Key result
A decrease in end-tidal CO2 >26% during hyperventilation strongly predicted changes in cerebral oximetry measured by near-infrared spectroscopy (AUC-ROC 0.93, p<0.0001).
Why the study?
The hyperventilation test lacks a standardized protocol, varying significantly and risking cerebral hypoxia or ischemia, prompting evaluation of near-infrared spectroscopy to identify the minimum end-tidal CO2 decrease needed to induce cerebral oximetry changes.
Can Near-Infrared Spectroscopy (NIRS) and ETCO2 monitoring identify the minimum decrease in ETCO2 necessary to induce cerebral vasoconstriction during hyperventilation?
Observational (n=46)
Can Near-Infrared Spectroscopy (NIRS) and ETCO2 monitoring identify the minimum decrease in ETCO2 necessary to induce cerebral vasoconstriction during hyperventilation?
Synchronous ETCO2 and NIRS monitoring can effectively predict cerebral vasoconstriction during hyperventilation, with an ETCO2 decrease >26% serving as a reliable cutoff.
ETCO2 drop >26% may flag cerebral vasoconstriction risk with NIRS; hypothesis-generating and requires prospective validation before clinical use.
Background: The hyperventilation test is used in clinical practice for diagnosis and therapeutic purposes; however, in the absence of a standardized protocol, the procedure varies significantly, predisposing tested subjects to risks such as cerebral hypoxia and ischemia. Near-infrared spectroscopy (NIRS), a noninvasive technique performed for cerebral oximetry monitoring, was used in the present study to identify the minimum decrease in the end-tidal CO2 (ETCO2) during hyperventilation necessary to induce changes on NIRS. Materials and Methods: We recruited 46 volunteers with no preexisting medical conditions. Each subject was asked to breathe at a baseline rate (8−14 breaths/min) for 2 min and then to hyperventilate at a double respiratory rate for the next 4 min. The parameters recorded during the procedure were the regional cerebral oxyhemoglobin and deoxyhemoglobin concentrations via NIRS, ETCO2, and the respiratory rate. Results: During hyperventilation, ETCO2 values dropped (31.4 ± 12.2%) vs. baseline in all subjects. Changes in cerebral oximetry were observed only in those subjects (n = 30) who registered a decrease (%) in ETCO2 of 37.58 ± 10.34%, but not in the subjects (n = 16) for which the decrease in ETCO2 was 20.31 ± 5.6%. According to AUC-ROC analysis, a cutoff value of ETCO2 decrease >26% was found to predict changes in oximetry (AUC-ROC = 0.93, p < 0.0001). Seven subjects reported symptoms, such as dizziness, vertigo, and numbness, throughout the procedure. Conclusions: The rise in the respiratory rate alone cannot effectively predict the occurrence of a cerebral vasoconstrictor response induced by hyperventilation, and synchronous ETCO2 and cerebral oximetry monitoring could be used to validate this clinical test. NIRS seems to be a useful tool in predicting vasoconstriction following hyperventilation.
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Sandru et al. (2022) conducted an observational in Healthy volunteers (n=46). Hyperventilation vs. Baseline breathing was evaluated on Changes in cerebral oximetry predicted by ETCO2 decrease (AUC-ROC 0.93, p=< 0.0001). A decrease in end-tidal CO2 >26% during hyperventilation strongly predicted changes in cerebral oximetry measured by near-infrared spectroscopy (AUC-ROC 0.93, p<0.0001).
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