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Lignocaine

Therapeutic Function Local anesthetic, antiarrhythmic Chemical Name 2-(diethylamino)-N-(2,6-dimethylphenyl)acetamide Common Name Lignocaine... [Pg.874]

Fluoreszein 0,15 % Thilo Minims lignocaine and Fluores (Showa Yakuhin)... [Pg.896]

SH, Gendeh BS IgE-mediated hypersensitivity reaction to lignocaine - a case report. Trop Biomed 30 2005 22 179-183. [Pg.199]

Lignocaine (lidocaine) A local anaesthetic and voltage-operated Na+ channel blocker. [Pg.244]

Organic Substances Cephalexin, Lignocaine hydrochloride, Griseofulvin, Diazoxide, Medazapam, Saccharin. [Pg.24]

Lidocaine (lignocaine, 4.128, Fig. 4.5) is a typical representative of the class of aminoacylanilides. Lidocaine is a local anesthetic and an anti-arrhythmic agent that is very resistant to chemical hydrolysis even in strongly acidic or basic media. Only at higher temperature does lidocaine... [Pg.131]

Lignocaine, originally introduced as a local anesthetic, is now widely used for the treatment and prevention of ventricular arrhythmias. When used for this purpose, it is usually administered either by intramuscular injection, or as a bolus intravenously, or, more commonly, by constant intravenous infusion. For clinical purposes, lignocaine measurements arc usually carried out on plasma collected either while the patient is receiving a constant intravenous infusion or at a specified time after the last intramuscular injection. Colorimetric methods have been used in the past (S29), but, because they lack both sensitivity and specificity, may yield false and misleading results. They have largely been replaced by GLC techniques (A3, El, K5). [Pg.83]

Despite reports to the contrary (P2), lignocaine is not therapeutically effective when given orally and does not achieve satisfactory blood levels when these are measured by specific techniques. Moreover, since the oral route of administration is associated with an unacceptably high incidence of side effects, which are probably due to metabolites of lignocaine rather than to the drug itself, this mode of administration has not gained widespread acceptance. [Pg.83]

Ventricular arrhythmias are well controlled when the plasma ligno-caine concentration lies between 2 and 6 /ig/ml (H8, SIO). The efiBcacy of the drug is low at blood levels of less than 2 /ig/ml and side effects, predominantly affecting the nervous system, begin to increase in frequency as plasma lignocaine levels exceed 6 /ig/ml. [Pg.84]

Plasma steady-state levels of up to 10 /ig/ml are occasionally necessary for control of ventricular arrhythmias but cannot always be tolerated without serious toxic effects. Of thirteen patients referred to a specialist coronary care unit because of reputed refractoriness to the therapeutic effect of lignocaine, in only four was the diagnosis substantiated by demonstrating failure of therapeutic response to blood lignocaine concentrations in excess of 10 /tg/ml (H8). In four patients a therapeutic response was observed at blood lignocaine levels between 5 and 10 /xg/ml, and another five patients were responsive to lignocaine blood levels within the usual therapeutic range. [Pg.84]

Animal experiments have shown (A3) that equilibration of lignocaine between blood and brain occurs relatively slowly. This may explain why plasma levels of lignocaine that can readily be tolerated, without cerebral side effects, after intravenous bolus injection nevertheless are associated with serious toxic symptoms when produced by constant intravenous infusion or when resulting from impaired metabolic degradation. [Pg.84]

Lignocaine s clearance by the liver is flow dependent. In heart failure cardiac output may be very low and therefore hepatic blood flow through both the hepatic artery and the portal venous system is also low. This meant a lower extraction of the drug from the blood and accumulation of lignocaine until the high plasma concentration produced the central nervous system toxicity. [Pg.127]

Metabolism of drug during the first-pass through the liver may be reduced if its extraction depends on blood flow as hepatic blood flow is characteristically low in heart failure. This mechanism leads to a higher Cp of drugs in this group (e.g., lignocaine, an example discussed earlier in the chapter). [Pg.155]

Mrs. Chen is 68 and has suffered a myocardial infarction. An ECG showed ventricular tachycardia, she was successfully defibrillated and now, to maintain sinus rhythm, your consultant asks you to load her with lignocaine. She weighs 85 kg and the Cp he wants you to achieve is 1.5 mg/1. You lookup the Vd... [Pg.159]

In this case an intravenous infusion of just under 150 mg lignocaine given over a few minutes should bring the Cp into the therapeutic range. [Pg.160]


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