Arterio-jugular Oxygen Content Difference Research Articles

Cerebral Oxygenation and Metabolism in Patients Undergoing Clipping of Cerebral Aneurysm: A Comparative Study between Propofol-based total intravenous anesthesia and Sevoflurane-based inhalational anesthesia.

ABSTRACT Background: Sevoflurane unfortunately increases the cranial blood flow, blood volume, and pressure changes cope with cerebral aneurysmal neuroanesthesia goals. Propofol decreases the brain metabolism, blood flow, preserve cerebral reactivity to carbon dioxide, creates neuroprotective effect during cerebral ischemia. Hypothesis: Propofol-based total intravenous anesthesia would be more appropriate than sevoflurane-based inhalational technique during surgical clipping of cerebral aneurysm. Methods: A prospective, randomized, comparative study on 50 patients subjected for elective clipping of cerebral aneurysm, randomly allocated into two equal groups of 25 patients each: propofol-dormicum total intravenous only group and sevoflurane based inhalational group. Results: Jugular oxygen saturation (primary outcome), cerebral blood flow equivalent, heart rate, mean arterial blood pressure, and end tidal carbon dioxide tension were statistically significantly decreased in propofol group compared to sevoflurane group at basal, just after dura opening, at 1,2,3 hours later, and after scalp closure. Arterio-Jugular oxygen content difference, cerebral extraction ratio of O2, estimated cerebral metabolic rate for O2, serum lactate (mg/dl) showed significant increase in propofol group compared to sevoflurane group at basal, 1, 2, 3 h, and after scalp closure. Duration of surgery, time of recovery, blood loss, blood transfusion, intraoperative complications, urine output, total midazolam consumption, surgeon satisfaction, intensive care unit stay time, and Ramsay sedation scale difference was not significant in between both studied groups during the early postoperative period. Conclusion: Propofol based total intravenous anesthesia has better cerebral oxygenation and neuro anesthesia profile compared to sevoflurane-based inhalational anesthesia during cerebral aneurysm clipping surgery with systemic hemodynamic stability.

Impact of pyrexia on neurochemistry and cerebral oxygenation after acute brain injury

Background: Postischaemic pyrexia exacerbates neuronal damage. Hyperthermia related cerebral changes have still not been well investigated in humans. Objective: To study how pyrexia affects neurochemistry and cerebral oxygenation after acute...

Assessment of Cerebrovascular Autoregulation in Head-Injured Patients

Cerebrovascular autoregulation is frequently measured in head-injured patients. We attempted to validate 4 bedside methods used for assessment of autoregulation. PET was performed at a cerebral perfusion pressure (CPP) of 70 and 90 mm Hg in 20 patients. Cerebral blood flow (CBF) and cerebral metabolic rate for oxygen (CMRo2) were determined at each CPP level. Patients were sedated with propofol and fentanyl. Norepinephrine was used to control CPP. During PET scanning, transcranial Doppler (TCD) flow velocity in the middle cerebral artery was monitored, and the arterio-jugular oxygen content difference (AJDo2) was measured at each CPP. Autoregulation was determined as the static rate of autoregulation based on PET (SROR(PET)) and TCD (SROR(TCD)) data, based on changes in AJDo2, and with 2 indexes based on the relationship between slow waves of CPP and flow velocity (mean velocity index, Mx) and between arterial blood pressure and intracranial pressure (pressure reactivity index, PRx) We found significant correlations between SROR(PET) and SROR(TCD) (r2=0.32; P<0.01) and between SROR(PET) and PRx (r2=0.31; P<0.05). There were no significant associations between PET data and autoregulation as assessed by changes in AJDo2. Global CMRo2 was significantly lower at the higher CPP (P<0.01). Despite some variability, SROR(TCD) and PRx may provide useful approximations of autoregulation in head-injured patients. At least with our methods, CMRo2 changes with the increase in CPP; hence, flow-metabolism coupling may affect the results of autoregulation testing.

