Phenylephrine increases cerebral perfusion pressure without increasing intracranial pressure in rabbits with balloon-elevated intracranial pressure.

Using a rabbit model of intracranial hypertension, we studied the effects of infusion of phenylephrine on intracranial pressure (ICP) and cerebral perfusion pressure (CPP). Seven New Zealand white rabbits were anesthetized with isoflurane and normocapnia was maintained. An extradural balloon was used to raise ICP to 25 +/- 1 mm Hg. Infusion of phenylephrine increased mean arterial blood pressure (MAP) (77 +/- 6 --> 95 +/- 8 mm Hg) and CPP (52 +/- 7 --> 70 +/- 7 mm Hg). ICP was unchanged during infusion of phenylephrine (25 +/- 1 vs. 25 +/- 2 mm Hg). The phenylephrine infusion was stopped after 45 minutes and MAP returned to baseline (76 +/- 8 mm Hg). We conclude that phenylephrine increased CPP because of its effect on MAP, but did not alter ICP. Phenylephrine may be used to increase CPP without raising ICP when autoregulation is intact.     

Adverse impact of a calcium entry-blocker (verapamil) on intracranial pressure in patients with brain tumors

In order to examine the effects of verapamil on intracranial pressure (ICP) in patients with compromised intracranial compliance, five hypertensive patients with supratentorial tumors were given verapamil, 5 mg intravenously, at the time of anesthesia induction. Within 4 minutes, ICP increased 67% from 18 +/- 4 mm Hg (standard error) to 27 +/- 5 mm Hg (p less than 0.05), whereas mean arterial pressure decreased 20% from 111 +/- 7 mm Hg to 89 +/- 4 mm Hg (p less than 0.05), and cerebral perfusion pressure (CPP) decreased 33% from 93 +/- 11 mm Hg to 62 +/- 6 mm Hg (p less than 0.05). The increases in ICP responded promptly to hyperventilation and intravenous lidocaine (1.5 mg/kg). A control group of five hypertensive patients with supratentorial tumors received the same anesthetic agents without verapamil. In this group, ICP and CPP were unchanged. The authors conclude that calcium entry-blockers, such as verapamil, should be avoided in patients with compromised intracranial compliance unless ICP is being monitored and proper therapy for intracranial hypertension can be rapidly instituted.     

Intracranial effects of endotracheal suctioning in the acute phase of head injury.

In patients with head injury, endotracheal suctioning (ETS) is a potentially dangerous procedure, because it can increase intracranial pressure (ICP). The purpose of this prospective nonrandomized study was to evaluate the impact of ETS on intracranial dynamics in the acute phase of head injury. Seventeen patients with severe head injury (Glasgow Coma Score < or = 8, range 4-8), sedated and mechanically ventilated, were studied during the first week after trauma. Single-pass ETS maneuver (with a 16-French catheter, negative pressure of 100 mm Hg, and duration of less than 30 seconds) was performed 60 seconds after the FiO2 was increased to 100%. After ETS, FiO2 was maintained at 100% for another 30 seconds. Before and after ETS, arterial blood gases and jugular oxygen saturation (S(j)O2), ICP, and mean arterial pressure (MAP) were measured and cerebral perfusion pressure (CPP) was calculated. A total of 131 ETS episodes, which consisted of repeated assessment of each patient, were analyzed. Six patients in 20 cases coughed and/or moved during ETS because of inadequate sedation. After ETS, ICP increased from 20 +/- 12 to 22 +/- 13 mm Hg in well-sedated patients and from 15 +/- 9 to 28 +/- 9 mm Hg in patients who coughed and/or moved (mean change, 2 +/- 6 versus 13 +/- 6 mm Hg, P <.0001). CPP and S(j)O2 increased in well-sedated patients (from 78 +/- 16 to 83 +/- 19 mm Hg, and from 71 +/- 10 to 73 +/- 13%, respectively) and decreased in patients who reacted to ETS (from 79 +/- 14 to 72 +/- 14 mm Hg and from 69 +/- 7 to 66 +/- 9%, respectively), and the differences were significant (mean change, CPP: 5 +/- 14 versus -7 +/- 15 mm Hg, P =.003; (S(j)O2) 2 +/- 5 vs. -3 +/- 5%, P <.0001). In well-sedated patients, endotracheal suctioning caused an increase in ICP, CPP, and S j O 2 without evidence of ischemia. In contrast, in patients who coughed or moved in response to suctioning, there was a slight and significant decrease in CPP and S(j)O2. In the case of patients with head injuries who coughed or moved during endotracheal suctioning, we strongly suggest deepening the level of sedation before completing the procedure to reduce the risk of adverse effects.     

