Effect of Hyperoxia on Cerebral Blood Flow Velocity and Regional Oxygen Saturation in Patients Operated on for Severe Traumatic Brain Injury-The Influence of Cerebral Blood Flow Autoregulation.

BACKGROUND: The effect of normobaric hyperoxia on brain oxygenation in the presence or absence of intact autoregulation has not been studied previously in acute traumatic brain injury (TBI). METHODS: In this prospective clinical investigation of 50 patients operated on for severe TBI, cerebral blood flow (CBF) velocity in the middle cerebral artery was measured using transcranial Doppler. Regional cerebral oxygen saturation using near-infrared spectroscopy at 3 different fractions of inspired oxygen (Fio2) (0.4, 0.6, and 1) was measured in the last 25 of these patients. RESULTS: There was no difference in the hemodynamic and respiratory variables except for Pao2, which increased with increasing Fio2. The CBF velocities and pulsatility indices did not vary at different levels of Fio2 (0.4, 0.6, and 1) both on the operated and on the nonoperated side. The regional cerebral oxygen saturation as evaluated by bifrontal near-infrared spectroscopy sensors increased with increasing Fio2 on the operated (pathologic) side with impaired cerebral autoregulation and not with intact autoregulation. CONCLUSIONS: In severe TBI, middle cerebral artery CBF velocity is not affected by hyperoxia in both the pathologic and the normal side. The cerebral oxygen saturation increased with increasing arterial hyperoxia in the operated cerebral hemisphere and remained within baseline range in the nonoperated hemisphere. Impairment in the cerebral autoregulation in the pathologic hemisphere contributes to this luxury oxygenation.

Moderate hyperoxic versus near-physiological oxygen targets during and after coronary artery bypass surgery: a randomised controlled trial.

BACKGROUND: The 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. METHODS: This 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. RESULTS: Weighted 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. CONCLUSIONS: Compared 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 REGISTRATION: Netherlands Trial Registry NTR4375, registered on 30 January 2014.

Pre-treatment with hyperoxia before coronary artery bypass grafting - effects on myocardial injury and inflammatory response.

BACKGROUND: In experimental studies, exposure to hyperoxia for a limited time before ischaemia induces a low-grade systemic oxidative stress and evokes an (ischaemic) preconditioning-like effect of the myocardium. We hypothesised that hyperoxia before cardioplegia could protect the myocardium against necrosis and stunning caused by ischaemia-reperfusion. METHODS: Forty patients undergoing coronary artery bypass grafting were randomly exposed to an oxygen fraction of 0.4 or > 0.96 in inspired air on an average of 120 min before cardioplegia. Blood for troponin I, creatine kinase-MB, lactate, glutathione and interleukin-6 was sampled from arterial and coronary sinus cannulae during 20 min of reperfusion. Additional arterial samples were drawn 60 min after declamping and in the first post-operative morning. The cardiac index and right and left ventricular stroke work indices were measured before sternotomy and up to 12 h post-operatively. RESULTS: Troponin I, creatine kinase-MB and lactate did not differ between the groups. Hyperoxic pre-treatment had no impact on the post-operative haemodynamic indices measured with the thermodilution pulmonary artery catheter. More oxidised glutathione was released in the hyperoxia group in the first minute of reperfusion (P = 0.015). Hyperoxic pre-treatment abolished the myocardial release of interleukin-6 during 20 min of reperfusion (P = 0.021 vs. controls). In the first post-operative morning, interleukin-6 was higher in the hyperoxia group [127.0 (86.0-140.0) vs. 85.2 pg/ml (66.6-94.5 pg/ml); P = 0.016]. CONCLUSIONS: Exposure to >96% oxygen before cardioplegia did not attenuate ischaemia-reperfusion injury of the heart in patients undergoing coronary artery bypass grafting. The only potentially beneficial effect observed was the decreased transmyocardial release of interleukin-6.