Can Hyperoxia Overcome Hyperventilation-Induced Cerebral Ischemia?
March 1, 1999 3 minutes read
Can Hyperoxia Overcome Hyperventilation-Induced Cerebral Ischemia?
Abstract & Commentary
Synopsis: Jugular venous oxygen saturation (SjO2) falls during hyperventilation, possibly reflecting a decrease in cerebral blood flow. Increasing the PaO2 to greater than 200 torr during hyperventilation reversed the decline in SjO2 in a group of severely head-injured patients.
Source: Thiagarajan A, et al. Anesth Analg 1998; 87:850-853.
Hyperventilation is frequently used to control intracranial pressure in head-injured patients. The resulting decrease in cerebral blood flow may result in cerebral ischemia in normal brain areas and contribute to a worse patient outcome. Jugular venous oxygen saturation (SjO2) reflects the global balance between arterial oxygen delivery and brain oxygen uptake. It is often monitored in patients subjected to extreme hyperventilation and during vascular occlusive surgery.
Thiagarajan and colleagues studied the effect on SjO2 of raising arterial PaO2 from 100-150 to 200-250 torr during acute hyperventilation in 18 young patients (age, 28 ± 11 years; 12 males) with severe head injuries (Glasgow Coma Scale score, 5-8). All patients were normothermic and normotensive, with a hemoglobin level between 10 and 14 g/dL.
In addition to arterial catheters, jugular bulb venous catheters were placed and their location confirmed radiographically. Samples for saturation and PO2 were obtained at baseline (PaO2 = 100-150 torr, PaCO2 = 30 torr), after 30 minutes of hyperventilation to a PaCO2 of 25 torr, and again after return to baseline. The sequence was repeated after the FiO2 was adjusted to produce a PaO2 of 200-250 torr. Arterial-(jugular) venous oxygen content difference (AVDO2) was calculated in each experimental condition and compared.
SjO2 fell from 66% to 56% when PaCO2 was reduced from 30 to 25 torr during normoxia. During hyperoxia, initial SjO2 was 77% and fell to 64% with hyperventilation. At normoxia, when PaCO2 was reduced from 30 to 25 torr, AVDO2 rose from 5.3 to 7 volume percent. When PaO2 was elevated to more than 200 torr, AVDO2 was reduced from control to 4.2 volume percent; with hyperventilation to a PaCO2 of 25 torr, it rose to 5.9 volume percent. Thus, increasing the PaO2 to more than 200 torr returned the SjO2 and AVDO2 to baseline values, implying improved global oxygen uptake in the brain during hyperventilation in patients with severe head inury.
COMMENT BY CHARLES G. DURBIN, Jr, MD, FCCM
The importance of this study, which was performed in India, is its use of patients to study relevant clinical interventions. The data and conclusions are provocative. However, using moderate hyperventilation in head injury—the baseline condition in this study—has generally been abandoned due to studies demonstrating a worse outcome in less severely injured patients. Acute hyperventilation for abrupt increases in intracranial pressure remains an accepted, although unproven, therapeutic intervention. In this study, ICP was not monitored.
Several additional issues about this study need mentioning. The effects of hyperventilation on hemoglobin saturation and binding of oxygen may affect the results. Alkalosis increases the affinity of hemoglobin for oxygen, making it less available to tissues. This means that if the same amount of O2 is taken up, the venous saturation will be lower with hyperventilation since less dissolved O2 (leading to a lower venous PO2) will be available to meet organ demands. This means that the fall in SjO2 and rise in AVDO2 could be related to shifts in hemoglobin affinity for oxygen, not just to changes in cerebral blood flow. The equation Thiagarajan et al used to calculate oxygen content employed the same constant for oxygen binding in calculating venous and arterial values. This does not negate the finding that increasing arterial saturation increased jugular venous saturation during hyperventilation, but it does bring into question the importance of the findings.
Another issue is the implication that cerebral ischemia occurred with hyperventilation and that increasing the SjO2 improved ischemia. No evidence was presented that suggested inadequate oxygen uptake in any of the experimental conditions. Tissue oxygen demands should have been met by the increased AVDO2 observed. Jugular venous lactate or creatine kinase brain fraction (CK-BB) would have been an interesting correlate to evaluate whether severe ischemia was occurring. Direct or indirect measurements of cerebral blood flow would have improved the interpretation of the observations in this study.
These criticisms aside, this study may have important implications to the everyday care of the head-injured patient. Increasing PaO2 to greater than 200 torr during acute hyperventilation seems to have a salient effect on cerebral oxygen kinetics. Based on this preliminary study, increasing the inspired oxygen concentration during episodes of acute hyperventilation in head-injured patients is reasonable.
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