Cerebrovascular CO2 reactivity during isoflurane-nitrous oxide anesthesia in patients with chronic renal failure

• Published in: Journal of anesthesia 2018-02, Vol.32 (1), p.15-22
• Main Authors: Ishida, Kazuyoshi, Uchida, Masato, Utada, Kohji, Yamashita, Atsuo, Yamashita, Satoshi, Fukuda, Shiro, Matsumoto, Mishiya, Sakabe, Takefumi
• Format: Article
• Language: English
• Subjects: Anesthesiology; Critical Care Medicine; Emergency Medicine; Intensive; Medicine; Medicine & Public Health; Original Article; Pain Medicine
• ISSN: 0913-8668; 1438-8359
• DOI: 10.1007/s00540-017-2422-3

Purpose We assessed the cerebrovascular CO 2 reactivity (CO 2 R) in chronic renal failure (CRF) patients without diabetes mellitus (DM), uncontrolled hypertension, peripheral vascular disease, or neurological disease under isoflurane-nitrous oxide anesthesia. Methods Forty-nine patients undergoing surgery, including 36 CRF patients (30 receiving dialysis and six pre-dialysis patients) and 13 patients without CRF (controls). Middle cerebral artery flow velocity (VMCA) was measured by transcranial Doppler ultrasonography at an end-tidal CO 2 of 35 to 45 mmHg. CO 2 R was calculated as an absolute value (change in VMCA per mmHg PaCO 2 ) and a relative value (absolute CO 2 R/baseline VMCA × 100). Factors associated with CO 2 R were evaluated simultaneously. Results Despite no significant differences in the absolute and relative values of CO 2 R between the CRF (mean 2.5 cm/s/mmHg; median 5.0%/mmHg) and control (2.4 cm/s/mmHg; 5.0%/mmHg) groups, blood urea nitrogen (BUN) concentrations in the CRF group correlated inversely with both absolute and relative CO 2 R. BUN concentration was higher (mean 72 versus 53 mg/dl, p  = 0.006) and relative CO 2 R was lower (mean 2.6 versus 5.7%/mmHg, p  = 0.011) in patients with pre-dialysis CRF ( n  = 6) versus CRF patients receiving dialysis ( n  = 30). Conclusions CO 2 R in CRF patients was not significantly different from that in controls. However, in CRF patients with high BUN concentrations, CO 2 R might be impaired, leading to reduced cerebrovascular reserve capacity. Because DM is a major cause of CRF and we excluded DM patients, our results might not be applicable to patients with DM-induced CRF.