Cerebral perfusion and metabolism during profound hypothermia in children. A study of middle cerebral artery ultrasonic variables and cerebral extraction of oxygen

Flow velocity of the right middle cerebral artery was studied in eight children during cardiac operations performed with profound hypothermia. Cerebral oxygen consumption was estimated by relating the difference in oxygen content between arterial and venous blood (jugular bulb) to flow velocity. In another six children, also during profound hypothermic procedures, the diameter of the middle cerebral artery was studied with an electronic echo-tracking instrument connected to a real-time ultrasound scanner. Flow velocity and estimated oxygen consumption decreased during cooling in proportion to the temperature decrease (r = 0.67, p less than 0.001, and r = 0.86, p less than 0.001, respectively), whereas the diameter was unaffected by temperature. At a nasopharyngeal temperature of 16.9 degrees +/- 1.9 degrees C flow velocity was reduced to 33.1% +/- 7.0% of the value obtained at 35 degrees C after induction of anesthesia. Correspondingly, the oxygen consumption decreased to 20.1% +/- 6.4%. The increase in oxygen consumption per 10 degrees C change in temperature was 3.6 (2.0 to 3.9) during surface cooling, 2.6 (1.9 to 2.7) during cardiopulmonary bypass cooling, and 2.7 (1.5 to 4.6) during rewarming. Flow velocity was not influenced by perfusion pressure during profound hypothermia within the range of 20 to 42 mm Hg (r = 0.14, p = 0.52) but was related to pump flow (r = 0.73, p less than 0.001). A pump flow down to 0.5 L/min/m2 was found to be adequate during stable profound hypothermia, as judged from the maintained high jugular bulb venous oxygen saturation (70% to 80%). It is concluded that flow velocity is reduced at hypothermia in proportion to the reduced metabolic rate, although modified by other factors that influence cerebral blood flow.     

Cerebral blood flow and oxygen metabolism during cardiopulmonary bypass with moderate hypothermic selective cerebral perfusion

Cerebral blood flow was measured using transcranial doppler during cardiopulmonary bypass in nine patients with selective cerebral perfusion for surgery of arch aorta (group S). For comparison, 11 adult open heart patients (group C) were also measured. The authors' selective cerebral perfusion at 28 degrees C resulted in moderate hypothermia and antegrade perfusion using independent pumps for three branches. Total flow in the three branches was 500 ml/min. A Labodop DP-100 doppler ultrasound velocimeter was used to measure middle cerebral arterial blood flow velocity. Hemoglobin concentration and oxygen saturation were also measured in arterial and jugular venous blood. The arteriovenous oxygen content difference (Ca-vO2) was calculated and multiplied by the middle cerebral arterial blood flow velocity value, which resulted in the cerebral metabolic rate for oxygen (CMRO2). The cerebral perfusion pressure of group S was lower than in group C, and the arterial carbon-dioxide tension (PaCO2) of group S was higher than in group C during cardiopulmonary bypass. Middle cerebral arterial blood flow velocity values of both groups remained constant before, during and after cardiopulmonary bypass. The CMRO2 decreased during cardiopulmonary bypass and showed no difference between the two groups. The changes in PaCO2 might be significant factors in the increase in cerebral blood flow during selective cerebral perfusion. This study supports the conclusion that, compared with our routine open heart surgery procedures, our selective cerebral perfusion procedures had the same cerebral blood flow and oxygen metabolism during cardiopulmonary bypass.     

Cerebral oxygen extraction and autoregulation during extracorporeal whole body hyperthermia in humans

BACKGROUND: The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans. METHODS: Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8 degrees C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release. RESULTS: For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40 degrees C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration. CONCLUSION: Profound hyperthermia during propofol anesthesia is associated with decreased cerebral oxygen extraction, increased cerebral blood flow velocity, and impaired pressure-flow autoregulation, indicating transient partial vasoparalysis.     

