Lidocaine Smoking

Smoking cessation, with or without nicotine substitutes, may alter response to concomitant medication in ex-smokers. Smoking may affect alcohol, benzodiazepines, beta-adrenergic blockers, caffeine, clozapine, fluvoxamine, olanzapine, tacrine, theophylline, clorazepate, lidocaine (oral), estradiol, flecanide, imipramine, heparin, insulin, mexiletine, opioids, propranolol, catecholamines, and cortisol. 

Beta-blockers interact with a large number of other medications. The combination of beta-blockers with calcium antagonists should be avoided, given the risk for hypotension and cardiac arrhythmias. Cimetidine, hydralazine, and alcohol all increase blood levels of beta-blockers, whereas rifampicin decreases their concentrations. Beta-blockers may increase blood levels of phenothiazines and other neuroleptics, clonidine, phen-ytoin, anesthetics, lidocaine, epinephrine, monoamine oxidase inhibitors and other antidepressants, benzodiazepines, and thyroxine. Beta-blockers decrease the effects of insulin and oral hypoglycemic agents. Smoking, oral contraceptives, carbamazepine, and nonsteroidal anti-inflammatory analgesics decrease the effects of beta-blockers (Coffey, 1990). 

Aluminum salts, cholestyramine, and colestipol may decrease absorption of /3 blockers. Pheny-toin, rifampin, and phenobarbital, as well as smoking, induce hepatic biotransformation enzymes and may decrease plasma concentrations of /3 receptor antagonists that are metabolized extensively (e.g., propranolol). Cimetidine and hydralazine may increase bioavailability of propranolol and metoprolol by affecting hepatic blood flow, fi Receptor antagonists can impair the clearance o/lidocaine. 

Rifampicin may also increase the metabolism of lidocaine to a minor extent, see Lidocaine + Rifampicin (Rifampin) , p.267, and smoking may reduce the oral bioavailability of lidocaine , (p.267). 

Tobacco smoking reduces the bioavailability of oral but not intravenous lidocaine. 

A study in healthy subjects found that the bioavailability of oral lidocaine was markedly lower in smokers (mean AUCs of 15.2 and 47.9 micrograms/mL per minute in 4 smokers and 5 non-smokers respectively), but when the lidocaine was given intravenously only moderate differences were seen. The reason for the differences is probably due to liver enzyme induction caused by components of tobacco smoke. With oral lidocaine this could result in increased first-pass hepatic clearance. In the case of intravenous lidocaine, first-pass clearance is bypassed, and the enzyme induction was opposed by a smoking-related decrease in hepatic flow. In practical terms this interaction is unlikely to be of much importance since lidocaine is not usually given orally. 

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