Lidocaine Unit Conversion

Lidocaine is an antiarrhythmic agent administered intravenously by either injection or continuous infusion. It is specifically indicated in the acute management of ventricular arrhythmias such as those occuring in relation to acute myocardial infarction, or during cardiac manipulation, such as cardiac surgery. Lidocaine is metabolized primarily by the liver. N‑ethylglycyl-2,6-xylidide (MEGX), glycyl-2, 6-xylidide (GX), and 4-hydroxy-2,6-xylidine (4-OH-XY) are the major metabolites. The primary metabolite, 4‑OH‑XY, which comprises 73 % of the dose is found in urine. Other metabolic products recovered in urine in amounts of less than 1% are 3-hydroxy lidocaine, 3-hydroxy MEGX, and 2,6-xylidine. MEGX has 80 to 90 % and GX has 10 to 26 % of the antiarrhythmic potency of lidocaine. Concentration monitoring is warranted by lidocaine’s extensive interpatient variability in disposition and by its narrow therapeutic index.

The therapeutic range for total concentration is stated as 1.5 to 6 μg/mL (6.4 to 25.6 μmol/L). Suppression of ventricular arrhythmias at concentrations above 2 μg/mL (8.5 μmol/L) are likely, but prevention of primary ventricular fibrillation may require higher concentrations in AMI patients. At concentrations exceeding 6 μg/mL (25.6 μmol/L) the frequency of CNS toxicity increases. A significant number of patients may require concentrations of 6 to 9 μg/mL (25.6 to 38.4 μmol/L) for arrhythmia control. The benefits and risks of lidocaine concentrations above 6 μg/mL (25.6 μmol/L) must be determined carefully. Lidocaine metabolites may contribute to toxicity in patients receiving prolonged (> 24 hours) infusions or in patients with renal insufficiency. Lidocaine is 60 to 80 % bound to plasma proteins. Of the fraction bound, approximately 70 % is associated with alpha-1-acid-glycoprotein (AAGP) and 30 % with albumin. AAGP concentrations have been reported to increase two fold by the third postbypass day. Plasma concentrations of AAGP have been reported higher in patients receiving phenytoin, carbamazepine, primidone and phenytoin plus phenobarbital. Females receiving estrogen-progestogen oral contraceptives have lower AAGP concentrations and higher free lidocaine concentrations. Cardiopulmonary bypass patients receive very large doses of heparin. Heparin releases lipoprotein lipase from tissues, which in turn increases free fatty acids and alters free lidocaine concentrations. Therapeutic concentrations of quinidine and disopyramide significantly increase the concentrations of free lidocaine.