Correlation between cerebral oxygen saturation measured by near-infrared spectroscopy and jugular oxygen saturation in patients with severe closed head injury.

Near-infrared spectroscopy has been used to monitor cerebral oxygen saturation during cerebral circulatory arrest and carotid clamping. However, its utility has not been demonstrated in more complex situations, such as in patients with head injuries. The authors tested this method during conditions that may alter the arteriovenous partition of cerebral blood in different ways. METHODS: The authors compared changes in measured cerebral oxygen saturation and other hemodynamic parameters, including jugular venous oxygen saturation, in nine patients with severe closed head injury during manipulation of arterial carbon dioxide partial pressure and after mean arterial pressure was altered by vasopressors. RESULTS: The Bland and Altman representation of cerebral oxygen saturation versus jugular oxygen saturation showed a uniform scatter. Values for changing arterial carbon dioxide partial pressure were: bias = 1.1%, 2 SD = +/-21%, absolute value; and those for alterations in mean arterial pressure: bias = 3.7%, 2 SD = +/-24%, absolute value. However, a Bland and Altman plot of changes in cerebral oxygen saturation versus changes in jugular oxygen saturation had a negative slope (alteration in arterial carbon dioxide partial pressure: bias = 2.4%, 2 SD = +/-17%, absolute value; alteration in mean arterial pressure: bias = -4.9%, 2 SD = +/-31%, absolute value). Regression analysis showed that changes in cerebral oxygen saturation were positively correlated with changes in jugular venous oxygen saturation during the carbon dioxide challenge, whereas correlation was negative during the arterial pressure challenge. CONCLUSIONS: Cerebral oxygen saturation assessed by near-infrared spectroscopy does not adequately reflect changes in jugular venous oxygen saturation in patients with severe head injury. Changes in arteriovenous partitioning, infrared-spectroscopy contamination by extracerebral signal, algorithm errors, and dissimilar tissue sampling may explain these findings.     

The effect of temperature on cerebral metabolism and blood flow in adults during cardiopulmonary bypass.

The effect of temperature on cerebral blood flow and metabolism was studied in 41 adult patients scheduled for operations requiring cardiopulmonary bypass. Plasma levels of midazolam and fentanyl were kept constant by a pharmacokinetic model-driven infusion system. Cerebral blood flow was measured by xenon 133 clearance (initial slope index) methods. Cerebral blood flow determinations were made at 27 degrees C (hypothermia) and 37 degrees C (normothermia) at constant cardiopulmonary bypass pump flows of 2 L/min/m2. Blood gas management was conducted to maintain arterial carbon dioxide tension (not corrected for temperature) 35 to 40 mm Hg and arterial oxygen tension of 150 to 250 mm Hg. Blood gas samples were taken from the radial artery and the jugular bulb. With decreased temperature there was a significant (p less than 0.0001) decrease in the arterial venous-oxygen content difference, suggesting brain flow in excess of metabolic need. For each patient, the cerebral metabolic rate of oxygen consumption at 37 degrees C and 27 degrees C was calculated from the two measured points at normothermia and hypothermia with the use of a linear relationship between the logarithm of cerebral metabolic rate of oxygen consumption and temperature. The temperature coefficient was then computed as the ratio of cerebral metabolic rate of oxygen consumption at 37 degrees C to that at 27 degrees C. The median temperature coefficient for man on nonpulsatile cardiopulmonary bypass is 2.8. Thus reducing the temperature from 37 degrees to 27 degrees C reduces cerebral metabolic rate of oxygen consumption by 64%.     

Continuous monitoring of blood oxygen saturation of internal jugular vein as a useful indicator for selective cerebral perfusion during aortic arch replacement.

