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Changes in cerebral oxygenation based on intraoperative ventilation strategy

INTRODUCTION: Cerebral oxygenation can be monitored clinically by cerebral oximetry (regional oxygen saturation, rSO(2)) using near-infrared spectroscopy (NIRS). Changes in rSO(2) have been shown to precede changes in pulse oximetry, providing an early detection of clinical deterioration. Cerebral o...

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Detalles Bibliográficos
Autores principales: Dewhirst, Elisabeth, Walia, Hina, Samora, Walter P, Beebe, Allan C, Klamar, Jan E, Tobias, Joseph D
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Dove Medical Press 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6065577/
https://www.ncbi.nlm.nih.gov/pubmed/30100768
http://dx.doi.org/10.2147/MDER.S158262
Descripción
Sumario:INTRODUCTION: Cerebral oxygenation can be monitored clinically by cerebral oximetry (regional oxygen saturation, rSO(2)) using near-infrared spectroscopy (NIRS). Changes in rSO(2) have been shown to precede changes in pulse oximetry, providing an early detection of clinical deterioration. Cerebral oximetry values may be affected by various factors, including changes in ventilation. The aim of this study was to evaluate the changes in rSO(2) during intraoperative changes in mechanical ventilation. PATIENTS AND METHODS: Following the approval of the institutional review board (IRB), tissue and cerebral oxygenation were monitored intraoperatively using NIRS. Prior to anesthetic induction, the NIRS monitor was placed on the forehead and over the deltoid muscle to obtain baseline values. NIRS measurements were recorded each minute over a 5-min period during general anesthesia at four phases of ventilation: 1) normocarbia (35–40 mmHg) with a low fraction of inspired oxygen (FiO(2)) of 0.3; 2) hypocarbia (25–30 mmHg) and low FiO(2) of 0.3; 3) hypocarbia and a high FiO(2) of 0.6; and 4) normocarbia and a high FiO(2). NIRS measurements during each phase were compared with sequential phases using paired t-tests. RESULTS: The study cohort included 30 adolescents. Baseline cerebral and tissue oxygenation were 81% ± 9% and 87% ± 5%, respectively. During phase 1, cerebral rSO(2) was 83% ± 8%, which decreased to 79% ± 8% in phase 2 (hypocarbia and low FiO(2)). Cerebral oxygenation partially recovered during phase 3 (81% ± 9%) with the increase in FiO(2) and then returned to baseline during phase 4 (83% ± 8%). Each sequential change (e.g., phase 1 to phase 2) in cerebral oxygenation was statistically significant (p < 0.01). Tissue oxygenation remained at 87%–88% throughout the study. CONCLUSION: Cerebral oxygenation declined slightly during general anesthesia with the transition from normocarbia to hypocarbic conditions. The rSO(2) decrease related to hypocarbia was easily reversed with a return to baseline values by the administration of supplemental oxygen (60% vs. 30%).