Lidocaine Tobacco

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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