Effect of pH-adjustment of bupivacaine on onset and duration of epidural analgesia in parturients

McMorland, G. H.; Douglas, M. Joanne; Jeffery, Wayne K.; Ross, P. L. E.; Axelson, James E.; Kim, James H. K.; Gambling, David R.; Robertson, Kerri M.

doi:10.1007/bf03014257

Cited by 67 publications

(13 citation statements)

References 10 publications

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“…However, although some authors reported a faster onset of action with lignocaine and bupivacaine (DiFazio et al 1976;McMorland et al 1986), others have noted disappointing results with chloroprocaine Ross et al 1987).…”

Section: Alkalisation and Carbonativnmentioning

confidence: 97%

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Burm

1989

Clinical Pharmacokinetics

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Epidural and spinal anaesthesia results from the interaction of local anaesthetics with nerve structures, primarily those located within the subarachnoid space. Local anaesthetics can reach the sites of action along various distribution pathways. Uptake into extraneural tissues (in particular epidural fat) and systemic absorption compete with neural tissue distribution and thereby affect the clinical potency and duration of action. Consequently, epidural doses must be much higher than spinal doses. The systemic absorption of lignocaine (lidocaine), bupivacaine and etidocaine following lumbar epidural administration has been shown to be biphasic, with a rapid initial absorption phase followed by a much slower absorption phase. Initial absorption rates of lignocaine and bupivacaine following subarachnoid injection are much slower, but the late absorption rates are similar to those after epidural administration. The tissue distribution characteristics of various amide-type agents are similar, because more extensive plasma binding offsets the greater tissue affinity of the more lipophilic compounds bupivacaine and etidocaine. The amide-type agents are predominantly eliminated by hepatic metabolism, except prilocaine, which is also metabolised elsewhere in the body. Ester-type agents are rapidly hydrolysed in blood and liver and are eliminated much faster than amide-type agents. The blood concentrations attained depend primarily upon the dose administered. The addition of adrenaline (epinephrine) reduces the peak plasma drug concentrations; similarly, the age of the patient, disease states and drug interactions may alter the pharmacokinetics to various extents. Because of the low dose requirements, systemic toxicity is not a problem during spinal anaesthesia. During epidural anaesthesia, however, the safety margin is relatively small, and systemic toxicity is very likely to occur after inadvertent intravascular injection of an epidural dose.

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Section: Alkalisation and Carbonativnmentioning

confidence: 97%

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Burm

1989

Clinical Pharmacokinetics

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“…Aucun brnrfice n'a 6t6 mis en 6vidence, que ce soit sur l'installation, la durre ou la qualit6 de l'analgrsie. McMorland et al 26 apr~s tamponnement de ce m~me anesthdsique local, /~ la m~me concentration, retrouve lui un effet favorable ~ l'alcalinisation: le temps de latence 6tait diminu6 de moiti6 (3 vs 6 min), la dur6e d'analgrsie prolongre (96 vs 79 min). I1 faut souligner que dans cette 6tude le pH de la solution tamponnre 6tait plus proche du pKa de la bupivaca'ine que dans celle de Jacquinot et al (7,26 contre 7,07).…”

Section: Alcalinisation Pour Analggsie Pdridurale Pendant L' Accoucheunclassified

Alcalinisation des anesthésiques locaux: théoriquement justifiée mais inutile cliniquement

1996

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“…This is in accordance with the clinical experience of many obstetric anesthesiologists as well as with previous studies. 16 When a conventional analysis (hours after epidural insertion) is used, the VAS curves are consistent with those of previous investigations 8,17,18 but could not show the same increase of pain as patients approach delivery, since women are at different stages of labor relative to insertion of the epidural catheter. The effectiveness of the loading dose can be assessed this way but not the effectiveness of the PCEA.…”

Section: Discussionmentioning

confidence: 57%

“…The time of onset of epidural analgesia with this technique is not known. McMorland and coworkers 16 showed that the time to onset of epidural analgesia of 8 mL of 0.25% bupivacaine, as defined by the first painless contraction, is 6.0 € 0.53 min using a solution that was not pH-adjusted and 3.2 € 0.24 min in a pH-adjusted solution. The times to peak effect in that study were 16.5 € 1.15 and 14.2 € 1.1 min respectively.…”

Section: Discussionmentioning

confidence: 99%