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This class 1B agent depresses automaticity and reduces refractory period duration in the HIS-Purkinje system and ventricles but has little effect on atrial tissue. Therapeutic doses do not slow AV nodal or intraventricular conduction velocity except in the ischemic myocardium. Lidocaine can cause hyperpolarization and significant increases in conduction velocity in tissues depolarized by stretch or low extracellular potassium concentrations.
Because it acts rapidly and moderate doses usually do not depress myocardial contractility or AV conduction; intravenous lidocaine has been used for immediate suppression of ventricular ectopy and hemodynamically stable ventricular tachycardia during acute myocardial infarction; however, prophylactic use is no longer recommended, because it does not improve the survival rate. Lidocaine may control ventricular arrhythmias caused by digitalis toxicity and those that develop during cardiac surgery, cardiac catheterization, or cardioversion. It usually does not correct supraventricular arrhythmias and may increase the ventricular rate.
Therapeutic: 1.5−5.0 μg/mL
This drug is used in therapy of ventricular but not supraventricular arrhythmias. Following initial parenteral administration of a bolus, lidocaine is rapidly cleared with a short half-life of approximately 10 minutes (first-pass effect). After approximately 30 minutes, there is a slower elimination phase about 90 minutes long. With continuous intravenous administration, a half-life of about 1.5 to 2 hours may be achieved, hence, prolonged administration by the I.V. route is often necessary to achieve the desired therapeutic result. Time to reach steady-state by I.V. is 6 to 12 hours. In most cases, a relatively constant plasma level may be maintained by slow intravenous infusion administered over a period of 6 to 10 hours. Blood levels are also elevated by impaired cardiac or hepatic function. The drug is metabolized by the liver to two active metabolites, monoethylglycinexylidide (MEGX) and glycinexylidide (GX). Both accumulate and MEGX most likely contributes to toxicity. Toxic symptoms may include confusion, respiratory depression, seizures, dizziness, drowsiness, paresthesias, hypotension, bradycardia, and double vision. Convulsions, cardiac and respiratory arrest may occur. Barbiturates and phenytoin seem to enhance drug metabolism and lower serum levels, whereas propranolol, cimetidine, and norepinephrine increase levels.
Lidocaine is approximately 70% bound to plasma proteins, especially α1 acid glycoprotein (the concentration of which is variable) and to albumin.
Serum or plasma
Red-top tube or green-top (heparin) tube. Do not use a gel-barrier tube. The use of gel-barrier tubes is not recommended due to slow absorption of the drug by the gel. Depending on the specimen volume and storage time, the decrease in drug level due to absorption may be clinically significant.
Transfer separated serum or plasma to a plastic transport tube. Draw specimens 12 hours after initiating therapy for arrhythmia prophylaxis, then every 24 hours thereafter. Obtain specimens every 12 hours when cardiac or hepatic insufficiency exists.
Causes for Rejection
Gel-barrier tube; hemolysis; gross lipemia; icteric specimen
|Order Code||Order Code Name||Order Loinc||Result Code||Result Code Name||UofM||Result LOINC|
|007013||Lidocaine (Xylocaine), Serum||3714-3||007013||Lidocaine (Xylocaine), Serum||ug/mL||3714-3|