Cerebral Arteriovenous Oxygen Difference Research Articles

Analysis of postprocedural microembolic infarctions and global oxygen extraction fraction during balloon-protected carotid artery stenting: Preliminary study.

Background: Atherosclerotic carotid stenosis with impaired cerebral perfusion is a risk factor for cerebral ischemia. In major carotid stenoocclusive diseases, increased oxygen extraction fraction (OEF) is associated with ischemic stroke. Balloon-protected carotid artery stenting (CAS) is valuable for high-grade carotid stenosis. However, while balloon-protected CAS can effectively reduce the occurrence of ischemic complications by blocking carotid flow, cerebral hypoperfusion may result in simultaneous cerebral ischemia. We sought to evaluate whether increased OEF during balloon-protected CAS can predict postprocedural microembolic infarction (MI).Methods: Eighty-four patients who underwent balloon-protected CAS were enrolled. Initial, intraprocedural, and postprocedural OEFs were calculated from the cerebral arteriovenous oxygen differences obtained from blood sampled just before the temporary occlusion and reperfusion of the internal carotid artery during and after the procedure. MIs were evaluated by diffusion-weighted imaging (DWI). Patients were classified into two groups based on the presence or absence of new MIs, and the relationship between the OEF and postprocedural MIs was analyzed.Results: New DWI-positive lesions were found in 37 cases (44.0%). Age, signal intensity ratio (SIR) of carotid plaque on T1-weighted black blood magnetic resonance imaging, and intraprocedural OEF were significantly higher in the DWI-positive group. The high SIR and intraprocedural OEF were significantly associated with the development of postprocedural MIs in multivariate analysis. MIs were correlated with the increase in OEF.Conclusion: Increased intraprocedural OEF, obtained by blood sampling during balloon-protected CAS, could predict the incidence of postprocedural MIs. Patients with carotid stenosis could be hemodynamically compromised by carotid flow blockage during balloon-protected CAS.

Cerebral metabolic rate of oxygen in obstructive sleep apnea at rest and in response to breath-hold challenge

Obstructive sleep apnea (OSA) is associated with extensive neurologic comorbidities. It is hypothesized that the repeated nocturnal apneas experienced in patients with OSA may inhibit the normal apneic response, resulting in hypoxic brain injury and subsequent neurologic dysfunction. In this study, we applied the recently developed OxFlow MRI method for rapid quantification of cerebral metabolic rate of oxygen (CMRO2) during a volitional apnea paradigm. MRI data were analyzed in 11 OSA subjects and 10 controls (mean ± SD apnea-hypopnea index (AHI): 43.9 ± 18.1 vs. 2.9 ± 1.6 events/hour, P < 0.0001; age: 53.8 ± 8.2 vs. 45.3 ± 8.5 years, P = 0.027; BMI: 36.6 ± 4.4 vs. 31.9 ± 2.2 kg/m2, P = 0.0064). Although total cerebral blood flow and arteriovenous oxygen difference were not significantly different between apneics and controls (P > 0.05), apneics displayed reduced baseline CMRO2 (117.4 ± 37.5 vs. 151.6 ± 29.4 µmol/100 g/min, P = 0.013). In response to apnea, CMRO2 decreased more in apneics than controls (−10.9 ± 8.8 % vs. −4.0 ± 6.7 %, P = 0.036). In contrast, group differences in flow-based cerebrovascular reactivity were not significant. Results should be interpreted with caution given the small sample size, and future studies with larger independent samples should examine the observed associations, including potential independent effects of age or BMI. Overall, these data suggest that dysregulation of the apneic response may be a mechanism for OSA-associated neuropathology.

Abstract W P115: Utilization of Blood Sampling Global Oxygen Extraction Fraction and SPECT to Anticipate Cerebral Hyperperfusion Syndrome Following Elective Carotid Artery Stenting

