Daniela Chalo1,2, Sara Pedrosa2, Pedro Amorim3, Aura Silva4, Paula Guedes de Pinho4, Rui Correia5, Sonia Gouveia6,7, Consuelo Sancho8. 1. Institute of Neurosciences of Castilla y Leon, INCyL, IBSAL, University of Salamanca, Salamanca, Spain. 2. Anesthesiology Department, Centro Hospitalar do Baixo Vouga, Aveiro, Portugal. 3. Anesthesiology Department, Centro Hospitalar do Porto, Porto, Portugal. 4. UCIBIO-REQUIMTE, Toxicology Laboratory, Biological Sciences Department, Faculty of Pharmacy of the University of Porto, Porto, Portugal. 5. Anesthesiology Department, Anesthesiology Centre for Investigation, Centro Hospitalar do Porto, Porto, Portugal. 6. Institute of Electronics and Informatics Engineering of Aveiro (IEETA), University of Aveiro, Aveiro, Portugal. 7. Center for R&D in Mathematics and Applications (CIDMA), University of Aveiro, Aveiro, Portugal. 8. Physiology and Pharmacology Department, INCyL, IBSAL, University of Salamanca, Salamanca, Spain.
Abstract
BACKGROUND: Anesthesia induction and maintenance with propofol can be guided by target-controlled infusion (TCI) systems using pharmacokinetic (Pk) models. Physiological variables, such as changes in cardiac output (CO), can influence propofol pharmacokinetics. Knee-chest (KC) surgical positioning can result in CO changes. OBJECTIVES: This study aimed to evaluate the relationship between propofol plasma concentration prediction and CO changes after induction and KC positioning. METHODS: This two-phase prospective cohort study included 20 patients scheduled for spinal surgery. Two different TCI anesthesia protocols were administered after induction. In phase I (n = 9), the loss of consciousness (LOC) concentration was set as the propofol target concentration and CO changes following induction and KC positioning were quantified. In phase II (n = 11), based on data from phase I, two reductions in the propofol target concentration on the pump were applied after LOC and before KC positioning. Propofol plasma concentrations were measured at different moments in both phases: after induction and after KC positioning. RESULTS: Schnider Pk model showed a good performance in predicting propofol concentration after induction; however, after KC positioning, when a significant drop in CO occurred, the measured propofol concentrations were markedly underestimated. Intended reductions in the propofol target concentration did not attenuate HD changes. In the KC position, there was no correlation between the propofol concentration estimated by the Pk model and the measured concentration in plasma, as the latter was much higher (P = 0.013) while CO and BIS decreased significantly (P < 0.001 and P = 0.004, respectively). CONCLUSIONS: Our study showed that the measured propofol plasma concentrations during the KC position were significantly underestimated by the Schnider Pk model and were associated with significant CO decrease. When placing patients in the KC position, anesthesiologists must be aware of pharmacokinetic changes and, in addition to standard monitoring, the use of depth of anesthesia and cardiac output monitors may be considered in high-risk patients.
BACKGROUND: Anesthesia induction and maintenance with propofol can be guided by target-controlled infusion (TCI) systems using pharmacokinetic (Pk) models. Physiological variables, such as changes in cardiac output (CO), can influence propofol pharmacokinetics. Knee-chest (KC) surgical positioning can result in CO changes. OBJECTIVES: This study aimed to evaluate the relationship between propofol plasma concentration prediction and CO changes after induction and KC positioning. METHODS: This two-phase prospective cohort study included 20 patients scheduled for spinal surgery. Two different TCI anesthesia protocols were administered after induction. In phase I (n = 9), the loss of consciousness (LOC) concentration was set as the propofol target concentration and CO changes following induction and KC positioning were quantified. In phase II (n = 11), based on data from phase I, two reductions in the propofol target concentration on the pump were applied after LOC and before KC positioning. Propofol plasma concentrations were measured at different moments in both phases: after induction and after KC positioning. RESULTS: Schnider Pk model showed a good performance in predicting propofol concentration after induction; however, after KC positioning, when a significant drop in CO occurred, the measured propofol concentrations were markedly underestimated. Intended reductions in the propofol target concentration did not attenuate HD changes. In the KC position, there was no correlation between the propofol concentration estimated by the Pk model and the measured concentration in plasma, as the latter was much higher (P = 0.013) while CO and BIS decreased significantly (P < 0.001 and P = 0.004, respectively). CONCLUSIONS: Our study showed that the measured propofol plasma concentrations during the KC position were significantly underestimated by the Schnider Pk model and were associated with significant CO decrease. When placing patients in the KC position, anesthesiologists must be aware of pharmacokinetic changes and, in addition to standard monitoring, the use of depth of anesthesia and cardiac output monitors may be considered in high-risk patients.
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