Graded Hypercapnia and Cerebral Autoregulation during Sevoflurane or Propofol Anesthesia

Background Hypercapnia abolishes cerebral autoregulation, but little is known about the interaction between hypercapnia and autoregulation during general anesthesia. With normocapnia, sevoflurane (up to 1.5 minimum alveolar concentration) and propofol do not impair cerebral autoregulation. This study aimed to document the level of hypercapnia required to impair cerebral autoregulation during propofol or sevoflurane anesthesia. Methods Eight healthy subjects received a remifentanil infusion and were anesthetized with propofol (140 microg. kg-1. min-1) and sevoflurane (1.0-1.1% end tidal) in a randomized crossover study. Ventilation was adjusted to achieve incremental increases in arterial carbon dioxide partial pressure (Paco2) until autoregulation was impaired. Cerebral autoregulation was tested by increasing the mean arterial pressure (MAP) from 80 to 100 mmHg with phenylephrine while measuring middle cerebral artery flow velocity by transcranial Doppler. The autoregulation index, which has a value ranging from 0 to 1, representing absent to perfect autoregulation, was calculated, and an autoregulation index of 0.4 or less represented significantly impaired autoregulation. Results The threshold Paco2 to significantly impair cerebral autoregulation ranged from 50 to 66 mmHg. The threshold averaged 56 +/- 4 mmHg (mean +/- SD) during sevoflurane anesthesia and 61 +/- 4 mmHg during propofol anesthesia (P = 0.03). Carbon dioxide reactivity measured at a MAP of 100 mmHg was 30% greater than that at a MAP of 80 mmHg. Conclusions Even mild hypercapnia can significantly impair cerebral autoregulation during general anesthesia. There is a significant difference between propofol anesthesia and sevoflurane anesthesia with respect to the effect of hypercapnia on cerebral autoregulation. This difference occurs at clinically relevant levels of Paco2. When inducing hypercapnia, carbon dioxide reactivity is significantly affected by the MAP.

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Faculty Opinions recommendation of The influence of inspired oxygen fraction and end-tidal carbon dioxide on post-cross-clamp cerebral oxygenation during carotid endarterectomy under general anesthesia.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.3232960.2917060 ◽

2010 ◽

Author(s):

Ian Herrick

Keyword(s):

Carbon Dioxide ◽

General Anesthesia ◽

Carotid Endarterectomy ◽

Cerebral Oxygenation ◽

Oxygen Fraction ◽

End Tidal Carbon Dioxide ◽

End Tidal ◽

Inspired Oxygen

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Cerebrovascular Carbon Dioxide Reactivity During General Anesthesia: A Comparison Between Sevoflurane and Isoflurane

Anesthesia & Analgesia ◽

10.1097/00000539-199912000-00021 ◽

1999 ◽

Vol 89 (6) ◽

pp. 1437 ◽

Cited By ~ 6

Author(s):

Tomoki Nishiyama ◽

Takashi Matsukawa ◽

Takeshi Yokoyama ◽

Kazuo Hanaoka

Keyword(s):

Carbon Dioxide ◽

General Anesthesia ◽

Carbon Dioxide Reactivity ◽

Cerebrovascular Carbon Dioxide Reactivity

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Low levels of end-tidal carbon dioxide during general anesthesia and postoperative mortality

Canadian Journal of Anesthesia/Journal canadien d anesthésie ◽

10.1007/s12630-021-02154-4 ◽

2021 ◽

Author(s):

Ali Solhpour

Keyword(s):

Carbon Dioxide ◽

General Anesthesia ◽

Postoperative Mortality ◽

End Tidal Carbon Dioxide ◽

Low Levels ◽

End Tidal

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Comparisons of the Nonlinear Relationship of Cerebral Blood Flow Response and Cerebral Vasomotor Reactivity to Carbon Dioxide under Hyperventilation between Postural Orthostatic Tachycardia Syndrome Patients and Healthy Subjects

Journal of Clinical Medicine ◽

10.3390/jcm9124088 ◽

2020 ◽

Vol 9 (12) ◽

pp. 4088

Author(s):

Shyan-Lung Lin ◽

Shoou-Jeng Yeh ◽

Ching-Kun Chen ◽

Yu-Liang Hsu ◽

Chih-En Kuo ◽

...

Keyword(s):

Carbon Dioxide ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Blood Flow Velocity ◽

Cerebral Blood Flow Velocity ◽

Postural Orthostatic Tachycardia Syndrome ◽

Significant Difference ◽

Cerebral Vasomotor Reactivity ◽

End Tidal ◽

Fitting Model

Postural orthostatic tachycardia syndrome (POTS) typically occurs in youths, and early accurate POTS diagnosis is challenging. A recent hypothesis suggests that upright cognitive impairment in POTS occurs because reduced cerebral blood flow velocity (CBFV) and cerebrovascular response to carbon dioxide (CO2) are nonlinear during transient changes in end-tidal CO2 (PETCO2). This novel study aimed to reveal the interaction between cerebral autoregulation and ventilatory control in POTS patients by using tilt table and hyperventilation to alter the CO2 tension between 10 and 30 mmHg. The cerebral blood flow velocity (CBFV), partial pressure of end-tidal carbon dioxide (PETCO2), and other cardiopulmonary signals were recorded for POTS patients and two healthy groups including those aged >45 years (Healthy-Elder) and aged <45 years (Healthy-Youth) throughout the experiment. Two nonlinear regression functions, Models I and II, were applied to evaluate their CBFV-PETCO2 relationship and cerebral vasomotor reactivity (CVMR). Among the estimated parameters, the curve-fitting Model I for CBFV and CVMR responses to CO2 for POTS patients demonstrated an observable dissimilarity in CBFVmax (p = 0.011), mid-PETCO2 (p = 0.013), and PETCO2 range (p = 0.023) compared with those of Healthy-Youth and in CBFVmax (p = 0.015) and CVMRmax compared with those of Healthy-Elder. With curve-fitting Model II for POTS patients, the fit parameters of curvilinear (p = 0.036) and PETCO2 level (p = 0.033) displayed significant difference in comparison with Healthy-Youth parameters; range of change (p = 0.042), PETCO2 level, and CBFVmax also displayed a significant difference in comparison with Healthy-Elder parameters. The results of this study contribute toward developing an early accurate diagnosis of impaired CBFV responses to CO2 for POTS patients.

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