Background: It is required to anticipate cerebral hyperperfusion syndrome (CHS) following carotid artery stenting (CAS). Purpose: The purpose of our retrospective study was to investigate whether or not blood sampling oxygen extraction fraction (OEF) and post-CAS CBF increase in SPECT had relation to CHS following CAS. Methods: Included in our analysis were patients (1) who underwent elective CAS in our institution between October 2010 and May 2014, and (2) who underwent blood sampling for OEF calculation before and immediately after CAS, and (3) who underwent SPECT before and just after CAS. OEF was calculated from cerebral arteriovenous oxygen difference. Arterial blood was sampled from the common carotid artery and venous blood from the dominant-sided superior jugular bulb. CHS was defined as pulsatile headaches, restlessness, convulsion, and/or new neurological symptoms not due to cerebral ischemia within seven days following CAS. CBF was measured before and just after CAS. CBF increase in the CAS side was defined as follows; (post-CAS CBF ratio - pre-CAS CBF ratio) of more than 10%, where CBF ratio was defined as CAS-sided fronto-parietal CBF divided by ipsilateral cerebellar CBF (%). Evaluated were baseline features in patients, pre-CAS OEF, post-CAS OEF, CBF ratio, CBF increase and CHS. Results: During the study period, 134 patients matched our criteria for analysis. Pre-CAS OEF was 0.41+-0.06, post-CAS OEF was 0.42+-0.08, pre-CAS CBF ratio: 88.7+-15.4%, CBF increase: 1.86+-12.3%. Nine patients presented CHS. Among them, pre-CAS OEF, CBF ratio and CBF increase were significant. ROC curves showed that pre-CAS OEF of 0.46 (p&lt;0.001, OR: 9.3), CBF ratio of 92%(p&lt;0.05, OR: 6.5), CBF increase of 8.8% (p&lt;0.005, OR: 6.6) were cut-off values. Among 10 patients with pre-CAS OEF of more than 0.46 and CBF increase of more than 8.8%, 4 patients presented CHS (p&lt;0.0001, OR;15.9). Conclusion: Elevation of pre-CAS OEF and increase of post-CAS CBF were strongly related to CHS.

Selective Brain Cooling with Endovascular Intracarotid Infusion of Cold Saline: A Pilot Feasibility Study

Endovascular brain cooling as a method for rapid and selective induction of hypothermic neuroprotection has not been systematically studied in humans. In this clinical pilot study we investigated the feasibility, safety, and physiologic responses of short-term brain cooling with IC-CSI. We studied 18 patients (50 +/- 10 years old, 9 women) undergoing follow-up cerebral angiography after previous treatment of vascular malformations. Isotonic saline (4-17 degrees C) was infused into 1 internal carotid artery at 33 mL/min for 10 minutes. Brain (JVB) and bladder/esophageal temperature measurements (n = 9) were performed. Both MCAs were monitored with transcranial Doppler sonography (n = 13). Arterial and JV blood were sampled to estimate hemodilution and brain oxygen extraction. JVB temperature dropped approximately 0.84 +/- 0.13 degrees C and systemic temperature by 0.15 +/- 0.08 degrees C from baseline (JVB versus systemic temperature: P = .0006). Systolic MCA-flow velocities decreased from 101 +/- 27 to 73 +/- 18 cm/s on the infused side and from 83 +/- 24 to 78 +/- 21 cm/s on the contralateral side (relative changes, -26 +/- 8% versus -4 +/- 27%; P = .009). Changes in hematocrit (-1.2 +/- 1.1%) and cerebral arteriovenous oxygen difference (0.2 +/- 1.0 mL O(2)/100 mL) were not significant. Doppler data showed no signs of vascular spasm or microemboli. No focal neurologic deficits occurred. Pain was not reported. The results of this pilot study suggest that brain cooling can be achieved safely, rapidly, and selectively by means of IC-CSI, opening a new potential avenue for acute neuroprotection. Clinical investigations with control of infusion parameters and measurements of CBF, oxygen consumption, and brain temperature are warranted.

Effect of Equiosmolar Solutions of Mannitol versus Hypertonic Saline on Intraoperative Brain Relaxation and Electrolyte Balance

