RESUMEN
BACKGROUND AND OBJECTIVES: The aim of our study was to assess systemic and cerebral hemodynamic changes as well as cerebral CO2-reactivity during propofol anesthesia. METHODS: 27 patients undergoing general anesthesia were enrolled. Anesthesia was maintained using the Target-Controlled Infusion (TCI) method according to the Schnider model, effect site propofol concentration of 4 µg.mL-1. Ventilatory settings (respiratory rate and tidal volume) were adjusted to reach and maintain 40, 35, and 30 mmHg EtCO2 for 5 minutes, respectively. At the end of each period, transcranial Doppler and hemodynamic parameters using applanation tonometry were recorded. RESULTS: Systemic mean arterial pressure significantly decreased during anesthetic induction and remained unchanged during the entire study period. Central aortic and peripherial pulse pressure did not change significantly during anesthetic induction and maintenance, whereas augmentation index as marker of arterial stiffness significantly decreased during the anesthetic induction and remained stable at the time points when target CO2 levels were reached. Both cerebral autoregulation and cerebral CO2-reactivity was maintained during propofol anesthesia. CONCLUSIONS: Propofol at clinically administered doses using the Total Intravenous Anesthesia (TIVA/TCI) technique decreases systemic blood pressure, but does not affect static cerebral autoregulation, flow-metabolism coupling and cerebrovascular CO2 reactivity. According to our measurements, propofol may exert its systemic hemodynamic effect through venodilation. TRIAL REGISTRATION: The study was registered at http://www.clinicaltrials.gov, identifier: NCT02203097, registration date: July 29, 2014.