Background Obstructive sleep apnea (OSA) is a common disorder that is highly associated with postoperative complications. The STOP-Bang questionnaire is a simple screening tool for OSA. The objective of this systematic review and meta-analysis is to evaluate the validity of the STOP-Bang questionnaire for screening OSA in the surgical population cohort. Methods A systematic search of the following databases was performed from 2008 to May 2021: MEDLINE, Medline-in-process, Embase, Cochrane Central Register of Controlled Trials, Cochrane Database of Systematic Reviews, PsycINFO, Journals @ Ovid, Web of Science, Scopus, and CINAHL. Continued literature surveillance was performed through October 2021. Results The systematic search identified 4641 articles, from which 10 studies with 3247 surgical participants were included in the final analysis. The mean age was 57.3 ± 15.2 years, and the mean BMI was 32.5 ± 10.1 kg/m2 with 47.4% male. The prevalence of all, moderate-to-severe, and severe OSA were 65.2, 37.7, and 17.0%, respectively. The pooled sensitivity of the STOP-Bang questionnaire for all, moderate-to-severe, and severe OSA was 85, 88, and 90%, and the pooled specificities were 47, 29, and 27%, respectively. The area under the curve for all, moderate-to-severe, and severe OSA was 0.84, 0.67, and 0.63. Conclusions In the preoperative setting, the STOP-Bang questionnaire is a valid screening tool to detect OSA in patients undergoing surgery, with a high sensitivity and a high discriminative power to reasonably exclude severe OSA with a negative predictive value of 93.2%. Trial registration PROSPERO registration CRD42021260451.
In the absence of central chemoreceptor input, the slope of the hypoxic ventilatory response (HVR) to progressive oxyhemoglobin desaturation (L·min-1·mmHg-1·%SaO2-1) – a measure of peripheral chemoreflex sensitivity – increases linearly with carbon dioxide tension (PCO2). We assessed whether this relationship remains linear with increasing central PCO2 in humans. Over four days, 20 participants (10 females; mean±SD age: 24±4 years) completed three repetitions of modified rebreathing with end-tidal PO2 (PETO2) clamped at 150, 70, 60, and 45 mmHg. End-tidal PCO2 (PETCO2), PETO2, ventilation (V̇E), and SaO2 were measured breath-by-breath by dual gas analyser, pneumotach, and pulse oximetry. The V̇E vs PETCO2 relationship in the hyperoxic test gave the central chemoreflex response to PCO2 and the hypoxic tests provided a combined central-peripheral chemoreflex response. The V̇E vs PETCO2 relationship of repeated trials were linear-interpolated, combined, averaged into 1 mmHg bins, and fit with a linear function (V̇ES, L·min-1·mmHg-1) to provide hyperoxic and hypoxic profiles. HVR was computed at 1 mmHg intervals of PETCO2 as follows: the difference in V̇E between the three hypoxic profiles and the hyperoxic profile (ΔV̇E) was calculated; these three ΔV̇E values were plotted against their corresponding SaO2; and linear regression determined HVR (L·min-1·mmHg-1·%SaO2-1). Steps were repeated at each PETCO2 to produce the HVR vs PCO2 relationship. Each participant’s HVR vs PETCO2 relationship was fit with a linear and polynomial function and Akaike Information Criterion identified the best-fit model. One-way repeated measures analysis of variance assessed between-condition differences. V̇ES rose (p<0.001) with isoxic PO2 from 3.7±1.5 L·min-1·mmHg-1 at 150 mmHg to 4.4±1.8, 5.0±1.6, and 6.0±2.2 L·min-1·mmHg-1 at 70, 60, and 45 mmHg, respectively. Mean SaO2 fell progressively (99.3%, 93.7%, 90.4%, and 80.5% for 150, 70, 60, and 45 mmHg, respectively; p<0.001). In all individuals, HVR increased with PETCO2 and this relationship was best described by a linear model in 75% of participants. In most participants, the peripheral chemoreflex-mediated HVR maintained a linear relationship with PETCO2 despite increasing central chemoreflex activation. Data suggest that central chemoreceptors did not alter the peripheral chemoreflex response to low O2. Natural Sciences and Engineering Research Council of Canada This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
Hyperoxia has been shown to stimulate ventilation (V̇E) in a dose-dependent manner. Whether this occurs due to an oxygen (O2)-specific mechanism or secondary to carbon dioxide (CO2) retention at the central chemoreceptors (via the Haldane effect) remains unclear. This study measured the ventilatory response to isoxic-hyperoxic CO2 modified rebreathing (an estimate of central chemoreflex sensitivity) with O2 clamped at increasingly higher hyperoxic pressures. We hypothesized that the slope of the V̇E versus PCO2 relationship is fixed and independent of hyperoxic severity. Fourteen healthy participants (6 females; mean ± SD age: 25 ±7 years) visited the laboratory on four occasions to perform three repetitions of modified rebreathing in four isoxic-hyperoxic conditions: “mild”: PO2=150 mmHg; “moderate”: PO2=200 mmHg; “high”: PO2=300 mmHg; and “extreme”: PO2=700 mmHg. The level of isoxic-hyperoxic PO2 was randomized between visits. Throughout rebreathing, breath-by-breath V̇E, end-tidal PCO2 (PETCO2) and O2 (PETO2) were measured by pneumotach and dual gas analyser. For each trial, the PETCO2 at which V̇E began to rise was identified as the ventilatory recruitment threshold (VRT, mmHg). The V̇E data prior to VRT provided baseline V̇E (V̇Ebsl, L∙min-1) and the slope of the linear response above VRT estimated central respiratory chemoreflex sensitivity (V̇ES, L∙min-1∙mmHg-1). For each hyperoxic condition, VRT, V̇Ebsl, and V̇ES from like-trials were averaged and between condition comparisons were assessed by repeated measures analysis of variance. There was no effect of PETO2 on V̇Ebsl (mild: 6.7±3.4 L∙min-1; moderate: 5.9±3.0 L∙min-1; heavy: 5.5±1.6 L∙min-1; extreme: 6.1±3.2 L∙min-1; p=0.35), VRT (mild: 42.7±3.2 mmHg; moderate: 42.0±2.2 mmHg; heavy: 42.2 ±2.4 mmHg; extreme: 41.5±2.4 mmHg; p=0.17) or V̇ES (mild: 5.04±2.78 L∙min-1∙mmHg-1; moderate: 4.64±1.90 L∙min-1∙mmHg-1; heavy: 4.68±1.92 L∙min-1∙mmHg-1; extreme: 4.49±1.72 L∙min-1∙mmHg-1; p=0.47). The hyperoxic V̇E versus PCO2 relationship was unaltered across a range of PO2 spanning mild to extreme. These data indicate that hyperoxia is not an independent stimulant of breathing. Supported by NSERC This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.
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