Hyperoxia may considerably decrease cardiac output and increase systemic vascular resistance, but effects differ between patient categories. Heart failure patients were the most sensitive while no hemodynamic effects were seen in septic patients. There is currently no evidence supporting the notion that oxygen supplementation increases oxygen delivery.

BackgroundThe safety of perioperative hyperoxia is currently unclear. Previous studies in patients undergoing coronary artery bypass surgery suggest reduced myocardial damage when avoiding extreme perioperative hyperoxia (>400 mmHg). In this study we investigated whether an oxygenation strategy from moderate hyperoxia to a near-physiological oxygen tension reduces myocardial damage and improves haemodynamics, organ dysfunction and oxidative stress.MethodsThis was a single-blind, single-centre, open-label, randomised controlled trial in patients undergoing elective coronary artery bypass surgery. Fifty patients were randomised to a partial pressure of oxygen in arterial blood (PaO2) target of 200–220 mmHg during cardiopulmonary bypass and 130–150 mmHg during intensive care unit (ICU) admission (control group) versus lower targets of 130–150 mmHg during cardiopulmonary bypass and 80–100 mmHg at the ICU (conservative group). Primary outcome was myocardial injury (CK-MB and Troponin-T) at ICU admission and 2, 6 and 12 hours thereafter.ResultsWeighted PaO2 during cardiopulmonary bypass was 220 mmHg (interquartile range (IQR) 211–233) vs. 157 (151–162) in the control and conservative group, respectively (P < 0.0001). During ICU admission, weighted PaO2 was 107 mmHg (86–141) vs. 90 (84–98) (P = 0.03), respectively. Area under the curve of CK-MB was median 23.5 μg/L/h (IQR 18.4–28.1) vs. 21.5 (15.8–26.6) (P = 0.35) and 0.30 μg/L/h (0.25–0.44) vs. 0.39 (0.24–0.43) (P = 0.81) for Troponin-T. Cardiac index, systemic vascular resistance index, creatinine, lactate and F2-isoprostane levels were not different between groups.ConclusionsCompared to moderate hyperoxia, a near-physiological oxygen strategy does not reduce myocardial damage in patients undergoing coronary artery bypass surgery. Conservative oxygen administration was not associated with increased lactate levels or hypoxic events.Trial registrationNetherlands Trial Registry NTR4375, registered on 30 January 2014Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-016-1240-6) contains supplementary material, which is available to authorized users.

IMPORTANCE Hyperoxemia may increase organ dysfunction in critically ill patients, but optimal oxygenation targets are unknown.OBJECTIVE To determine whether a low-normal PaO 2 target compared with a high-normal target reduces organ dysfunction in critically ill patients with systemic inflammatory response syndrome (SIRS).DESIGN, SETTING, AND PARTICIPANTS Multicenter randomized clinical trial in 4 intensive care units in the Netherlands. Enrollment was from February 2015 to October 2018, with end of follow-up to January 2019, and included adult patients admitted with 2 or more SIRS criteria and expected stay of longer than 48 hours. A total of 9925 patients were screened for eligibility, of whom 574 fulfilled the enrollment criteria and were randomized.INTERVENTIONS Target PaO 2 ranges were 8 to 12 kPa (low-normal, n = 205) and 14 to 18 kPa (high-normal, n = 195). An inspired oxygen fraction greater than 0.60 was applied only when clinically indicated.MAIN OUTCOMES AND MEASURES Primary end point was SOFA RANK , a ranked outcome of nonrespiratory organ failure quantified by the nonrespiratory components of the Sequential Organ Failure Assessment (SOFA) score, summed over the first 14 study days. Participants were ranked from fastest organ failure improvement (lowest scores) to worsening organ failure or death (highest scores). Secondary end points were duration of mechanical ventilation, in-hospital mortality, and hypoxemic measurements. RESULTS Among the 574 patients who were randomized, 400 (70%) were enrolled within 24 hours (median age, 68 years; 140 women [35%]), all of whom completed the trial. The median PaO 2 difference between the groups was −1.93 kPa (95% CI, −2.12 to −1.74; P < .001). The median SOFA RANK score was −35 points in the low-normal PaO 2 group vs −40 in the high-normal PaO 2 group (median difference, 10 [95% CI, 0 to 21]; P = .06). There was no significant difference in median duration of mechanical ventilation (3.4 vs 3.1 days; median difference, −0.15 [95% CI, −0.88 to 0.47]; P = .59) and in-hospital mortality (32% vs 31%; odds ratio, 1.04 [95% CI, 0.67 to 1.63]; P = .91). Mild hypoxemic measurements occurred more often in the low-normal group (1.9% vs 1.2%; median difference, 0.73 [95% CI, 0.30 to 1.20]; P < .001). Acute kidney failure developed in 20 patients (10%) in the low-normal PaO 2 group and 21 patients (11%) in the high-normal PaO 2 group, and acute myocardial infarction in 6 patients (2.9%) in the low-normal PaO 2 group and 7 patients (3.6%) in the high-normal PaO 2 group.CONCLUSIONS AND RELEVANCE Among critically ill patients with 2 or more SIRS criteria, treatment with a low-normal PaO 2 target compared with a high-normal PaO 2 target did not result in a statistically significant reduction in organ dysfunction. However, the study may have had limited power to detect a smaller treatment effect than was hypothesized.

SummaryDuring and after cardiac surgery with cardiopulmonary bypass, high concentrations of oxygen are routinely administered, with the intention of preventing cellular hypoxia. We systematically reviewed the literature addressing the effects of arterial hyperoxia. Extensive evidence from pre-clinical experiments and clinical studies in other patient groups suggests predominant harm, caused by oxidative stress, vasoconstriction, perfusion heterogeneity and myocardial injury.