We continuously monitored blood oxygen saturation in the internal jugular vein during selective cerebral perfusion for aortic arch operations and evaluated its efficacy as an indicator of cerebral oxygen metabolism. The selective cerebral perfusion method was applied in 11 patients who underwent operations for aortic arch replacement. Blood oxygen saturation in the internal jugular vein was continuously monitored at the bulbus jugularis with a fiberoptic catheter during the operation. Perfusion flow of 500 ml/min was continued for 134.7 +/- 14.9 minutes under moderate hypothermia at 25 degrees C, and bilateral temporal arterial pressure was 40 to 60 mm Hg. Blood gas data were used to estimate oxygen consumption, oxygen extraction ratio, and lactate uptake in the cerebrum. No patients had postoperative cerebral complications. Cerebral oxygen consumption was 2.93 +/- 0.4 ml/min/100 gm under general anesthesia at 36 degrees C. While selective cerebral perfusion at 25 degrees C decreased consumption to 0.92 +/- 0.39 ml/min/100 gm, it fell to about 30% of its former value. Blood oxygen tension in the internal jugular vein showed no significant correlation with rectal temperature. Selective cerebral perfusion did not significantly affect cerebral lactate uptake. In contrast, blood oxygen saturation in the internal jugular vein was significantly affected by temperature and cerebral flow during selective cerebral perfusion, and blood oxygen saturation in the internal jugular vein correlated closely with cerebral oxygen extraction ratio (r = 0.91). Cerebral oxygen metabolism was thus well maintained, and continuous monitoring of blood oxygen saturation in the internal jugular vein was found to serve as a useful indicator under selective cerebral perfusion during operations for aortic arch replacement.     

Cerebrovascular and cerebral metabolic effects of alterations in perfusion flow rate during hypothermic cardiopulmonary bypass in man.

Recent experimental and clinical investigations provide conflicting evidence regarding the effects of changes in the systemic flow rate from the pump oxygenator on cerebral blood flow and the cerebral metabolic rate of oxygen consumption. However, the results of existing clinical studies are difficult to interpret because of the confounding effects of differences in management of arterial carbon dioxide tension and use of anesthetic and vasoactive agents during cardiopulmonary bypass. To clarify the relationship among perfusion flow rate, cerebral blood flow, and cerebral metabolic rate of oxygen consumption in man during hypothermic cardiopulmonary bypass, we varied perfusion flow rate in random order to either 1.75 or 2.25 L.min-1.m-2 and studied cerebral blood flow (measured by clearance of xenon 133) and cerebral metabolic rate of oxygen consumption (estimated as the product of cerebral blood flow and the cerebral arteriovenous oxygen content difference) in patients managed with both the alpha-stat (group 1) and the pH-stat (group 2) methods of pH and arterial carbon dioxide tension adjustment. We measured the cerebral arteriovenous oxygen content difference using radial arterial and jugular venous bulb blood samples. In each patient other variables known to exert effects on cerebral blood flow and cerebral metabolic rate of oxygen consumption, including temperature, arterial carbon dioxide tension, arterial oxygen tension, mean arterial pressure, and hematocrit, were maintained constant between measurements. In both groups, mean arterial pressure at both pump flow rates was similar because of spontaneous reciprocal alterations in systemic vascular resistance, that is, as perfusion flow rate declined, systemic vascular resistance increased; as perfusion flow rate increased, systemic vascular resistance declined. Under these tightly controlled conditions, pump flow variation per se exerted no effect on cerebral blood flow or cerebral metabolic rate of oxygen consumption in either group.     

Influence of aortic blood flow velocity on changes of middle cerebral artery blood flow velocity during isoflurane and sevoflurane anaesthesia