The effects of propofol bolus administration on the intracranial pressure in craniocerebral trauma

Previous investigations have revealed that propofol has a beneficial effect on intracranial dynamics in patients undergoing elective neurosurgery. In the present study we evaluated the impact of propofol in patients with normal or compromised intracranial compliance. METHODS. Epidural ICP probes were implanted in 14 patients with head injury. The heart rate, mean arterial pressure (MAP), intracranial pressure (ICP) and end-tidal CO2 were recorded continuously, and propofol was given in doses of 0.5, 1.0 and 2.0 mg/kg; there were 15 min between each application. The data were evaluated 1, 2, 5 and 10 min after each application. The patients were allocated to group I (ICP less than 20 mmHg) or group II (ICP greater than 20 mmHg) according to their ICP baseline level. A statistical analysis was performed by one-way ANOVA. A P value of less than 0.05 was regarded as significant. RESULTS. In group I decreases in MAP at all measuring points were detected with 1.0 and 2.0 mg/kg propofol; ICP with 1.0 and 2.0 mg/kg and CPP with 2.0 mg/kg fell significantly. In group II MAP decreased with all doses studied, as did ICP with 1.0 and 2.0 mg/kg; however, CPP was not particularly influenced. CONCLUSION. Propofol decreased ICP in patients with normal and compromised intracranial compliance, particularly with 2.0 mg/kg. As the responses to the hypotensive effects of propofol were mild and almost similar in both groups, no inadvertent CPP drops were observed with any of the doses studied. Thus, propofol as a bolus can be used safely for the sedation of ICU patients with head injury and normal or compromised intracranial compliance.     

Cerebral oxygenation following decompressive hemicraniectomy for the treatment of refractory intracranial hypertension

OBJECT: Medically intractable intracranial hypertension is a major cause of morbidity and mortality after severe brain injury. One potential treatment for intracranial hypertension is decompressive hemicraniectomy (DCH). Whether and when to use DCH, however, remain unclear. The authors therefore studied the effects of DCH on cerebral O2 to develop a better understanding of the effects of this treatment on the recovery from injury and disease. METHODS: The study focused on seven patients (mean age 30.6 +/- 9.7 years) admitted to the hospital after traumatic brain injury (five patients) or subarachnoid hemorrhage (two patients) as part of a prospective observational database at a Level I trauma center. At admission the Glasgow Coma Scale (GCS) score was 6 or less in all patients. Patients received continuous monitoring of intracranial pressure (ICP), cerebral perfusion pressure (CPP), blood pressure, and arterial O2 saturation. Cerebral oxygenation was measured using the commercially available Licox Brain Tissue Oxygen Monitoring System manufactured by Integra NeuroSciences. A DCH was performed when the patient's ICP remained elevated despite maximal medical management. CONCLUSIONS: All patients tolerated DCH without complications. Before the operation, the mean ICP was elevated in all patients (26 +/- 4 mm Hg), despite maximal medical management. After surgery, there was an immediate and sustained decrease in ICP (19 +/- 11 mm Hg) and an increase in CPP (81 +/- 17 mm Hg). Following DCH, cerebral oxygenation improved from a mean of 21.2 +/- 13.8 mm Hg to 45.5 +/- 25.4 mm Hg, a 114.8% increase. The change in brain tissue O2 and the change in ICP after DCH demonstrated only a modest relationship (r2 = 0.3). These results indicate that the use of DCH in the treatment of severe brain injury is associated with a significant improvement in brain O2.     

Treatment of intracranial hypertension using nonsurgical abdominal decompression

BACKGROUND: Elevated intra-abdominal pressure (IAP) increases intracranial pressure (ICP) and reduces cerebral perfusion pressure (CPP). We evaluated a nonsurgical means of reducing IAP to reverse this process. METHODS: Swine with a baseline ICP of 25 mm Hg produced by an intracranial balloon catheter were studied. In group 1 (n = 5), IAP was increased by 25 mm Hg. Continuous negative abdominal pressure (CNAP) was then applied. Group 2 (n = 4) had neither IAP elevation nor CNAP. Group 3 (n = 4) had CNAP without IAP elevation. RESULTS: Elevation of IAP by 25 mm Hg above baseline led to deleterious changes in ICP (25.8+/-0.8 to 39.0+/-2.8; p < 0.05) and CPP (85.2+/-2.0 to 64.8+/-2.6; p < 0.05). CNAP led to a reduction in IAP (30.2+/-1.2 to 20.4+/-1.3; p < 0.05) and improvements in cerebral perfusion (ICP, 33+/-2.7; CPP, 74.4+/-1.2; both p < 0.05). Group 2 had stable ICP (25.8+/-0.25 to 28.7+/-1.7; p > 0.05) and CPP (80.8+/-1.4 to 80.5+/-1.8; p > 0.05). In group 3, CNAP decreased cardiac index (2.9+/-0.2 to 1.1+/-0.4; p < 0.05), mean arterial pressure (105.2+/-4.0 to 38.2+/-12.0; p < 0.05), and CPP (74.2+/-4.7 to 14.5+/-12.2; p < 0.05). CONCLUSION: Elevations in IAP led to increased ICP and decreased CPP. CNAP ameliorated these intracranial disturbances. With normal IAP, CNAP impaired cerebral perfusion.     

