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 (r_cSo₂) with blood volume index (CBVI) would detect hypocapnia-induced cerebral tissue hypoxia and hypoperfusion.

Patients requiring mechanical ventilation underwent end-tidal CO₂ (ETco₂), r_cSo₂, and CBVI monitoring. Baseline data was analyzed and then the effect of varying ETco₂ on r_cSo₂ and CBVI readings was analyzed. Median r_cSo₂ and CBVI values were compared when above and below the ETco₂ 30 mmHg threshold. Subgroup analysis and descriptive statistics were also calculated.

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 r_cSO₂ 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 r_cSO₂ 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 r_cSo₂ and CBVI consistent with decreased cerebral blood flow. While left and right r_cSO₂ and CBVI decreased quickly once ETCO₂​ was below 30 mmHg, increase once ETCO₂​ was above 30 mmHg was much slower.

This preliminary study has demonstrated the ability of r_cSo₂ 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.