Changes in cerebrospinal fluid pressure and spinal cord perfusion pressure prior to cross-clamping of the thoracic aorta in humans

Little is known about what influences cerebrospinal fluid pressure (CSFP) during anesthesia prior to aortic cross-clamping (AXC). Therefore, this study measured the effect of anesthetic induction, of various drugs administered during the course of surgery prior to AXC, and of hemodynamic changes on CSFP, and calculated spinal cord perfusion pressure (SCPP = mean arterial pressure [MAP] - CSFP) in 11 patients undergoing surgery on the descending thoracic aorta. A lumbar drainage catheter was placed to facilitate drainage of CSF and to measure CSFP. Anesthesia was induced with fentanyl, 50 micrograms/kg, and midazolam, 1 mg, using a pancuronium-metocurine mixture for neuromuscular blockade. Data were collected prior to and after (1) anesthetic induction, (2) mannitol to augment diuresis, (3) sequential use of sodium nitroprusside (SNP) and isoflurane (ISO) to lower MAP by 20%, (4) drainage of spinal fluid, (5) intrathecal injection of papaverine (IP), and (6) AXC. Statistical comparisons of recorded data were made using the least squares mean method and Friedman test. Linear regression was used to test for correlation between CSFP and hemodynamics. Anesthetic induction affected neither hemodynamics nor CSFP. Mannitol significantly increased heart rate, central venous pressure (CVP), pulmonary capillary wedge pressure (PCWP), cardiac output (CO), and CSFP (P less than 0.05). SNP or ISO altered neither CVP, PCWP, CO, nor CSFP, which remained elevated at the postmannitol infusion level. ISO, unlike SNP, caused a significant decrease in SCPP (P less than 0.005). Subsequent drainage of 20 mL of CSF improved SCPP (P less than 0.05). IP did not have any effect on hemodynamics or CSFP. CSFP showed a strong correlation with CVP (r = 0.86).(ABSTRACT TRUNCATED AT 250 WORDS)     

Treatment of proximal aortic hypertension after thoracic aortic cross-clamping in dogs. Phlebotomy versus sodium nitroprusside/isoflurane.

Thoracic aortic cross-clamping causes proximal aortic hypertension. Theoretically, the method used to treat hypertension can influence spinal cord perfusion pressure and neurologic outcome. Phlebotomy was compared to sodium nitroprusside/isoflurane in terms of ability to treat increased proximal mean aortic pressure (MAPp) after thoracic aortic cross-clamping in dogs. Dogs were assigned randomly to one of three groups depending on the method used to treat hypertension after cross clamping: 1) phlebotomy (n = 10); 2) sodium nitroprusside/isoflurane (n = 11); and 3) control (no treatment) (n = 8). In each dog, anesthesia was maintained with isoflurane in oxygen, 1.4% end-tidal. The thoracic aorta was occluded 2.5 cm distal to the left subclavian artery for 50 min and then was released. Hemodynamics, cerebrospinal fluid pressure (CSFP), and regional blood flows by the radioactive microsphere technique, were measured at 1) baseline; 2) 2 min after aortic cross-clamping; 3) after treatment of proximal aortic hypertension; 4) 5 min after aortic unclamping; and 5) 30 min after resuscitation. At 24 h, a neurologic assessment was performed. Thoracic aortic cross-clamping increased MAPp, decreased distal MAP (MAPd), and reduced lumbar spinal cord perfusion pressure (SCPPl), [SCPPl = MAPd - CSFP], in all three groups. Control of increased MAPp necessitated removal of 36 +/- 9 ml/kg of blood in the phlebotomy group. In the sodium nitroprusside/isoflurane group, sodium nitroprusside (16 micrograms.kg-1.min-1) was infused and end-tidal isoflurane concentration increased to 2.5 +/- 0.7%, restoring MAPp to baseline level.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of Cerebrospinal Fluid Drainage and/or PartiaI Exsanguination on Tolerance to Prolonged Aortic Cross-Clamping