Cerebral CO2 Vasoreactivity Evaluation With and Without Changes in Intrathoracic Pressure in Comatose Patients

It is well established that cerebral blood flow (CBF) is sensitive to variations in arterial PCO2 (PaCO2) and can be influenced by changes in jugular venous return due to elevated intrathoracic pressure. Therefore, we compared cerebral CO2 vasoreactivity when PaCO2 was altered either by changing inspired PCO2 or tidal volume. In addition, we sought to determine if noninvasive transcranial Doppler ultrasonography can be used instead of invasive CBF measurement to determine cerebral CO2 vasoreactivity. In 36 mechanically ventilated patients in coma due to acute brain lesion, we evaluated CBF by continuous jugular thermodilution, middle cerebral artery flow velocity (Vm) by transcranial Doppler ultrasonography, intracranial pressure (ICP; in only 23 of them) by intraventricular catheter, systemic and pulmonary hemodynamic variables, and arterial and jugular bulb blood gases. Measurements were taken at four levels of PaCO2 (25, 30, 35, and 40 mmHg) by modifying in a random order either tidal volume or inspired PCO2. Cerebral, pulmonary, and systemic hemodynamic changes were similar in magnitude during both methods of altering PaCO2. From the highest to the lowest PaCO2, CBF decreased from 61+/-7 to 36+/-4 ml/min/100 g (p < 0.001, mean +/- SE), Vm from 89+/-7 to 65+/-5 cm/s (p < 0.001), and ICP from 29+/-2 to 12+/-2 mmHg (p < 0.001), but cerebral perfusion pressure remained constant, ranging from 65+/-3 to 67+/-4 mmHg (p = NS). Arteriojugular oxygen content difference increased from 3.2+/-0.2 to 5.7+/-0.4 ml/dl (p < 0.001). Eleven of the 20 patients with a preserved CBF response to CO2 survived to 6 months, whereas only two of the 16 patients with an altered response were alive at 6 months (p < 0.05). When compared with CBF by jugular thermodilution, the rates of sensitivity and specificity of transcranial Doppler ultrasonography to detect impaired cerebral CO2 vasoreactivity were 69% and 65%, respectively. In conclusion, the reduction of PaCO2 from 40 to 25 mmHg by modifying either tidal volume or inspired PCO2 resulted in similar effects on cerebral, pulmonary, and systemic circulations. Cerebral CO2 vasoreactivity is of prognostic value in brain-injured patients when determined using CBF but may be misleading when evaluated using velocities measured by transcranial Doppler ultrasonography.

Cerebrospinal fluid and plasma nitrite and nitrate concentrations after head injury in humans

To measure cerebrospinal fluid and plasma nitrite and nitrate concentrations as indicators of nitric oxide production in adults after severe closed-head injury. To determine if there is an association between cerebrospinal fluid and plasma nitrite and nitrate concentrations, and cerebral blood flow, arterio-jugular oxygen content difference, injury severity, and outcome after severe closed-head injury. A prospective, clinical study. Multidisciplinary intensive care unit. Fifteen comatose (Glasgow Coma Scale score of < or = 7) adult patients with severe closed-head injury were studied during the prospective, randomized evaluation of the effect of moderate hypothermia (32 degrees C for 24 hrs) on neurologic outcome after closed-head injury. Seven patients were in the hypothermic group and eight patients were in the normothermic treatment group. None. Patients were examined sequentially, every 12 hrs for 2 days. Intraventricular cerebrospinal fluid was assayed for nitrite and nitrate concentrations. Cerebral blood flow was measured by the 133xenon intravenous method. Simultaneous blood samples were obtained for measurements of arterio-jugular oxygen content difference and plasma nitrite and nitrate concentrations. Cerebral metabolic rate for oxygen was calculated. Cerebrospinal fluid nitrite and nitrate concentrations were highest at 30 to 42 hrs vs. 6 to 18, 18 to 30, and 42 to 54 hrs (26.4 +/- 3.3 vs. 17.3 +/- 2.1, 20.0 +/- 2.2, and 18.8 +/- 2.4 microM, respectively, p < .05). There was no difference over time in plasma nitrite and nitrate concentrations. Cerebral blood flow was increased and arterio-jugular oxygen content difference was reduced at 18 to 30, 30 to 42, and 42 to 54 hrs vs. 6 to 18 hrs (p < .05). At 30 to 42 hrs, cerebrospinal fluid nitrite and nitrate concentrations were 80% higher in patients who died vs. survivors (36.4 +/- 3.2 vs. 20.2 +/- 3.6, p < .05). Using a generalized, multivariate, linear regression model, both plasma nitrite and nitrate concentrations and injury Severity Score independently predicted cerebrospinal fluid nitrite and nitrate concentrations (p < .00001 and p = .0053, respectively). Cerebral blood flow and arterio-jugular oxygen content difference were not associated with cerebrospinal fluid or plasma nitrite and nitrate concentrations using this model. Cerebrospinal fluid nitrite and nitrate concentrations were increased over time in hypothermic vs. normothermic patients. But, where this difference occurred could not be determined by multiple comparisons (p = .03). The hypothermic patients had lower admission Glasgow Coma Scale scores than normothermic patients (p = .04) and tended to have higher injury Severity Scores (p = .09). Increases in cerebrospinal fluid nitrite and nitrate concentrations peaked at 30 to 42 hrs after severe closed-head injury. This increase in cerebrospinal fluid nitrite and nitrate concentrations was greater in nonsurvivors. Also, cerebrospinal fluid and plasma nitrite and nitrate concentrations were associated with injury Severity Score, suggesting that increased nitric oxide production in the brain is associated with injury severity and death. Hypothermia did not prevent the increase in cerebrospinal fluid nitrite and nitrate concentrations. Further study is required to determine the source of this increase in cerebrospinal fluid nitrite and nitrate concentrations and to further define the relationship to outcome and the effect of hypothermia on this process.

