The effects of propofol on cerebral blood flow velocity and cerebral oxygen extraction during cardiopulmonary bypass.

UNLABELLED: We investigated the effects of burst-suppression doses of propofol on cerebral blood flow velocity (CBFV), cerebral oxygen extraction (COE), and dynamic autoregulation in 20 patients undergoing cardiac surgery. The experimental procedure was performed during nonpulsatile cardiopulmonary bypass (CPB) with stable hypothermia (32 degrees C) in fentanyl-anesthetized patients. Middle cerebral artery transcranial Doppler flow velocity, right jugular bulb oxygen saturation, and jugular venous pressure (JVP) were continuously measured. Dynamic autoregulation was tested by stepwise changes in mean arterial pressure (MAP) within a range of 40-80 mm Hg by sodium nitroprusside and phenylephrine before (control) and during propofol infusion, with a stable plasma concentration (approximately 9 microg/mL). Propofol induced a 35% decrease in CBFV (P < 0.0001) and a 10% decrease in COE (P < 0.05) compared with control. The slopes of the curves relating CBFV and COE to cerebral perfusion pressure (CPP = MAP - JVP) were less pronounced with propofol (P < 0.01 and P < 0.05, respectively). We conclude that propofol decreases CBFV and improves dynamic autoregulation during moderate hypothermic CPB. Furthermore, during propofol infusion, cerebral blood flow was in excess relative to oxygen demand, as indicated by the decrease in COE. IMPLICATIONS: In this study, we evaluated the effects of propofol on continuously measured cerebral blood flow velocity (CBFV) and cerebral oxygen extraction as a function of perfusion pressure. Propofol induced 35% and 10% decreases in CBFV and cerebral oxygen extraction, respectively. The slope of the curve relating cerebral perfusion pressure to CBFV decreased with propofol.

Do changes in cardiac output affect the inspiratory to end-trial oxygen difference?

BACKGROUND: The paramagnetic technique has made it possible to monitor the end-tidal oxygen concentration and P(1-ET)O2, i.e. inspiratory to end-tidal oxygen difference, breath-by-breath. Little is known about the implications of a changing P(1-ET)O2, but so far studies have shown it to be a quick and sensitive variable to detect hypoventilation. This study was designed to observe the circulatory effects on P(1-ET)O2 in an experimental setting but monitored as in a clinical situation. METHODS: We assessed the oxygen difference during changes in cardiac output induced by intravenous ephedrine-hydrochloride in 12 healthy male volunteers. P(1-ET)O2 was measured with a fast-response paramagnetic differential oxygen sensor. Cardiac output was measured with non-invasive transthoracic electrical bioimpedance. As simultaneous changes in metabolism and ventilation will also influence P(1-ET)O2 oxygen uptake and expired minute volume were monitored. After a rest period, the subjects had an intravenous injection of ephedrine-hydrochloride 0.1 mg.kg-1 followed by a 30-min observation period. RESULTS: Cardiac output increased significantly as did the oxygen uptake and the ventilation. We found no biological significant correlation between cardiac output and P(1-ET)O2. The P(1-ET)O2 was influenced by ventilation and metabolism.

Effects of ephedrine on oxygen consumption and cardiac output.

Bolus doses of ephedrine are often used by anaesthesiologists for intraoperative hypotension. This randomized single-blind cross-over study was designed to simultaneously evaluate circulatory, respiratory and metabolic effects of intravenously given ephedrine in 12 healthy male volunteers. Oxygen uptake and carbon dioxide excretion were measured with indirect calorimetry and non-invasive transthoracic electrical bioimpedance was used for cardiac output measurements. The maximum effect on most variables was reached at 4-5 min. At 5 min after the administration of ephedrine 0.1 mg per kilogram body weight, there were significant increases in cardiac index, systolic and mean arterial blood pressure, expired minute volume, oxygen uptake and carbon dioxide excretion rates. There were no significant changes in the quotient between oxygen uptake rate and cardiac index, VO2/CI during the 30 min study period. The O2 saturation was not altered. The present study indicates that ephedrine increases oxygen demand and supply in a similar magnitude.