Ketamine, Not Propofol, Attenuates Cerebrovascular Response to Carbon Dioxide in Humans With Isoflurane Anesthesia

Study Objectives: To investigate the effects of ketamine and propofol on the cerebrovascular response to carbon dioxide (CO₂) in humans during isoflurane anesthesia.Design: Randomized clinical investigation.Settings: University hospital of a medical school.Patients: 30 ASA physical status I and II adult, elective surgical patients.Interventions and Measurements: With each patient given air/oxygen/isoflurane anesthesia, the flow velocity in the middle cerebral artery (Vmca) and pulsatility index were measured using the transcranial Doppler method under hypocapnic [arterial CO₂tension (Paco₂) 28–32 mmHg], normocapnic (Paco₂ 38–42 mmHg), and hypercapnic conditions (Paco₂ 48–52 mmHg). Paco₂ was altered by supplementing the inspired gas with CO₂ without changing the respiratory conditions. Patients were then randomly assigned to receive either ketamine 1 mg · kg⁻¹ or propofol (2 mg · kg⁻¹followed by an infusion of 6–10 mg · kg⁻¹ · hr⁻¹) (n = 15 for each drug), and the measurements were repeated.Main Results: Ketamine reduced both absolute and relative cerebrovascular reactivity to CO₂ significantly [2.9 ± 0.8 (control) vs. 2.6 ± 1.0 (ketamine) cm · sec⁻¹ · mmHg⁻¹: p < 0.05; and 3.5 ± 0.7 (control) vs. 2.8 ± 0.9 (ketamine) % · mmHg⁻¹: p < 0.01, respectively]. However, ketamine did not reduce Vmca during hypercapnic conditions (117 ± 29 cm · sec⁻¹) compared with controls (120 ± 28 cm · sec⁻¹). Although propofol decreased Vmca during all conditions, it did not cause any change in either absolute or relative CO₂ reactivity [2.5 ± 0.8 (control) vs. 2.5 ± 1.0 (propofol) cm · sec⁻¹ · mmHg⁻¹, and 3.3 ± 1.3 (control) vs. 4.1 ± 1.0 (propofol) % · mmHg⁻¹, respectively].Conclusions: In humans given isoflurane anesthesia, a) ketamine reduced cerebrovascular response to CO₂, but cerebral blood flow (CBF) during hypercapnic conditions was comparable with controls, and b) although propofol decreases CBF, it maintains the cerebrovascular response to CO₂.