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Aim: Ventilation with pure oxygen (hyperoxic ventilation: HV) is thought to decrease whole body oxygen consumption (VO(2)). However, the validity and impact of this phenomenon remain ambiguous; until now, under hyperoxic conditions, VO(2) has only been determined by the reverse Fick principle, a method with inherent methodological problems. The goal of this study was to determine changes of VO(2), carbon dioxide production (VCO(2)), and the respiratory quotient (RQ) during normoxic and hyperoxic ventilation, using a metabolic monitor., Methods: After providing signed informed consent and institutional acceptance, 14 healthy volunteers were asked to sequentially breathe room air, pure oxygen, and room air again. VO(2), VCO(2), RQ, and energy expenditure (EE) were determined by indirect calorimetry using a modified metabolic monitor during HV., Results: HV reduced VO(2) from 3.4 (3.0/4.0) mL/kg/min to 2.8 (2.5/3.6) mL/kg/min (P < 0.05), whereas VCO(2) remained constant (3.0 [2.6/3.6] mL/kg/min versus 3.0 [2.6/3.5] mL/kg/min, n.s.). After onset of HV, RQ increased from 0.9 (0.8/0.9) to 1.1 (1.0/1.1). Most changes during HV were immediately reversed during subsequent normoxic ventilation., Conclusion: HV not only reduces VO(2), but also increases the respiratory quotient. This might be interpreted as an indicator of the substantial metabolic changes induced by HV. However, the impact of this phenomenon requires further study.

Aim of the Study: Recently it has been demonstrated that short term hyperoxic ventilation (HV) can improve glucose metabolism, reduce pulmonary and hepatic apoptosis, and improve gastrointestinal perfusion during acute sepsis. However, it is unknown whether additional O(2) improves survival. Therefore we investigated the effects of increased plasma O(2) on survival during extreme anaemia and concomitant endotoxaemia in order to quantify the efficacy of HV., Methods: Endotoxaemia (Salmonella abortus equi-LPS) was induced in 14 anesthetized pigs ventilated with room air (FiO(2)=0.21). Simultaneously, animals were haemodiluted by exchange of whole blood for 6% hydroxyethyl starch (200,000:0.5) until the individual critical hemoglobin concentration (Hb(crit)) was achieved (outermost limit of tissue oxygenation). Subsequently, animals were either ventilated with an FiO(2) of 0.21 (NOX, n=7) or an FiO(2) of 1.0 (HOX, n=7), and observed thereafter for 6 h without further intervention., Results: HV significantly prolonged survival time at Hb(crit) (NOX, 30 [27/35] min; HOX, 172 [111/235] min, p<0.05). In contrast to the NOX group, HV maintained MAP, and improved DO(2) and tissue oxygenation in the HOX group., Conclusion: The improvement of survival, oxygen transport and tissue oxygenation seems to underline the efficacy of HV during endotoxaemia and concomitant acute anaemia. Further studies are needed to transfer these results into daily clinical practice., (Copyright © 2010 Elsevier Ireland Ltd. All rights reserved.)

Background: When initiated in anemic hypoxia, hyperoxic ventilation (ventilation with pure O2, FiO2 1.0, HV) reverses hypoxia-induced ECG-changes and enables survival for several hours. The quantification of the HV-induced gain in anemia tolerance and particularly the Hb-equivalent of HV in this situation are unknown., Methods: Nine anaesthetized pigs were hemodiluted under normoxia (FiO2 0.21) by exchange of whole blood for hydroxyethyl starch (HES) until predefined, ischemia associated ECG-changes occurred (timepoint Hb(crit)). From that time on all animals were ventilated with 100% O2 (FiO2 1.0). In the case of disappearance of the ECG changes with onset of HV, the animals were further hemodiluted until ECG changes reoccurred., Results: HV initiated in anemic hypoxia (Hb 2.3 +/- 0.2 g/dl) improved ECG-readings of all animals, and allowed for a further exchange of 14 +/- 11 ml/kg blood until ECG-changes reoccurred at Hb 1.2 +/- 0.4 g/dl., Conclusion: HV initiated in anemic hypoxia creates a margin of safety for myocardial tissue oxygenation and thus further increases anemia tolerance. The Hb equivalent of HV in this situation amounts to approximately 1g/dl.

