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Pharmacokinetics lidocaine

Lidocaine pharmacokinetics tend to follow a single compartment model in neonates, with an increased half-life, and substantially reduced protein binding, leading to a much larger volume of distribution than in adults, but an increased proportion of unbound drug (56). [Pg.2056]

That sex differences can affect lidocaine pharmacokinetics is suggested by a report of higher blood concentrations in men than in women after administration of the same dose (SED-12, 256) (58). [Pg.2056]

Thomson PD, Melmon KL, Richardson JA, el al. Lidocaine pharmacokinetics in advanced heart failure, liver disease, and renal failure in humans. Ann Intern Med 1973 78 499-508. [Pg.72]

Chow MS, Ronfeld RA, Ruggett D, Fieldman A. Lidocaine pharmacokinetics during cardiac arrest and external cardiopulmonary resuscitation. AmHeartJ 1981 102 799-801. [Pg.183]

Hendrie J, O Callaghan CJ. Lidocaine pharmacokinetics after cardiac arrest and external cardiopulmonary resuscitation. Am J Cardiol 1996 78 1322-1323. [Pg.183]

Gawronska-Szklarz B, Zarzycki M, Musial HD, Pudlo A, Loniewski 1, Drozdzik M. Lidocaine pharmacokinetics in postmenopausal women on hormone therapy. Menopause 2006 13(5) 793-798. [Pg.283]

The local anesthetics can be broadly categorized on the basis of the chemical nature of the linkage contained within the intermediate alkyl chain group. The amide local anesthetics include lidocaine (7.5), mepivacaine (7.6), bupivacaine (7.7), etidocaine (7.8), prilocaine (7.9), and ropivacaine (7.10) the ester local anesthetics include cocaine (7.11), procaine (7.12), benzocaine (7.13), and tetracaine (7.14). Since the pharmacodynamic interaction of both amide and ester local anesthetics with the same Na" channel receptor is essentially idenhcal, the amide and ester functional groups are bioisosterically equivalent. However, amide and ester local anesthetics are not equal from a pharmacokinetic perspective. Since ester links are more susceptible to hydrolysis than amide links. [Pg.416]

Pharmacokinetics Lidocaine is given intravenously because of extensive first-pass transformation by the liver, which precludes oral administration. The drug is dealkylated and eliminated almost entirely by the liver, consequently dosage adjustment may be necessary in patients with liver dysfunction. [Pg.180]

Pharmacokinetic. Agents metabolised in the liver provide higher plasma concentrations when another drug that inhibits hepatic metabolism, e.g. cimetidine, is added. Enzyme inducers enhance the metabolism of this class of P-blockers. P-adrenoceptor blockers themselves reduce hepatic blood flow (fall in cardiac output) and reduce the metabolism of p-blockers and other drugs whose metabolic elimination is dependent on the rate of delivery to the liver, e.g. lignocaine (lidocaine), chlorpromazine. [Pg.479]

The pharmacokinetics and safety of the 5% lidocaine patches have been studied in 20 healthy volunteers, who applied four patches to the skin either every 24 hours or every 12 hours for 3 days (67). Mean steady-state plasma concentrations were 186 and 225 ng/ml respectively, well below those required for an antidysrhythmic effect (1500 ng/ml) or a risk of toxicity (5000 ng/ml). The patches were well tolerated, with no major cutaneous adverse effects. This is in line with data from postmarketing surveillance studies, which have shown that since the availability of lidocaine patches in 1999, no adverse cardiac or other serious adverse events have been reported (68). [Pg.2057]

The pharmacokinetics of lidocaine in patches have been investigated in two studies. In 20 healthy volunteers, 5% lidocaine patches were applied for 18 hours/day on 3 consecutive days (69). The mean peak concentrations on days 1, 2, and 3 were 145,153, and 154 ng/ml respectively the median values of were 18.0, 16.5, and 16.5 hours and the mean trough concentrations were 83, 86, and 77 ng/ml. The patches were well tolerated local skin reactions were generally minimal and self-limiting. In 20 healthy volunteers, 4 lidocaine patches were applied every 12 or 24 hours on 3 consecutive days (67). The mean maximum-plasma lidocaine concentrations at steady state were 225 and 186 ng/ml respectively. There was no loss of sensation at the site of application. No patient had edema and most cases of erythema were very slight. No systemic adverse events were judged to be related to the patches. [Pg.2057]

The thrombin inhibitor argatroban had no effect on the pharmacokinetics of intravenous lidocaine 1.5 mg/kg for 10 minutes followed by 2 mg/kg/hour for 16 hours in 12 healthy volunteers the argatroban was given as an intravenous infusion of 2 pg/kg/minute for 16 hours (73). [Pg.2057]

