Cerebral Oxygenation In Patients Research Articles

Increased Oxygen Administration Improves Cerebral Oxygenation in Patients Undergoing Awake Carotid Surgery

Increased Oxygen Administration Improves Cerebral Oxygenation in Patients Undergoing Awake Carotid Surgery

Effect of mannitol and hypertonic saline on cerebral oxygenation in patients with severe traumatic brain injury and refractory intracranial hypertension

Background:The impact of osmotic therapies on brain oxygen has not been extensively studied in humans. We examined the effects on brain tissue oxygen tension (PbtO2) of mannitol and hypertonic saline...

Increased Oxygen Administration Improves Cerebral Oxygenation in Patients Undergoing Awake Carotid Surgery

During regional anesthesia for carotid endarterectomy (CEA), 10% to 15% of patients develop signs of cerebral hypoxia after cross-clamping, manifested as changes in speech, cerebration or contralateral motor power. Reversal of such neurological deficits using administration of 100% O2 has been described. We used near-infrared cerebral oximetry to assess whether 100% O2 reliably improves regional cerebral oxygenation (rSO2) during carotid cross-clamping. Sixteen patients undergoing awake CEA were studied. Bilateral rSO2 optodes were applied before the initiation of sedation and the conduct of the regional blockade. Patients received 28% oxygen by Venturi facemask. Perioperative blood pressure was maintained at or within 10% above the patient's normal limits during carotid cross-clamping. After cross-clamping, 100% O2 was administered for 5 min by a close-fitting anesthetic facemask. The O2 mask was then removed and the patient breathed room air. The effects on rSO2 readings and arterial blood gases were observed after each intervention. Data were analyzed for 15 patients. Ipsilateral rSO2 values decreased by 7.4% +/- 5% after carotid cross-clamping. Administration of 100% O2 resulted in an increase in ipsilateral rSO2 in all patients of 6.9% +/- 3.3% (range, 1%-12%) (paired t-test, P < 0.001) over the cross-clamped value while receiving 28% O2. Hemodynamic variables and arterial PaCO2 values were unaltered. With the carotid cross-clamped, ipsilateral rSO2 was reliably increased by the administration of 100% O(2) compared with 28% O2. The etiology of this increase is unclear, but may relate to the associated increase in O2 content of the blood or to an improvement in cerebral blood flow. Thus administration of 100% O2 during carotid cross-clamping may be beneficial for all patients undergoing CEA.

Impact of age of transfused blood on cerebral oxygenation in male patients with severe traumatic brain injury*

Prolonged erythrocyte storage time might reduce the efficacy of transfusion. In this study, the effects of transfusion of erythrocytes with four different storage periods (<10 days, n = 18; 10-14 days, n = 15; 15-19 days, n = 17; and >19 days, n = 16 patients) on brain tissue oxygen tension (PtiO2) in stable male patients with severe traumatic brain injury were investigated during a 24-hr follow-up period. Prospective, observational study. Neurotrauma critical care unit of a university hospital. Sixty-six male, nonbleeding, hemodynamically stable anemic patients (hemoglobin <95 g/L) with Glasgow Coma Scale score <9. None. PtiO2, cerebral perfusion pressure, mean arterial pressure, intracranial pressure, peripheral oxygen saturation, CO2 pressure at the end of expiration, and intracerebral temperature were recorded in all patients at baseline, immediately after the completion of transfusion, and 1, 2, 3, 4, 5, 6, 12, and 24 hrs posttransfusion. All four groups were homogeneous with respect to multiple baseline variables, except for storage time of transfused erythrocytes (p < .0001). There was a significant short-lasting (3-4 hrs) increase in PtiO2 values after transfusion of erythrocytes stored for <10 days, 10-14 days, or 15-19 days, compared with those at baseline. In contrast, no significant changes in PtiO2 were observed after transfusion of erythrocytes stored >19 days. Transfusion of erythrocytes increased cerebral oxygenation in patients with severe traumatic brain injury, except in those transfused with erythrocytes stored >19 days.