Cerebral blood flow, vascular resistance, and oxygen metabolism in acute brain trauma: redefining the role of cerebral perfusion pressure?

To evaluate normal or high cerebral perfusion pressure in relation to cerebral blood flow and oxygen metabolism, as well as other multivariate cerebral hemodynamic and metabolic interrelationships, in acute brain trauma in humans. Prospective, observational study. Neuroscience intensive care unit of a university hospital. Adults (n = 66) with severe acute brain trauma (Glasgow Coma Scale scores from 4 to 8), undergoing multivariate physiologic studies involving cerebral perfusion pressure, cerebral blood flow, cerebral metabolic rate of oxygen consumption, total hemoglobin content, arterio-jugular oxygen content difference, and cerebral vascular resistance, along with other routine procedures. None. Statistical analysis did not demonstrate any correlation between cerebral perfusion pressure and cerebral blood flow, between cerebral perfusion pressure and arterio-jugular oxygen content difference, and between cerebral perfusion pressure and cerebral metabolic rate of oxygen consumption, over a broad spectrum of perfusion pressures ranging from 60 to 130 mm Hg. In contrast, a significant negative correlation was found between cerebral vascular resistance and cerebral blood flow, where higher values of cerebral vascular resistance were associated with lower blood flow levels, and vice versa. In severe acute brain trauma, cerebral hemodynamic and oxygen metabolic variables are not necessarily correlated with normal or even high levels of cerebral perfusion pressure. Under these circumstances, cerebral vascular resistance (not perfusion pressure) is more closely correlated with different patterns of cerebral blood flow and metabolism.

Estimated cerebral metabolic rate of oxygen in severely brain-injured patients

To evaluate a novel parameter of global cerebral oxygen metabolism, the estimated cerebral metabolic rate of oxygen, for its clinical utility in monitoring acute, severely brain-injured patients. Prospective, observational study. Neuroscience intensive care unit of a university hospital. Sixty-six adults with acute brain trauma undergoing 133Xe regional cerebral blood flow and global cerebral oxygen metabolic studies, in conjunction with other routine monitoring techniques. None. Estimated cerebral metabolic rate of oxygen was calculated as the product of PaCO2 and arterio-jugular oxygen content difference, and compared with the measured cerebral metabolic rate of oxygen (the product of mean regional cerebral blood flow and arterio-jugular oxygen content difference). Good correlations were found between the estimated and the true values (r2 = .56/.67, p < .0001) in 91 studies performed in 66 patients. These findings suggest that the estimated cerebral metabolic rate of oxygen is a useful substitute for the traditional cerebral metabolic rate of oxygen when cerebral blood flow information is not available. In addition, with this parameter, the patient's metabolic status can be assessed more frequently than with cerebral blood flow studies. These measurements do not require special instrumentation and can be done in any intensive care setting.