Efficacy of hyperventilation,blood pressure elevation,and metabolic suppression therapy in controlling intracranial pressure after head injury

OBJECT: Hyperventilation therapy, blood pressure augmentation, and metabolic suppression therapy are often used to reduce intracranial pressure (ICP) and improve cerebral perfusion pressure (CPP) in intubated head-injured patients. In this study, as part of routine vasoreactivity testing, these three therapies were assessed in their effectiveness in reducing ICP. METHODS: Thirty-three patients with a mean age of 33 +/- 13 years and a median Glasgow Coma Scale (GCS) score of 7 underwent a total of 70 vasoreactivity testing sessions from postinjury Days 0 to 13. After an initial 133Xe cerebral blood flow (CBF) assessment, transcranial Doppler ultrasonography recordings of the middle cerebral arteries were obtained to assess blood flow velocity changes resulting from transient hyperventilation (57 studies in 27 patients), phenylephrine-induced hypertension (55 studies in 26 patients), and propofol-induced metabolic suppression (43 studies in 21 patients). Changes in ICP, mean arterial blood pressure (MABP), CPP, PaCO2, and jugular venous oxygen saturation (SjvO2) were recorded. With hyperventilation therapy, patients experienced a mean decrease in PaCO2 from 35 +/- 5 to 27 +/- 5 mm Hg and in ICP from 20 +/- 11 to 13 +/- 8 mm Hg (p < 0.001). In no patient who underwent hyperventilation therapy did SjvO2 fall below 55%. With induced hypertension, MABP in patients increased by 14 +/- 5 mm Hg and ICP increased from 16 +/- 9 to 19 +/- 9 mm Hg (p = 0.001). With the aid of metabolic suppression, MABP remained stable and ICP decreased from 20 +/- 10 to 16 +/- 11 mm Hg (p < 0.001). A decrease in ICP of more than 20% below the baseline value was observed in 77.2, 5.5, and 48.8% of hyperventilation, induced-hypertension, and metabolic suppression tests, respectively (p < 0.001 for all comparisons). Predictors of an effective reduction in ICP included a high PaCO2 for hyperventilation, a high study GCS score for induced hypertension, and a high PaCO2 and a high CBF for metabolic suppression. CONCLUSIONS: Of the three modalities tested to reduce ICP, hyperventilation therapy was the most consistently effective, metabolic suppression therapy was variably effective, and induced hypertension was generally ineffective and in some instances significantly raised ICP. The results of this study suggest that hyperventilation may be used more aggressively to control ICP in head-injured patients, provided it is performed in conjunction with monitoring of SjvO2.     

Effects of nifedipine on intracranial pressure in neurosurgical patients with arterial hypertension

The effects of nifedipine, 20 mg administered via a nasogastric tube, on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) were examined. Nifedipine was administered to treat arterial hypertension (greater than 180 mm Hg, systolic). Ten measurements were made in eight patients with cerebrovascular disease or head trauma. The mean arterial blood pressure (MABP) and ICP were measured before and for 30 minutes after the administration of nifedipine. The MABP gradually decreased and reached its lowest value at approximately 10 minutes after initiation of nifedipine administration, and thereafter remained unchanged. The MABP decreased significantly from 128 +/- 8 (mean +/- standard deviation) to 109 +/- 7 mm Hg, and the CPP decreased from 105 +/- 11 to 84 +/- 10 mm Hg. The ICP increased by 1 to 10 mm Hg in eight of 10 measurements, and the mean change of ICP from 19 +/- 7 to 22 +/- 6 mm Hg was statistically significant. These changes were not accompanied by alterations in neurological signs. The results suggest that enteral nifedipine produces a small but statistically significant increase in ICP. Accordingly, neurological signs must be closely observed to detect deterioration, which can be caused by an increase in ICP and/or a decrease in CPP.     

