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Diffuse Optical Monitoring of Cerebral Hemodynamics and Oxygen Metabolism during and after Cardiopulmonary Bypass: Hematocrit Correction and Neurological Vulnerability

Cardiopulmonary bypass (CPB) provides cerebral oxygenation and blood flow (CBF) during neonatal congenital heart surgery, but the impacts of CPB on brain oxygen supply and metabolic demands are generally unknown. To elucidate this physiology, we used diffuse correlation spectroscopy and frequency-do...

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Detalles Bibliográficos
Autores principales: Benson, Emilie J., Aronowitz, Danielle I., Forti, Rodrigo M., Lafontant, Alec, Ranieri, Nicolina R., Starr, Jonathan P., Melchior, Richard W., Lewis, Alistair, Jahnavi, Jharna, Breimann, Jake, Yun, Bohyun, Laurent, Gerard H., Lynch, Jennifer M., White, Brian R., Gaynor, J. William, Licht, Daniel J., Yodh, Arjun G., Kilbaugh, Todd J., Mavroudis, Constantine D., Baker, Wesley B., Ko, Tiffany S.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10672802/
https://www.ncbi.nlm.nih.gov/pubmed/37999249
http://dx.doi.org/10.3390/metabo13111153
Descripción
Sumario:Cardiopulmonary bypass (CPB) provides cerebral oxygenation and blood flow (CBF) during neonatal congenital heart surgery, but the impacts of CPB on brain oxygen supply and metabolic demands are generally unknown. To elucidate this physiology, we used diffuse correlation spectroscopy and frequency-domain diffuse optical spectroscopy to continuously measure CBF, oxygen extraction fraction (OEF), and oxygen metabolism (CMRO(2)) in 27 neonatal swine before, during, and up to 24 h after CPB. Concurrently, we sampled cerebral microdialysis biomarkers of metabolic distress (lactate–pyruvate ratio) and injury (glycerol). We applied a novel theoretical approach to correct for hematocrit variation during optical quantification of CBF in vivo. Without correction, a mean (95% CI) +53% (42, 63) increase in hematocrit resulted in a physiologically improbable +58% (27, 90) increase in CMRO(2) relative to baseline at CPB initiation; following correction, CMRO(2) did not differ from baseline at this timepoint. After CPB initiation, OEF increased but CBF and CMRO(2) decreased with CPB time; these temporal trends persisted for 0–8 h following CPB and coincided with a 48% (7, 90) elevation of glycerol. The temporal trends and glycerol elevation resolved by 8–24 h. The hematocrit correction improved quantification of cerebral physiologic trends that precede and coincide with neurological injury following CPB.