Sequestration of propofol in an extracorporeal circuit

Tarr, T.J.; Kent, A.P.

doi:10.1016/0888-6296(89)90818-1

Cited by 12 publications

(6 citation statements)

References 3 publications

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“…As propofol is a highly lipophilic and highly protein bound drug (68), it is anticipated to be significantly sequestered within the ECMO circuitry (21,77,(88)(89)(90). In an in vitro study, Hynynen et al showed that approximately 35% and 75% of propofol were lost within the ECMO circuits after 5 and 120 minutes of the experiment, respectively (89).…”

Section: Propofolmentioning

confidence: 99%

Optimising drug dosing in patients receiving extracorporeal membrane oxygenation

et al. 2018

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Optimal pharmacological management during extracorporeal membrane oxygenation (ECMO) involves more than administering drugs to reverse underlying disease. ECMO is a complex therapy that should be administered in a goal-directed manner to achieve therapeutic endpoints that allow reversal of disease and ECMO wean, minimisation of complications (treatment of complications when they do occur), early interruption of sedation and rehabilitation, maximising patient comfort and minimising risks of delirium. ECMO can alter both the pharmacokinetics (PK) and pharmacodynamics (PD) of administered drugs and our understanding of these alterations is still evolving. Based on available data it appears that modern ECMO circuitry probably has a less significant impact on PK when compared with critical illness itself. However, these findings need further confirmation in clinical population PK studies and such studies are underway. The altered PD associated with ECMO is less understood and more research is indicated. Until robust dosing guidelines become available, clinicians will have to rely on the principles of drug dosing in critically ill and known PK alterations induced by ECMO itself. This article summarises the PK alterations and makes preliminary recommendations on possible dosing approaches.

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Section: Propofolmentioning

confidence: 99%

Optimising drug dosing in patients receiving extracorporeal membrane oxygenation

et al. 2018

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“…ANH does not confer any additional benefit. Introduction: The sequestration of drugs, such as fentanyl [1,2], thiopental, nitroglycerine and propofol [3] in the extracorporeal circuit in vitro has been well described. This phenomenon can change the pharmacokinetic behaviour of drugs during cardiopulmonary bypass, thus potentially leading to problems in achieving adequate dosing regimens.…”

Section: Discussionmentioning

confidence: 99%

Does a remifentanil bolus attenuate the haemodynamic response to rigid bronchoscopy?

et al. 2001

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It has been suggested that mild hypothermia during cardiopulmonary bypass (CPB) may attenuate, but not completely suppress, the production of interleukin-8 (IL-8) in the brain [1]. This study examined the effect of repeated deep hypothermic circulatory arrest (DHCA) on production of IL-8 and myeloperoxidase (MPO) in the cerebrovascular bed in patients undergoing pulmonary thromboendarterectomy (PTE). Methods: After LREC approval and written informed consent, we studied eight patients undergoing PTE. Anaesthetic and surgical technique were strictly standardized [2] and all patients had a jugular bulb catheter inserted after induction. After initiation of CPB, all patients were cooled to below 20°C and underwent at least two periods of DHCA for 20 min. Each DHCA period was separated by a 10-min reperfusion interval. The levels of IL-8 and MPO were measured in paired arterial and jugular samples drawn simultaneously at specific time points, using enzyme-linked immunoassay kits. Juguloarterial (j-a) gradients were then calculated. All data are expressed as median (interquartile range) and were compared with the baseline values using the Wilcoxon signed rank sum test. J-a gradients were compared with zero using one-sample t-test. Results: The baseline arterial values before CPB [T1] for IL-8 and MPO were 12.9 (11.5-21.4) pg/ml and 4.5 (3.1-6.6) ng/ml, respectively (Fig. 1). For both IL-8 and MPO, arterial levels significantly increased before the first DHCA [T3] to 28.3 (21.6-43.1) pg/ml and 31.2 (26.1-11.7) ng/ml, respectively, and remained elevated until 8 min following the second DHCA [T7]. However, no significant j-a differences for IL-8 and MPO were found throughout this period. Conclusions: These data imply that the cerebral activation of inflammatory processes represented as specific IL-8 and MPO production in the cerebrovascular bed are suppressed during repeated DHCA in the present study.

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“…Adsorption of Diprivan onto uncoated extracorporeal surfaces was first investigated by Tarr et al 7 when they measured total propofol levels during a normothermic in vitro study using four uncoated oxygenators and circuits. Using HPLC, they found a 50% drop in total propofol levels after 15 minutes of circulation, which continued to decrease over the remaining four-hour study period.…”

Section: Introductionmentioning

confidence: 99%

The effect of Diprivan (propofol) on phosphorylcholine surfaces during cardiopulmonary bypass — an in vitro investigation

Myers¹,

Voorhees²,

Eke³

et al. 2009

Perfusion

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It is well known that extracorporeal surfaces have the ability to bind such drugs as fentanyl, nitroglycerine and propofol. Adsorption of the injectable anesthetic agent Diprivan (propofol) onto uncoated and heparin-coated extracorporeal surfaces during cardiopulmonary bypass (CPB) has been previously investigated; however, propofol adsorption onto synthetic-coated extracorporeal surfaces has not been published previously. The focus of this investigation was on the interaction of propofol and the synthetic biomimetic coating from the Sorin Group called Mimesys (phosphorylcholine (PC)). A randomized series of six in vitro experiments were done with propofol using both PC-coated circuits without arterial filters and those with arterial filters. The circuits were identical in all experiments and priming remained the same, with 750 mls of normal saline and 1250 mls of fresh bovine blood (hematocrit 41.0 +/- 1.0%). After circulation and collection of baseline samples, the first (low) dose of 4 mg (4000 mcg) of Diprivan 1% was added to the perfusate, followed by the second (high) dose of 40 mg (40,000 mcg) and the final challenge (extreme dose) of 356 mg (356,000 mcg) of Diprivan. Drug assay was done by an independent laboratory, using the standardized method of High Performance Liquid Chromatography (HPLC). Measurements of total propofol were done at baseline, 20 minutes, 40 minutes and 60 minutes after each injection. Oxygenator performance was also measured prior to the addition of propofol and repeated after exposure to 4 mg, 40mg and 356 mg propofol for 60 min, 120 min and 180 minutes of circulation. Results indicate that phosphorylcholine coating does not prevent the adsorption of propofol during extracorporeal circulation and the oxygenator's gas exchange ability is not affected by prolonged exposure to an extreme dose of the medication during high flow extracorporeal circulation.

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Sequestration of propofol in an extracorporeal circuit

Cited by 12 publications

References 3 publications

Optimising drug dosing in patients receiving extracorporeal membrane oxygenation

Optimising drug dosing in patients receiving extracorporeal membrane oxygenation

Does a remifentanil bolus attenuate the haemodynamic response to rigid bronchoscopy?

The effect of Diprivan (propofol) on phosphorylcholine surfaces during cardiopulmonary bypass — an in vitro investigation

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