The effect of the substance is based on the blockade of voltage-dependent sodium channels located in the membranes of nerve cells. Sodium channels are significantly involved in the transmission of stimuli in the human body. If they are blocked at certain points in the body, no stimuli (e.g. pain) are transmitted from there to the brain. This is the reason for the local anaesthesia of Lidocaine. The antiarrhythmic effect is based on the same principle. Here, however, sodium channels in the heart muscle cells are blocked. This results in a prolongation of the action potential, whereby certain arrhythmias can be remedied. However, lidocaine itself can also cause arrhythmias, which is why it is now rarely considered for this application.
Lidocaine is well absorbed in the GI tract, but a large portion of the given dose is immediately cleared due to the significant "first pass effect," which is why oral bioavailability is only 35%. Therefore, lidocaine for systemic use (antiarrhythmic) is administered intravenously only. This circumvents the "first pass effect". Lidocaine is 60-80% bound to plasma proteins and is relatively rapidly cleared by the liver. The elimination half-life is 1.5-2 hours. The majority of the given dose is excreted via the kidneys.
Drug interactions are not expected when used as a topical anesthetic. When used as an antiarrhythmic agent, class III antiarrhythmic agents should not be given concomitantly under any circumstances.