The influence of nitroglycerin and prostaglandin E1 on dynamic cerebral autoregulation in adult patients during propofol and fentanyl anaesthesia.

We investigated dynamic cerebral autoregulation in 24 normocapnic adult patients during propofol and fentanyl anaesthesia. Hypotension was induced, to a mean arterial pressure (MAP) of 60-65 mmHg, using nitroglycerin or prostaglandin E1. Time-averaged mean cerebral blood flow velocity in the right middle cerebral artery was measured continuously using transcranial Doppler sonography. Dynamic autoregulatory response was activated by a sudden decrease in MAP following release of bilateral thigh cuffs (thigh cuff test) and evaluated as a dynamic rate of autoregulation (dRoR in % x s(-1)). The cuff test was repeated to obtain two values of dRoR during baseline and during induced hypotension; the data were then averaged. The mean value of dRoR during baseline and during induced hypotension was 14.2 (2.9) and 14.2 (1.6) % x s(-1), respectively, in the nitroglycerin group, and 14.6 (2.6) and 14.4 (2.4) % x s(-1), in the prostaglandin E1 group. We were unable to demonstrate significant between- or within-group differences in dRoR. Thus, we conclude that nitroglycerin and prostaglandin E1 do not attenuate dynamic cerebral autoregulation.

Continuous intra-jugular venous blood-gas monitoring with the Paratrend 7 during hypothermic cardiopulmonary bypass.

We measured the accuracy of the continuous intra-vascular blood-gas monitoring system (Paratrend 7, PT7) placed in the jugular venous bulb in 18 adult patients having cardiac or aortic surgery with hypothermic cardiopulmonary bypass (CPB). After induction of anaesthesia, a PT7 sensor was inserted through a 20-gauge venous catheter into the right jugular venous bulb. Blood samples were drawn from the venous catheter and measured with a blood gas analyser (BGA). Five to eight paired measurements using the PT7 and blood samples were made per patient, and bias and precision were calculated for each patient using the Bland-Altman method. The ranges for the blood sample measurements were: pH 7.12 to 7.59, PCO(2) 3.7 to 9.6 kPa, PO(2) 3.5 to 16.0 kPa, oxygen saturation 40 to 99%, bicarbonate 18.6 to 34.4 mmol l(-1), and base excess -7.8 to 12.5 mmol l(-1). Bias and precision values were 0.014/0.071 for pH, 0/0.90 kPa for PCO(2), and -0.16/1.18 kPa for PO(2). These values were comparable with those previously made on arterial blood. However, precision for oxygen saturation in each patient varied 2.3 to 23.6% (95% CI: 6.3 to 12.9%), which was unsatisfactory for clinical measurements. Deep hypothermia ( approximately 19.6 degrees C) and marked haemodilution ( approximately 13.5%) during CPB did not influence the reliability of the PT7 sensor. Thus, we concluded that continuous intra-jugular venous blood-gas monitoring is clinically feasible using the PT7 and may provide valuable information during CPB.

The effects of nicardipine on dynamic cerebral autoregulation in patients anesthetized with propofol and fentanyl.

UNLABELLED: We investigated the effects of nicardipine on dynamic cerebral pressure autoregulation in 13 normal adult patients undergoing gynecologic or orthopedic surgery. Anesthesia was induced and maintained with propofol and fentanyl. Hypotension to a mean arterial pressure of 60-65 mm Hg was induced and maintained with a continuous infusion of nicardipine. Time-averaged mean blood flow velocity in the right middle cerebral artery was measured continuously by using transcranial Doppler ultrasonography. The cerebral autoregulatory responses were activated by releasing thigh cuffs. The actual blood flow velocity in the right middle cerebral artery response to acute change in mean arterial pressure was fitted to 1 of 10 computer-generated curves to determine the dynamic rate of cerebral autoregulation (dRoR), and the best fitting curve was used. The autoregulation test was repeated until two values of dRoR were obtained at baseline and during induced hypotension. Nicardipine significantly reduced dRoR values of 13.1% +/- 3.6%/s at baseline to 8.3% +/- 2.6%/s during hypotension (P: < 0.01). During deliberate hypotension induced by nicardipine, the cerebral dynamic autoregulatory response is impaired in normal adult patients. IMPLICATIONS: During deliberate hypotension induced by nicardipine, the cerebral dynamic autoregulatory response is impaired in normal adult patients.