The purpose of the study was to compare the effect of equiosmolar solutions of mannitol and hypertonic saline (HS) on brain relaxation and electrolyte balance. After institutional review board approval and informed consent, patients with American Society of Anesthesiologists physical status II-IV, scheduled to undergo craniotomy for various brain pathologies, were enrolled into this prospective, randomized, double-blind study. Patients received 5 ml/kg 20% mannitol (n = 20) or 3% HS (n = 20). Partial pressure of carbon dioxide in arterial blood was maintained at 35-40 mmHg, and central venous pressure was maintained at 5 mmHg or greater. Hemodynamic variables, fluid balance, blood gases, electrolytes, lactate, and osmolality (blood, cerebrospinal fluid, urine) were measured at 0, 15, 30, and 60 min and 6 h after infusion; arteriovenous difference of oxygen, glucose, and lactate were calculated. The surgeon assessed brain relaxation on a four-point scale (1 = relaxed, 2 = satisfactory, 3 = firm, 4 = bulging). Appropriate statistical tests were used for comparison; P < 0.05 was considered significant. There was no difference in brain relaxation (mannitol = 2, HS = 2 points; P = 0.8) or cerebral arteriovenous oxygen and lactate difference between HS and mannitol groups. Urine output with mannitol was higher than with HS (P < 0.03) and was associated with higher blood lactate over time (P < 0.001, compared with HS). Cerebrospinal fluid osmolality increased at 6 h in both groups (P < 0.05, compared with baseline). HS caused an increase in sodium in cerebrospinal fluid over time (P < 0.001, compared with mannitol). Mannitol and HS cause an increase in cerebrospinal fluid osmolality, and are associated with similar brain relaxation scores and arteriovenous oxygen and lactate difference during craniotomy.

Hypertonic Saline for Craniotomy?

Hypertonic Saline for Craniotomy?

Cerebral hemodynamic and metabolic profiles in fulminant hepatic failure: Relationship to outcome

The purpose of this retrospective study was to examine the potential role of cerebral hemodynamic and metabolic factors in the outcome of patients with fulminant hepatic failure (FHF). Based on the literature, a hypothetical model was proposed in which physiologic changes progress sequentially in five phases, as defined by intracranial pressure (ICP) and cerebral blood flow (CBF) measurements. Seventy-six cerebral physiologic profiles were obtained in 26 patients (2 to 5 studies each) within 6 days of FHF diagnosis. ICP was continuously measured by an extradural fiber optic monitor. Global CBF estimates were obtained by xenon clearance techniques. Jugular venous and peripheral artery catheters permitted calculation of cerebral arteriovenous oxygen differences (AVDO2), from which cerebral metabolic rate for oxygen (CMRO2) was derived. A depressed CMRO2 was found in all patients. There was no evidence of cerebral ischemia as indicated by elevated AVDO2s. Instead, over 65% of the patients revealed cerebral hyperemia. Eight of the 26 patients underwent orthotopic liver transplantation-all recovered neurologically, including 6 with elevated ICPs. Of the 18 patients receiving medical treatment only, all 7 with increased ICP died in contrast to 9 survivors whose ICP remained normal (P < 0.004). Hyperemia, per se, was not related to outcome, although it occurred more frequently at the time of ICP elevations. Six patients were studied during brain death. All 6 revealed malignant intracranial hypertension, preceded by hyperemia. In conclusion, the above findings are consistent with the hypothetical model proposed. Prospective longitudinal studies are recommended to determine the precise evolution of the pathophysiologic changes.

Activation-induced resetting of cerebral metabolism and flow is abolished by beta-adrenergic blockade with propranolol.

It has previously been shown that activation will increase cerebral blood flow (CBF) and cerebral glucose uptake (CMR(glc)) in excess of cerebral oxygen uptake (CMRO(2)). Our purpose was to investigate the influence of beta-adrenergic blockade with propranolol on the activation-induced uncoupling of cerebral glucose and oxygen metabolism. Using awake rats, we determined the cerebral arteriovenous differences of oxygen [(a-v)(O2)], glucose [(a-v)(glc)], and lactate [(a-v)(lac)] both under baseline conditions and during activation. The molar ratio between CMRO(2) and CMR(glc), the oxygen-glucose index (OGI), was calculated. Without beta-adrenergic blockade, activation decreased the (a-v)(O2) but not the (a-v)(glc), reducing the OGI from 6.1 during baseline conditions to 4.0 under activation (P<0.01). The (a-v)(O2) decreased, indicating that the ratio CBF/CMRO(2) had increased. Under baseline conditions, a slight flux of lactate from the brain was observed. Activation increased the arterial lactate concentration, and during this condition, the lactate flux from the brain was reversed into a slight lactate uptake. Propranolol administration did not change the behavior of the animals during activation. After administration of propranolol, baseline values were unaffected, but beta-adrenergic blockade totally abolished the activation-induced uncoupling of (a-v)(O2) from (a-v)(glc), because both remained constant with an unchanged OGI. The unchanged (a-v)(O2) indicates that CBF remained unchanged compared with CMRO(2). beta-Adrenergic blockade by propranolol abolishes the activation-induced uncoupling of cerebral oxygen to glucose metabolism and the changes in (a-v)(O2). This may be of most significance to studies of cerebral activation by the blood oxygen level-dependent fMRI method.

Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm.

The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO[2]) and cerebral metabolic rate of oxygen (CMRO[2]). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF calculated from cerebral clearance curves integrated to 15 minutes (mean CBF 32.3 +/- 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean V[MCA] 56.7 +/- 2.9 cm/second), normal hemispheric index ([HI], mean HI 1.67 +/- 0.11), and normal AVDO(2) (mean AVDO[2] 5.4 +/- 0.5 vol%). The CMRO, is approximately 50% of normal (mean CMRO(2) 1.77 +/- 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 +/- 3 ml/100 g/minute), AVDO(2) falls (3.8 +/- 0.1 vol%), V(MCA) rises (86 +/- 3.7 cm/second), and the HI remains less than 3 (2.41 +/- 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 +/- 3.8 ml/100 g/minute), a further increase in V(MCA) (96.7 +/- 6.3 cm/second), and a pronounced rise in the HI (2.87 +/- 0.22). This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

Cerebral arteriovenous oxygen difference: a predictor of cerebral infarction and outcome in patients with severe head injury

Jugular bulb oxygen monitoring can be used to estimate the adequacy of cerebral blood flow to support cerebral metabolism after severe head injury. In the present study, the authors studied the cerebral arteriovenous oxygen difference (AVDO2) before and after treatment in 32 head-injured patients (Glasgow Coma Scale scores ¾ 8) to examine the relationships among AVDO2 and cerebral perfusion pressure (CPP), delayed cerebral infarction, and outcome. Fifteen patients (Group A) underwent craniotomy for hematoma evacuation and 17 (Group B) received mannitol for sustained intracranial hypertension (intracranial pressure &gt; 20 mm Hg, &gt; 10 minutes). Radiographic evidence of delayed cerebral infarction was observed in 14 patients. Overall, 17 patients died or were severely disabled. Cerebral AVDO2 was elevated before craniotomy or mannitol administration; the mean AVDO2 for all patients before treatment was 8.6 ± 1.8 vol%. Following craniotomy or mannitol administration, the AVDO2 decreased in 27 patients and increased in five patients (mean AVDO2 6.2 ± 2.1 vol% in all patients; 6 ± 1.9 vol% in Group A; and 6.4 ± 2.4 vol% in Group B). The mean CPP was 75 ± 9.8 mm Hg and no relationship with AVDO2 was demonstrated. Before treatment, the AVDO2 was not associated with delayed cerebral infarction or outcome. By contrast, a limited improvement in elevated AVDO2 after craniotomy or mannitol administration was significantly associated with delayed cerebral infarction (Group A: p &lt; 0.001; Group B: p &lt; 0.01). Similarly, a limited improvement in elevated AVDO2 after treatment was significantly associated with an unfavorable outcome (Group A: p &lt; 0.01; Group B: p &lt; 0.001). In conclusion, these findings strongly indicate that, despite adequate cerebral perfusion, limited improvement in elevated cerebral AVDO2 after treatment consisting of either craniotomy or mannitol administration may be used to help predict delayed cerebral infarction and poor outcome after traumatic brain injury.

Characterization of cerebral hemodynamic phases following severe head trauma: hypoperfusion, hyperemia, and vasospasm