Paraplegia as a consequence of spinal cord ischemia associated with procedures on the thoracic and thoracoabdominai aorta has been linked to the interaction of proximal hypertension with elevated cerebrospinal fluid pressure (CSFP) during aortic cross-clamping (AXC). CSFP reduction via cerebrospinal fluid (CSF) drainage is thought to significantly prolong the cord's tolerance to AXC. Likewise, partial exsanguination is reported to effectively reduce ischemic injury by controlling proximal hypertension. To evaluate the individual and collective efficacy of both techniques, 18 mongrel dogs (25 to 35 kg), divided into three equal groups, underwent a fourth interspace left thoracotomy AXC. Baseline proximal arterial blood pressure (PABP), distal arterial blood pressure (DABP), and CSFP were established and monitored at 5-minute intervals during 120 minutes of AXC, and for 30 minutes thereafter. Group I animals were partially exsanguinated prior to AXC to maintain PABP at a mean of 115 to 120 mmHg. Group II animals had sufficient (16 ± 5 cc) CSF withdrawn to maintain a DABP-CSFP gradient, i.e., spinal cord perfusion pressure (SCPP) of 20 mmHg. Group III animals were treated with both CSF drainage and partial exsanguination in the same manner as groups I and II, respectively. Periop-erative somatosensory evoked potential (SEP) monitoring evaluated cord function. Postoperative neurological outcome was assessed with Tariov's criteria. SEPs degenerated approximately 22 minutes following AXC for groups II and III. In contrast, group I exhibited rapid (10 ± 7 min) SEP loss. All five surviving group I animals displayed paralysis 48 hours postopera-tively. Mean PABP was significantly higher in group II (155 ±18 mmHg) than in either group 1 (117 ± 9 mmHg) or Ill (120 ± 14 mmHg) (p < 0.001). CSFP was significantly higher in group I (14 ± 4 mmHg) than in either group II or III (5 ± 2 mmHg) (p < 0.0001). The only parameter associated with neurological injury was low SCPP, which inversely correlated with CSF dynamics. Group I animals, with a mean SCPP of 4.6 mmHg, exhibited paraplegia, while groups II and Ill, with SCPP values above 20 mmHg, were free of neurological injury. Proximal hypertension did not play a role in cord injury. This study underscores the potential of CSF drainage to protect the ischemic spinal cord. (J Card Surg 7994;9:637–637)     

Effects of exsanguination and sodium nitroprusside on compliance of the spinal canal during aortic occlusion.

To evaluate the effects of sodium nitroprusside (SNP) and partial exsanguination (EXS) on systemic hemodynamics and cerebrospinal fluid dynamics, we monitored proximal and distal blood pressure (BP), cerebrospinal fluid pressure (CSFP), spinal cord perfusion pressure (SCPP), and compliance of the spinal canal (CSC) in 10 mongrel dogs during aortic cross-clamping of the descending thoracic aorta. CSC was measured by serial injections of 2 ml of saline solution into the cisterna cerebellomedullaris via a percutaneously placed catheter with simultaneous measurements of CSFP. Data were acquired at baseline (BL), during aortic cross-clamping with proximal hypertension (AXC), and after control of proximal hypertension with EXS and SNP. During the cross-clamp interval, mean proximal aortic pressure (PxBP) rose from 114 +/- 6 to 150 +/- 3 mm Hg (P less than 0.001), whereas mean blood pressure decreased to 88 +/- 5 and 82 +/- 4 mm Hg during the SNP and EXS intervals, respectively (P less than 0.05 vs BL). EXS and SNP were equally effective in controlling PxBP (82 +/- 4 vs 88 +/- 5 mm Hg, P greater than 0.05). Mean distal aortic pressure (DsBP) decreased from systemic values to 21.5 +/- 1.9 mm Hg during AXC, and to 12.4 +/- 1.0 and to 8 +/- 0.8 mm Hg during EXS and SNP, respectively (P less than 0.05 AXC vs EXS and SNP). SNP lowered DsBP significantly more than EXS, 8 +/- 0.8 vs 12.4 +/- 1.0 mm Hg (P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)     

Reconstructive surgery in 59-year-old patient with coarctation of aorta under the monitoring of somatosensory evoked potential and spinal cord perfusion pressure]