The effects of erythromycin, an inhibitor of CYP3A4, on the pharmacokinetics of lidocaine have been studied in nine healthy volunteers. Steady-state oral erythromycin had no effect on the plasma concentration versus time curve of lidocaine after intravenous administration, but erythromycin increased the plasma concentrations of the major metabolite of lidocaine, MEGX (78). It is not clear what the interpretation of these results is, particularly since the authors did not study enough subjects to detect what might have been small but significant changes in various disposition parameters of lidocaine and did not report unbound concentrations of Udocaine or its metabolites. However, whatever the pharmacokinetic explanation, the clinical relevance is that one would expect that erythromycin would potentiate the toxic effects of lidocaine that are mediated by MEGX. [Pg.2057]

The effects of itraconazole, an inhibitor of CYP3A4, on the pharmacokinetics of lidocaine have been studied in nine healthy volunteers. Steady-state oral itraconazole had no effect on the plasma concentration versus time curve of lidocaine after intravenous administration nor on the plasma concentrations of the major metabolite of lidocaine, MEGX (78). [Pg.2057]

Gammaitoni AR, Davis MW. Pharmacokinetics and tolerability of lidocaine patch 5% tvith extended dosing. Ann Pharmacother 2002 36(2) 236-40. [Pg.2060]

Maeda Y, Funakoshi S, Nakamura M, Fukuzawa M, Kugaya Y, Yamasaki M, Tsukiai S, Murakami T, Takano M. Possible mechanism for pharmacokinetic interaction between lidocaine and mexiletine. Clin Pharmacol Ther 2002 7I(5) 389-97. [Pg.2060]

Ujhelyi MR, O Rangers EA, Fan C, Kluger J, Pharand C, Chow MS. The pharmacokinetic and pharmacodynamic interaction between propafenone and lidocaine. Clin Pharmacol Ther I993 53(I) 38-48. [Pg.2060]

Mexiletine is a class Ib antidysrhythmic drug, similar in action to lidocaine, but it can be given orally. Its adverse effects occur in up to 50% of patients (1) and withdrawal is often necessary (2). The most common adverse effects are on the cardiovascular and central nervous systems. The pharmacokinetics, clinical use, and adverse effects and interactions of mexiletine have been reviewed widely (3-8). [Pg.2329]

Example Lidocaine (Xylocaine) Moderate-acting amide (1-3 hours) Route IM/SC/I V Topical Pregnancy category B Pharmacokinetic Metabolized in liver PB 60%-80% ... [Pg.205]

Engelking, L.R., Blyden, G.T., Lofstedt, J. Greenblatt, D.J. (1987) Pharmacokinetics of antipyrine, acetaminophen and lidocaine in fed and fasted horses. Journal of Veterinary Pharmacology and Therapeutics, 10, 73-82. [Pg.131]

Pharmacokinetic parameters of digoxin and other cardioactive drugs are summarized in Table 33-2. Digoxin, disopyra-mide, lidocaine, procainamide, and quinidine are usually quantified by immunoassay. HPLC methods to quantify the other cardioactive drugs are reviewed in a previous edition of this chapter. ... [Pg.1256]

T. W. Schnider, R. Gaeta, W. Brose, C. F. Minto, K. M. Gregg, and S. L. Shafer, Derivation and cross-vahdation of pharmacokinetic parameters for computer controlled infusion of lidocaine in pain therapy. Anesthesiology 84 1043-1050 (1996). [Pg.417]

Rutledge, D.R. Abadi, A.H. Lopez, L.M. Beaudreau, C.A. High-performance liquid chromatographic determination of diltiazem and two of its metabolites in plasma using a short alkyl chain silanol deactivated column. J.Chromatogr., 1993, 615, 111-116 [plasma extracted metabolites imipramine IS LOD 4 n mL pharmacokinetics interfering theophylline simultaneous desipramine, propranolol, verapamil non-interfering aspirin, atenolol, caffeine, ibuprofen, lidocaine, metoprolol, nifedipine]... [Pg.528]

Johnson, K.E. Pieper, J.A. An HPLC method for the determination of diltiazem and three of its metabolites in serum. J.Liq.Chromatogr., 1990, 13, 951-960 [extracted metabolites serum doxepin (IS) LOD 3 ng/mL non-interfering carbamazepine, chlorpromazine, gedlopamil, imipramine, lidocaine, prochlorperazine, quinidine, thioridazine, trimeprazine pharmacokinetics]... [Pg.529]


See other pages where Pharmacokinetics lidocaine is mentioned: [Pg.396]    [Pg.178]    [Pg.267]    [Pg.396]    [Pg.178]    [Pg.267]    [Pg.128]    [Pg.177]    [Pg.71]    [Pg.66]    [Pg.352]    [Pg.2054]    [Pg.2059]    [Pg.213]    [Pg.302]    [Pg.164]    [Pg.183]    [Pg.1246]    [Pg.271]    [Pg.202]    [Pg.863]    [Pg.530]    [Pg.599]    [Pg.601]    [Pg.28]   
See also in sourсe #XX -- [ Pg.51 ]

See also in sourсe #XX -- [ Pg.178 , Pg.329 ]

See also in sourсe #XX -- [ Pg.593 , Pg.599 ]




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