The extent and timing of posttraumatic cerebral hemodynamic disturbances have significant implications for the monitoring and treatment of patients with head injury. This prospective study of cerebral blood flow (CBF) (measured using 133Xe clearance) and transcranial Doppler (TCD) measurements in 125 patients with severe head trauma has defined three distinct hemodynamic phases during the first 2 weeks after injury. The phases are further characterized by measurements of cerebral arteriovenous oxygen difference (AVDO2) and cerebral metabolic rate of oxygen (CMRO2). Phase I (hypoperfusion phase) occurs on the day of injury (Day 0) and is defined by a low CBF15 calculated from cerebral clearance curves integrated to 15 minutes (mean CBF15 32.3 ± 2 ml/100 g/minute), normal middle cerebral artery (MCA) velocity (mean VMCA 56.7 ± 2.9 cm/second), normal hemispheric index (mean HI 1.67 ± 0.11), and normal AVDO2 (mean AVDO2 5.4 ± 0.5 vol%). The CMRO2 is approximately 50% of normal (mean CMRO2 1.77 ± 0.18 ml/100 g/minute) during this phase and remains depressed during the second and third phases. In Phase II (hyperemia phase, Days 1-3), CBF increases (46.8 ± 3 ml/100 g/minute), AVDO2 falls (3.8 ± 0.1 vol%), VMCA velocity rises (86 ± 3.7 cm/second), and the HI remains less than 3 (2.41 ± 0.1). In Phase III (vasospasm phase, Days 4-15), there is a fall in CBF (35.7 ± 3.8 ml/100 g/minute), a further increase in VMCA (96.7 ± 6.3 cm/second), and a pronounced rise in the HI (2.87 ± 0.22). This is the first study in which CBF, metabolic, and TCD measurements are combined to define the characteristics and time courses of, and to suggest etiological factors for, the distinct cerebral hemodynamic phases that occur after severe craniocerebral trauma. This research is consistent with and builds on the findings of previous investigations and may provide a useful temporal framework for the organization of existing knowledge regarding posttraumatic cerebrovascular and metabolic pathophysiology.

Altered energy metabolism in Alzheimer's disease

To evaluate the energy metabolism in Alzheimer's disease (AD), the cerebral arteriovenous differences of oxygen, glucose, lactate, pyruvate, ketone bodies and free fatty acids, and regional cerebral blood flow (rCBF) were examined in 7 patients with Alzheimer's disease (AD). The ratio of oxygen and glucose molar utilization was significantly elevated to 9.86 in AD, compared with 5.63 for 7 age matched controls. Single-photon emission computed tomography revealed that the patients had significantly decreased rCBF only in the parietotemporal region. The glucose extraction fraction and global cerebral metabolic rate of glucose were significantly decreased, whereas the global cerebral metabolic rate of oxygen was slightly decreased. However, the elevated oxygen/glucose utilization ratio is not due to the oxygenation of ketone bodies or free fatty acids, because the cerebral metabolic rates of these substrates did not alter. We concluded that the marked elevated value of the oxygen/glucose utilization ratio suggests an altered energy metabolism in AD.

Altered energy metabolism in Alzheimer's disease

To evaluate the energy metabolic status of Alzheimer's disease, we examined the cerebral arteriovenous differences of glucose, oxygen, lactate, pyruvate, ketone bodies, and free fatty acids and N-isopropyl-p-(123I) iodoamphetamine (IMP) single-photon emission computed tomography in 5 patients with Alzheimer's disease (4 male and 1 female patients; mean age of 64.80 +/- 8.47 years). Compared with 5 age matched normal control subjects (4 males and 1 female; mean age of 63.20 +/- 10.76 years), the patients showed significantly decreased regional cerebral blood flow only in the parietotemporal region. The global cerebral glucose metabolic rate (CMRGlu) had significantly low value, whereas the global cerebral oxygen metabolic rate (CMRO2) was not changed. The metabolic ratio (CMRO2/CMRGlu) was significantly elevated to 9.73 in the patients with Alzheimer's disease, compared with 5.50 in the normal controls. The cerebral metabolic rates of ketone bodies and free fatty acids were unchanged. The cerebral pyruvate output was significantly decreased. The cerebral lactate output became negative, but the decrease did not reach statistical significance. We concluded that the markedly elevated metabolic ratio suggests an altered energy metabolism in Alzheimer's disease.

Cerebral blood flow, oxygen metabolism and transcranial Doppler sonography during high-volume plasmapheresis in fulminant hepatic failure