Postoperative paraplegia is a relatively rare complication in reconstructive surgery for coarctation of the aorta and the operative treatment is usually performed without any adjuncts. A 59-year-old male patient underwent replacement of descending thoracic aorta with vascular prosthesis under the monitoring of SEP and spinal cord perfusion pressure (SCPP) [pressure difference between mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP)]. During cross-clamping of the aorta, MDAP decreased from 61 to 40 mmHg and CSFP increased from 6 to 15 mmHg, SCPP was 25 mmHg, and the amplitude of the SEP waves rapidly decreased. As the ischemic changes of spinal cord were suspected, the aortic cross-clamping was released. The amplitude of SEP recovered to the preoperative level immediately after de-clamping. In order to prevent spinal cord ischemia, the partial cardio-pulmonary bypass was employed, and SCPP was maintained above 60 mmHg, so that SEP did not show any ischemic changes during cross-clamping of the aorta. The patient did not develop any neurological deficit postoperatively. The monitoring of SEP and SCPP appears to be useful for prevention of postoperative paraplegia in the surgical treatment for coarctation of the aorta.     

Prevention of spinal cord ischemia after cross-clamping of the thoracic aorta--monitoring of spinal cord perfusion pressure and somatosensory evoked potentials

The pressure difference between the mean distal aortic pressure (MDAP) and the cerebrospinal fluid pressure (CSFP), defined as the spinal cord perfusion pressure (SCPP), as well as somatosensory evoked potentials (SEP) were monitored intraoperatively to detect and prevent intraoperative spinal cord ischemia in 24 patients who required cross-clamping of the descending thoracic aorta. A temporary axillo-femoral shunt, utilizing a 10 mm woven Dacron tube graft, was employed in 10 patients and partial cardiopulmonary bypass was employed in fourteen. Ischemic SEP changes were seen in six patients. Two patients, whose SCPPs were 32 and 35 mmHg, showed a complete loss of SEP and subsequently developed paraplegia. In the other four cases, increase of the MDAP and/or withdrawal of cerebrospinal fluid were performed to increase the SCPP to more than 60 mmHg when ischemic SEP changes occurred. The SEP gradually recovered in two of these cases. The ischemic SEP changes seen in one patient, who had the longest aortic cross-clamping time, (175 minutes) returned to normal immediately after unclamping. In another case, who had a thoracoabdominal aortic aneurysm, the intercostal arteries were reimplanted since the ischemic SEP changes did not revert. These four patients recovered without any neurological deficit. In the other 18 cases without ischemic SEP change, SCPP was kept at more than 40 mmHg during aortic cross-clamping. We conclude that the SCPP should be maintained at more than 40 mmHg during aortic occlusion, and increased to more than 60 mmHg when ischemic SEP changes occur, by increasing MDAP and/or withdrawing cerebrospinal fluid in order to prevent postoperative paraplegia.     

Correlation of peripheral venous pressure and central venous pressure in surgical patients

OBJECTIVE: To determine the degree of agreement between central venous pressure (CVP) and peripheral venous pressure (PVP) in surgical patients. DESIGN: Prospective study. SETTING: University hospital. PARTICIPANTS: Patients without cardiac dysfunction undergoing major elective noncardiac surgery (n = 150). MEASUREMENTS AND MAIN RESULTS: Simultaneous CVP and PVP measurements were obtained at random points in mechanically ventilated patients during surgery (n = 100) and in spontaneously ventilating patients in the postanesthesia care unit (n = 50). In a subset of 10 intraoperative patients, measurements were made before and after a 2-L fluid challenge. During surgery, PVP correlated highly to CVP (r = 0.86), and the bias (mean difference between CVP and PVP) was -1.6 +/- 1.7 mmHg (mean +/- SD). In the postanesthesia care unit, PVP also correlated highly to CVP (r = 0.88), and the bias was -2.2 +/- 1.9 (mean +/- SD). When adjusted by the average bias of -2, PVP predicted the observed CVP to within +/-3 mmHg in both populations of patients with 95% probability. In patients receiving a fluid challenge, PVP and CVP increased similarly from 6 +/- 2 to 11 +/- 2 mmHg and 4 +/- 2 to 9 +/- 2 mmHg. CONCLUSION: Under the conditions of this study, PVP showed a consistent and high degree of agreement with CVP in the perioperative period in patients without significant cardiac dysfunction. PVP -2 was useful in predicting CVP over common clinical ranges of CVP. PVP is a rapid noninvasive tool to estimate volume status in surgical patients.     

