Cardiac or central nervous system toxicity may result when standard lidocaine doses are administered to patients with circulatory failure. This may be due to the following reason:
A i.e. Lidocaine concentration are initially higher in relatively well perfused tissues such as brain and hea - The highly perfused organs (as Brain, Lung, Liver, Kidney, hea) are responsible for initial rapid uptake (Alpha phase) which is followed by a slower redistribution (Beta phase) to moderately perfused tissues (muscle and gut). Amide Local anaesthetics (lidocaine) are metabolzied by Microsomal enzymes in liver Decrease in hepatic function (eg cirrhosis) or blood flow (eg. congestive Hea failure) will reduce metabolic rate and predispose patients to systemic toxicityQ Toxicity of Lidocaine is due to it's own concentration in blood not due to it's toxic metabolite that is why option 4 is wrong.
Lidocaine concentration are initially higher in relatively well perfused tissues such as brain and hea
Histamine receptors in brain and hea gets suddenly activated in circulatory failure
There is a sudden out-burst of release of adreneline, noradreneline and dopamine in brain and hea
Lidocaine is conveed into a toxic meta-bolite due to its longer stay in liver.