Cerebral oximetry with blood volume index and capnography in intubated and hyperventilated patients

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Abstract

Objective:

Hyperventilation-induced hypocapnia leads to cerebral vasoconstriction and hypoperfusion. Intubated patients are often inadvertently hyperventilated during resuscitations, causing theoretical risk for ischemic brain injury. Current emergency department monitoring systems do not detect these changes. The purpose of this study was to determine if cerebral oximetry (rcSo2) with blood volume index (CBVI) would detect hypocapnia-induced cerebral tissue hypoxia and hypoperfusion.

Methods:

Patients requiring mechanical ventilation underwent end-tidal CO2 (ETco2), rcSo2, and CBVI monitoring. Baseline data was analyzed and then the effect of varying ETco2 on rcSo2 and CBVI readings was analyzed. Median rcSo2 and CBVI values were compared when above and below the ETco2 30 mmHg threshold. Subgroup analysis and descriptive statistics were also calculated.

Results:

Thirty-two patients with neurologic emergencies and potential increased intracranial pressure were included. Age ranged from 6 days to 15 years (mean age, 3.1 years; SD, 3.9 years; median age, 1.5 years: 0.46-4.94 years). Diagnoses included bacterial meningitis, viral meningitis, and seizures. ETco2 crossed 30 mm Hg 80 times. Median left and right rcSO2 when ETCO2 was below 30 mmhg was 40.98 (35.3, 45.04) and 39.84 (34.64, 41) respectively. Median left and right CBVI when ETCO2 was below 30 mmhg was -24.86 (-29.92, -19.71) and -22.74 (-27.23, - 13.55) respectively. Median left and right CBVI when ETCO2 was below 30 mmHg was −24.86 (−29.92, −19.71) and −22.74 (−27.23, −13.55) respectively. Median left and right rcSO2 when ETCO2 was above 30 mmHg was 63.53 (61.41, 66.92) and 63.95 (60.23, 67.58) respectively. Median left and right CBVI when ETCO2 was above 30 mmHg was 12.26 (0.97, 20.16) and 8.11 (−0.2, 21.09) respectively. Median duration ETco2 was below 30 mmHg was 17.9 minutes (11.4, 26.59). Each time ETco2 fell below the threshold, there was a significant decrease in rcSo2 and CBVI consistent with decreased cerebral blood flow. While left and right rcSO2 and CBVI decreased quickly once ETCO2 was below 30 mmHg, increase once ETCO2 was above 30 mmHg was much slower.

Conclusion:

This preliminary study has demonstrated the ability of rcSo2 with CBVI to noninvasively detect the real-time effects of excessive hyperventilation producing ETco2 < 30 mmHg on cerebral physiology in an emergency department. We have demonstrated in patients with suspected increased intracranial pressure that ETco2 < 30 mmHg causes a significant decrease in cerebral blood flow and regional tissue oxygenation.

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