Abstract
Background/aim:To examine the effects of active and passive smoking on perioperative anesthetic and analgesic consumption.Materials and methods:Patients were divided into three groups: group S, smokers; group PS, passive smokers; and group NS, individuals who did not have a history of smoking and were not exposed to smoke. All patients underwent the standard total intravenous anesthesia method. The primary endpoint of this study was determination of the total amount of propofol and remifentanil consumed.Results:The amount of propofol used in induction of anesthesia was significantly higher in group S compared to groups PS and NS. Moreover, the total consumption of propofol was significantly higher in group S compared to groups PS and NS. The total propofol consumption of group PS was significantly higher than that of group NS (P = 0.00). Analysis of total remifentanil consumption showed that remifentanil use was significantly higher in group S compared to group NS (P = 0.00).Conclusion:The amount of the anesthetic required to ensure equal anesthetic depth in similar surgeries was higher in active smokers and passive smokers compared to nonsmokers.
Highlights
Tobacco smoke consists of more than 4000 particles of toxic, ciliatoxic, and carcinogenic properties in gas and particle phases [1,2]
Materials and methods: Patients were divided into three groups: group S, smokers; group PS, passive smokers; and group NS, individuals who did not have a history of smoking and were not exposed to smoke
The amount of propofol used in induction of anesthesia was significantly higher in group S compared to groups PS and NS
Summary
Tobacco smoke consists of more than 4000 particles of toxic, ciliatoxic, and carcinogenic properties in gas and particle phases [1,2]. Nonsmokers exposed to secondhand smoke in their environments are described as passive smokers. The risk for anesthesia-associated reintubation, laryngospasm, bronchospasm, aspiration, hypoventilation, and hypoxemia is 1.8 times greater in smokers compared to nonsmokers. This rate is 2.3 times higher in younger smokers and 6.3 times higher in obese smokers. Tobacco smoke induces hepatic microsomal enzymes and increases the metabolism of drugs such as phenytoin, chlorpromazine, fentanyl, theophylline, and others. While it has been shown that the dose requirements for benzodiazepine increase in smokers, there has been no change reported in lidocaine and corticosteroids requirements [2].
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