Effects of 15% Mannitol, 10% NaCl and HyperHAES on the ICP, oxygen delivery and cerebral oxygenation in patients with the intracranial haemorrhage

Effects of 15% Mannitol, 10% NaCl and HyperHAES on the ICP, oxygen delivery and cerebral oxygenation in patients with the intracranial haemorrhage

Influence of Cerebrovascular Arteriosclerosis on Cerebral Oxygenation During Exercise

Although it is assumed that cerebral oxygenation during exercise is influenced by both cardiopulmonary function and cerebrovascular arteriosclerosis, the latter factor has not been fully clarified. In the present study the relationship between the degree of cerebrovascular arteriosclerosis and cerebral oxygenation during exercise was investigated. A total of 109 patients (69 patients with coronary artery disease, 40 patients with hypertensive heart disease) (61.7+/-9.7 years) performed a symptom-limited exercise test with respiratory gas measurements (CPX). From the respiratory gas analysis, peak O(2) uptake (VO(2)), the slope of the increase in VO(2) to the increase in work rate (DeltaVO (2)/DeltaWR), and the slope of the increase in ventilation to the increase in CO(2) output (VE/VCO(2) slope) were calculated. Oxyhemoglobin (O(2)Hb) at the forehead was monitored using near-infrared spectroscopy. The brain ischemic score was counted based upon fluid-attenuated inversion recovery images of magnetic resonance imaging and expressed from 0 to 4. When compared with patients with a lower ischemic score (<2, n=67), those with a higher ischemic score (> or =2, n=42) had a lower increase in brain O(2)Hb during exercise (-1.08 +/-2.7 vs 0.77+/-4.1 micromol/L, p=0.011). Of brain ischemic score, left ventricular ejection fraction, peak VO(2), DeltaVO(2)/DeltaWR, and the VE/VCO(2) slope, DeltaVO(2)/ DeltaWR was found to be the sole independent index determining cerebral O(2)Hb during exercise. The CPX parameters were also significantly related to the degree of cerebrovascular arteriosclerosis. Although cerebral oxygenation during exercise is mainly related to cardiopulmonary function, the degree of cerebrovascular arteriosclerosis partly influences cerebral oxygenation in patients with risk factors for atherosclerosis.

Transfusion of erythrocyte concentrates produces a variable increment on cerebral oxygenation in patients with severe traumatic brain injury

To investigate the long-term influence of erythrocyte transfusion on cerebral oxygenation in patients with severe traumatic brain injury. Prospective and observational study. Neurotrauma intensive care unit of trauma center level I. Sixty consecutive, hemodynamically stable patients with severe traumatic brain injury, pretransfusion hemoglobin<100g/l, non-bleeding and monitored through intracranial pressure and brain tissue partial pressure of oxygen (PtiO(2)) catheters were included. Transfusion of 1-2 units of red blood cells. Ten sets of variables (pretransfusion, end of transfusion, and 1, 2, 3, 4, 5, 6, 12 and 24h after transfusion) were recorded, including: PtiO(2), cerebral perfusion pressure (CPP), end-tidal CO(2), peripheral saturation of oxygen, temperature, hemoglobin, lactate and PaO(2)/FiO(2) ratio. Transfusion was associated with an increase in PtiO(2) during a 6-h period, with a peak at 3h (26.2%; p=0.0001) in 78.3% of the patients. No relationship was observed between PtiO(2), CPP and hemoglobin increments. The relative increment in PtiO(2) at hour 3 was only correlated with baseline PtiO(2) (r(2) 0.166; p=0.001). All of the patients with basal PtiO(2)<15mmHg showed an increment in PtiO(2) versus 74.5% of patients with basal PtiO(2)>or=15mmHg (p<0.01, hour 3). Erythrocyte transfusion is associated with a variable and prolonged increment of cerebral tissue oxygenation in anemic patients with severe traumatic brain injury. Low baseline PtiO(2) levels (<15mmHg) could define those patients who benefit the most from erythrocyte transfusion.

