Cerebral arteriovenous oxygen difference as an estimate of cerebral blood flow in comatose patients

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✓ The hypothesis that cerebral arteriovenous difference of oxygen content (AVDO2) can be used to predict cerebral blood flow (CBF) was tested in patients who were comatose due to head injury, subarachnoid hemorrhage, or cerebrovascular disease. In 51 patients CBF was measured daily for 3 to 5 days, and in 49 patients CBF was measured every 8 hours for 5 to 10 days after injury. In the latter group of patients, when a low CBF (≤ 0.2 ml/gm/min) or an increased level of cerebral lactate production (CMRL) (≤ −0.06 µmol/gm/min) was encountered, therapy was instituted to increase CBF, and measurements of CBF, AVDO2, and arteriovenous difference of lactate content (AVDL) were repeated. When data from all patients were analyzed, including those with cerebral ischemia and those without, AVDO2 had only a modest correlation with CBF (r = −0.24 in 578 measurements, p < 0.01). When patients with ischemia, indicated by an increased CMRL, were excluded from the analysis, CBF and AVDO2 had a much improved correlation (r = −0.74 in 313 measurements, p < 0.01). Most patients with a very low CBF would have been misclassified as having a normal or increased CBF based on the AVDO2 alone. However, when measurements of AVDO2 were supplemented with AVDL, four distinct CBF patterns could be distinguished. Patients with an ischemia/infarction pattern typically had a lactate-oxygen index (LOI = −AVDL/AVDO2) of 0.08 or greater and a variable AVDO2. The three nonischemic CBF patterns had an LOI of less than 0.08, and could be classified according to the AVDO2. Patients with a normal CBF (mean 0.42 ± 0.12 ml/gm/min) had an AVDO2 between 1.3 and 3.0 µmol/ml. A CBF pattern of hyperemia (mean 0.53 ± 0.18 ml/gm/min) was characterized by an AVDO2 of less than 1.3 µmol/ml. A compensated hypoperfusion CBF pattern (mean 0.23 ± 0.07 ml/gm/min) was identified by an AVDO2 of more than 3.0 µmol/min. These studies suggest that reliable estimates of CBF may be made from AVDO2 and AVDL measurements, which can be easily obtained in the intensive care unit.

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Address reprint requests to: Claudia S. Robertson, M.D., Department of Neurosurgery, Baylor College of Medicine, One Baylor Plaza, Houston, Texas 77030.

© AANS, except where prohibited by US copyright law.

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    Relationship between arteriovenous oxygen difference (AVDO2) and cerebral blood flow (CBF). If a coupled change in cerebral metabolic rate of oxygen (CMRO2) and CBF occurs, then AVDO2 remains unchanged and the relationship between CBF and AVDO2 shifts to a new CMRO2 curve (horizontal arrows). If CMRO2 remains constant, then changes in AVDO2 reflect uncoupled changes in CBF (curved arrows).

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    Correlation between arteriovenous oxygen difference (AVDO2) and cerebral blood flow (CBF) in 100 comatose patients with and without cerebral ischemia (r = −0.24 in 578 measurements, p < 0.01).

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    Correlation between arteriovenous oxygen difference (AVDO2) and cerebral blood flow (CBF) in 55 comatose patients without cerebral ischemia (r = −0.74 in 313 measurements, p < 0.01).

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    Findings in a patient with a transient episode of hyperemia. Left: Graphs showing changes in cerebral blood flow (CBF) and arteriovenous oxygen difference (AVDO2) over time after injury. On Day 2, CBF increased with no change in the cerebral metabolic oxygen rate (CMRO2). Right: The relationship between AVDO2 and CBF is shown for each CBF measurement. All of the points fall close to the 0.9-µmol/gm/min CMRO2 curve. The increase in CBF on Day 2 is easily identifiable by the decrease in AVDO2.

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    Summary of treatment of compensated hypoperfusion in 11 patients. Left: Graphs showing the mean values for cerebral blood flow (CBF) and cerebral metabolic oxygen rate (CMRO2) before and after treatment. The CBF increased with treatment, while CMRO2 remained unchanged. Right: The relationship between CBF and the arteriovenous oxygen difference (AVDO2) is shown before and after treatment for the individual patients. The changes in CBF did not alter cerebral metabolism and were accompanied by reciprocal changes in AVDO2.

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    Findings during the development of cerebral ischemia in four patients who initially had a normal cerebral blood flow (CBF). Left: Graphs showing the mean values for CBF and cerebral metabolic oxygen rate (CMRO2). Over a period of 8 hours, CBF and CMRO2 decreased, while cerebral lactate production increased from −0.020 to −0.042 µmol/gm/min. Right: The relationship between CBF and the arteriovenous oxygen difference (AVDO2) is shown for the individual patients. As the CBF decreased, the AVDO2 also decreased.

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    Treatment of cerebral ischemia in nine patients. When cerebral blood flow (CBF) increased, cerebral metabolic oxygen rate (CMRO2) increased in five patients (upper) and remained unchanged in four (lower). Left: Graphs showing the mean CBF and CMRO2 values before and after treatment. When an increase in CBF improved CMRO2, cerebral lactate production decreased (upper pair). When the ischemic changes were irreversible, CMRO2 and cerebral metabolic lactate rate were unchanged by treatment (lower pair). Right: The relationship between CBF and the arteriovenous oxygen difference (AVDO2) is shown for the individual patients. The changes in AVDO2 as CBF increased were variable and not predictive of whether or not CMRO2 was improved.

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    Model diagramming the relationship between cerebral blood flow (CBF) and cerebral metabolism in comatose patients. In the absence of cerebral ischemia, the arteriovenous oxygen difference (AVDO2) and CBF have the relationship illustrated by the solid curve, with cerebral metabolic rate of oxygen (CMRO2) averaging 0.9 µmol/gm/min. In the presence of cerebral ischemia/infarction (open arrows), AVDO2 and CBF have an unpredictable relationship.

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