The effect of high-volume plasmapheresis on hepatic encephalopathy, cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRO2) was investigated in patients with fulminant hepatic failure (FHF). Twelve consecutive patients (8 women, 4 men, median age 34 years (range 19-51), were studied before and after high-volume plasmapheresis with 10-16 litres fresh frozen plasma, while PaCO2 and body temperature were maintained at 30 (23-34) mmHg and 37.6 degrees C (36.6-38.4), respectively. Blood samples from the internal jugular vein and a radial artery allowed calculation of the cerebral arteriovenous oxygen difference (AVDO2) and oxygen extraction (AVDO2 divided by arterial oxygen content). CBF was determined by a xenon-133 clearance method in eight patients and CMRO2 calculated as AVDO2 times CBF. Cerebral perfusion pressure (CPP) was determined as the difference between mean arterial and subdural pressures in eight patients. High-volume plasmapheresis was initiated 22 (6-168) h after the development of hepatic encephalopathy and 11 patients had grade 4 encephalopathy. Following high-volume plasmapheresis the grade of encephalopathy improved in four patients. The CBF increased from a median of 31 (16-86) to 45 (18-97) ml/100 g/min and as oxygen extraction remained unchanged (32 (9-41) vs. 29 (7-39)%), CMRO2 increased from 1.24 (0.96-1.82) to 1.86 (1.00-2.07) ml/100 g/min (P < 0.05). The CPP increased from 62 (19-76) to 92 (50-105) mmHg (P < 0.01), whereas the intracranial pressure remained unchanged (19 (3-45) vs. 11 (5-33) mmHg). No statistical difference was found between the relative changes in the above parameters in survivors compared to non-survivors. Although the clinical status did not improve in all patients, both CBF and CMRO2 increased after high-volume plasmapheresis. The alleviation of brain oxygen metabolism by high-volume plasmapheresis may reflect partial removal of neuroinhibitory plasma factors.

Effects of intravenous nitroglycerin combined with dopamine on intracranial pressure and cerebral arteriovenous oxygen difference in patients with acute subarachnoid haemorrhage.

The effects of intravenous nitroglycerin (NTG) combined with dopamine on intracranial pressure (ICP) and cerebral arteriovenous oxygen difference (AVDO2) were studied in 11 patients with acute subarachnoid haemorrhage (SAH). The study was performed on Days 1 to 3 of SAH after aneurysmal clipping. Treatment consisted of an intravenous drip infusion of NTG in increasing incremental doses of 0.5, 1.0, 1.5, 2.0, and 2.5 micrograms/kg/min at one-hour intervals. Dopamine (5 to 10 micrograms/kg/min) was also given concurrently to maintain systemic blood pressure. ICP values before NTG administration ranged from 7 to 24 mmHg (mean. 11.91 +/- 5.30 mmHg). ICP began to increase immediately after the administration of NTG 0.5 microgram/kg/min and peaked at 14.64 +/- 5.93 mmHg 10 minutes after onset of infusion. Thereafter, ICP gradually returned to pretreatment levels. Increasing the dose of NTG failed to induce further significant rises in ICP. Mean AVDO2 before NTG administration was 4.69 +/- 0.62 ml/dl. This parameter showed no significant change during NTG infusion, although cerebral perfusion pressure decreased to between 75% to 94% of the control value after NTG administration. These results indicate that continuous NTG infusion combined with dopamine does not have adverse effects on ICP (the ICP increase is minimal and transient) and may even have beneficial effects on CBF in patients with acute SAH.

Transcranial Doppler is valid for determination of the lower limit of cerebral blood flow autoregulation.

This study validates transcranial Doppler sonography (TCD) for determination of the lower limit of cerebral blood flow (CBF) autoregulation and establishes a relation between global CBF and mean flow velocity (Vmean) in the middle cerebral artery. Relative changes in CBF and in Vmean were compared in 12 normal volunteers (2 women and 10 men; median age, 30 years [range, 21 to 61 years]). Catheters was placed in the left radial artery and in the bulb of the right internal jugular vein, respectively. Baseline CBF was measured by single-photon emission computed tomography scanning; concomitantly, blood samples were drawn for calculation of the cerebral arteriovenous oxygen difference. Then changes in mean arterial pressure (MAP) were induced, and relative changes in global CBF were calculated according to Fick's principle assuming a constant cerebral oxygen metabolism. MAP was increased 30 mm Hg by norepinephrine infusion and was decreased by lower body negative pressure. Vmean was measured in the right middle cerebral artery by a 2-MHz probe, and blood samples were drawn at intervals of 5 mm Hg. MAP values between 122 (range, 110 to 140) and 48 (range, 34 to 75) mm Hg were measured. The lower limit of autoregulation (the blood pressure under which autoregulation is off) as determined by Vmean did not differ significantly from that determined by relative changes in global CBF: 91 (range, 41 to 108) and 79 (range, 53 to 113) mm Hg, respectively. A significant correlation between Vmean and relative changes in global CBF was demonstrated below the lower limit of autoregulation (R2 = .73, P < .001; CBF = -6.3 + 1.0.Vmean). Above the lower limit both values were stable. TCD is valid for determination of the lower limit of CBF autoregulation, and changes in CBF may be reliably evaluated by TCD during changes in cerebral perfusion pressure in normal subjects.

