Cerebral autoregulation in subjects adapted and not adapted to high altitude.

BACKGROUND AND PURPOSE: Impaired cerebral autoregulation (CA) from high-altitude hypoxia may cause high-altitude cerebral edema in newcomers to a higher altitude. Furthermore, it is assumed that high-altitude natives have preserved CA. However, cerebral autoregulation has not been studied at altitude. METHODS: We studied CA in 10 subjects at sea level and in 9 Sherpas and 10 newcomers at an altitude of 4243 m by evaluating the effect of an increase of mean arterial blood pressure (MABP) with phenylephrine infusion on the blood flow velocity in the middle cerebral artery (Vmca), using transcranial Doppler. Theoretically, no change of Vmca in response to an increase in MABP would imply perfect autoregulation. Complete loss of autoregulation is present if Vmca changes proportionally with changes of MABP. RESULTS: In the sea-level group, at a relative MABP increase of 23+/-4% during phenylephrine infusion, relative Vmca did not change essentially from baseline Vmca (2+/-7%, P=0.36), which indicated intact autoregulation. In the Sherpa group, at a relative MABP increase of 29+/-7%, there was a uniform and significant increase of Vmca of 24+/-9% (P<0.0001) from baseline Vmca, which indicated loss of autoregulation. The newcomers showed large variations of Vmca in response to a relative MABP increase of 21+/-6%. Five subjects showed increases of Vmca of 22% to 35%, and 2 subjects showed decreases of Vmca of 21% and 23%. CONCLUSIONS: All Sherpas and the majority of the newcomers showed impaired CA. It indicates that an intact autoregulatory response to changes in blood pressure is probably not a hallmark of the normal human cerebral vasculature at altitude and that impaired CA does not play a major role in the occurrence of cerebral edema in newcomers to the altitude.

Jugular bulb oxygen saturation during propofol and isoflurane/nitrous oxide anesthesia in patients undergoing brain tumor surgery.

UNLABELLED: We investigated, in brain tumor patients, the jugular bulb venous oxygen partial pressure (PjO2) and hemoglobin saturation (SjO2), the arterial to jugular bulb venous oxygen content difference (AJDO2), and middle cerebral artery blood flow velocity (Vmca) during anesthesia, and the effect of hyperventilation on these variables. Twenty patients were randomized to receive either isoflurane/ nitrous oxide/fentanyl (Group 1) or propofol/fentanyl (Group 2). At normoventilation (PacO2 35 +/- 2 mm Hg in Group 1 and 33 +/- 3 mm Hg in Group 2), SjO2 and PjO2 were significantly higher in Group 1 than in Group 2 (SjO2 60% +/- 6% and 49% +/- 13%, respectively; P = 0.019) (PjO2 32 +/- 3 and 27 +/- 5 mm Hg, respectively; P = 0.027). In Group 2, 5 of 10 patients had SjO2 < 50%, and 3 of these patients had SjO2 < 40% and AJDO2 > 9 mL/dL. All patients in Group 1 had SjO2 > 50%. During hyperventilation, there were no differences in SjO2, PjO2, or AJDO2 between the two groups. On hyperventilation, there was no correlation between the relative decreases of Vmca and 1/AJDO2 (r = 0.21, P = 0.41). The results indicate during propofol anesthesia, half of the brain tumor patients showed signs of cerebral hypoperfusion, but not during isoflurane/nitrous oxide anesthesia. Furthermore, during PacO2 manipulations, shifts in Vmca are inadequate to evaluate brian oxygen delivery in these patients. IMPLICATIONS: During propofol anesthesia at normoventilation, 50% of brain tumor patients showed signs suggesting cerebral hypoperfusion, but this could not be demonstrated during isoflurane/nitrous oxide anesthesia. During PacO2 manipulations, consecutive measurements of the cerebral blood flow velocity may be inadequate to assess cerebral oxygenation.

Laparoscopic fundoplication: a new technique with new complications?

We report pneumomediastinum, pneumopericardium, and subcutaneous emphysema occurring in patients who underwent laparoscopic fundoplication in our clinic. These complications might adversely affect hemodynamics during this procedure.