BACKGROUND AND OBJECTIVE: We studied the influence of systemic (aortic) blood flow velocity on changes of cerebral blood flow velocity under isoflurane or sevoflurane anaesthesia. METHODS: Forty patients (age: isoflurane 24-62 years; sevoflurane 24-61 years; ASA I-III) requiring general anaesthesia undergoing routine spinal surgery were randomly assigned to either group. Cerebral blood flow velocity was measured in the middle cerebral artery by transcranial Doppler sonography (depth: 50-60 mm). Systemic blood flow velocity was determined by transthoracic Doppler sonography at the aortic valve. Heart rate, arterial pressure, arterial oxygen saturation and body temperature were monitored. After standardized anaesthesia induction (propofol, remifentanil, vecuronium) sevoflurane or isoflurane were used as single agent anaesthetics. Cerebral blood flow velocity and systemic blood flow velocity were measured in the awake patient (baseline) and repeated 5 min after reaching a steady state of inspiratory and end-expiratory concentrations of 0.75, 1.00, and 1.25 mean alveolar concentrations of either anaesthetic. To calculate the influence of systemic blood flow velocity on cerebral blood flow velocity, we defined the cerebral-systemic blood flow velocity index (CSvI). CSvI of 100% indicates a 1:1 relationship of changes of cerebral blood flow velocity and systemic blood flow velocity. RESULTS: Isoflurane and sevoflurane reduced both cerebral blood flow velocity and systemic blood flow velocity. The CSvI decreased significantly at all three concentrations vs. 100% (isoflurane/sevoflurane: 0.75 MAC: 85 +/- 25%/81 +/- 23%, 1.0 MAC: 79 +/- 19%/74 +/- 16%, 1.25 MAC: 71 +/- 16%/79 +/- 21%; [mean +/- SD] P = 0.0001). CONCLUSIONS: The reduction of the CSvI vs. 100% indicates a direct reduction of cerebral blood flow velocity caused by isoflurane/sevoflurane, independently of systemic blood flow velocity.     

Middle cerebral artery flow velocity during coronary surgery; influence of clinical variables

The flow velocity in the middle cerebral artery was measured continuously with a noninvasive transcranial Doppler in 18 patients during coronary artery surgery. Neurolept anesthesia and alpha-static acid-base management were employed. The flow velocity data were expressed as a percent of the awake level. During intubation, there was a transient flow velocity increase, which was related to a concomitant increase in mean arterial pressure (r = 0.67, p less than 0.01). Prior to cardiopulmonary bypass, flow velocity had decreased to 52.4% +/- 3.0% (mean +/- SEM). At the onset of cardiopulmonary bypass, flow velocity values were transiently doubled. Flow velocity then reached a stable level of 63% to 65% during hypothermia (25 degrees C to 30 degrees C). The increase from 52.4% to 63% to 65% was related to the reduction in hematocrit (r = -0.62, p less than 0.02). With rewarming, flow velocity increased to 101% +/- 5.2%. Flow velocity was found to correlate with temperature during cardiopulmonary bypass (median rs = 0.84, range 0.61 to 0.99, p less than 0.0001). No positive correlation was found between mean arterial pressure (MAP) and flow velocity during cardiopulmonary bypass. Although no direct metabolic measurements were performed, it is concluded that these findings are compatible with a maintained cerebral blood flow/metabolic coupling during cardiopulmonary bypass.     

Middle cerebral artery flow velocity and cerebral oxygenation during abdominal aortic surgery

Cerebral perfusion was evaluated in twelve patients undergoing elective infra-renal abdominal aortic aneurysmectomy by transcranial Doppler ultrasonography-determined middle cerebral artery mean flow velocity, near-infrared spectroscopy-assessed cerebral oxygen saturation and systemic haemodynamic variables. The middle cerebral artery mean flow velocity and cerebral oxygen saturation decreased during cross-clamping of the aorta, and both increased upon declamping of the aorta with the oxygen saturation change lagging behind the change in the flow velocity. The changes in cerebral flow velocity and oxygen saturation paralleled the deviations in cardiac output and end-tidal carbon dioxide tension.     

Ketamine Decreases Intracranial Pressure and Electroencephalographic Activity in Traumatic Brain Injury Patients during Propofol Sedation

Background: The potential adverse effects of ketamine in neurosurgical anesthesia have been well established and involve increased intracranial pressure (ICP) and cerebral blood flow. However, reexamination of ketamine is warranted because data regarding the effects of ketamine on cerebral hemodynamics are conflicting.