Cerebral Arteriovenous Oxygen and Acid-Base Differences during Callosotomy in Pediatrics

Cerebral Arteriovenous Oxygen and Acid-Base Differences during Callosotomy in Pediatrics

Cerebral Arteriovenous Oxygen Difference and Lactate-Oxygen Index: A Case of Bilateral Monitoring

We report a case of ruptured cerebral aneurysm that had uneven bilateral cerebral arteriovenous oxygen differences and lactate oxygen indexes. Guidelines are offered for determining which side to choose for jugular bulb catheterization. We conclude that bilateral catheterization may be useful in patients with severe hemispheric damage.

Changes in Cerebral Blood Flow and Metabolism Related to the Presence of Subdural Hematoma

Acute subdural hematoma (SDH) remains an important factor in head injury. The early effects of SDH on cerebral blood flow (CBF) and cerebral metabolic rate of oxygen consumption (CMRO2) in humans have not been clearly demonstrated. Patients admitted to the Medical College of Virginia with severe closed-head injury between 1982 and 1990 were studied with Xenon-133 regional CBF measurement. Data were reviewed retrospectively with regard to the presence of SDH (n = 54). A comparison group consisted of patients with head injuries without mass lesions or midline shift on admission computed tomographic scans (n = 76). CBF measurements made in patients less than 16 years of age, with concurrent administrations of mannitol or vasopressors, or with cerebral perfusion pressure under 50 mm Hg were excluded. CBF measurements were made on multiple occasions during the first 6 days after injury, and in many instances, simultaneous determinations of cerebral arteriovenous oxygen difference (AVDO2) were made through sampling of jugular bulb and arterial oxygen content. Not all patients underwent CBF measurements on each day. Differences in mean CBF, CMRO2, and AVDO2 were evaluated on each day after injury with the application of Student's t-test for independent groups. Significant reductions in CBF were demonstrated in patients with SDH on Days 1 (P < 0.0005) and 2 (P < 0.01). CMRO2 differed notably on Days 1 (P < 0.005) and 2 (P < 0.05) in patients with SDH, but when corrected for the lower Glasgow Coma Score in patients with SDH, the P values were only 0.07 and 0.12, respectively (analysis of covariance).(ABSTRACT TRUNCATED AT 250 WORDS)

Cerebral blood flow, arteriovenous oxygen difference, and outcome in head injured patients.

Cerebral blood flow (CBF) and other physiological variables were measured repeatedly for up to 10 days after severe head injury in 102 patients, and CBF levels were related to outcome. Twenty five of the patients had a reduced CBF [mean (SD) 0.29 (0.05) ml/g/min]; 47 had a normal CBF, (0.41 (0.10) ml/g/min); and 30 had a raised CBF (0.62 (0.14) ml/g/min). Cerebral arteriovenous oxygen differences were inversely related to CBF and averaged 2.1 (0.7) mumol/ml in the group with reduced CBF, 1.9 (0.5) mumol/ml in the group with normal CBF, and 1.6 (0.4) mumol/ml in the group with raised CBF. Patients with a reduced CBF had a poorer outcome than patients with a normal or raised CBF. Mortality was highest in patients with a reduced CBF, and was 32% at three months after injury, whereas only 21% of the patients with a normal CBF and 20% of the patients with a raised CBF died. There were no differences in the type of injury, initial score on the Glasgow Coma Scale, mean intracranial pressure (ICP), highest ICP, or the amount of medical treatment required to keep the ICP less than 20 mm Hg in each group. Systemic factors did not significantly contribute to the differences in CBF among the three groups. A logistic regression model of the effect of CBF on neurological outcome was developed. When adjusted for variables which were found to be significant confounders, including age, initial Glasgow Coma Score, haemoglobin concentration, cerebral perfusion pressure and cerebral metabolic rate of oxygen, a reduced CBF remained significantly associated with an unfavourable neurological outcome.