Haemodynamic effects of pneumoperitoneum for laparoscopic surgery: a comparison of CO2 with N2O insufflation.

We studied the haemodynamic effects of intra-abdominal insufflation with either CO2 (n = 15) or N2O (n = 15) in patients undergoing laparoscopic surgery. Haemodynamic variables were measured at increasing levels of intra-abdominal pressure up to 20 mmHg. In the CO2 group cardiac index decreased from 2.6 +/- 0.6 to 2.0 +/- 0.4 litre min-1 m-2 (mean +/- SD, P < 0.001) and in the N2O group from 2.6 +/- 0.5 to 1.8 +/- 0.4 litre min-1 m-2 (P < 0.001)). In the CO2 group, this was accompanied by increases in mean arterial pressure, systemic vascular resistance index and central venous pressure without change in heart rate. In contrast, during N2O insufflation mean arterial pressure decreased (from 77 +/- 8 to 63 +/- 15 mmHg (P < 0.001)) without change in vascular resistance. No further changes in haemodynamic variables were observed during head-up tilt in both groups. After desufflation mean arterial pressure increased in the N2O group to pre-insufflation levels and cardiac index increased in both groups (P < 0.001), but reached pre-insufflation levels only in the CO2 group. In both groups central venous O2 tension and saturation decreased at maximum intra-abdominal pressure and increased after release of the pneumoperitoneum. The results indicate that laparoscopic insufflation with either CO2 or N2O results in cardiovascular depression. Insufflation with N2O may decrease blood pressure, whereas mean arterial pressure is better preserved with CO2 insufflation.

Intraperitoneal local anaesthetics after laparoscopic cholecystectomy: effects on postoperative pain, metabolic responses and lung function.

We have compared the efficacy of 0.9% NaCl 20 ml (n = 15), 0.25% bupivacaine 20 ml (n = 15) and 0.5% lignocaine 20 ml (n = 15), administered i.p., in reducing postoperative pain and opioid requirements, and modifying the metabolic response to surgery and postoperative lung function after laparoscopic cholecystectomy. There were no differences in postoperative pain scores (visual analogue scale and verbal rating scale) between the three groups in the first 4 h after operation and in analgesic requirements during the first 24 h. In all groups, forced vital capacity, peak expiratory flow and forced expiratory volume in 1 s decreased 2 h after surgery (P < 0.001). Ventilatory values recovered only partially in the first 2 days after operation (P < 0.05), with no significant differences between groups. Plasma concentrations of glucose and cortisol increased after surgery (P < 0.05). Cortisol concentrations returned to baseline 48 h after operation. There were no significant differences between the groups in any measured variable. These data suggest that the administration of 20 ml of local anaesthetics i.p. is not effective in reducing postoperative pain, improving lung function, or attenuating the metabolic endocrine response after laparoscopic cholecystectomy.

A comparison of the effects of propofol and nitrous oxide on the electroencephalogram in epileptic patients during conscious sedation for dental procedures.

The influence of sedative doses of propofol or nitrous oxide on the electroencephalogram was studied in 11 mentally handicapped patients with treated epilepsy undergoing dental procedures. At one session, propofol was titrated to achieve conscious sedation. The mean (+/- SD) dose requirements were 5.5 +/- 1.1 mg.kg-1.h-1. In six patients, the electroencephalogram was unchanged during propofol administration. In three patients, there was a decrease in epileptic activity, and in two patients, paroxysmal discharges disappeared. At another session, nitrous oxide was administered by nasal mask. The mean (+/- SD) concentration of nitrous oxide needed was 43.6% +/- 4.8%. The electroencephalogram did not change in nine patients, whereas in two patients epileptic activity decreased. There were no clinical epileptoid or other adverse manifestations during any treatment or up to 48 h thereafter. The results of the present study suggest that propofol or nitrous oxide can be administered in subanesthetic doses for conscious sedation in mentally handicapped patients with treated epilepsy.

Pulmonary function and stress response after laparoscopic cholecystectomy: comparison with subcostal incision and influence of thoracic epidural analgesia.