Characterization of Cerebral Oxygenation in Patients with Traumatic Brain Injury before and after Brain Tissue Oxygen-guided Therapy

Characterization of Cerebral Oxygenation in Patients with Traumatic Brain Injury before and after Brain Tissue Oxygen-guided Therapy

Characterization of Cerebral Oxygenation in Patients with Traumatic Brain Injury before and after Brain Tissue Oxygen-guided Therapy

Characterization of Cerebral Oxygenation in Patients with Traumatic Brain Injury before and after Brain Tissue Oxygen-guided Therapy

Relative importance of hypertension compared with hypervolemia for increasing cerebral oxygenation in patients with cerebral vasospasm after subarachnoid hemorrhage

Hypervolemia and hypertension therapy is routinely used for prophylaxis and treatment of symptomatic cerebral vasospasm at many institutions. Nevertheless, there is an ongoing debate about the preferred modality (hypervolemia, hypertension, or both), the degree of therapy (moderate or aggressive), and the risk or benefit of hypervolemia, moderate hypertension, and aggressive hypertension in patients following subarachnoid hemorrhage. Monitoring data and patient charts for 45 patients were retrospectively searched to identify periods of hypervolemia, moderate hypertension, or aggressive hypertension. Measurements of central venous pressure, fluid input, urine output, arterial blood pressure, intracranial pressure, and oxygen partial pressure (PO2) in the brain tissue were extracted from periods ranging from 1 hour to 24 hours. For these periods, the change in brain tissue PO2 and the incidence of complications were analyzed. During the 55 periods of moderate hypertension, an increase in brain tissue PO2 was found in 50 cases (90%), with complications occurring in three patients (8%). During the 25 periods of hypervolemia, an increase in brain oxygenation was found during three intervals (12%), with complications occurring in nine patients (53%). During the 10 periods of aggressive hypervolemic hypertension, an increase in brain oxygenation was found during six of the intervals (60%), with complications in five patients (50%). When hypervolemia treatment is applied as in this study, it may be associated with increased risks. Note, however, that further studies are needed to determine the role of this therapeutic modality in the care of patients with cerebral vasospasm. In poor-grade patients, moderate hypertension (cerebral perfusion pressure 80-120 mm Hg) in a normovolemic, hemodiluted patient is an effective method of improving cerebral oxygenation and is associated with a lower complication rate compared with hypervolemia or aggressive hypertension therapy.

Effects of hydroxyurea treatment on cerebral oxygenation in adult patients with sickle cell disease: an open-label pilot study

