metricas
Revista Española de Anestesiología y Reanimación (English Edition) Comparison of the Cortínez and the Schnider models with a targeted effect-site ...
Journal Information
Vol. 63. Issue 10.
Pages 553-612 (December 2016)
Cite
Cite
Share
Download PDF
More article options
Visits
755
Vol. 63. Issue 10.
Pages 553-612 (December 2016)
Original article

Comparison of the Cortínez and the Schnider models with a targeted effect-site TCI of 3mcg/ml in biophase in healthy volunteers

Comparación del modelo de Cortínez y de Schnider en perfusión de propofol controlada por objetivo de 3 mcg/ml, a biofase, en voluntarios sanos
Visits
755
C. Frederico Avendañoa,
Corresponding author
carolinafrederico@gmail.com

Corresponding author.
, L.I. Cortínezb, C.R. Ramírez-Paesanoc
a Departamento de Anestesiología, Clínica Santiago de León, Caracas, Venezuela
b Departamento de Anestesiología, Escuela de Medicina, Pontificia Universidad Católica de Chile, Santiago, Chile
c Departamento de Anestesiología Clínica Ávila, Caracas, Venezuela
This item has received
Article information
Abstract
Full Text
Bibliography
Download PDF
Statistics
Abstract
Objective

To compare the Cortínez and Schnider models in effect-site TCI mode (3mcg/ml) in healthy volunteers.

Methods

Ten healthy volunteers were prospectively studied on 2 occasions. Propofol was administered with the Cortínez or the Schnider models, as randomly assigned. Times and predicted concentrations at the time of loss and recovery of consciousness (LOC and ROC), mass of drug administered, BIS, and haemodynamic variables were compared. Statistical analysis was with paired Wilcoxon test. A P<.05 was considered significant.

Results

The propofol bolo was higher (1.4 [1.3–1.6] versus 0.9 [0.7–1.3] mg/kg, P=.005) and the LOC occurred earlier (1.33 [0.67–6.83] versus 3.87 [1.66–11.08] minutes, P=.02) with the Cortínez model compared to the Schnider model. With the Cortínez model, LOC occurred at an effect site concentrations of 2.6 (1.65–3.0)mcg/ml. With the Schnider model, LOC occurred at 3.87min (1.66–11.8) after reaching the target of 3 mcg/ml. (P=.001). BIS values, infusion rates, and haemodynamic variables were similar between models after 20min of infusion (P>.5). Recovery (ROC) was longer with the Cortínez model (11.6 [8.1–16.2] vs. 8.5 [4.7–15.5] min, P=.003).

Conclusions

The Cortínez model is a good alternative to the Schnider model for use in effect-site TCI mode in normal weight subjects. With the target used in this study (3mcg/ml), the slower Ke0 incorporated into the Cortínez model better discriminated the LOC time.

Keywords:
Propofol
Pharmacokinetics
Target controlled infusion
Ke0
Resumen
Objetivo

Comparar clínicamente los modelos de Schnider y Cortínez con sistemas «TCI», para la perfusión de propofol a concentración en biofase de 3 mcg/ml en voluntarios sanos.

Material y método

Se estudió prospectivamente a 10 voluntarios sanos en 2 ocasiones. Se administró propofol con el modelo de Cortínez o Schnider según asignación aleatorizada. Se compararon tiempos y concentraciones de propofol alcanzadas al momento de pérdida y recuperación de consciencia (LOC y ROC), masa de fármaco administrada, valores de BIS y variables hemodinámicas. El análisis estadístico fue con Wilcoxon pareado. Una p ≤ 0,05 fue considerada significativa.

Resultados

El bolo inicial de propofol fue mayor (1,4 [1,3–1,6] versus 0,9 [0,7–1,3] mg/kg; p=0,005) y el LOC ocurrió antes (1,33 [0,67–6,83] versus 3,87 [1,66–11,08] min; p=0,02) con el modelo de Cortínez comparado con el modelo de Schnider. El modelo de Cortínez predice una concentración en biofase al LOC de 2,6mcg/ml (1,65–3,0). Con Schnider, el LOC ocurre 3,87min (1,66–11,8) después de alcanzado el objetivo de 3mcg/ml (p=0,001). Los valores de BIS, las velocidades de perfusión y las variables hemodinámicas fueron similares con ambos modelos a los 20min de perfusión (p>0,5). La recuperación (ROC) fue más larga con el modelo de Cortínez (11,6 [8,1–16,2] vs. 8,5 [4,7–15,5] min; p=0,003).

Conclusiones

El modelo de Cortínez es una buena alternativa al modelo de Schnider para su uso en TCI con objetivo en biofase en sujetos normopeso. Con el objetivo utilizado, las concentraciones en biofase predichas con la Ke0 más lenta incorporada en el modelo de Cortínez permiten discriminar mejor el momento del LOC en la inducción.

Palabras clave:
Propofol
Farmacocinética
Perfusión controlada por objetivo
Ke0

Article

These are the options to access the full texts of the publication Revista Española de Anestesiología y Reanimación (English Edition)
Subscriber
Subscriber

If you already have your login data, please click here .