Propofol vs. thiopental-isoflurane for neurosurgical anesthesia: comparison of hemodynamics, CSF pressure, and recovery

Sixty otherwise healthy patients with no clinical signs of intracranial hypertension who were undergoing elective intracranial surgery were randomly assigned to receive anesthesia with either thiopental, 3-6 mg/kg i.v., and isoflurane, 0.5-1.5% (group 1, N = 30) or propofol, 1-2.5 mg/kg i.v., and propofol infusion, 40-200 microg/kg/h (group 2, N = 30). Both groups received 50% nitrous oxide in O2 subsequent to dural opening. During induction, the changes in heart rate (HR), mean arterial pressure (MAP), cerebrospinal fluid pressure (CSFP), and cerebral perfusion pressure (CPP) were similar between the groups, except at 3 min when the findings (mean +/- SEM) for CPP (81 +/- 3.3 vs. 70.3 +/- 2.8 mm Hg, p <0.05) were significantly lower in group 2. At intubation, the highest level of MAP (103.1 +/- 3.3 vs. 88.9 +/- 2.7 mm Hg, p <0.05) was significantly greater in group 1. At pinhead-holder application, the highest values of HR (81.8 +/- 3 vs. 73.9 +/- 2.1 beats/min, p <0.05), MAP (112.2 +/- 3.6 vs. 98.3 +/- 3 mm Hg, p <0.05), CSFP (15.2 +/- 1.3 vs. 11.6 +/- 1.1 mm Hg, p <0.05), and CPP (97.0 +/- 3.9 vs. 86.7 +/- 3.3 mm Hg, p <0.05) were significantly greater in group 1. During early (20-30 min) recovery, group 2 had higher Glasgow Coma Scale scores and a greater percentage of patients in whom eye opening, response to commands, extubation, speech, and time/space orientation were present. In conclusion, when compared to thiopentalisoflurane for intracranial surgery, propofol produces similar HR, MAP, CSFP, and CPP responses during induction, adequate control of these responses during nociceptive stimulation, and faster recovery for cerebral function postoperatively.     

The effects of isoflurane and desflurane on intracranial pressure,cerebral perfusion pressure,and cerebral arteriovenous oxygen content difference in normocapnic patients with supratentorial brain tumors

BACKGROUND: Desflurane is a volatile anesthetic agent with low solubility whose use in neurosurgery has been debated because of its effect on intracranial pressure and cerebral blood flow. The purpose of this study was to determine the variations on intracranial pressure (ICP) and cerebral perfusion pressure (CPP) as well as on cerebral arteriovenous oxygen content difference (AVDo(2)) in normocapnic patients scheduled to undergo removal of supratentorial brain tumors with no evidence of mass effect during anesthesia with isoflurane or desflurane. METHODS: In 60 patients scheduled to undergo craniotomy and removal of supratentorial brain tumors with no evidence of midline shift, anesthesia was induced with intravenous fentanyl, thiopental, and vecuronium and was maintained with 60% nitrous oxide in oxygen. Patients were assigned to two groups randomized to receive 1 minimum alveolar concentration isoflurane or desflurane for 30 min. Heart rate, mean arterial pressure, intraparenchymal ICP, and CPP were monitored continuously. Before and after 30 min of continuous administration of the inhaled agents, AVDo(2) was calculated. RESULTS: There were no significant differences between groups in heart rate, mean arterial pressure, ICP, and CPP. ICP measurements throughout the study did not change within each group compared to baseline values. Mean arterial pressure decreased significantly in all patients compared to baseline values, changing from 105 +/- 14 mmHg (mean +/- SD) to 85 +/- 10 mmHg in the isoflurane group and from 107 +/- 11 mmHg to 86 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). CPP also decreased within each group compared with baseline values, changing from 95 +/- 15 mmHg to 74 +/- 11 mmHg in the isoflurane group and from 95 +/- 16 mmHg to 74 +/- 10 mmHg in the desflurane group (P < 0.05 in both groups). Cerebral AVDo(2) decreased significantly in both groups throughout the study, changing from 2.35 +/- 0.77 mm to 1.82 +/- 0.61 mm (mmol/l) in the isoflurane group (P < 0.05) and from 2.23 +/- 0.72 mm to 1.94 +/- 0.76 mm in the desflurane group (P < 0.05), without differences between groups. CONCLUSIONS: The results of this study indicate that there are no variations on ICP in normocapnic patients undergoing removal of supratentorial brain tumors without midline shift, as they were anesthetized with isoflurane or desflurane. CPP and cerebral AVDo(2) decreased with both agents.     