Somatosensory evoked potentials and spinal cord perfusion pressure are significant predictors of postoperative neurologic dysfunction

Paraplegia after thoracoabdominal aneurysm repair can occur in 3% to 40% of patients. This study investigated the efficacy of cerebrospinal fluid (CSF) drainage to protect the spinal cord during aortic cross-clamping (AXC) and the interrelationship between drainage, spinal cord perfusion pressure (SCPP), and changes in somatosensory evoked potentials (SEP) in a canine model of spinal cord ischemia. SCPP was defined as the mean distal aortic pressure minus the CSF pressure. In the experimental group, CSF was drained before AXC. SEP changes were quantitated as time to latency increase of 10% (L-10) and time to complete SEP loss. Drainage of CSF had no significant effect on the distal aortic pressure but significantly increased SCPP from 9.4 to 21.8 mm Hg and decreased the incidence of postoperative neurologic injury. Ischemic SEP changes were highly significant predictors of postoperative neurologic injury, occurring more than two times earlier in the paralyzed and paraparetic animals. Dogs without neurologic injury had significantly higher SCPP, delayed L-10 time, and delayed SEP loss.     

Influence of low proximal aortic pressure on spinal cord oxygenation in experimental thoracic aortic occlusion

BACKGROUND: To evaluate the effect of low proximal aortic pressure on cerebrospinal fluid (CSF) oxygenation in an experimental thoracic occlusion model. METHODS: In nine pigs, continuous intrathecal pO(2), pCO(2) and pH monitoring was used during double descending thoracic aortic clamping following insertion of an aorto-aortic shunt. In five pigs, the shunt was connected to a citrated bag adjusted at approximately 40-45 cm above the heart for partial exsanguination in order to decrease mean proximal aortic pressure (MPAP) to below 50 mmHg. In four animals, sodium nitroprusside infusion was used for this purpose. RESULTS: Intrathecal pO(2) demonstrated a significant decrease from 4.9+/-2.1 to 2.9+/-2.4 kPa after 10 minutes of aortic cross-clamping. Lowering proximal aortic pressure caused a further significant decrease to 1.2+/-1.7 kPa (p<0.05). In seven pigs (5 in the exsanguination and 2 in the vasodilator group), restoration of mean proximal aortic pressure to 94.0+/-27.7 caused a recovery of CSF pO(2) from 1.2+/-1.9 to 2.8+/-3.0 (p<0.05). CONCLUSIONS: The results of this study demonstrate that MPAP which provides spinal cord perfusion through subclavian-vertebral arteries are crucial for maintenance of spinal cord oxygenation during thoracic aortic occlusion in this pig model.     

Fentanyl increases cerebrospinal fluid pressure in normocapnic volunteers.

In a double blind randomized study, the effect of fentanyl 1 microgram kg-1 i.v. or placebo on mean lumbar cerebrospinal fluid pressure (CSFP), mean arterial pressure, cerebral perfusion pressure, transcutaneous PCO2 and heart rate was studied in 10 spontaneously breathing volunteers in the lateral decubitus position via a 22-gauge spinal needle inserted into the subarachnoidal space at level L3/L4. Fentanyl increased mean CSFP (+/- SD) from 12.4 +/- 2.7 mmHg to 16.0 +/- 2.3 mmHg (P < 0.05) without significant changes in the other variables. No significant changes in any of the measured variables were seen after administration of placebo. Cerebral perfusion pressure decreased significantly after fentanyl (P < 0.05).     

