Pharmacokinetic Aspects of Intravenous Regional Anesthesia

Tucker, Geoffrey T.; Boas, Robert A.

doi:10.1097/00000542-197106000-00014

Cited by 123 publications

(50 citation statements)

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“…The efficacy of this technique to decrease the maximal arterial concentration and/or the incidence of symptomatic patients is a controversial issue [57]. Maximal arterial concentrations may occur as early as 30 seconds after tourniquet deflation [58,59]. Cyclic deflation may delay the occurrence of the maximal arterial concentration but does not significantly affect its value [57].…”

Section: Discussionmentioning

confidence: 99%

Adverse events associated with intravenous regional anesthesia (Bier block): a systematic review of complications

Guay

2009

Journal of Clinical Anesthesia

114

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Section: Discussionmentioning

confidence: 99%

Adverse events associated with intravenous regional anesthesia (Bier block): a systematic review of complications

Guay

2009

Journal of Clinical Anesthesia

114

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“…At appropriate doses, lidocaine can be administered locally without central nervous system (CNS) or cardiac toxicity because local tissue concentrations reach a thousand-fold higher levels than blood concentrations (8). If lidocaine does enter the systemic circulation following local injection, peak arterial lidocaine concentrations are blunted due to the considerable uptake in the lungs (9,10). This is followed by back diffusion of lidocaine into the circulation, occurring within 30 s (10).…”

Section: Discussionmentioning

confidence: 99%

Lidocaine-induced altered mental status and seizure after hematoma block

Dorf

Kuntz

Kelsey

et al. 2006

The Journal of Emergency Medicine

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“…However, considerable arterio-venous concentration differences exist for lignocaine after its rapid i.v. input (Tucker & Boas, 1971 (Tucker, 1978 …”

Section: Intrinsic Clearancementioning

confidence: 99%

Effects of beta‐adrenoceptor antagonists on the pharmacokinetics of lignocaine.

Tucker¹,

Bax²,

Lennard³

et al. 1984

Brit J Clinical Pharma

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1 In theory, 3-adrenoceptor antagonists could lower the clearance of free lignocaine in three ways (a) by decreasing hepatic blood flow, (b) by competing for plasma binding sites or (c) by inhibiting the enzymes responsible for metabolising lignocaine. 2 The first mechanism has been demonstrated for propranolol and is probably common to all agents lacking intrinsic sympathomimetic activity.3 The second mechanism is discounted by data showing that propranolol, one of the more highly bound f8-adrenoceptor antagonists, does not alter the free fraction of lignocaine in plasma.4 In vitro studies support the third mechanism for the more lipid-soluble ,8-adrenoceptor antagonists, as does the fact that observed decreases in the clearance of lignocaine in vivo are generally greater than the anticipated maximum lowering of hepatic blood flow.

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Pharmacokinetic Aspects of Intravenous Regional Anesthesia

Cited by 123 publications

References 0 publications

Adverse events associated with intravenous regional anesthesia (Bier block): a systematic review of complications

Adverse events associated with intravenous regional anesthesia (Bier block): a systematic review of complications

Lidocaine-induced altered mental status and seizure after hematoma block

Effects of beta‐adrenoceptor antagonists on the pharmacokinetics of lignocaine.

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