Methods: Eight patients with traumatic brain injury were studied. In all patients, ICP monitoring was instituted before the study. Control of ICP (less than 25 mmHg), hemodynamic values, and blood gas tension (partial pressure of carbon dioxide in arterial blood between 35-38 mmHg) was obtained with propofol infusion (3 mg [center dot] kg sup -1 [center dot] h sup -1) and mechanical ventilation. The effects of three doses of ketamine, 1.5, 3, and 5 mg/ kg, respectively, on ICP, cerebral perfusion pressure, jugular vein bulb oxygen saturation, middle cerebral artery blood flow velocity, and electric activity of the brain (EEG) were measured. The three doses were administered intravenously at 6-h intervals over 30 s through a central venous line. Systemic and cerebral hemodynamics and end-tidal carbon dioxide were continuously monitored and recorded at 1-min intervals throughout the 30-min study periods.

Results: Ketamine, in all three doses studied (1.5, 3, and 5 mg/kg) was associated with a significant decrease in ICP (mean +/- SD: 2 +/- 0.5 mmHg [P < 0.05], 4 +/- 1 mmHg [P < 0.05], and 5 +/- 2 mmHg [P < 0.05]) among the study patients regardless of the ketamine dose used. There were no significant differences in cerebral perfusion pressure, jugular vein bulb oxygen saturation, and middle cerebral artery blood flow velocity. Ketamine induced a low-amplitude fast-activity electroencephalogram, with marked depression, such as burst suppression.     

Correlation between Cerebral Oxygen Saturation Measured by Near-infrared Spectroscopy and Jugular Oxygen Saturation in Patients with Severe Closed Head Injury

Background: Near-infrared spectroscopy has been used to monitor cerebral oxygen saturation during cerebral circulatory arrest and carotid clamping. However, its utility has not been demonstrated in more complex situations, such as in patients with head injuries. The authors tested this method during conditions that may alter the arteriovenous partition of cerebral blood in different ways.

Methods: The authors compared changes in measured cerebral oxygen saturation and other hemodynamic parameters, including jugular venous oxygen saturation, in nine patients with severe closed head injury during manipulation of arterial carbon dioxide partial pressure and after mean arterial pressure was altered by vasopressors.

Results: The Bland and Altman representation of cerebral oxygen saturation versus jugular oxygen saturation showed a uniform scatter. Values for changing arterial carbon dioxide partial pressure were: bias = 1.1%, 2 SD = +/-21%, absolute value; and those for alterations in mean arterial pressure: bias = 3.7%, 2 SD = +/-24%, absolute value. However, a Bland and Altman plot of changes in cerebral oxygen saturation versuschanges in jugular oxygen saturation had a negative slope (alteration in arterial carbon dioxide partial pressure: bias = 2.4%, 2 SD = +/-17%, absolute value; alteration in mean arterial pressure: bias = -4.9%, 2 SD = +/-31%, absolute value). Regression analysis showed that changes in cerebral oxygen saturation were positively correlated with changes in jugular venous oxygen saturation during the carbon dioxide challenge, whereas correlation was negative during the arterial pressure challenge.     

Cerebral Oxygen Extraction and Autoregulation during Extracorporeal Whole Body Hyperthermia in Humans

Background: The effects of hyperthermia on the human brain are incompletely understood. This study assessed the effects of whole body hyperthermia on cerebral oxygen extraction and autoregulation in humans.

Methods: Nineteen patients with chronic hepatitis C virus infection, not responding to interferon treatment, were subjected to experimental therapy with extracorporeal whole body hyperthermia at 41.8[degrees]C for 120 min under propofol anesthesia (23 sessions total). During treatment series A (13 sessions), end-tidal carbon dioxide was allowed to increase during heating. During series B (10 sessions), end-tidal carbon dioxide was maintained approximately constant. Cerebral oxygen extraction (arterial to jugular venous difference of oxygen content) and middle cerebral artery blood flow velocity were continuously measured. Cerebral pressure-flow autoregulation was assessed by static tests using phenylephrine infusion and by assessing the transient hyperemic response to carotid compression and release.