Effects of ethanol on spinal cord blood flow in the rat

This study examines the effects of low and high concentrations of ethanol on spinal cord blood flow (SCBF) in the rat. SCBF was measured in the following blood pressure ranges: (a) <60 mm Hg, (b) 60-90 mm Hg, (c) 90-120 mm Hg, (d) 120-150 mm Hg, and (e) >150 mm Hg. Rats were anesthetized with 1.4% isoflurane in air and randomly assigned to the following treatment groups: group 1 (n = 12), intraperitoneal (i.p.) saline injection; group 2 (n = 10), 1 g/kg of ethanol i.p.; and group 3 (n = 14), 4 g/kg of ethanol i.p. Blood pressure was increased by intravenous phenylephrine infusion or lowered by a combination of intravenous trimethaphan and blood withdrawal. The SCBF was measured in cervical, thoracic, and lumbar segments using radioactive microspheres. The plasma ethanol concentration was 0 mg/ml for group 1, 0.64 +/- 0.06 mg/ml (mean +/- SEM) in group 2, and 4.18 +/- 0.11 mg/ml in group 3. In control rats, the cervical SCBF was higher than the thoracic or lumbar SCBF, evaluated over the entire blood pressure range (analysis of variance, p <0.05). This difference in regional SCBF was abolished by ethanol. Ethanol produced a significant decrease in cervical and lumbar SCBF (p <0.05) but not thoracic SCBF (p = 0.07). This decrease in SCBF was most pronounced at high blood pressures. These results suggest that ethanol produces vasoconstriction in the spinal cord that is countered by autoregulatory vasodilation at low blood pressures.     

The effect of desflurane and isoflurane on cerebrospinal fluid pressure in humans with supratentorial mass lesions.

Desflurane, a new volatile anesthetic, produces cerebral vasodilation. The purpose of this study was to compare the effects of 1 MAC desflurane with those of isoflurane on cerebrospinal fluid pressure (CSFP) in patients with supratentorial mass lesions and a mass effect on computerized tomography (CT scan). Twenty adult patients undergoing craniotomy for removal of supratentorial mass lesions were studied. Ten patients received desflurane and 10 patients received isoflurane. Prior to induction of anesthesia, a radial artery catheter was inserted and a 19-G needle was inserted into the lumbar subarachnoid space to measure CSFP. Baseline arterial blood gases and CSFP were measured with the patient awake and unmedicated. Anesthesia was induced with thiopental (6-9 mg/kg) and muscle relaxation achieved with vecuronium (0.2 mg/kg). The lungs of all patients were hyperventilated to achieve an arterial CO2 tension of 24-28 mmHg. Anesthesia was maintained with 1 MAC volatile anesthetic, either 7.0% desflurane or 1.2% isoflurane in an air:O2 mixture to maintain an inspired O2 fraction (FIO2) of 0.50. Patients were not administered any other anesthetic until the dura was incised. Mean arterial pressure was kept within 20% of the patient's mean ward values with the use of esmolol or phenylephrine. CSFP, mean arterial pressure, end-tidal CO2 concentration (PETCO2), hemoglobin O2 saturation, and cerebral perfusion pressure were recorded with the patient awake, immediately postinduction with thiopental, postintubation, after institution of the volatile anesthetic, and every 5 min until the dura was incised. There was no difference in the mean (+/- SD) awake CSFP between the desflurane (11 +/- 4 mmHg) and the isoflurane (10 +/- 2 mmHg) groups.(ABSTRACT TRUNCATED AT 250 WORDS)     

Peripheral venous pressure as a predictor of central venous pressure during orthotopic liver transplantation

STUDY OBJECTIVE: To assess the reliability of peripheral venous pressure (PVP) as a predictor of central venous pressure (CVP) in the setting of rapidly fluctuating hemodynamics during orthotopic liver transplant surgery. DESIGN: Prospective clinical trial. SETTING: UCLA Medical Center, main operating room-liver transplant surgery. PATIENTS: Nine adult patients with liver failure undergoing orthotopic liver transplant surgery. INTERVENTIONS: A pulmonary artery catheter and a 20-g antecubital peripheral intravenous catheter dedicated to measuring PVP were placed in all patients after standard general endotracheal anesthesia induction and institution of mechanical ventilation. MEASUREMENTS: Peripheral venous pressure and CVP were recorded every 5 minutes and/or during predetermined, well-defined surgical events (skin incision, venovenous bypass initiation, portal vein anastamosis, 5 minute post graft reperfusion, abdominal closure). Pulmonary artery pressure and cardiac output (via thermodilution) were recorded every 15 and 30 minutes, respectively. MAIN RESULTS: Peripheral venous pressure (mean +/- SD) was 11.0 +/- 4.5 mmHg vs a CVP of 9.5 +/- 5.0; the two measurements differed by an average of 1.5 +/- 1.6 mmHg. Peripheral venous pressure correlated highly with CVP in every patient, and the overall correlation among all nine patients calculated using a random-effects regression model was r = 0.95 (P < 0.0001). A Bland-Altman analysis used to determine the accuracy of PVP in comparison to CVP yielded a bias of -1.5 mmHg and a precision of +/-3.1 mm Hg. CONCLUSION: Our study confirms that PVP correlates with CVP even under adverse hemodynamic conditions in patients undergoing liver transplantation.     