In patients with sickle cell disease (SCD), cerebral oxygen saturation (rSO(2)) has been reported to be below normal and to increase after red blood cell transfusion. This study was designed to determine the effects of long-term and short-term hydroxyurea (HU) treatment on cerebral oxygenation in patients with SCD. This open-label pilot study was conducted at the Department of Anesthesiology and the Center for Sickle Cell Disease, College of Medicine, Howard University, Washington, DC. Adult African American outpatients with SCD and hemoglobin (Hb) genotype HbSS (homozygous sickle Hb) who were receiving long-term (>6 months) HU treatment (15-30 mg/kg . d PO) or who had never received this treatment (control group) were enrolled. Patients in the treated and control groups were matched for age, sex, race, and Hb genotype. Cerebral oximetry (near-infrared spectroscopy) was performed to determine rSO(2) index. In a separate analysis to determine the effects of short-term HU treatment on cerebral oxygenation, hospitalized patients with SCD and vaso-occlusive crisis (VOC)receiving long-term therapy with HU were enrolled. We performed cerebral and pulse (fingernail) oximetry to determine rSO (2)index and arterial oxygen saturation (SpO(2)) after the administration of a single oral dose of HU (500-mg tablet) alone and again after dosing concomitantly with inhaled oxygen. The study enrolled 11 patients in the HU group (6 women, 5 men; mean [SD] age, 37 [8] years) and 20 controls (8 women, 12 men; mean [SD] age, 35 [6] years). Mean (SD) rSO(2) index was significantly increased (but still low) in patients receiving long-term HU treatment compared with controls (46.1% [6.6%] vs 41.2% [7.6%]; P< 0.025). Hb concentration (9.6 [1.4] g/dL vs 8.5 [1.2] g/dL; P< 0.027), hematocrit (28% [3%] vs 24% [4%]; P < 0.028), and mean corpuscular volume (102% [7%] vs 89% [8%]; P < 0.027) also were significantly higher in the HU group compared with controls. In 8 patients with SCD and VOC (6 men, 2 women; mean [SD] age, 28 [5] years), single-dose HU, either alone or in combination with inhaled oxygen, did not significantly affect cerebral oxygenation, and SpO(2) failed to correlate with rSO(2) index in these patients. The results of this open-label pilot study in patients with SCD suggest that the low cerebral oxygenation in these patients is significantly improved but not normalized with long-term HU treatment. A single dose of HU, either alone or in combination with inhaled oxygen, did not appear to influence cerebral oxygenation in patients with VOC.

Effects of furosemide versus captopril on postprandial and orthostatic blood pressure and on cerebral oxygenation in patients ≥70 years of age with heart failure

Elderly patients with heart failure are at risk of postprandial hypotension (PPH), orthostatic hypotension (OH), and concomitant cerebral oxygenation changes because of altered cardiovascular balance and the use of cardiovascular medications, such as furosemide and captopril. In 24 patients with heart failure (New York Heart Association class II to III, in stable condition, and receiving cardiovascular medication [aged 70 to 83 years]), blood pressure (BP) was measured by Finapres, and cortical concentrations of oxyhemoglobin and deoxyhemoglobin were measured using near-infrared spectroscopy during standing and after a 292-kcal carbohydrate meal. Tests were performed before and during therapy with furosemide 40 mg once daily (n = 11) or captopril 6.25 and 12.5 mg twice daily (n = 13) in a double-blind randomized trial. Before treatment, 13 of 24 patients had PPH, and 2 of 24 patients had OH. The first dose of furosemide significantly decreased postprandial systolic BP (p <0.05) and postprandial frontal cortical oxygenation (p <0.05), whereas the first dose of captopril did not. Furosemide and captopril did not significantly affect postprandial or orthostatic BP or cortical oxygenation after 2 weeks of treatment. Thus, PPH is a common phenomenon in elderly patients with heart failure, whereas OH is not. The first dose of furosemide 40 mg decreased postprandial systolic BP and frontal cortical oxygenation, in contrast with the first dose of captopril 6.25 mg and 2-week treatment with furosemide 40 mg once daily or captopril 12.5 mg twice daily. These findings indicate that initiating furosemide treatment worsens PPH, and furosemide is less safe in elderly patients with heart failure.

Effect of endotracheal suctioning on cerebral oxygenation in traumatic brain-injured patients.