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BackgroundHyperoxia, an arterial oxygen pressure of more than 100 mmHg or 13% O2, frequently occurs in hospitalized patients due to administration of supplemental oxygen. Increasing evidence suggests that hyperoxia induces vasoconstriction in the systemic (micro)circulation, potentially affecting organ perfusion. This study addresses effects of hyperoxia on viability, proliferative capacity, and on pathways affecting vascular tone in cultured human microvascular endothelial cells (hMVEC).MethodshMVEC of the systemic circulation were exposed to graded oxygen fractions of 20, 30, 50, and 95% O2 for 8, 24, and 72 h. These fractions correspond to 152, 228, 380, and 722 mmHg, respectively. Cell proliferation and viability was measured via a proliferation assay, peroxynitrite formation via anti-nitrotyrosine levels, endothelial nitric oxide synthase (eNOS), and endothelin-1 (ET-1) levels via q-PCR and western blot analysis.ResultsExposing hMVEC to 50 and 95% O2 for more than 24 h impaired cell viability and proliferation. Hyperoxia did not significantly affect nitrotyrosine levels, nor eNOS mRNA and protein levels, regardless of the exposure time or oxygen concentration used. Phosphorylation of eNOS at the serine 1177 (S1177) residue and ET-1 mRNA levels were also not significantly affected.ConclusionsExposure of isolated human microvascular endothelial cells to marked hyperoxia for more than 24 h decreases cell viability and proliferation. Our results do not support a role of eNOS mRNA and protein or ET-1 mRNA in the potential vasoconstrictive effects of hyperoxia on isolated hMVEC.Electronic supplementary materialThe online version of this article (doi:10.1186/s40635-017-0135-4) contains supplementary material, which is available to authorized users.

Vitamin C deficiency is common in critically ill patients. Vitamin C, the most important antioxidant, is likely consumed during oxidative stress and deficiency is associated with organ dysfunction and mortality. Assessment of vitamin C status may be important to identify patients who might benefit from vitamin C administration. Up to now, vitamin C concentrations are not available in daily clinical practice. Recently, a point-of-care device has been developed that measures the static oxidation-reduction potential (sORP), reflecting oxidative stress, and antioxidant capacity (AOC). The aim of this study was to determine whether plasma vitamin C concentrations were associated with plasma sORP and AOC. Plasma vitamin C concentration, sORP and AOC were measured in three groups: healthy volunteers, critically ill patients, and critically ill patients receiving 2- or 10-g vitamin C infusion. Its association was analyzed using regression models and by assessment of concordance. We measured 211 samples obtained from 103 subjects. Vitamin C concentrations were negatively associated with sORP (R2 = 0.816) and positively associated with AOC (R2 = 0.842). A high concordance of 94–100% was found between vitamin C concentration and sORP/AOC. Thus, plasma vitamin C concentrations are strongly associated with plasma sORP and AOC, as measured with a novel point-of-care device. Therefore, measuring sORP and AOC at the bedside has the potential to identify and monitor patients with oxidative stress and vitamin C deficiency.

BackgroundIn spite of the introduction of mild therapeutic hypothermia (MTH), mortality rates remain high in patients with return of spontaneous circulation (ROSC) after cardiac arrest (CA). To date, no accurate and independent biomarker to predict survival in these patients exists. B-type natriuretic peptide (BNP) was found to provide both prognostic and diagnostic value in various cardiovascular diseases, including survival to hospital discharge in patients with ROSC. However, the biologically inactive counterpart of BNP, NT-proBNP, was found to be a more stable and accurate analyte. The current retrospective observational study investigates the value of NT-proBNP to predict 28-day mortality in post-CA patients treated with MTH, as well as the dynamics of NT-proBNP during MTH.MethodsNT-proBNP levels were measured in post-CA patients cooled via cold intravenous saline infusion and water-circulating body wraps (Medi-Therm®, Gaymar). Plasma samples were obtained before cooling was started, at the start and end of the maintenance phase and at the end of rewarming.Results250 patients, admitted between 2009 and 2013, had NT-proBNP levels measured on ICU admission and were included for the evaluation of NT-proBNP as a prognostic marker. In the 28 days following ICU admission, 114 patients died (46%). Non-survivors had significantly higher NT-proBNP (median 1448 ng/l, IQR 366–4623 vs median 567 ng/1, IQR 148–1899; P < 0.001) levels on ICU admission. Unadjusted odds ratios for 28-day mortality were 1.7 (95% CI 0.8-3.5), 1.6 (0.8-3.3) and 3.6 (1.7-7.5) for increasing quartiles of NT-proBNP as compared to the lowest quartile. Adjusted odds ratios were 1.1 (95% CI 0.5-2.5), 1.1 (0.5-2.5) and 1.6 (0.7-3.8), respectively. A cut-off value of 834 ng/l achieved a sensitivity of 58% and a specificity of 58% to predict 28-day mortality. Of 113 patients, NT-proBNP values of each MTH phase were available and grouped in decreased or increased levels in time. Both decreases and increases of NT-proBNP values were observed during the MTH phases, but presence of either was not associated with outcome.ConclusionsHigh NT-proBNP plasma concentrations on ICU admission are associated with high 28-day mortality in post-CA patients treated with MTH in a univariate analysis, but not in a multivariate analysis. Increases or decreases of NT-proBNP levels during MTH appear unrelated to 28 day mortality.