TY - JOUR
T1 - The Influence of Carbon Dioxide on Cerebral Autoregulation during Sevoflurane-based Anesthesia in Patients with Type 2 Diabetes
AU - van den Dool, Rokus E. C.
AU - Immink, Rogier V.
AU - van der Ster, Bjorn P.
AU - Hermanides, Jeroen
AU - Hollmann, Markus W.
AU - Preckel, Prof. dr. , Benedikt
AU - van Lieshout, Johannes J.
AU - Sperna Weiland, Niek H.
N1 - Funding Information: The study was investigator-initiated and was supported by a €51,000 grant from the European Society of Anaesthesiology. Publisher Copyright: © 2023 Lippincott Williams and Wilkins. All rights reserved.
PY - 2023/1/1
Y1 - 2023/1/1
N2 - Background: Cerebral autoregulation (CA) continuously adjusts cerebrovascular resistance to maintain cerebral blood flow (CBF) constant despite changes in blood pressure. Also, CBF is proportional to changes in arterial carbon dioxide (CO2) (cerebrovascular CO2reactivity). Hypercapnia elicits cerebral vasodilation that attenuates CA efficacy, while hypocapnia produces cerebral vasoconstriction that enhances CA efficacy. In this study, we quantified the influence of sevoflurane anesthesia on CO2reactivity and the CA-CO2relationship. Methods: We studied patients with type 2 diabetes mellitus (DM), prone to cerebrovascular disease, and compared them to control subjects. In 33 patients (19 DM, 14 control), end-tidal CO2, blood pressure, and CBF velocity were monitored awake and during sevoflurane-based anesthesia. CA, calculated with transfer function analysis assessing phase lead (degrees) between low-frequency oscillations in CBF velocity and mean arterial blood pressure, was quantified during hypocapnia, normocapnia, and hypercapnia. Results: In both control and DM patients, awake CO2reactivity was smaller (2.8%/mm Hg CO2) than during sevoflurane anesthesia (3.9%/mm Hg; P<0.005). Hyperventilation increased CA efficacy more (3 deg./mm Hg CO2) in controls than in DM patients (1.8 deg./mm Hg CO2; P<0.001) in both awake and sevoflurane-anesthetized states. Conclusions: The CA-CO2relationship is impaired in awake patients with type 2 DM. Sevoflurane-based anesthesia does not further impair this relationship. In patients with DM, hypocapnia induces cerebral vasoconstriction, but CA efficacy does not improve as observed in healthy subjects.
AB - Background: Cerebral autoregulation (CA) continuously adjusts cerebrovascular resistance to maintain cerebral blood flow (CBF) constant despite changes in blood pressure. Also, CBF is proportional to changes in arterial carbon dioxide (CO2) (cerebrovascular CO2reactivity). Hypercapnia elicits cerebral vasodilation that attenuates CA efficacy, while hypocapnia produces cerebral vasoconstriction that enhances CA efficacy. In this study, we quantified the influence of sevoflurane anesthesia on CO2reactivity and the CA-CO2relationship. Methods: We studied patients with type 2 diabetes mellitus (DM), prone to cerebrovascular disease, and compared them to control subjects. In 33 patients (19 DM, 14 control), end-tidal CO2, blood pressure, and CBF velocity were monitored awake and during sevoflurane-based anesthesia. CA, calculated with transfer function analysis assessing phase lead (degrees) between low-frequency oscillations in CBF velocity and mean arterial blood pressure, was quantified during hypocapnia, normocapnia, and hypercapnia. Results: In both control and DM patients, awake CO2reactivity was smaller (2.8%/mm Hg CO2) than during sevoflurane anesthesia (3.9%/mm Hg; P<0.005). Hyperventilation increased CA efficacy more (3 deg./mm Hg CO2) in controls than in DM patients (1.8 deg./mm Hg CO2; P<0.001) in both awake and sevoflurane-anesthetized states. Conclusions: The CA-CO2relationship is impaired in awake patients with type 2 DM. Sevoflurane-based anesthesia does not further impair this relationship. In patients with DM, hypocapnia induces cerebral vasoconstriction, but CA efficacy does not improve as observed in healthy subjects.
KW - carbon dioxide/blood
KW - cerebrovascular circulation/physiology
KW - diabetes mellitus type 2
KW - sevoflurane
UR - http://www.scopus.com/inward/record.url?scp=85132977806&partnerID=8YFLogxK
U2 - https://doi.org/10.1097/ANA.0000000000000794
DO - https://doi.org/10.1097/ANA.0000000000000794
M3 - Article
C2 - 34387283
SN - 0898-4921
VL - 35
SP - 65
EP - 73
JO - Journal of Neurosurgical Anesthesiology
JF - Journal of Neurosurgical Anesthesiology
IS - 1
ER -