Background: Treatment of severe methemoglobinemia includes the avoidance of methemoglobin-inducing drugs, the application of methylene blue, and the administration of supplementary oxygen. However, the efficacy of the latter on oxygen transport, tissue oxygenation, and survival in the treatment of extreme methemoglobinemia is ambiguous. The objective was to assess whether using hyperoxic ventilation as the sole therapeutic intervention (i.e., ventilation with pure oxygen, Fio2 1.0) improves the short-term (6-hr) survival rate during otherwise lethal methemoglobinemia., Design: Prospective, randomized, controlled study., Setting: Experimental animal laboratory of a university hospital., Subjects: Fourteen anesthetized, mechanically ventilated pigs., Interventions: After induction of profound methemoglobinemia (60 +/- 2%) by the injection of 15 mg/kg 4-dimethylaminophenol, artificial ventilation either was continued with room air (G 0.21, n = 7) or was changed over to hyperoxic ventilation (G 1.0, n = 7). A constant level of methemoglobinemia was maintained by continuous infusion of 4-dimethylaminophenol throughout a 6-hr follow-up period., Measurements and Main Results: All animals died within the 6-hr follow-up period, but survival time was prolonged in animals ventilated with pure oxygen (G 0.21, 105 +/- 30 mins; G 1.0, 210 +/- 64 mins, p < .05). No differences were encountered between G 0.21 and G 1.0 with respect to the investigated variables of macrohemodynamics, oxygen transport, and tissue oxygenation., Conclusions: Hyperoxic ventilation has negligible effects on oxygen transport and tissue oxygenation during lethal methemoglobinemia; nevertheless, survival was increased without severe adverse reactions provoked by hyperoxic ventilation.

Background: Hemodilution reduces hematocrit (Hct) and blood oxygen content. Tissue oxygenation is mainly preserved by increased cardiac output. As myocardial O2-demands increase, coronary vasodilatation becomes necessary to increase myocardial blood flow. Myocardial ischemia occurs at a critical Hct-value (Hctcrit), with accompanying exhaustion of coronary reserve. Hyperoxic ventilation is known to both reverse peripheral tissue hypoxia at Hctcrit and also to induce coronary vasoconstriction. This study aimed to determine whether hyperoxic ventilation at Hctcrit further exacerbates myocardial ischemia and dysfunction., Methods: Nine anesthetized pigs ventilated on room air were hemodiluted by 1:1 exchange of blood with pentastarch (6%HES) to Hctcrit, defined as onset of myocardial ischemia (ECG changes). At Hctcrit, hyperoxic ventilation was started. Measurements were performed at baseline, at Hctcrit, and after 15 min of hyperoxic ventilation. We determined myocardial blood flow (microsphere method), arterial O2-content, subendocardial O2-delivery and myocardial function (left ventricular pressure increase)., Results: At Hctcrit 7 (6;8)%, O2-content was reduced [3.7 (3.1;3.9) ml dl(-1)]. Despite a compensatory increase of myocardial blood flow [531 (449;573), ml min(-1)100 g(-1)], all pigs displayed myocardial ischemia and compromised myocardial function (P < 0.05). Hyperoxic ventilation produced increased coronary vascular resistance secondary to vasoconstriction, and reduced myocardial blood flow [426 (404;464), ml min(-1)100 g(-1); P < 0.05]. Myocardial oxygenation was found to be maintained by increased O2-content [4.4 (4.2;4.8), ml dl(-1); P < 0.05], the contribution of dissolved O2 to subendocardial O2-delivery increased (32 vs. 8%; P < 0.05), which preserved myocardial function., Conclusion: Hyperoxic ventilation at Hctcrit is followed by coronary vasoconstriction and reduction of coronary blood flow. However, myocardial oxygenation and function is maintained, as increased O2-content (in particular dissolved O2) preserves myocardial oxygenation.