In patients with severe head injuries, brain damage occurs not only from the primary trauma but also secondarily from a reduction in cerebral oxygenation as a result of brain swelling, ischemia, and elevated intracranial pressure (ICP). However, routine interventions designed to maintain oxygenation, such as endotracheal suctioning (ETS), also may negatively affect the cerebrovascular status by increasing the ICP. The purpose of this study was to determine whether ETS influences cerebral oxygenation in patients with traumatic brain injury. Descriptive, prospective, with repeated assessments within each patient. Ten-bed trauma intensive care unit in a university Level I trauma center. Nineteen patients who were 16 yrs or older, had acute head injury, a Glasgow Coma Scale score < or =8; external ventricular drain and arterial pressure devices in place, and were intubated and mechanically ventilated. ETS protocol consisting of administration of four ventilator-delivered breaths at 135% of the patients' actual tidal volume, 100% F(IO)2, before and after suctioning with a standardized catheter at a 16-L flow rate. This study examined cerebrovascular responses as measured by the traditional measures of ICP and cerebral perfusion pressure, as well as middle cerebral artery velocity and jugular venous oxygen tension that occurred during ETS in head-injured adults. The results of this study show that both ICP and cerebral perfusion pressure are increased during ETS. In the majority of patients (84%), the ICP returned to baseline values within 2 mins. The increase in jugular venous oxygen tension associated with increases in middle cerebral artery velocity and mean arterial pressure suggests that cerebral oxygen delivery was maintained during ETS. Cerebral changes associated with ETS using the described protocol are consistent with the preservation of cerebral oxygenation.

Cerebral oxygenation in patients after severe head injury: monitoring and effects of arterial hyperoxia on cerebral blood flow, metabolism and intracranial pressure.

Early impaired cerebral blood flow (CBF) after severe head injury (SHI) leads to poor brain tissue oxygen delivery and lactate accumulation. The purpose of this investigation was to elucidate the relationship between CBF, local dialysate lactate (lact(md)) and dialysate glucose (gluc(md)), and brain tissue oxygen levels (PtiO2) under arterial normoxia. The effect of increased brain tissue oxygenation due to high fractions of inspired oxygen (FiO2) on lact(md) and CBF was explored. A total of 47 patients with SHI were enrolled in this studies (Glasgow Coma Score [GCS] < 8). CBF was first assessed in 40 patients at one time point in the first 96 hours (27 +/- 28 hours) after SHI using stable xenon computed tomography (Xe-CT) (30% inspired xenon [FiXe] and 35% FiO2). In a second study, sequential double CBF measurements were performed in 7 patients with 35% FiO2 and 60% FiO2, respectively, with an interval of 30 minutes. In a subsequent study, 14 patients underwent normobaric hyperoxia by increasing FiO2 from 35 +/- 5% to 60% and then 100% over a period of 6 hours. This was done to test the effect of normobaric hyperoxia on lact(md) and brain gluc(md), as measured by local microdialysis. Changes in PtiO2 in response to changes in FiO2 were analyzed by calculating the oxygen reactivity. Oxygen reactivity was then related to the 3-month outcome data. The levels of lact(md) and gluc(md) under hyperoxia were compared with the baseline levels, measured at 35% FiO2. Under normoxic conditions, there was a significant correlation between CBF and PtiO2 (R = 0.7; P < .001). In the sequential double CBF study, however, FiO2 was inversely correlated with CBF (P < .05). In the 14 patients undergoing the 6-hour 100% FiO2 challenge, the mean PtiO2 levels increased to 353 (87% compared with baseline), although the mean lact(md) levels decreased by 38 +/- 16% (P < .05). The PtiO2 response to 100% FiO2 (oxygen reactivity) was inversely correlated with outcome (P < .01). Monitoring PtiO2 after SHI provides valuable information about cerebral oxygenation and substrate delivery. Increasing arterial oxygen tension (PaO2) effectively increased PtiO2, and brain lact(md) was reduced by the same maneuver.

Monitoring of cerebral oxygenation in patients with severe head injuries: brain tissue PO2 versus jugular vein oxygen saturation.

