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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Article Info
Publication History
Published online: March 04, 2016
Accepted:
March 1,
2016
Received in revised form:
February 29,
2016
Received:
January 9,
2016
Footnotes
☆Work previously presented at the 22nd Pediatric Critical Care Colloquium; poster session; September 11-13, 2015; Little Rock, AR.
☆☆Grants/funding: none obtained for this study.
★Conflicts of interest: The authors declare that they have no conflict of interest.
★★Author contributions: TAB and TJA conceived the study, designed the trial, ensured data collection, and drafted figures/tables and manuscript. TJA, GWA, JWO, EAS, NWHP, TMT, and EO assisted with conduction of the study and data collection. ZH and TN provided statistical planning/design and data analysis. All authors contributed significantly to manuscript revision and editing.
Identification
Copyright
© 2016 Elsevier Inc. All rights reserved.