Intraoperative surgical blood loss is initially replaced by infusion of red cell-free, cristalloidal or colloidal solutions. When normovolemia is maintained the ensuing dilutional anemia is compensated by an increase of cardiac output and of arterial oxygen extraction. In the ideal case, a surgical blood loss can entirely be 'bridged' without transfusion by intraoperative normovolemic hemodilution. However major blood loss results in extreme hemodilution and the transfusion of red blood cells may finally become necessary to increase arterial oxygen content and to preserve tissue oxygenation. When transfusion has to be started before surgical control of bleeding has been achieved, parts of the red blood cells transfused will get lost, thereby increasing intraoperative transfusion needs. Beside red blood cell transfusion, arterial oxygen content can be rapidly increased by ventilating the patient with 100% oxygen (hyperoxic ventilation), thus enhancing the amount of physically dissolved oxygen in plasma (hyperoxia). In experimental and clinical studies hyperoxic ventilation has emerged as a simple, safe and effective intervention to enlarge the margin of safety for hemodynamic compensation and tissue oxygenation in hemodiluted subjects experiencing major bleeding. The hyperoxia-associated microcirculatory dysregulation and impaired tissue oxygenation known to take place in the presence of a physiologic hemoglobin concentration are not encountered in hemodiluted subjects. Hyperoxic hemodilution i.e. the combination of intraoperative extreme hemodilution and hyperoxic ventilation may therefore be considered a cost-effective, safe and efficient supplement to reduce allogeneic transfusion during surgical interventions associated with high blood losses. The vast majority of the experimental and clinical investigations this new concept is based on was initiated and performed under the guidance of Prof. Konrad Messmer., (Copyright 2002 S. Karger AG, Basel)

Hypervolaemic haemodilution makes myocardial perfusion more homogenous as reflected by reduced fractal dimension of regional myocardial perfusion. The clinically more commonly performed acute normovolaemic haemodilution, however, has not yet been studied in this respect. Hyperoxic ventilation with 100% oxygen is used in conjunction with haemodilution to compensate for low oxygen content by increasing physically dissolved oxygen in plasma. Since hyperoxia is known to cause disturbance in microcirculatory regulation we studied the effects of acute normovolaemic haemodilution to haematocrit (hct) 20 +/- 1% and hyperoxia on regional myocardial perfusion heterogeneity in 22 anaesthetized dogs using fractal and correlation analysis. Regional myocardial perfusion was assessed with radioactive microspheres. The results of the study were that heart rate, blood volume and arterial pressure were unchanged during haemodilution. Cardiac index was 3.6 +/- 0.7 L min-1 m-2 before and 4.6 +/- 0.7 L min-1 m-2 after haemodilution (P < 0.05). Fractal dimension (D) of regional myocardial perfusion was 1.17 +/- 0.10 at baseline. Neither haemodilution (D = 1.19 +/- 0.10) nor hyperoxia (D = 1.17 +/- 0.10) altered fractal properties of regional myocardial perfusion. Spatial correlation of blood flow to adjacent tissue samples before haemodilution was 0.58 +/- 0.15. Haemodilution and hyperoxia did not significantly influence spatial correlation (0.57 +/- 0.12 vs. 0.60 +/- 0.09; ns). We conclude that neither acute normovolaemic haemodilution nor haemodilution in combination with hyperoxic ventilation alter physiological myocardial perfusion heterogeneity.

In seven anesthetized dogs, the effects of acute normovolemic hemodilution (ANH) to a hematocrit of 20 and 8% and the effects of hyperoxic ventilation (100% oxygen) on distribution of regional pulmonary blood flow (rPBF; radioactive microspheres) were investigated. Normovolemia was monitored with blood volume measurements (indocyanine green dilution kinetics). Before ANH, fractal dimension (D) of rPBF in the whole lung was 1.19 +/- 0.09 (mean +/- SD). Spatial correlation (rho) of rPBF in the whole lung was 0.6 +/- 0.08. D is a resolution-independent measure for global rPBF distribution, and rho is the averaged flow relationship of directly neighboring lung samples. With regard to the entire lung, neither ANH nor hyperoxia changed D or rho. With regard to horizontal, isogravitational planes, ANH induced opposite changes of rPBF heterogeneity depending on the vertical location of the plane and the parameter used. In ventral planes, a change in relative dispersion (SD/mean) indicated decreased homogeneity. However, rho suggested more homogeneous perfusion. Hyperoxia restored baseline rPBF distribution. Our data suggest that ANH causes different alterations of heterogeneity of rPBF depending on location within the lung.