Effects of nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension on human cerebrovascular carbon dioxide reactivity during propofol-fentanyl anesthesia.

STUDY OBJECTIVE: To investigate the effects of nicardipine-, nitroglycerin-, and prostaglandine E1-induced hypotension on cerebrovascular carbon dioxide (CO2) reactivity over a wide range of arterial CO2 tension (PaCO2) (PaCO2; range 25 to 50 mmHg). DESIGN: Prospective, randomized study. SETTING: Operating room of a university-affiliated hospital. PATIENTS: 36 ASA physical status I and II patients without cerebrovascular disease, hypertension, or diabetes mellitus, undergoing an elective abdominal surgery. INTERVENTIONS: Patients were randomly allocated to one of three groups (nicardipine-, nitroglycerin-, or prostaglandin E1-induced hypotension group; 12 in each group). Anesthesia was induced and maintained with a bolus dose, followed by a continuous infusion of propofol (6.7 +/- 1.5 mg/kg/hr) and fentanyl (1.68 +/- 0.4 micrograms/kg/hr). Deliberate hypotension of mean arterial pressure 55 to 60 mmHg was induced and maintained with a bolus dose, followed by a continuous infusion of nicardipine (6.80 +/- 0.75 micrograms/kg/min), nitroglycerin (3.20 +/- 1.10 micrograms/kg/min), or prostaglandin E1 (0.103 +/- 0.052 microgram/kg/min). MEASUREMENTS AND MAIN RESULTS: Time-averaged mean red blood cell velocity in the right middle cerebral artery (Vmca) at PaCO2 ranging from 25 to 50 mmHg was measured with transcranial Doppler ultrasonography. A minimum of six simultaneous measurements of Vmca and PaCO2 were obtained during baseline and deliberate hypotension in each patient. Absolute slope between Vmca and PaCO2 during baseline and deliberate hypotension was determined individually by linear regression analysis. Absolute slope was treated as the variable, because it yielded a significant close correlation coefficient (r > 0.95; p < 0.05). Comparisons between baseline and deliberate hypotension were made by analysis of variance for repeated measures. Mean absolute slope was significantly reduced from 1.88 +/- 0.57 cm/sec/mmHg (mean +/- SD) to 1.21 +/- 0.46 in the nicardipine group (p < 0.05), from 1.75 +/- 0.69 to 1.35 +/- 0.47 in the nitroglycerin group (p < 0.05), and from 1.95 +/- 0.89 to 1.33 +/- 0.70 (p < 0.05) in the prostaglandin E1 group, respectively. CONCLUSION: Nicardipine-, nitroglycerin-, and prostaglandin E1-induced hypotension attenuate the human cerebrovascular CO2 reactivity during propofol-fentanyl anesthesia.

[A comparative study of transcranial Doppler sonography and near-infrared spectroscopy for the assessment of cerebrovascular CO2 reactivity].

Simultaneous measurements of time averaged mean blood flow velocity in the right middle cerebral artery (Vmca) by transcranial Doppler sonography (TCD) and regional cerebral oxygen saturation (rSo2) by near-infrared spectroscopy (NIRS) were performed in 30 subjects under propofol /fentanyl/ oxygen anesthesia. End-tidal CO2 pressure (PetCO2) was controlled by adjusting minute ventilation. A paired measurements of Vmca and rSo2 was repeated at PetCO2 of 50, 45, 40, 35, 30, and 25 mmHg in each subject. Relative Vmca (rVmca) was also calculated as a relative expression of Vmca at PetCO2 of 40 mmHg. Linear regression analysis was applied to determine the individual best fit relationship of these, parameters. There were significant linear correlations between PetCO2 and Vmca (R > 0.94, P < 0.01), between PetCO2 and rVmca (R > 0.94, P < 0.01), between PetCO2 and rSo2 (R > 0.92, P < 0.01), and between rSo2 and Vmca (R > 0.88, P < 0.05) in each subject. Furthermore, there was a significant linear correlation between rVmca based CO2 reactivity and rSo2 based CO2 reactivity (R = 0.60, P < 0.001). These results indicate that measurements of rSo2 may be an alternative method for evaluating cerebrovascular CO2 reactivity when poor ultrasound window.