Laparoscopic cholecystectomy (LPC) is increasingly used to treat symptomatic cholelithiasis. We compared the effects of cholecystectomy by subcostal incision to those of LPC on lung function and endocrine metabolic response. The effects of thoracic epidural analgesia for LPC were studied as well. Thirty patients undergoing elective cholecystectomy under general anesthesia were allocated to three study groups: group I, cholecystectomy by subcostal incision; group II, LPC; group III, LPC and epidural analgesia with 0.5% bupivacaine with epinephrine, followed by continuous epidural infusion of 6 mL of 0.5% bupivacaine. Forced vital capacity (FVC), peak expiratory flow, and forced expiratory volume in 1 s were measured with the patients in a half-sitting position. In all groups, sustained decreases in FVC, forced expiratory volume in 1 s, and peak expiratory flow were observed up to 24 h after surgery. Reduction of FVC was significantly more in group I compared with groups II and III (P less than 0.05). The FVC in group I decreased from 3.8 +/- 0.42 (SD) to 1.1 +/- 0.27 L (P less than 0.01), in group II from 3.6 +/- 1.46 to 2.1 +/- 0.94 L (P less than 0.05), and in group III from 3.8 +/- 0.92 to 2.8 +/- 0.90 L (P less than 0.05). In all groups, plasma glucose and cortisol increased after surgery compared with baseline levels (P less than 0.05). At 240 min after surgery, a small but significant decrease of cortisol was measured in group III (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of epidural and spinal anesthesia on blood rheology.

This study was designed to compare the influence of epidural and spinal anesthesia on blood viscosity. We studied 22 patients, ASA classification I, who underwent elective knee or ankle arthroscopy and received epidural (n = 11) or spinal (n = 11) anesthesia with plain bupivacaine, and 10 control volunteers, who did not undergo surgery or receive anesthesia. There were significant decreases in hematocrit, plasma viscosity, and whole-blood viscosity at high (70 s-1), medium (0.5 s-1), and low (0.05 s-1) shear rates. The magnitude of changes was similar in all groups but occurred earlier in the control group (between 10 and 30 min) and after spinal administration (between 10 and 30 min) rather than after epidural administration (between 30 and 60 min) of bupivacaine. Only spinal anesthesia was associated with a decrease in erythrocyte deformability. The observed rheologic changes are attributed to hemodilution from the intravenous administration of fluids and the redistribution of fluid in the intravascular and extravascular compartments after sympathetic blockade and to postural changes rather than the effect of bupivacaine on blood elements.

The effects of bupivacaine and pipecoloxylidide on platelet function in vitro.

The influence of bupivacaine and its major metabolite, pipecoloxylidide, on human platelet function was studied in vitro. Significant inhibition of ADP and collagen-induced platelet aggregation occurred only with concentrations of bupivacaine above 10 micrograms.ml-1. This concentration (10-25 micrograms.ml-1) is much higher than would be expected in routine clinical use of bupivacaine for epidural analgesia. The inhibition of platelet aggregation was associated with a significant decrease in beta-thromboglobulin secretion. In contrast, pipecoloxylidide had no effect on platelet aggregation or the beta-thromboglobulin release. We conclude that the previously reported 30-min time-lag between the maximal plasma concentration of bupivacaine and the inhibition of platelet aggregation is unlikely to be due to a metabolism of bupivacaine to pipecoloxylidide.

The influence of epidural analgesia on platelet function and correlation with plasma bupivacaine concentrations.

The effect of epidural anaesthesia with bupivacaine 0.5% on platelet aggregation was studied in seven patients undergoing transurethral resection of the prostate. Peak plasma concentrations of bupivacaine 470 +/- 270 ng ml-1 occurred at 30 min after administration. At that time there were no significant changes in platelet aggregation. However, the maximum rate of the primary- and secondary-aggregation velocities induced by 1.0 microM ADP were significantly decreased at 1 h and 3 h after bupivacaine administration. The maximum percentage ADP-induced platelet aggregation was also decreased significantly at 1 h and 3 h. The minimum concentration of ADP required to induce secondary-phase platelet aggregation was significantly increased at 1 h but not at 3 h. There was a significant correlation between bupivacaine concentrations and all platelet aggregation parameters except the maximum ADP-induced aggregation. Platelet inhibition occurred at plasma bupivacaine concentrations that were considerably lower than those needed to produce similar inhibition in vitro.