Results: For treatment series A, cerebral oxygen extraction decreased 2.2-fold and cerebral blood flow velocity increased 2.0-fold during heating. For series B, oxygen extraction decreased 1.6-fold and flow velocity increased 1.5-fold. Jugular venous oxygen saturation and lactate measurements did not indicate cerebral ischemia at any temperature. Static autoregulation test results indicated loss of cerebrovascular reactivity during hyperthermia for both series A and series B. The transient hyperemic response ratio did not decrease until the temperature reached approximately 40[degrees]C. Per degree Celsius temperature increase, the transient hyperemic response ratio decreased 0.07 (95% confidence interval, 0.05-0.09; P = 0.000). This association remained after adjustment for variations in arterial partial pressure of carbon dioxide, mean arterial pressure, and propofol blood concentration.     

Cerebral blood flow response to changes in arterial carbon dioxide tension during hypothermic cardiopulmonary bypass in children

We examined the relationship of changes in partial pressure of carbon dioxide on cerebral blood flow responsiveness in 20 pediatric patients undergoing hypothermic cardiopulmonary bypass. Cerebral blood flow was measured during steady-state hypothermic cardiopulmonary bypass with the use of xenon 133 clearance methodology at two different arterial carbon dioxide tensions. During these measurements there was no significant change in mean arterial pressure, nasopharyngeal temperature, pump flow rate, or hematocrit value. Cerebral blood flow was found to be significantly greater at higher arterial carbon dioxide tensions (p less than 0.01), so that for every millimeter of mercury rise in arterial carbon dioxide tension there was a 1.2 ml.100 gm-1.min-1 increase in cerebral blood flow. Two factors, deep hypothermia (18 degrees to 22 degrees C) and reduced age (less than 1 year), diminished the effect carbon dioxide had on cerebral blood flow responsiveness but did not eliminate it. We conclude that cerebral blood flow remains responsive to changes in arterial carbon dioxide tension during hypothermic cardiopulmonary bypass in infants and children; that is, increasing arterial carbon dioxide tension will independently increase cerebral blood flow.     

The effects of isoflurane-induced electroencephalographic burst suppression on cerebral blood flow velocity and cerebral oxygen extraction during cardiopulmonary bypass

We investigated the effects of isoflurane-induced burst suppression, monitored with electroencephalography (EEG), on cerebral blood flow velocity (CBFV), cerebral oxygen extraction (COE), and autoregulation in 16 patients undergoing cardiac surgery. The experimental procedure was performed during nonpulsatile cardiopulmonary bypass (CPB) with mild hypothermia (32 degrees C) in fentanyl-anesthestized patients. Middle cerebral artery transcranial Doppler flow velocity, right jugular vein bulb oxygen saturation, and jugular venous pressure (JVP) were continuously measured. Autoregulation was tested during changes in mean arterial blood pressure (MAP) within a range of 40-80 mm Hg, induced by sodium nitroprusside and phenylephrine before (control) and during additional isoflurane administration to an EEG burst-suppression level of 6-9/min. Isoflurane induced a 27% decrease in CBFV (P < 0.05) and a 13% decrease in COE (P < 0.05) compared with control. The slope of the positive relationship between CBFV and cerebral perfusion pressure (CPP = MAP - JVP) was steeper with isoflurane (P < 0.05) compared with control, as was the slope of the negative relationship between CPP and COE (P < 0.05). We conclude that burst-suppression doses of isoflurane decrease CBFV and impair autoregulation of cerebral blood flow during mildly hypothermic CPB. Furthermore, during isoflurane administration, blood flow was in excess relative to oxygen demand, indicating a loss of metabolic autoregulation of flow. IMPLICATIONS: The effects of isoflurane on cerebral blood flow velocity (CBFV) and oxygen extraction (COE) as a function of perfusion pressure were studied. When added to fentanyl anesthesia, isoflurane induced a 27% and 13% decrease in CBFV and COE, respectively. CBFV became more pressure-dependent with isoflurane indicating an impaired autoregulation.     

