Revista espanola de anestesiologia y reanimacion · 2021
Influence of rate of administration on the mechanism behind propofol induced loss of consciousness.
СтатьяНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Sepúlveda P, Acosta I, Hoppe A, Lobo F A, Carrasco E
Аннотация
BACKGROUND: Propofol effect-site time course models included in TCI systems have been under discussion. We hypothesized that the rate of administration is a major contributor affecting the construction of a useful effect-site model: yielding different plasmatic concentrations, loss of consciousness may occur by different mechanisms more complex than the pharmacological effect-site.
METHODOLOGY: ASA I-II patients were randomized in two groups: rapid induction (RI) received TCI of propofol effect-site (CeCALC) 5.4μg/mL (modified Marsh model), and slow induction (SI) propofol infusion of 10mg/kg/hour. A neurologist, blinded to induction method, performed neurological assessments using the FOUR score until the loss of consciousness (LOC). At LOC, the presence of brain stem reflexes, EEG index (PSI) and infusion time/mass of drug were registered. Fisher's exact test was used to describe differences between brain stem reflexes and respiration components of the FOUR score and CeCALC for 4 propofol models at LOC time.
RESULTS: 16 patients divided in two groups were included. All patient in SI had brainstem reflexes free at LOC. In the RI, all patients had brain stem reflexes abolished and 1 patient had B and R of 4 points in the FOUR score (brain stem reflexes unaffected; P<.001). CeCALC at LOC time were contradictory at LOC in both groups and using 4 different Pk/Pd models.
CONCLUSIONS: Depending of the infusion rate, propofol CeCALC at LOC calculated by different Pk/Pd models could be the source of confuse data to be used to guide the state of general anesthesia.
METHODOLOGY: ASA I-II patients were randomized in two groups: rapid induction (RI) received TCI of propofol effect-site (CeCALC) 5.4μg/mL (modified Marsh model), and slow induction (SI) propofol infusion of 10mg/kg/hour. A neurologist, blinded to induction method, performed neurological assessments using the FOUR score until the loss of consciousness (LOC). At LOC, the presence of brain stem reflexes, EEG index (PSI) and infusion time/mass of drug were registered. Fisher's exact test was used to describe differences between brain stem reflexes and respiration components of the FOUR score and CeCALC for 4 propofol models at LOC time.
RESULTS: 16 patients divided in two groups were included. All patient in SI had brainstem reflexes free at LOC. In the RI, all patients had brain stem reflexes abolished and 1 patient had B and R of 4 points in the FOUR score (brain stem reflexes unaffected; P<.001). CeCALC at LOC time were contradictory at LOC in both groups and using 4 different Pk/Pd models.
CONCLUSIONS: Depending of the infusion rate, propofol CeCALC at LOC calculated by different Pk/Pd models could be the source of confuse data to be used to guide the state of general anesthesia.