Cerebral lactate-oxygen index in acute brain injury with acute anemia: assessment of false versus true ischemia.

To evaluate the occurrence of global cerebral ischemia in acute brain trauma with acute anemia by combined measurements of cerebral hemodynamics, oxygenation, and lactate production. Prospective, intervention study. Neuroscience intensive care unit of a university hospital. Adults (n = 22) with severe acute brain trauma (Glasgow Coma Scores ranging from 4 to 8), undergoing frequent serial measurements of total hemoglobin content, jugular oxyhemoglobin saturation, arteriojugular oxygen content difference, arteriojugular lactate concentration difference, lactate-oxygen index, and cerebral blood flow, along with other routine procedures. Acute anemia (disclosed by a total hemoglobin content of < 11 g/dL in at least three measurements) was found in 19 (86%) of 22 patients. In 211 serial multivariate physiologic observations, only one (0.4%) disclosed abnormally negative arteriojugular lactate difference consistent with global cerebral ischemia. However, in 18 (8.5%) studies in seven (31.8%) patients, acute anemia resulted in markedly decreased values of arteriojugular oxygen content difference. The latter, in turn, yielded abnormally high values of lactate-oxygen index despite normal cerebral lactate production (arteriojugular lactate difference) and oxygenation (jugular oxyhemoglobin saturation). In acute brain injury with acute anemia, global cerebral ischemia is a rare finding. However, false cerebral ischemia may be frequently found, if assessed by the lactate-oxygen index, because the denominator of the index (the arteriojugular oxygen content difference) frequently decreases as a function of decreasing hemoglobin, thus yielding false calculated ischemic high values for lactate-oxygen index despite normal cerebral oxygenation and lactate production.

Cerebral blood flow and oxygen consumption in acute brain injury with acute anemia

To comparatively evaluate cerebral metabolic rate of oxygen consumption and a modification of it, cerebral consumption of oxygen, in patients with acute brain injury with acute anemia. Prospective, observational study. Neuroscience intensive care unit (ICU) of a university hospital. Adults (n = 62) with acute brain trauma, undergoing serial 133xenon studies of regional cerebral blood flow and global cerebral oxygen metabolism, along with other routine monitoring techniques. In 173 combined studies of blood flow and oxygen metabolism, in the presence of spontaneous decreases in hemoglobin, cerebral metabolic rate of oxygen consumption and cerebral consumption of oxygen were comparatively evaluated in three groups with different hemoglobin levels. Cerebral metabolic rate of oxygen consumption was calculated as the product of averaged regional cerebral blood flow and arterio-jugular oxygen content difference, while cerebral consumption of oxygen was calculated as the product of averaged regional cerebral blood flow and the arterio-jugular oxyhemoglobin saturation difference, i.e., cerebral extraction of oxygen. Results indicated that a decrease of hemoglobin content is paralleled by a decrease in cerebral metabolic rate of oxygen consumption, even though the level of consciousness (coma score) is essentially unchanged across three hemoglobin groups. On the other hand, cerebral consumption of oxygen does not follow the decrease in hemoglobin and cerebral metabolic rate of oxygen consumption, thus demonstrating better stability to changing hemoglobin content. The low cerebral metabolic rate of oxygen consumption is due to a decrease in arterio-jugular oxygen content difference in anemia, while the cerebral extraction of oxygen does not follow the trend of the arterio-jugular oxygen content difference. In acute brain trauma with acute anemia, calculated arterio-jugular oxygen content difference and cerebral metabolic rate of oxygen consumption tend to be progressively lower, depending on the extent of anemia, which is in disagreement with coma scores. These changes in hemoglobin tend to have an inverse influence on cerebral consumption of oxygen, which, therefore, constitutes an alternative and independent measure of cerebral oxygen and independent measure of cerebral oxygen consumption under these limiting circumstances.