Cerebral Blood Flow and Oxygen Metabolism During Mild Hypothermia in Patients with Subarachnoid Haemorrhage

Cerebral blood flow and O2 metabolism during hypothermia (33-34 degrees C) was evaluated in 5 patients with aneurysmal subarachnoid haemorrhage by positron emission tomography (PET). Their preoperative clinical condition was WFNS scale IV or V. The patients received surface cooling postoperatively, and were maintained in a hypothermic state during transfer for radiological examination. Positron emission tomography revealed a decrease in cerebral blood flow and O2 metabolic rate. Cerebral blood flow was 34.8+/-15.1 ml/100 ml/min and the O2 metabolic rate was 1.85+/-0.61 ml/100 ml/min in areas of the middle cerebral artery ipsilateral to the ruptured aneurysms, whereas these values were 30.8+/-7.1 and 2.21+/-0.45 ml/100 ml/min, respectively, on the contralateral side. This represents a decrease of 37+/-27% compared to normal cerebral blood flow and 52+/-16% compared to normal O2 metabolic rate (p < 0.02) in the ipsilateral areas, and decreases of 44+/-13% and 43+/-12%, respectively, on the contralateral side. The present results reflected the luxury perfusion state in almost all cases and provide the first PET evidence of decreased cerebral blood flow and metabolic rate of O2 during hypothermia in humans.     

Cerebral blood flow and metabolism during cardiopulmonary bypass with special reference to effects of hypotension induced by prostacyclin

Cerebral blood flow and metabolism of oxygen, glucose, and lactate were studied in 43 patients undergoing aortocoronary bypass. Twenty-five patients received prostacyclin infusion, 50 ng per kilogram of body weight per minute, during cardiopulmonary bypass (CPB), and 18 patients served as a control group. Regional cerebral blood flow (CBF) was studied by intraarterially injected xenon 133 and a single scintillation detector. Oxygen tension, carbon dioxide tension, oxygen saturation, glucose, and lactate were measured in arterial and cerebral venous blood. Mean arterial blood pressure decreased during hypothermia and prostacyclin infusion to less than 30 mm Hg. The regional CBF was, on average, 22 (standard deviation [SD] 4) ml/100 gm/min before CPB. It increased in the control group during hypothermia to 34 (SD 12) ml/100 gm/min, but decreased in the prostacyclin group to 15 (SD 5) ml/100 gm/min. It increased during rewarming in the prostacyclin group. After CPB, regional CBF was about 40 ml/100 gm/min in both groups. The cerebral arteriovenous oxygen pressure difference decreased more in the control group than in the prostacyclin group during hypothermia. The cerebral metabolic rate of oxygen decreased in both groups from approximately 2 ml/100 gm/min to about 1 ml/100 gm/min during hypothermia, increased again during rewarming, and after CPB was at the levels measured before bypass in both groups. There was no difference between the groups in regard to glucose and lactate metabolism.     

Changes in jugular bulb oxygenation in patients undergoing warm coronary artery bypass surgery (34-37 degrees C)

BACKGROUND AND OBJECTIVE: Imbalance between cerebral oxygen supply and demand is thought to play an important role in the development of cerebral injury during cardiac surgery with cardiopulmonary bypass. METHODS: We studied jugular bulb oxygen saturation, jugular bulb oxygen tension, arterial-jugular bulb oxygen content difference and oxygen extraction ratio in 20 patients undergoing warm coronary artery bypass surgery (34-37 degrees C) with pH-stat blood gas management. RESULTS: Only two patients showed desaturation (jugular bulb oxygen saturation < 50%) at 5 min on bypass, and none from 20 min onwards. Multiple regression models were performed after using bypass temperature, mean arterial pressure, cerebral perfusion pressure, haemoglobin concentration and arterial carbon dioxide tension as independent variables, and arterial-jugular bulb oxygen content difference, jugular bulb oxygen saturation, oxygen extraction ratio and jugular bulb oxygen tension as individual dependent variables. CONCLUSIONS: We found that jugular bulb oxygen saturation, jugular bulb oxygen tension and oxygen extraction ratio are mainly dependent on arterial carbon dioxide tension, and arterial-jugular bulb oxygen content difference is dependent on arterial carbon dioxide tension and the bypass temperature. Our results suggest jugular bulb oxygenation is mainly dependent on arterial carbon dioxide tension during warm cardiopulmonary bypass.     