Monitoring of cerebral oxygenation is considered to be of great importance in minimizing secondary hypoxic and ischemic brain damage following severe head injury. Although the threshold for cerebral hypoxia in jugular bulb oximetry (measurement of O2 saturation in the jugular vein (SjvO2)) is generally accepted to be 50% oxygen saturation, a comparable value in brain tissue PO2 (PtiO2) monitoring, a new method for direct assessment of PO2 in the cerebral white matter, has not yet been established. Hence, the purpose of this study was to compare brain PtiO2 with SjvO2 in severely head injured patients during phases of reduced cerebral perfusion pressure (CPP) to define a threshold in brain PtiO2 monitoring. In addition, the safety and data quality of both SjvO2 and brain PtiO2 monitoring were studied. In 15 patients with severe head injuries, SjvO2 and brain PtiO2 were monitored simultaneously. For brain PtiO2 monitoring a polarographic microcatheter was inserted in the frontal cerebral white matter, whereas for SjvO2 measurements were obtained by using a fiberoptic catheter placed in the jugular bulb. Intracranial pressure was monitored by means of an intraparenchymal catheter. Mean arterial blood pressure, CPP, end-tidal CO2, and arterial oxygen saturation (pulse oximetry) were continuously recorded. All data were simultaneously stored and analyzed using a multimodal computer system. For specific analysis, phases of marked deterioration in systemic blood pressure and consecutive reductions in CPP were investigated. There were no complications that could be attributed to the PtiO2 catheters, that is, no intracranial bleeding or infection. The "time of good data quality" was 95% in brain PtiO2 compared to 43% in SjvO2; PtiO2 monitoring could be performed twice as long as SjvO2 monitoring. During marked decreases in CPP, SjvO2 and brain PtiO2 correlated closely. A significant second-order regression curve of SjvO2 versus brain PtiO2 (p < 0.01) was plotted. At a threshold of 50% in SjvO2, brain PtiO2 was found to be within the range of 3 to 12 mm Hg, with a regression curve "best fit" value of 8.5 mm Hg. There was a close correlation between CPP and oxygenation parameters (PtiO2 and SjvO2) when CPP fell below a breakpoint of 60 mm Hg, suggesting intact cerebral autoregulation in most patients. This study demonstrates that monitoring brain PtiO2 is a safe, reliable, and sensitive diagnostic method to follow cerebral oxygenation. In comparison to SjvO2, PtiO2 is more suitable for long-term monitoring. It can be used to minimize episodes of secondary cerebral maloxygenation after severe head injury and may, hopefully, improve the outcome in severely head injured patients.

Cerebral oxygenation monitoring by near-infrared spectroscopy is not clinically useful in patients with severe closed-head injury

To compare continuous jugular venous bulb oximetry and cerebral near-infrared spectroscopy in patients with severe closed head injury. A prospective observational study. Intensive care unit of a major teaching hospital. Adults (n = 10) with severe closed-head injury (Glasgow Coma Scale score of < or = 8). None. Jugular venous bulb oximetry, cerebral near-infrared spectroscopy, and cerebral perfusion pressure were measured continuously. A total of 3,691 paired measurements of near-infrared spectroscopy and jugular venous bulb oximetry were analyzed. Poor correlation (r2 = .04) between paired measurements and wide limits of agreement (-13% to +21%) were demonstrated. The mean difference between measurements was +/- 4% and the standard deviation of the mean difference was +/- 8.69%. The data were subsequently grouped according to three clinically significant subgroups of jugular venous bulb oxygen saturation reflecting low ( < 55%), normal (55% to 75%) and high ( > 75%) saturation values. Poor correlation and wide limits of agreement between the two methods of measurement were observed in all groups. Values recorded by near-infrared spectroscopy did not significantly change between the groups, and 14 clinically significant episodes of jugular venous bulb desaturation were not detected by near-infrared spectroscopy. Tissue oxygen saturation determined by near-infrared spectroscopy does not reflect significant changes in cerebral oxygenation detected by the global measurement of jugular venous bulb oximetry. This finding may be explained by inadequate signal detection and inaccuracies in the algorithm used to filter out extracranial components. Until these technical difficulties are addressed, near-infrared spectroscopy, as measured by the machine assessed in this study, cannot be routinely recommended for assessment of cerebral oxygenation in patients with acute head injury.

Cerebral blood flow and oxygen consumption in man.

Cerebral blood flow and oxygen consumption in man.