If you have forgotten your password you can you can recover it by clicking here and selecting the option “I have forgotten my password”
Purchase
Purchase article

Purchasing article the PDF version will be downloaded

Purchase now
Contact
Phone for subscriptions and reporting of errors
From Monday to Friday from 9 a.m. to 6 p.m. (GMT + 1) except for the months of July and August which will be from 9 a.m. to 3 p.m.
Calls from Spain
932 415 960
Calls from outside Spain
+34 932 415 960
E-mail
References
[1]
A.R. Absalom, V. Mani, T. de Smet, M.M. Struys.
Pharmacokinetic models for propofol – defining and illuminating the devil in the detail.
Br J Anaesth, 103 (2009), pp. 26-37
[2]
L.I. Cortínez, B.J. Anderson, A. Penna, L. Olivares, H.R. Muñoz, N.H. Holford, et al.
Influence of obesity on propofol pharmacokinetics: derivation of a pharmacokinetic model.
BJA, 105 (2010), pp. 448-456
[3]
T.W. Schnider, C.F. Minto, P.L. Gambus, C. Andresen, D.B. Goodale, S.L. Shafer, et al.
The influence of method of administration and covariates on the pharmacokinetics of propofol in adult volunteers.
Anesthesiology, 88 (1998), pp. 1170-1182
[4]
F. Servin, R. Farinotti, J.P. Haberer, J.M. Desmonts.
Propofol infusion for maintenance of anesthesia in morbidly obese patients receiving nitrous oxide. A clinical and pharmacokinetic study.
Anesthesiology, 78 (1993), pp. 657-665
[5]
D.J. Eleveld, J.H. Proost, L.I. Cortínez, A.R. Absalom, M.M. Struys.
A general purpose pharmacokinetic model for propofol.
Anesth Analg, 118 (2014), pp. 1221-1237
[6]
L.I. Cortínez, N. de la Fuente, D.J. Eleveld, A. Oliveros, F. Crovari, P. Sepúlveda, et al.
Performance of propofol target-controlled infusion models in the obese: pharmacokinetic and pharmacodynamic analysis.
Anesth Analg, 119 (2014), pp. 302-310
[7]
A.G. Doufas, M. Bakhshandeh, A.R. Bjorksten, S.I. Shafer, D.I. Sessler.
Induction speed is not a determinant of propofol pharmacodynamics.
Anesthesiology, 101 (2004), pp. 1112-1121
[8]
M. Coppens, J.G. Van Limmen, T. Schnider, B. Wyler, S. Bonte, F. Dewaele, et al.
Study of the time course of the clinical effect of propofol compared with the time course of the predicted effect-site concentration: performance of 3 pharmacokinetic-dynamic models.
BJA, 104 (2010), pp. 452-458
[9]
A.J. Thomson, A.F. Nimmo, F.H. Engbers, J.B. Glen.
A novel technique to determine an ‘apparent ke0’ value for use with the Marsh pharmacokinetic model for propofol.
Anaesthesia, 69 (2014), pp. 420-428
[10]
P.O. Sepúlveda, X. Mora.
Reevaluación del comportamiento del curso temporal del efecto de propofol descrito por el modelo farmacocinético de Schnider.
Rev Esp Anestesiol Reanim, 59 (2012), pp. 542-548
[11]
M.R. Struys, M.J. Coppens, N. de Neve, E.P. Mortier, A.G. Doufas, J.F. van Bocxlaer, et al.
Influence of administration rate on propofol plasma-effect site equilibration.
Anesthesiology, 107 (2007), pp. 386-396
[12]
P.O. Sepúlveda, L.I. Cortínez, A. Recart, H.R. Muñoz.
Predictive ability of propofol effect-site concentrations during fast and slow infusion rates.
Acta Anaesthesiol Scand, 54 (2010), pp. 447-452
[13]
D.A. McCormick, H.C. Pape, A. Williamson.
Actions of norepinephrine in the cerebral cortex and thalamus: implications for function of the central noradrenergic system.
Prog Brain Res, 88 (1991), pp. 293-305
[14]
M.B. Kelz, Y. Sun, J. Chen, Q. Cheng Meng, J.T. Moore, S.C. Veasey, et al.
An essential role for orexins in emergence from general anesthesia.
Proc Natl Acad Sci U S A, 105 (2008), pp. 1309-1314
[15]
E.B. Friedman, Y. Sun, J.T. Moore, H.T. Hung, Q.C. Meng, P. Perera, et al.
A conserved behavioral state barrier impedes transitions between anesthetic-induced unconsciousness and wakefulness: Evidence for neural inertia.
[16]
C.B. Saper, T.C. Chou, T.E. Scammell.
The sleep switch: hypothalamic control of sleep and wakefulness.
Trends Neurosci, 24 (2001), pp. 726-731
[17]
S. Van Kralingen, J. Diepstraten, M.Y. Peeters, V.H. Deneer, B. van Ramshorst, R.J. Wiezer, et al.
Population pharmacokinetics and pharmacodynamics of propofol in morbidly obese patients.
Clin Pharmacokinet, 50 (2011), pp. 739-750
[18]
J.F. Coetzee.
Allometric or lean body mass scaling of propofol pharmacokinetics: towards simplifying parameter sets for target-controlled infusions.
Clin Pharmacokinet, 51 (2012), pp. 137-145
asdasdasd
Article options
Tools