Phenylephrine increases regional cerebral blood flow following hemorrhage during isoflurane-oxygen anesthesia

Using the radioactive microsphere technique regional cerebral blood flow (rCBF) and total CBF (tCBF) were examined in rats at three time periods: baseline (CBF1) during 1.5 MAC inspired isoflurane-oxygen anesthesia, CBF2; during 1.5 MAC inspired isoflurane anesthesia combined with hypotension induced by hemorrhage and CBF3; during isoflurane and hemorrhage plus phenylephrine infused to restore mean arterial pressure (MAP) to baseline. For CBF1 MAP was 89 +/- 3 mmHg (mean +/- SEM, n = 9) with PaCO2 44 +/- 1 mmHg. For CBF2 following graded hemorrhage MAP was 48 +/- 2 mmHg and PaCO2 43 +/- 1 mmHg. For CBF3 MAP was 93 +/- 2 and PaCO2 45 +/- 1 mmHg, following infusion of phenylephrine (PE) at 13.9 +/- 4.0 micrograms.kg-1.min-1. Total CBF1 was 1.84 +/- 0.18 ml.g-1.min-1, tCBF2 1.32 +/- 0.09 ml.g-1.min-1 (P less than 0.05 vs. tCBF1) and tCBF3 2.60 +/- 0.18 (P less than 0.05 vs. tCBF1 and 2). For tCBF3 hemoglobin concentration had decreased 23% from 14.2 +/- 0.2 g.100 ml-1 to 11.0 +/- 0.5 g.100 ml-1 (P less than 0.05). Regional CBF decreased significantly in seven of 12 regions examined from CBF1 to CBF2 and was significantly higher in all regions for CBF3. For CBF1-3 infratentorial blood flows (cerebellar and brain stem) were significantly higher than flows to the supratentorial structures (cerebral cortical and basal ganglia). During isoflurane anesthesia, phenylephrine infused to support MAP following hemorrhagic hypotension effectively maintains rCBF and tCBF. There is no indication that phenylephrine infused to increase MAP following hemorrhage results in cerebral vasoconstriction in rats anesthetized with isoflurane.     

Epidural Anesthesia and Acutely Increased Intracranial Pressure: Lumbar Epidural Space Hydrodynamics in a Porcine Model

Background: The effects of epidural injection on intracranial pressure (ICP), lumbar epidural pressure, cerebral blood flow (CBF), and spinal cord blood flow (SCBF) were studied after acutely increased ICP in swine.

Methods: Twenty pigs, anesthetized with isoflurane and mechanically ventilated to maintain normocarbia, had two Tuohy needles placed in the lumbar epidural space. The ICP, lumbar epidural pressure, heart rate, mean arterial pressure, and central venous pressure were monitored. All animals had a Fogarty catheter placed in the parietal epidural space. Six pigs were randomized to a normal ICP group (group N) and eight pigs to an increased ICP group by inflation of the Fogarty catheter balloon (group R). Each pig had 0.33 ml [centered dot] kg sup -1 of 2.0% carbonated lidocaine injected over 20 s via an epidural needle placed at L3. The ICP and lumbar epidural pressure were then monitored continuously for 30 min. Pressure-time data were fit to traditional compartmental models. Epidural elastance and resistance were calculated using a derivation of the Windkessel theory. An additional six pigs had ICP elevated as in group R and CBF and SCBF measured using radioactive microspheres at five time periods: baseline, 0-60 s, 100-160 s, 200-260 s, and at 30 min after epidural injection.

