Simultaneous Systemic and Hepatic Hemodynamic Measurements During High Peridural Anesthesia In Normal Man

Kennedy, William F.; Everett, Gaither B.; Cobb, Leonard A.; Allen, Gerald D.

doi:10.1213/00000539-197150060-00029

Cited by 50 publications

(10 citation statements)

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“…Hepatic blood flow may also be decreased, an effect which has been demonstrated following epidural administration of lignocaine in volunteers (Kennedy et al 1971). Maintenance of fluid balance may attenuate or prevent the effects of sympathetic blockade.…”

Section: Effects Of Epidural and Spinal Blockadementioning

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: Effects Of Epidural and Spinal Blockadementioning

confidence: 97%

Clinical Pharmacokinetics of Epidural and Spinal Anaesthesia

Burm

1989

Clinical Pharmacokinetics

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“…For example, in two previous studies, an epidural technique was used for part of the clinical management, which may have had significant effect on HaBF or HBF. 15,16 It is important, therefore, to interpret the results of this study while bearing in mind that many anesthetics, or anesthetic techniques, can have a profound effect on hepatic blood flow.…”

Section: Effect Of Propofol Infusion On Hepatic Oxygen Balancementioning

confidence: 99%

Effect of propofol on hepatic blood flow and oxygen balance in rabbits

Zhu

Pang

McCluskey

et al. 2008

Can J Anesth/J Can Anesth

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reports of original investigations CAN J ANESTH 55: 6 www.cja-jca.org June, 2008 Purpose: Propofol has been reported to alter hepatic blood flow and to increase hepatic oxygen consumption. This study was designed to determine the effect of propofol on hepatic blood flow and oxygenation in rabbits, in order to establish its net effect on hepatic oxygen balance.Methods: Twenty, adult male, New Zealand white rabbits were randomly divided into two groups: Group P (propofol, 0.6 mg·kg). An electromagnetic flowmeter was used to measure hepatic blood flow, and blood, from the carotid artery, the portal vein, and the hepatic vein, was used to determine hepatic oxygenation. After we obtained baseline values, we repeated measurements ten, 30, and 60 min after initiating the infusion.Results: Intralipid did not affect systemic hemodynamics, hepatic blood flow, or oxygenation during the 60 min infusion; however, propofol caused a time-dependent decrease in mean arterial blood pressures and an increase in portal venous flow and total hepatic blood flow. In contrast, hepatic arterial blood flow remained unchanged during the propofol infusion. Hepatic oxygen delivery and consumption increased in a time-dependent manner to maximums of 25% and 21.4% (both, P < 0.05) above baseline, respectively. Hepatic venous oxygen saturation and extraction was unchanged throughout the study period. Conclusion:Propofol increases total hepatic blood flow, primarily by increasing hepatic portal venous flow. The increase in liver oxygen consumption was fully compensated by an increase in oxygen supply to the liver, resulting in a preserved, hepatic oxygen balance.

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“…The effect of high-lumbar epidural anesthesia on hepatic blood flow was evaluated in 3 human studies. Kennedy et al [8] reported that hepatic blood flow is decreased to 25% in healthy volunteers despite constant cardiac flow. Tanaka et al [9] reported that high-lumbar epidural anesthesia decreased hepatic blood flow by 35% according to measurement of PDR and ICG clearance.…”

Section: Discussionmentioning

confidence: 99%