhemoglobin (COHb) levels. In the early to mid-1990s, generation of CO within the anesthesia breathing circuit and patient exposure became more widely recognized. 7 Although it is over 50 years old, this work insightfully identified the patient's own alveolar gas as a potential source of CO. 7 In this study, the authors documented levels of CO as high as 810 parts per million (ppm) within the breathing circuit and concluded that “complete closure of the anesthetic system build up” of CO. The first report of CO detection within a closed circuit anesthesia system was published in 1965. Here we review the concept of CO exposure in the setting of an anesthetic and identify the sources of production, detail the mechanisms of overt CO toxicity, highlight the cellular effects of low dose CO, and discuss the potential therapeutic role for CO as a part of routine anesthetic management.ĬO Exposure During General Endotracheal Anesthesia 3– 6 Although the consequences of such anesthesia-related exposures are relatively unknown and investigative efforts to understand them are just beginning, low dose CO is being developed more generally to treat a variety of conditions. Anesthesiologists should be aware of CO and its effects given that CO exposure can occur during general endotracheal anesthesia. Such CO-mediated effects can be either cytoprotective or pathologic, depending on the context, duration, and concentration of exposure. 1, 2 However, CO also has biological activity at sub-toxic levels, affecting several cellular pathways in a more complex manner. 2 Classification of CO as a life-threatening toxin is certainly warranted given that it continues to be the major cause of poison-related death in the United States. 1, 2 Historically, CO was regarded as a poison due to the well-characterized tissue hypoxia and overt toxicity that result following exposure to high concentrations. Carbon monoxide (CO) is a colorless, odorless, and tasteless gas that exerts a number of biologic effects in a variety of different tissues and organs.
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