Results: The animals did not differ with respect to heart rate, central venous pressure, or mean arterial pressure at baseline. The ICP was 10 +/- 2 mmHg in group N, and 24 +/- 2 mmHg after balloon inflation in group R. After epidural injection, peak ICP was significantly greater in group R (76 +/- 22 vs. 54 +/- 17 mmHg) but not different by 30 min (17 +/- 5 vs. 11 +/- 1 mmHg). Epidural elastance in group N was 8.3 +/- 3.1 mmHg [centered dot] ml sup -1 and 12.8 +/- 3.0 mmHg [centered dot] ml sup -1 in group R (P = 0.045). Epidural resistance was 1,330 +/- 590 mmHg [centered dot] s [centered dot] ml sup -1 in group N and 2,220 +/- 600 mmHg [centered dot] s [centered dot] ml sup -1 in group R (P = 0.038). The CBF and SCBF were less than 10% of baseline during the 0- to 60-s time period after epidural injection. Thereafter, CBF and SCBF did not differ from baseline values.     

Sufentanil, alfentanil, and fentanyl: impact on cerebrospinal fluid pressure in patients with brain tumors

In order to evaluate the safety of the new synthetic opioids, alfentanil and sufentanil, in neurosurgical patients, we administered sufentanil 1 microg/kg i.v., alfentanil 50 microg/kg i.v. followed by an infusion of 1 microg/kg/min, or fentanyl 5 microg/kg i.v. to 30 patients with supratentorial tumors anesthetized with nitrous oxide (N2O), 60% in O2. Lumbar cerebrospinal fluid pressure (CSFP) and mean arterial pressure (MAP) responses were recorded for 10 min thereafter, while ventilation was held constant [mean PaCO2 = 36.1 +/- 1.0 mm Hg (SEM)]. There was no change in CSFP after fentanyl. In contrast, both sufentanil and alfentanil caused increases in CSFP, equal to 89 +/- 31 % SE (p < 0.05) and 22 +/- 5% (p < 0.05), respectively. MAP decreased after administration of each opioid. Peak decreases in cerebral perfusion pressure (MAP - CSFP) were 14 +/- 3% after fentanyl, 25 +/- 5% after sufentanil, and 37 +/- 3% after alfentanil. It is concluded that because sufentanil increased CSFP in patients who have brain tumors, it also may be contraindicated in other neurosurgical patients at risk for intracranial hypertension. Alfentanil may share this propensity, since CSFP increased despite a profound reduction in MAP. Among the three opioids evaluated, only fentanyl appears to be appropriate for supplementing N2O-2 anesthesia in patients who have compromised intracranial compliance.     

Spinal cord blood flow in the rat under normal physiological conditions

Regional spinal cord blood flow (SCBF) was measured in a group of rats under conditions of normothermia, normocarbia, normoxia, and normal blood pressure, using the hydrogen clearance technique. Regional SCBF in the cervical white matter was 26.8 +/- 1 (SE) ml/100 g/min and in the cervical gray matter 53.6 +/- 2.5; in the thoracic white matter it was 22.2 +/- 2.4 ml/100 g/min and in the thoracic gray matter 41.2 +/- 12/6 ml/100 g/min; and in the lumbar gray matter it was 52.3 +/- 1.9 ml/100 g/min. The effect of changes in blood pressure on SCBF (autoregulation) was investigated in nine rats. We have observed that SCBF remains relatively constant in the blood pressure range of 45 to 165 mm Hg and assumes a passive flow below or above this range.     

Spinal cord perfusion after extensive segmental artery sacrifice: can paraplegia be prevented?