Cerebral hemodynamics in neonates and infants undergoing cardiopulmonary bypass and profound hypothermic circulatory arrest: assessment by transcranial Doppler sonography

Profound hypothermic circulatory arrest (PHCA) is followed by a transient period of increased intracranial pressure and a longer period of neurophysiologic dysfunction. To investigate the effect of cardiopulmonary bypass (CPB) with PHCA on cerebral hemodynamics, we used transcranial Doppler sonography to measure cerebral blood flow velocity in 10 neonates and infants before and after PHCA. Cerebral blood flow velocity was compared before and after PHCA during normothermic cardiopulmonary bypass at the same mean arterial pressure, central venous pressure, hematocrit, and arterial carbon dioxide tension. Cerebral blood flow velocity decreased exponentially with decreasing nasopharyngeal temperature before PHCA (P less than 0.05) and remained decreased after PHCA during normothermic CPB, compared with values for normothermic CPB before PHCA (P less than 0.005). During normothermic CPB after PHCA, the modified cerebral vascular resistance (mm Hg.cm.s-1) was increased above values for normothermic CPB before PHCA (P less than 0.05). The results of this study suggest that the observed increase in intracranial pressure during PHCA is not caused by increased cerebral perfusion, but rather that cerebral perfusion is reduced in response to a decreased demand for cerebral metabolic oxygen.     

Effect of Dexmedetomidine on Cerebral Blood Flow Velocity, Cerebral Metabolic Rate, and Carbon Dioxide Response in Normal Humans

Background: Dexmedetomidine reduces cerebral blood flow (CBF) in humans and animals. In animal investigations, cerebral metabolic rate (CMR) was unchanged. Therefore, the authors hypothesized that dexmedetomidine would cause a decrease in the CBF/CMR ratio with even further reduction by superimposed hyperventilation. This reduction might be deleterious in patients with neurologic injuries.

Methods: Middle cerebral artery velocity (CBFV) was recorded continuously in six volunteers. CBFV, jugular bulb venous saturation (Sjvo2), CMR equivalent (CMRe), and CBFV/CMRe ratio were determined at six intervals before, during, and after administration of dexmedetomidine: (1) presedation; (2) presedation with hyperventilation; at steady state plasma levels of (3) 0.6 ng/ml and (4) 1.2 ng/ml; (5) 1.2 ng/ml with hyperventilation; and (6) 30 min after discontinuing dexmedetomidine. The slope of the arterial carbon dioxide tension (Paco2)-CBFV relation was determined presedation and at 1.2 ng/ml.

Results: CBFV and CMRe decreased in a dose-related manner. The CBFV/CMRe ratio was unchanged. The CBFV response to carbon dioxide decreased from 1.20 +/- 0.2 cm[middle dot]s-1[middle dot]mm Hg-1 presedation to 0.40 +/- 0.15 cm[middle dot]s-1[middle dot]mm Hg-1 at 1.2 ng/ml. Sjvo2 was statistically unchanged during hyperventilation at 1.2 ng/ml versus presedation (50 +/- 11 vs. 43 +/- 5%). Arousal for hyperventilation at 1.2 ng/ml resulted in increased CBFV (30 +/- 5 to 38 +/- 4) and Bispectral Index (43 +/- 10 to 94 +/- 3).