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Cerebrovascular Effects of Carbon Monoxide
Published in David G. Penney, Carbon Monoxide, 2019
Mark A. Helfaer, Richard J. Traystman
Understanding the pathophysiology of CO poisoning is most clinically germane as it applies to fires. During combustion, other toxic chemicals are released, so there has been research regarding the cerebral effects of these agents in combination with CO. Of particular interest is the combination of CO and cyanide (CN) (Pitt et al., 1979). Comatose states and confusion have been described in a number of experimental paradigms involving the administration of CN. This toxin seems to affect cerebral white matter. Early experiments demonstrated a rise in CBF, ICP, and CMRO2 in response to small doses of CN. It has been demonstrated that both CO and CN increase CBF and maintain CMRO2 constant at low doses. The combination however, additively increased CBF but decreased CMRO2 in a synergistic manner (Pitt et al., 1979). In addition to fires, CO poisoning has gained importance recently in the area of anesthesia. It has been discovered that there is an interaction between some inhalational anesthetics and dry baralyme (a CO2 absorber) that results in the liberation of CO. This has caused several cases of CO poisoning in patients. The inhalational anesthetics associated with this have been desflurane and enflurane, and to a lesser extent, isoflurane. Halothane and sevoflurane seem not to be affected by this interaction. Dryness and, to a lesser extent, elevated temperatures increase the rate of CO production (Fang and Eger, 1994).
A case report of personal exposures to isoflurane during animal anesthesia procedures
Published in Journal of Occupational and Environmental Hygiene, 2018
Isoflurane, CAS# 26675-46-7, is a halogenated anesthetic gas widely used for animal anesthesia in both research institutions and veterinary practices.[1] Exposure to waste anesthetic gas (WAG) has been associated with an increased risk of adverse health outcomes. At high concentrations, potential health effects of WAG exposure include headache, hypotension, tachycardia, respiratory depression, hepatotoxicity, and nephrotoxicity.[2] At low concentrations, potential health effects of WAG exposure consist of miscarriage, birth defects (genetic damage), and cancer in exposed workers.[2] Due to limited toxicological data on isoflurane, it is prudent to consider potential health effects to be similar to those of other anesthetic gases such as halothane, methoxyflurane, and enflurane.[3]
A new Cu(II)-based coordination polymer: crystal structure and protective effect on cardiac arrest induced by anesthesia via inducing SIRT1 signaling pathway
Published in Inorganic and Nano-Metal Chemistry, 2021
Minwei Liu, Shanyong Qin, Jing Qu
The incidence of arrhythmias caused by perioperative cardiac and non-cardiac surgery is very high [1]. The anesthesiologist should be able to identify changes in the ECG and also explain the cause of the arrhythmia, understand its severity and correct drug usage to reduce perioperative of complications and mortality [2]. The incidence of halothane anesthesia is higher than other inhaled anesthetics; Enflurane and isoflurane have a concentration-dependent inhibition of sinoatrial node autonomy and atrioventricular conduction; thiopental can lower blood pressure and cause reflex tachycardia; Sodium hydroxybutyrate and propofol excite the parasympathetic nerves and cause reduction of the heart rate [3, 4].