Influence of extradural blockade and ephedrine on transcutaneous oxygen tension.

The influence of lumbar extradural blockade with 0.5% pain bupivacaine on transcutaneous oxygen tension (PtcO2) and skin temperature was studied in 20 patients, 10 scheduled for vascular surgery and 10 for urological surgery. At the time of maximum extent of blockade, mean arterial pressure (MAP) had decreased significantly (P less than 0.001) from 96.6 +/- 18.8 mm Hg to 69.5 +/- 10.1 (mean +/- SD) in the vascular group and from 88.0 +/- 14.7 mm Hg to 71.1 +/- 12 mm Hg in the urological group. In the vascular group PtcO2 decreased significantly in the ischaemic (P less than 0.01) and non-ischaemic (P less than 0.001) limbs. In the urological group, there was a significant (P less than 0.001) decrease in PtcO2 in both limbs. There was no change in cutaneous temperature in the ischaemic limbs (vascular group), but the temperature in the non-ischaemic limbs increased significantly (P less than 0.01). In the urological group, the cutaneous temperature increased significantly (P less than 0.001) in both limbs. When ephedrine 10 mg was administered i.v., MAP increased significantly (P less than 0.001) in both groups to pre-blockade values. This was accompanied in both groups by significant increases in PtcO2' but not by a change in skin temperature. There was a significant correlation between change in MAP and change in PtcO2 in both groups after ephedrine.

Effects of extradural bupivacaine on the haemostatic system.

Twenty consecutive patients undergoing elective transurethral resection of the prostate were allocated randomly to one of two groups. Group I (n = 10) received lumbar extradural analgesia with 0.5% bupivacaine. Group II (n = 10) received general anaesthesia with spontaneous respiration, using 60% nitrous oxide and 1-2% halothane in oxygen. There was a significant inhibitory effect on platelet aggregation in the extradural group. No such effect was observed in the general anaesthesia group. Measured indices of coagulation and fibrinolysis showed no abnormalities compared with control in either group except for a significant decrease in alpha 2-antiplasmin during surgery in group II. These results suggest that the possible thromboprophylatic effect of extradural analgesia with bupivacaine may result from an inhibitory effect on platelet aggregation which is in addition to the increase in lower limb blood flow.

Plasma bupivacaine concentrations following psoas compartment block.

Fourteen patients undergoing hip replacement surgery under psoas compartment block combined with general anaesthesia were studied. Group 1 (n = 7) received plain and Group 2 (n = 7) received 0.25% bupivacaine with adrenaline. The mean maximum peak concentrations were 1.93 (SEM 0.46) micrograms/ml and 1.04 (SEM 0.19) micrograms/ml at 10 minutes in groups 1 and 2 respectively. Bupivacaine concentrations were higher at all times in the group which received plain than the group receiving solution containing adrenaline. These differences were statistically significant at 10, 15 (p less than 0.05) and 30 minutes (p less than 0.025). The highest recorded plasma bupivacaine concentration was 4.54 micrograms/ml in one patient receiving plain bupivacaine. No patient developed any signs of toxic symptoms. The duration of analgesia was longer (p less than 0.005) in the group receiving bupivacaine with adrenaline. Bupivacaine 0.25% with adrenaline 1:200 000 is safe for psoas compartment block, and is recommended for hip surgery.

Epidural analgesia and anticoagulant therapy. Experience with one thousand cases of continuous epidurals.

One thousand lumbar epidural blocks in 950 patients undergoing vascular surgery are reported. All patients were receiving oral anticoagulants pre-operatively. Mean thrombotest (TT) was 19.3% (normal range 70-130%). During surgery intravascular heparin was administered. At the end of surgery, the kaolin cephalin clotting time (KCCT) was 68 (+/- 0.8) seconds (normal range 35-60 seconds), and partial thromboplastin time (PTT) was 536 (77.9%, normal control of 100%). Despite the anticoagulant therapy, no side effects were observed in any patient which could be related to haemorrhage or haematoma formation in the epidural space. It is concluded that, provided adequate precautions are taken, epidural analgesia can be safely used in patients receiving anticoagulant therapy.