OBJECTIVE: Understanding the ability of the paraspinal anastomotic network to provide adequate spinal cord perfusion pressure (SCPP) critical for both surgical and endovascular repair of thoracoabdominal aortic aneurysms (TAAA). METHODS: To monitor pressure in the collateral circulation, a catheter was inserted into the distal end of the divided first lumbar segmental artery (SA) of 10 juvenile Yorkshire pigs (28.9+/-3.8kg). SA pairs from T3 through L5 were serially sacrificed at 32 degrees C; SCPP and function - using motor-evoked potentials (MEPs) - were continuously monitored until 1h after clamping the last SA. Intermittent aortic and SCPP monitoring was continued for 5 days postoperatively, along with evaluation of motor function. RESULTS: A mean of 14.4+/-0.7 SAs were sacrificed without loss of MEP. SCPP (mmHg) dropped from 68+/-7 before SA clamping (77% of aortic pressure) to 22+/-6 at end clamping, and 21+/-4 after 1h, reaching its lowest point - 19+/-4 - after 5h. Postoperatively, SCPP recovered to 33+/-6 at 24h; 42+/-10 at 48h; 56+/-14 at 72h; 62+/-15 at 96h, returning to baseline (63+/-20) at 120h. Despite comparable SCPP patterns, four pigs did not fully regain the ability to stand. Six animals recovered: two could stand and four could walk. CONCLUSIONS: Interruption of all SAs at 32 degrees C in this pig model results in a spectrum of cord injury, with normal function in a majority of pigs postoperatively. The short duration of low SCPP suggests that hemodynamic manipulation lasting only 24-48h may allow routine complete preservation of normal cord function despite sacrifice of all SAs.     

Hemodynamic effects of dopamine during thoracic epidural analgesia in man

The cardiovascular effects of dopamine were studied before and during thoracic epidural analgesia (TEA) in eight patients prior to abdominal aortic surgery. Dopamine was infused at rates of 2, 4, and 8 micrograms X kg-1 X min-1. Mean plasma dopamine concentration increased proportionally to the infusion rate. Before TEA, dopamine 8 micrograms X kg-1 X min-1 decreased systemic vascular resistance 4 +/- 4 mmHg min X 1-1 (m +/- SD) (P less than 0.05), but increased mean arterial pressure 15 +/- 12 mmHg (P less than 0.01), cardiac output 1.9 +/- 1.0 1 X min-1 (P less than 0.01), heart rate 10 +/- 9 beats X min-1 (P less than 0.05), and plasma norepinephrine concentration 544 +/- 252 pg X ml-1 (P less than 0.01). After the induction of TEA, which extended above the T2 dermatome and below the L2 dermatome, saline and albumin were infused to maintain central venous and pulmonary capillary wedge pressures. TEA reduced mean arterial pressure from 96 +/- 18 to 55 +/- 8 mmHg (P less than 0.01), cardiac output from 4.7 +/- 0.9 to 3.9 +/- 0.9 1 X min-1 (P = 0.05), systemic vascular resistance from 21 +/- 6 to 14 +/- 3 mmHg min X 1-1 (P less than 0.05), and plasma norepinephrine concentration from 394 +/- 141 to 207 +/- 73 pg X ml-1 (P less than 0.01). The plasma epinephrine concentration was reduced 49% after the induction of TEA.(ABSTRACT TRUNCATED AT 250 WORDS)     

Cerebral venous sinus pressure in seated dogs: impact of PEEP, cervical venous compression, and abdominal compression

The authors studied the effects of positive end-expiratory pressure (10 cmH2O PEEP), abdominal compression, and neck compression on dural venous sinus pressure (VSP) in seated dogs. Abdominal compression increased the central venous pressure (CVP) as well as both the systemic arterial pressure and the cardiac output and thus may offer a useful substitute for an antigravity suit. Except when CVP was greater than 8 mmHg, there was little or no correlation between CVP and VSP. Moreover, each method increased VSP, but this effect was closely related to VSP prior to application of the method (pre-VSP). On comparing the VSP changes in relation to the pre-VSP levels when they were either above or below -1.0 mmHg, significant differences were noted in VSP increases, i.e., -0.4 +/- 1.3 (mean +/- SEM) and 4.3 +/- 1.2 mmHg by PEEP, 1.9 +/- 0.3 and 6.4 +/- 0.4 mmHg by abdominal compression, and 10.2 +/- 1.3 and 1.5 +/- 0.5 mmHg by neck compression, respectively. This indicates that PEEP and abdominal compression were more effective in increasing relatively highly negative pre-VSP (less than -1.0 mmHg), while neck compression greatly increased pre-VSP when it was at or above a slightly negative pressure (-1.0 mmHg). The authors conclude that a single application of any one of these three methods during sitting-position surgery may not be effective in increasing cerebral dural sinus pressure.