In patients in coma due to trauma or metabolic encephalopathy, CMRO2 is typically reduced from a normal value of 1.5 µmol/gm/min to between 0.6 and 1.2 µmol/gm/min.7,10,12,16 If CBF remains coupled to CMRO2, then CBF will also be reduced. Normal coupling of CBF is retained in only 45% of comatose head-injured patients,10 however; in most of these patients, the CBF regulatory mechanisms are abnormal and, rather than being coupled to CMRO2, CBF is increased or decreased independently of the reduced CMRO2. In this situation, the ratio between CMRO2 and CBF will vary. As CBF changes occur, measurements of the reciprocal changes in AVDO2 might serve as an indicator of CBF adequacy. A normal AVDO2 would suggest that CBF is normally coupled to CMRO2, a decreased AVDO2 would indicate that CBF is excessive for cerebral metabolic requirements, and an elevated AVDO2 would indicate a decreased CBF. Figure 1 illustrates the nonlinear relationship between CBF and AVDO2 that would be expected in normal and pathophysiological conditions; a series of curves is displayed, each described by the formula: AVDO2 = CMRO2/CBF. Each individual curve defines the relationship between AVDO2 and CBF that would occur if CMRO2 were held constant at a particular value and CBF were varied. The brain extracts oxygen more completely than most tissues, and the normal cerebral AVDO2, shown by the horizontal dashed lines in Fig. 1, is 1.8 to 3.9 µmol/ml.6 If a coupled change in CMRO2 and CBF occurs, then AVDO2 remains unchanged, and the relationship between CBF and AVDO2 simply shifts to a new CMRO2 curve, as illustrated by the horizontal arrows. Assuming that CMRO2 remains constant, changes in AVDO2 (curved arrows) reflect uncoupled variations in CBF. A low AVDO2 suggests that CBF is elevated relative to cerebral metabolic requirements, while an increased AVDO2 suggests that CBF is low. This hypothesis is of particular interest, because technology has become available to monitor cerebral AVDO2 continuously.* Such continuous monitoring of CBF adequacy may allow early identification and treatment of secondary ischemic injury.
Two conditions are obviously required for this hypothesis to be valid: CMRO2 must be relatively constant and in the expected range; alternatively, if CMRO2 does change, there must be a marker that CMRO2 has moved out of the expected range. Previous studies have shown that when a head injury is accompanied by cerebral infarction, the first condition may not be true.12 In such cases, CMRO2 is typically less than 0.6 µmol/gm/min in the presence of ischemic injury. However, these studies also showed that the characteristic elevation of cerebral lactate production may provide a satisfactory marker of the presence of significant cerebral ischemia, and therefore that CMRO2 may not be in the expected range.
The purpose of the present study was to assess the value of AVDO2 in predicting CBF and, in particular, in identifying patients with a low CBF.
Monitoring system manufactured by Oximetrix, Inc., Mountain View, California.
Infrared N2O analyzer manufactured by Vital Signs, Inc., East Rutherford, New Jersey.
Blood gas analyzers manufactured by Ciba Corning Diagnostics Corp., Medfield, Massachusetts; co-oximeter manufactured by Instrumentation Laboratories, Lexington, Massachusetts.
YSI-23L lactate analyzer manufactured by Yellow Springs Instruments, Yellow Springs, Ohio.