Effects of PEEP on the intracranial system of patients with head injury and subarachnoid hemorrhage: the role of respiratory system compliance

BACKGROUND: Positive end-expiratory pressure (PEEP) can be effective in improving oxygenation, but it may worsen or induce intracranial hypertension. The authors hypothesized that the intracranial effects of PEEP could be related to the changes in respiratory system compliance (Crs). METHODS: A prospective study investigated 21 comatose patients with severe head injury or subarachnoid hemorrhage receiving intracranial pressure (ICP) monitoring who required mechanical ventilation and PEEP. The 13 patients with normal Crs were analyzed as group A and the 8 patients with low Crs as group B. During the study, 0, 5, 8, and 12 cm H2O of PEEP were applied in a random sequence. Jugular pressure, central venous pressure (CVP), cerebral perfusion pressure (CPP), intracranial pressure (ICP), cerebral compliance, mean velocity of the middle cerebral arteries, and jugular oxygen saturation were evaluated simultaneously. RESULTS: In the group A patients, the PEEP increase from 0 to 12 cm H2O significantly increased CVP (from 10.6 +/- 3.3 to 13.8 +/- 3.3 mm Hg; p < 0.001) and jugular pressure (from 16.6 +/- 3.1 to 18.8 +/- 3.2 mm Hg; p < 0.001), but reduced mean arterial pressure (from 96.3 +/- 6.7 to 91.3 +/- 6.5 mm Hg; p < 0.01), CPP (from 82.2 +/- 6.9 to 77.0 +/- 6.2 mm Hg; p < 0.01), and mean velocity of the middle cerebral arteries (from 73.1 +/- 27.9 to 67.4 +/- 27.1 cm/sec; F = 7.15; p < 0.001). No significant variation in these parameters was observed in group B patients. After the PEEP increase, ICP and cerebral compliance did not change in either group. Although jugular oxygen saturation decreased slightly, it in no case dropped below 50%. CONCLUSIONS: In patients with low Crs, PEEP has no significant effect on cerebral and systemic hemodynamics. Monitoring of Crs may be useful for avoiding deleterious effects of PEEP on the intracranial system of patients with normal Crs.     

七氟醚和异丙酚复合麻醉下妇科腹腔镜手术患者脑血流量和颅内压的比较

目的 比较七氟醚和异丙酚复合麻醉下妇科腹腔镜手术患者的脑血流量(CBF)和颅内压(ICP).方法 择期拟行妇科腹腔镜手术患者40例,年龄20～59岁,体重44～69kg,ASA Ⅰ或Ⅱ级,随机分为2组(n=20):七氟醚复合麻醉组(S组)和异丙酚复合麻醉组(P组).麻醉诱导:S组吸人8%七氟醚,P组TCI异丙酚(Ce 4μg/ml),两组均TCI瑞芬太尼(Ce 6ng/ml),睫毛反射消失后,静脉注射顺阿曲库铵0.15mg/kg,BIS<45时行气管插管.麻醉诱导后瑞芬太尼Ce下调为3 ng/ml,调节异丙酚Ce和七氟醚吸人浓度,维持BIS 45～50,于麻醉诱导前水平仰卧位稳定后5 min(T1)、水平截石位稳定后5 min(T2)、气管插管后即刻(T3)、气管插管后5 min(T4)、气腹头低位后即刻(T5)、气腹头低位后15 min(T6)及气腹放气后10 min(T7)时采用经颅多普勒超声测定大脑中动脉脑血流速率(CBFV)和搏动指数(PI).结果 与T1时比较,P组T3,4,7时CBFV降低,T3,4时P1降低,S组T4,7时CBFV降低,两组T5,6时PI升高(P<0.05);与T4时比较,两组T5,6时CBFV升高(P<0.05);与S组比较,P组T3时CBFV降低,T3,4时PI降低(P<0.05).结论 与七氟醚复合麻醉相比,异丙酚复合麻醉下妇科腹腔镜手术患者麻醉诱导后CBF和ICP明显降低;气腹后CBF和ICP均升高.     

Computed tomographic brain density measurement as a predictor of elevated intracranial pressure in blunt head trauma

There are no independent computed tomography (CT) findings predictive of elevated intracranial pressure (ICP). The purpose of this study was to evaluate brain density measurement on CT as a predictor of elevated ICP or decreased cerebral perfusion pressure (CPP). A prospectively collected database of patients with acute traumatic brain injury was used to identify patients who had a brain CT followed within 2 hours by ICP measurement. Blinded reviewers measured mean density in Hounsfield Units (HU) within a 100-mm2 elliptical region at four standardized positions. Brain density measurement was compared for patients with an ICP of 20 or greater versus less than 20 mm Hg and CPP of 70 or greater versus less than 70 mm Hg. During a 2-year period, 47 patients had ICP monitoring after brain CT. Average age was 40 +/- 18 years old; 93.6 per cent were male; mean Injury Severity Score was 25 +/- 10; and Glasgow Coma Scale was 6 +/- 4. There was no difference in brain density measurement for observer 1, ICP less than 20 (26.3 HU) versus ICP 20 or greater (27.4 HU, P = 0.545) or for CPP less than 70 (27.1 HU) versus CPP 70 or greater (26.2, P = 0.624). Similarly, there was no difference for observer 2, ICP less than 20 (26.8 HU) versus ICP 20 or greater (27.4, P = 0.753) and CPP less than 70 (27.6 HU) versus CPP 70 or greater (26.2, P = 0.436). CT-measured brain density does not correlate with elevated ICP or depressed CPP and cannot predict patients with traumatic brain injury who would benefit from invasive ICP monitoring.     

Intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension

Sympathetic hyperactivity during sudden intracranial hypertension leads to cardiovascular instability, myocardial dysfunction, and neurogenic pulmonary edema. Because spinal anesthesia is associated with sympatholysis, we investigated the protective effects of intrathecal lidocaine in a rodent model. Halothane-anesthetized rats were given a 10-microL intrathecal injection of saline (n = 10) or lidocaine 1% (n = 6). A subdural balloon catheter was inflated for 60 s to produce intracranial hypertension. Hemodynamics were monitored, and hearts and lungs were harvested for histological examination. In Saline versus Lidocaine-Treated rats, peak mean arterial blood pressure during balloon inflation was 115 +/- 4 mm Hg versus 78 +/- 8 mm Hg (P < 0.05), mean arterial blood pressure 30 min after balloon deflation was 47 +/- 2 mm Hg versus 67 +/- 3 mm Hg (P < 0.05), and lung weight was 1.54 +/- 0.03 g versus 1.41 +/- 0.04 g (P < 0.05), respectively. Cardiac dysrhythmias and electrocardiographic changes were more frequent in the Saline-Treated group (P < 0.05). Saline-Treated rats had extensive, hemorrhagic pulmonary edema, whereas the Lidocaine-Treated rats had only patchy areas of lung abnormality. Histological changes in the myocardium were rare, and no difference was found between the two groups. We conclude that intrathecal lidocaine prevents cardiovascular collapse and neurogenic pulmonary edema in a rat model of acute intracranial hypertension. IMPLICATIONS:In a rat model of intracranial balloon inflation, intrathecal lidocaine prevented cardiovascular collapse and neurogenic pulmonary edema. Descending neural pathways are involved in the development of cardiopulmonary complications associated with acute intracranial hypertension.     

"Defasciculation" with metocurine prevents succinylcholine-induced increases in intracranial pressure

In order to determine whether a small, "defasciculating" dose of metocurine could prevent increases in intracranial pressure (ICP) induced by succinylcholine (Sch), the authors studied 12 patients (ages 25-79 yr) undergoing craniotomy for excision of malignant supratentorial gliomas. After insertion of a subarachnoid bolt for ICP monitoring and a radial arterial cannula for determination of blood pressure and blood gas tensions, six patients (group I) were randomly allocated to receive MTC 0.03 mg/kg 3 min before induction of general anesthesia with thiopental 4 mg/kg and nitrous oxide 70% in O2. Six other patients (group II) received saline 0.015 ml/kg instead of MTC, followed by the same induction sequence. After induction of anesthesia, ventilation was controlled by mask (PaCO2 = 40 mmHg +/- 2 SE), and arterial and intracranial pressures were allowed to stabilize. Four minutes after thiopental administration (7 min after MTC), after a 1-min period of relatively stable arterial pressure and ICP, Sch 1 mg/kg was administered as a bolus. ICP and blood pressure were recorded continuously until normal twitch tension was restored. In group I (MTC pretreatment), ICP did not change significantly from the mean value observed before Sch, 14 mmHg +/- 2 SE. In group II (saline pretreatment), ICP increased from 11 mmHg +/- 2 SE to 23 mmHg +/- 4 SE (P less than .05). This study not only confirms previous work showing that Sch may induce marked ICP increases in lightly anesthetized patients with intracranial mass lesions, but also indicates that pretreatment with a "defasciculating" dose of MTC can prevent these potentially deleterious ICP increases in patients known to be at risk.     

The effects of indomethacin on intracranial pressure and cerebral hemodynamics during isoflurane or propofol anesthesia in sheep with intracranial hypertension

The effect of indomethacin in reducing intracranial pressure (ICP) may be dependent on the choice of anesthetic regimen. We studied the effects of indomethacin on ICP and cerebral blood flow (CBF) during isoflurane or propofol anesthesia in a sheep model of intracranial hypertension. A crossover design was applied in which six sheep were anesthetized with isoflurane and propofol in a random order. Anesthetic depth was measured with response and state entropy. Changes in CBF, ICP, mean arterial blood pressure, arterio-venous oxygen difference, and Paco2 were measured at specific times before and after an IV indomethacin bolus (0.2 mg/kg). Response and state entropy values during anesthesia were similar in both groups. Isoflurane and propofol reduced CBF by 11% and 34%, respectively. Indomethacin caused a reduction in ICP within 15 s during both anesthetic regimens, with the decrease in ICP being significantly more pronounced during isoflurane (P = 0.009). In both anesthetic groups, indomethacin caused a simultaneous increase in mean arterial blood pressure and a further 17% versus 14% decrease in CBF from predrug values for isoflurane and propofol, respectively. The reduction in CBF was significantly more pronounced for propofol (P = 0.02). The effect on ICP, however, was most pronounced during isoflurane anesthesia. We suggest that the effect of indomethacin is partly mediated by an autoregulatory response.     

