Milam, Adam J.

BACKGROUND: Arterial hyperoxemia may cause end-organ damage secondary to the increased formation of free oxygen radicals. The clinical evidence on postoperative lung toxicity from arterial hyperoxemia during cardiopulmonary bypass (CPB) is scarce, and the effect of arterial partial pressure of oxygen (Pa o 2 ) during cardiac surgery on lung injury has been underinvestigated. Thus, we aimed to examine the relationship between Pa o 2 during CPB and postoperative lung injury. Secondarily, we examined the relationship between Pa o 2 and global (lactate), and regional tissue malperfusion (acute kidney injury). We further explored the association with regional tissue malperfusion by examining markers of cardiac (troponin) and liver injury (bilirubin). METHODS: This was a retrospective cohort study including patients who underwent elective cardiac surgeries (coronary artery bypass, valve, aortic, or combined) requiring CPB between April 2015 and December 2021 at a large quaternary medical center. The primary outcome was postoperative lung function defined as the ratio of Pa o 2 to fractional inspired oxygen concentration (F io 2 ); P/F ratio 6 hours following surgery or before extubation. The association between CPB in-line sample monitor Pa o 2 and primary, secondary, and exploratory outcomes was evaluated using linear or logistic regression models adjusting for available baseline confounders. RESULTS: A total of 9141 patients met inclusion and exclusion criteria, and 8429 (92.2%) patients had complete baseline variables available and were included in the analysis. The mean age of the sample was 64 (SD = 13), and 68% were men (n = 6208). The time-weighted average (TWA) of in-line sample monitor Pa o 2 during CPB was weakly positively associated with the postoperative P/F ratio. With a 100-unit increase in Pa o 2 , the estimated increase in postoperative P/F ratio was 4.61 (95% CI, 0.71–8.50; P = .02). Our secondary analysis showed no significant association between Pa o 2 with peak lactate 6 hours post CPB (geometric mean ratio [GMR], 1.01; 98.3% CI, 0.98–1.03; P = .55), average lactate 6 hours post CPB (GMR, 1.00; 98.3% CI, 0.97–1.03; P = .93), or acute kidney injury by Kidney Disease Improving Global Outcomes (KDIGO) criteria (odds ratio, 0.91; 98.3% CI, 0.75–1.10; P = .23). CONCLUSIONS: Our investigation found no clinically significant association between Pa o 2 during CPB and postoperative lung function. Similarly, there was no association between Pa o 2 during CPB and lactate levels, postoperative renal function, or other exploratory outcomes.

BACKGROUND: A racial compensation disparity among physicians across numerous specialties is well documented and persists after adjustment for age, sex, experience, work hours, productivity, academic rank, and practice structure. This study examined national survey data to determine whether there are racial differences in compensation among anesthesiologists in the United States. METHODS: In 2018, 28,812 active members of the American Society of Anesthesiologists were surveyed to examine compensation among members. Compensation was defined as the amount reported as direct compensation on a W-2, 1099, or K-1, plus all voluntary salary reductions (eg, 401[k], health insurance). Covariates potentially associated with compensation were identified (eg, sex and academic rank) and included in regression models. Racial differences in outcome and model variables were assessed via Wilcoxon rank sum tests and Pearson’s χ 2 tests. Covariate adjusted ordinal logistic regression estimated an odds ratio (OR) for the relationship between race and ethnicity and compensation while adjusting for provider and practice characteristics. RESULTS: The final analytical sample consisted of 1952 anesthesiologists (78% non-Hispanic White). The analytic sample represented a higher percentage of White, female, and younger physicians compared to the demographic makeup of anesthesiologists in the United States. When comparing non-Hispanic White anesthesiologists with anesthesiologists from other racial and ethnic minority groups, (ie, American Indian/Alaska Native, Asian, Black, Hispanic, and Native Hawaiian/Pacific Islander), the dependent variable (compensation range) and 6 of the covariates (sex, age, spousal work status, region, practice type, and completed fellowship) had significant differences. In the adjusted model, anesthesiologists from racial and ethnic minority populations had 26% lower odds of being in a higher compensation range compared to White anesthesiologists (OR, 0.74; 95% confidence interval [CI], 0.61–0.91). CONCLUSIONS: Compensation for anesthesiologists showed a significant pay disparity associated with race and ethnicity even after adjusting for provider and practice characteristics. Our study raises concerns that processes, policies, or biases (either implicit or explicit) persist and may impact compensation for anesthesiologists from racial and ethnic minority populations. This disparity in compensation requires actionable solutions and calls for future studies that investigate contributing factors and to validate our findings given the low response rate.

Purpose To examine the relationship between experiences of discrimination, institutional responses to seminal race events, and depressive symptoms among Black medical students. Method This study collected data from a convenience sample of Black U.S. medical students via an anonymous electronic questionnaire in August 2020 that was distributed through the Student National Medical Association and Organization of Student Representatives listservs and an author’s social media accounts. It included questions on demographics, institutional responses to seminal race events, experiences of discrimination, and symptoms of depression. Path models were used to examine the relationship between experiences of discrimination, institutional responses to seminal race events, and depressive symptoms among Black medical students. Results Of the 750 students completing the survey, 733 (97.7%) were Black. Experiences of discrimination and a lack of institutional responses to seminal race events were associated with more depressive symptoms ( b = 0.19, 95% CI: 0.11, 0.26; P < .001 and b = 0.12, 95% CI: 0.04, 0.20; P = .01). After controlling for gender and clinical diagnosis of depression or anxiety before medical school, there was a relationship between experiences of discrimination and institutional responses to seminal race events such that students who reported more experiences of discrimination were more likely to report that their institution did not respond to seminal race events ( b = 0.41, 95% CI: 0.34, 0.48; P < .001). Experiences of discrimination moderated the relationship between institutional responses to seminal race events and depressive symptoms (i.e., the relationship between a lack of institutional responses to seminal race events and depressive symptoms was stronger among students who reported more frequent experiences of discrimination). Conclusions Institutions dedicated to supporting Black medical student wellness must be diligent in cultivating a culture intolerant of discrimination and deft in their responses to seminal race events in the larger culture.