In: Anesthesia21 Feb 2010
In moderate or heavy smokers, the forced expiratory volume-/second (FEV-l) is reduced following spinal anesthesia above T10. Also, the forced midexpiratory flow and the forced expiratory flow are markedly reduced. Thus, for prevention of accumulation of secretions in small airways, it is advised that patients be in structed to frequently take deep breaths and cough during the period of the block.
THE EFFECT ON POSTOPERATIVE MORBIDITY
Postoperatively, hypoxia occurs following both general anesthesia and spinal anesthesia. However, it is greater following general anesthesia. Hypoxia occurs more frequently in chronic smokers due to the increased closing volumes, giving rise to higher alveolar arterial oxygen differences, and increased carbon monoxide, decreasing the oxygen availability to tissues. Postoperative pulmonary complications were reported by Morton in 1944 to be six times higher in smokers compared with nonsmokers. Wellman and Smith reported that it was two times higher in smokers following abdominal and thoracic surgery. Bluman et al found it to be four times that of nonsmokers.
EFFECTS OF SMOKING CESSATION PRIOR TO SURGERY ON POSTOPERATIVE MORBIDITY
Warner et al reported pulmonary complications such as purulent sputum, atelectasis, and pleural effusion in those that had stopped smoking for 8 weeks or more prior to surgery to be only 14.5%, compared with 57.9% in those who stopped smoking less than 8 weeks before surgery, a four times higher incidence in those who stopped less than 8 weeks from surgery. Mitchell et al reported the incidence of postoperative purulent sputum to be 25% more for those that stopped smoking 8 weeks before surgery and 50% more in those who stopped smoking less than 8 weeks before surgery than in nonsmokers. Warner et al found that, if patients stopped smoking for 6 months or more prior to surgery, the incidence was the same as that in nonsmokers. Bluman et al found that risks were seven times higher in those that reduced smoking near surgery than for those who smoked continuously up to the time of surgery. These results indicate that stopping smoking less than 8 weeks before surgery is not beneficial with regard to postoperative morbidity.
EFFECT ON POSTOPERATIVE NAUSEA AND VOMITING
The incidence of postoperative nausea and vomiting is less in smokers compared with both nonsmoking males and in females. It is suggested that this may be due to an antiemetic in the constituents of smoke. canadian antibiotics
EFFECT ON THE GASTROINTESTINAL SYSTEM
Cigarette smoking does not increase the gastric volume or alter the pH of the gastric secretions. Smoking does make the gastroesophageal sphincter incompetent, which allows reflux, with accompanying risks of pulmonary aspiration. The incompetence in the gastroesophageal sphincter begins within 4 minutes of beginning to smoke and returns to normal within 8 minutes after the end of smoking. Usually patients are unable to smoke up to 8 minutes prior to surgery. Thus, in contrast to previous beliefs, there is no increased risk of acid pulmonary aspiration in smokers.
EFFECT ON THE IMMUNE SYSTEM
Smoking impairs the immune response. The result is an increased risk of infections and neoplasia. Anesthesia further impairs the immune response, leading to a compounded detrimental effect on the immune system.
EFFECT ON THE RENAL SYSTEM
Cigarette smoking results in an increased secretion of antidiuretic hormone (ADH), leading to dilutional hyponatremia.
EFFECT ON DRUG METABOLISM
Cigarette smoking induces liver microsomal enzymes, increasing the metabolism of some drugs. In chronic smokers, larger doses of benzodiazepines appear to be necessary to produce the same drowsiness as in non-smokers despite the pharmacokinetics of the drugs not exhibiting a significant difference in smokers and non-smokers. It is probably due to the decreased response of end organs rather than being due to increased metabolism. There is no effect on thiopentone, ligno-caine, or corticosteroids.
EFFECT ON PAIN AND ANALGESIC DRUGS
Chronic smokers exhibit a decreased tolerance to pain. Thus, independent of the action on the analgesic drugs, they require more analgesics for pain. Fentanyl and pentazocine are metabolized quicker in smokers. Morphine and meperidine have been metabolized quicker in rats in the presence of nicotine. However, in humans, mean total meperidine clearance has been shown not to differ significantly between smokers and nonsmokers. There is no effect on codeine or paracetamol. Phenylbutazone metabolism is increased.
EFFECTS ON NEUROMUSCULAR BLOCKERS
Nicotine in small doses (<100 ng/mL) stimulates the acetylcholine receptors, requiring larger doses of muscle relaxants to block the receptors. In large doses (>10 |xg/mL), it blocks the receptors. In smokers, the concentration of nicotine does not go beyond 75 ng/mL. Thus, in smokers, the action of nicotine is stimulation of the receptors. The reports on the effect of smoking on individual neuromuscular blocking drugs vary.
Teiria et al found the 95% effective dose (ED95) for vecuronium to be higher in smokers. Smokers also needed more frequent doses to maintain neuromuscular block, indicating an increased requirement at the receptor site. The reason is possibly because the smokers stopped smoking about 6 hours before the surgery. Thus, small doses of nicotine may have stimulated the receptors, requiring a higher dose to block the receptors. More frequent doses needed for maintenance may have been due to increased metabolism.
The reports on rocuronium differ in their findings. La-torre et al found that, in the case of rocuronium, there was no difference in onset of block or recovery times with the same dose used in smokers and nonsmokers. They attribute this to a longer period (12 hours) of refraining from smoking than in the previous study and to a possible different elimination pathway of rocuronium. However, Rautoma and Svartling have found the ED95 of rocuronium to be the same as in nonsmokers, as reported in the previous study, but the maintenance dose to be higher, indicating a higher metabolism of the drug in smokers. Apcalis Oral Jelly
Puura et al found even different results with atracurium. Smoking had no effect on neuromuscular blockade. However, in smokers who abstained from smoking for greater than 10 hours, recovery was prolonged and the maintenance doses required were smaller. When nicotine patches were used with these patients, the prolonged recovery was abolished and the maintenance doses required were the same as in nonsmokers. The probable explanation for this response is as follows: In humans, up and down regulation of nicotinic acetylcholine receptors continuously modify the transmission at the neuromuscular junction. Continuous agonistic stimulation of a receptor leads to down regulation of the receptor and the number of receptors decrease due to internalization. The chronic presence of nicotine may also down regulate the production of acetylcholine. Thus, chronic smokers require the same dose of atra-curium as nonsmokers. However, in those who abstain from smoking for more than 10 hours, the effect of nicotine is negligible—they have fewer receptors and the acetylcholine production is also less. Thus, the maintenance dose of atracurium needed is also less. Nicotine patch introduces nicotine, which stimulates the receptors and leads to the requirement of increased maintenance doses.
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