Cerebral and cardiovascular responses to changes in head elevation in patients with intracranial hypertension

To establish if an optimum level of head elevation exists in patients with intracranial hypertension, the authors examined changes in intracranial pressure (ICP), systemic and pulmonary pressures, systemic flows, and intrapulmonary shunt fraction with the patient lying flat, and then with the head elevated at 15 degrees, 30 degrees, and 60 degrees. Cerebral perfusion pressure (CPP) was calculated. The lowest mean ICP was found with elevation of the head to 15 degrees (a fall of -4.5 +/- 1.6 mm Hg, p less than 0.001) and 30 degrees (a fall of -6.1 +/- 3.5 mm Hg, p less than 0.001); the CPP and cardiac output were maintained. With elevation of the head to 60 degrees, the mean ICP increased to -3.8 +/- 9.3 mm Hg of baseline, while the CPP decreased -7.9 +/- 9.3 mm Hg (p less than 0.02), and the cardiac index also fell -0.25 +/- 0.28 liters/min/sq m (p less than 0.01). No significant change in filling pressures, arterial oxygen content, or heart rate was encountered at any level of head elevation. Therefore, a moderate degree (15 degrees or 30 degrees) of head elevation provides a consistent reduction of ICP without concomitant compromise of cardiac function. Lower (0 degrees) or higher (60 degrees) degrees of head elevation may be detrimental to the patient because of changes in the ICP, CPP, and cardiac output.     

右美托咪啶与异丙酚镇静下允许性高碳酸血症患者颅内压及脑氧代谢的比较

目的 比较右美托咪啶与异丙酚镇静下允许性高碳酸血症患者的颅内压及脑氧代谢情况.方法行允许性高碳酸血症通气、Ramsay评分≤2分的急性呼吸窘迫综合征患者24例,年龄28～64岁,APACHE-Ⅱ评分11～18分,采用随机数字表法,将患者随机分为2组(n=12):右美托咪啶组(D组)和异丙酚组(P组).调节右美托咪啶输注速率或异丙酚血浆靶浓度使D组和P组患者Ramsay评分逐步达到3、4、5分.于给药前(T0)、达各目标镇静水平后30 min(T1～3)时采用经颅多普勒超声测定大脑中动脉脑血流速率(CBFW)、搏动指数(PI)和阻力指数(RI),抽取桡动脉血样和颈内静脉球部血样行血气分析,计算脑氧代谢率(CNRO2)、动脉-颈内静脉氧含量差(Da-jvO2)、脑氧摄取率(CERO2).结果 与T0时比较,D组和P组T1～3时MAP、BIS值、CBFV、PI、RI和CMRO2降低(P＜0.05或0.01);两组各时点Da-jvO2、CERO2差异无统计学意义(P＞0.05);与P组比较,D组各时点BIS值和MAP差异无统计学意义(P＞0.05),CBF、PI和RI降低(P＜0.05).D组和P组CBFV与CMRO2均呈正相关(相关系数分别为0.80、0.76,P＜0.05).结论 在不同镇静水平,右美托咪啶较异丙酚可明显降低允许性高碳酸血症患者的颅内压,且可保持脑氧供需平衡.

Abstract：

Objective To compare the effects of sedation induced with dexmedetomidine and propofol on intracranial pressure and cerebral oxygen metabolism in patients with permissive hypercapnia. Methods Twentyfour patients with acute respiratory distress syndrome (ARDS) were randomly divided into 2 groups ( n = 12 each) :dexmedetomidine group (group D) and propofol group (group P) . Their APACHE Ⅱ scores were 11-18. The patients were mechanically ventilated (VT 5-7 ml/kg, RR 12-17 bpm, PEEP 6-10 cm H2O, FiO2 40-60%). PaCO2 was maintained at 50-65 mm Hg. Radial artery was cannulated for direct BP monitoring and blood sampling. Right internal jugular vein was cannulated and the catheter was advanced cephalad until jugular bulb. Continuous infusion of dexmedetomidine was started at 0.5 μg· kg-1· h-1 and TCI of propofol was started at target plasma concentration (Cp) of 0.4 μg/ml. The infusion of both drugs was gradually increased until Ramsay score (1= fully awake, 6 =asleep, unresponsive to loud verbal stimulus) reached 3,4,5. Transcranial Doppler monitoring was used to determine cerebral blood flow velocity (CBFV), pulsatility index (PI) and resistance index (RI) before administration of dexmedetomidine and propofol (T0 ) and at 30 min after the 3 levels of sedation were reached (T1-3) . Meanwhile blood samples were taken from radial artery and jugular bulb for blood gas analyses. Cerebral O2 metabolic rate (CMRO2), cerebral A-V O2 content differences (Da-jvO2) and cerebral O2 extraction rate (CERO2) were calculated .ResultsCBFV, PI, RI and CMRO2 were significantly decreased at T1-3 as compared with the baseline values at T0 in both groups. CBFV was positively correlated with CMRO2 in both group D (r = 0.80) and group P ( r = 0.76) . CBFV, PI and RI were significantly lower at T1-3 in group D than in group P. There was no significant change in Da-jvO2 and CERO2 at T1-3 as compared with the baseline values at T0 in both groups. Conclusion At different sedation levels, dexmedetomidine results in lower intracranial pressure than propofol and maintains the balance between cerebral O2 supply and demand in patients with permissive hypercapnia.     

Ephedrine, dopamine, or doubtamine to treat hypotension with propofol during epidural anesthesia

PURPOSE: To compare the efficacy of ephedrine, dopamine and dobutamine for circulatory support during thoracic epidural anesthesia after anesthetic induction with propofol. METHODS: Forty patients undergoing lobectomy or mastectomy were divided into four groups of 10: a control group received no vasopressor; an ephedrine group received 5 mg ephedrine when the mean arterial pressure (MAP), measured every 2.5 min, decreased by 10% from baseline; dopamine and dobutamine groups received 5 microg x kg(-1) x min(-1) dopamine or 3 microg x kg(-1) x min(-1) dobutamine from five minutes after epidural injection of local anesthetic to the end of tracheal intubation. Anesthesia was induced with 2 mg x kg(-1) propofol. The MAP and heart rate (HR) were measured at baseline, 20 min after epidural injection, three minutes after propofol, and one minute after tracheal intubation. RESULTS: In the control group, MAP and HR decreased from 86+/-9 mmHg, 74+/-8 bpm to 62+/-9 mm Hg; P<0.0001, 60+/-8 bpm; P = 0.0003 after propofol. After tracheal intubation, MAP was restored to (81+/-13 mmHg, 70+/-13 bpm). In the ephedrine, dopamine, and dobutamine groups, MAP and HR remained unchanged during epidural anesthesia and propofol induction. However, after tracheal intubation, MAP and HR increased in the ephedrine (104+/-11 mm Hg; P = 0.004, 87+/-11 bpm; P<0.0001) and dobutamine (117+/-13 mm Hg; P = 0.0005, 100+/-11 bpm; P<0.0001) groups, but not in the dopamine group compared with baseline. CONCLUSION: Dopamine is preferable to ephedrine and dobutamine in providing hemodynamic stability during propofol induction and tracheal intubation following epidural anesthesia.     

Effects of alterations in arterial CO2 tension on cerebral blood flow during acute intracranial hypertension in rats.

Cerebrovascular reactivity to CO2 in clinical and experimental studies has been found to be impaired during increased intracranial pressure (ICP). However, from previous study results it has not been possible to estimate whether the impairment was caused by elevated ICP, or caused by decreased cerebral perfusion pressure (CPP). The current study was carried out in a group of unmanipulated control rats and in six investigation groups of six rats each: two groups with elevated ICP (30 and 50 mm Hg) and spontaneous arterial blood pressure (MABP), two groups with spontaneous ICP and arterial hypotension (77 and 64 mm Hg), and two groups with elevated ICP (30 and 50 mm Hg) and arterial hypertension (124 mm Hg). Intracranial hypertension was induced by continuous infusion of lactated Ringer's solution into the cisterna magna, arterial hypotension by controlled bleeding, and arterial hypertension by continuous administration of norepinephrine intravenously. Cerebral blood flow (CBF) was measured repetitively by the intraarterial 133Xe method at different levels of arterial PCO2. In each individual animal, CO2 reactivity was calculated from an exponential regression line obtained from the corresponding CBF/PaCO2 values. By plotting each individual value of CO2 reactivity against the corresponding CPP value from the seven investigation groups, CPP was significantly and directly related to CO2 reactivity of CBF (P < .001). No correlation was found by plotting CO2 reactivity values against the corresponding MABP values or the corresponding ICP values. Thus, the results show that CO2 reactivity is at least partially determined by CPP and that the impaired CO2 reactivity observed at intracranial hypertension and arterial hypotension may be caused by reduced CPP.