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Background: During acellular replacement of an acute blood loss, hyperoxic ventilation (HV) increases the amount of O2 physically dissolved in the plasma and thereby improves O2 supply to the tissues. While this effect could be demonstrated for HV with inspiratory O2 fraction (FiO2) 0.6, it was unclear whether HV with pure oxygen (FiO2 1.0) would have an additional effect on the physiological limit of acute normovolemic anemia., Methods: Seven anesthetized domestic pigs were ventilated with FiO2 1.0 and subjected to an isovolemic hemodilution protocol. Blood was drawn and replaced by a 6% hydroxyethyl starch (HES) solution (130/0.4) until a sudden decrease of total body O2 consumption (VO2) indicated the onset of O2 supply dependency (primary endpoint). The corresponding hemoglobin (Hb) concentration was defined as 'critical Hb' (Hbcrit). Secondary endpoints were parameters of myocardial function, central hemodynamics, O2 transport and tissue oxygenation., Results: HV with FiO2 1.0 enabled a large blood-for-HES exchange (156 ± 28% of the circulating blood volume) until Hbcrit was met at 1.3 ± 0.3 g/dl. After termination of the hemodilution protocol, the contribution of O2 physically dissolved in the plasma to O2 delivery and VO2 had significantly increased from 11.7 ± 2 to 44.2 ± 9.7% and from 29.1 ± 4.2 to 66.2 ± 11.7%, respectively. However, at Hbcrit, cardiovascular performance was found to have severely deteriorated., Conclusion: HV with FiO2 1.0 maintains O2 supply to tissues during extensive blood-for-HES exchange. In acute situations, where profound anemia must be tolerated (e.g. bridging an acute blood loss until red blood cells become available for transfusion), O2 physically dissolved in the plasma becomes an essential source of oxygen. However, compromised cardiovascular performance might require additional treatment.

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.

Objective: To investigate the impact of prophylactic hyperoxic ventilation with Fio2 0.6 on the physiologic limit of acute normovolemic anemia., Design: Prospective, controlled, randomized experimental study., Setting: Experimental animal laboratory of a university hospital., Subjects: Fourteen anesthetized domestic pigs., Interventions: Animals were randomly ventilated with either Fio2 0.21 (group 0.21, n = 7) or Fio2 0.6 (group 0.6, n = 7), and acute anemia was induced by isovolemic blood-for-hydroxy-ethylstarch (HES) exchange using a 6% HES solution (130/0.4)., Measurements and Main Results: The blood-for-HES-exchange was continued until a sudden decrease of total body oxygen consumption indicated the onset of oxygen supply dependency (primary end point); the corresponding hemoglobin (Hb) concentration was defined as "critical" (Hb(crit)). Secondary end points were changes in myocardial function, central hemodynamics, oxygen transport, and tissue oxygenation. Compared with room air ventilation (Fio2 0.21), hyperoxic ventilation with Fio2 0.6 enabled a larger blood-for-HES-exchange (139%, 124/156) of circulating blood volume vs. 87% (68/94, p < .05), until Hb(crit) was reached (1.5 g/dL [1.4/2.1] vs. 2.4 g/dL [2.0/2.8], p < .05). At Hb 2.4 g/dL (i.e., Hb(crit) in group 0.21), animals of group 0.6 still presented with superior oxygen transport, tissue oxygenation, and hemodynamic stability. However, hemodynamic and oxygen transport variables were found deteriorated more severely at Hb 1.5 g/dL (i.e., Hb(crit) of group 0.6) compared with group 0.21 at Hb 2.4 g/dL., Conclusion: During cell-free volume replacement, hyperoxic ventilation with Fio2 0.6 generates a readily usable plasmatic oxygen reserve and thereby increases the tolerance toward acute normovolemic anemia.

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: Ventilation with pure oxygen (hyperoxic ventilation, HV) increases arterial oxygen content (CaO(2)). However HV induces arteriolar constriction and thus potentially affects O(2) supply. We therefore investigated the effects of HV on regional blood flow (RBF) and O(2) supply of different vital organs during moderate normovolaemic anaemia., Methods: Twenty-two anaesthetized dogs were haemodiluted under normoxia (i.e. FiO(2) = 0.21) to a target haemoglobin concentration (Hb) of 7 g dl(-1) and were subsequently ventilated with pure O(2). RBF was determined by use of the radioactive microspheres method in the myocardium, kidney, skeletal muscle, liver, intestine, stomach, and pancreas at Hb = 7 g dl(-1) and after subsequent initiation of HV. RBF in proportion to cardiac output (RBF(relative)), the variation coefficient of RBF (VC) and regional O(2) supply (rDO(2)) were calculated., Results: Initiation of HV at Hb = 7.0 +/- 0.3 g dl(-1) reduced cardiac index (-17%) as well as RBF within the myocardium (-21%), pancreas (-25%), and skeletal muscle (-25%), whereas renal, hepatic, and intestinal RBF remained unchanged. Consequently RBF(relative) of the latter organs increased. Heterogeneity of RBF was marginally affected by HV., Conclusion: The initiation of HV during moderate normovolaemic anaemia (Hb =7 g dl(-1)) was accompanied by RBF redistribution with preference for renal, hepatic and intestinal O(2) supply. Cardiac, pancreatic and muscular O(2) supply decreased, however without any critical restriction of organ function.

Under resting conditions oxygen consumption (VO2) of the tissues equals their O2 demand. However, when oxygen delivery (DO2) decreases below "a critical" value, the consecutive decline of VO2 reflects a critical restriction of DO2 resulting in the onset of tissue hypoxia. Reliable bedside detection of a significant VO2 decline requires continuous measurement of in- and exspiratory O2 concentrations with a metabolic monitor as well as a standardized online analysis of the data obtained. However, for this purpose no standardized procedure was available yet. Therefore, the DeltaCrit-System (DCS) has been developed enabling online detection of a significant VO2 decline indicating critical restriction of DO2. After a reference period with stable VO2 values the DCS tests whether a subsequently measured VO2 value is significantly lower than the mean baseline VO2. A significant VO2 decrease should indicate the onset of O2 supply dependency of VO2 due to a critical restriction of DO2. The DCS has been validated with nine different, artificially generated data sets and has been tested in one animal experiment. DCS has proven consistency and may therefore be considered a new tool allowing clinicians to recognize restrictions in DO2 at an early time, and to start early therapeutic interventions.

Objective: During normovolaemic haemodilution arterial O(2)-content decreases exponentially. Nevertheless, tissue oxygenation is first maintained initially by increased organ perfusion and O(2)-extraction. As soon as these compensatory mechanisms are exhausted, myocardial ischaemia and tissue hypoxia occur at an individual 'critical' haematocrit (Hct) value. This study was conducted in order to assess whether tissue hypoxia at the critical Hct is reversed by hyperoxic ventilation with 100% O(2)., Method: Eighteen anaesthetized pigs were ventilated with room air and were hemodiluted by 1:1 exchange of blood with 6% pentastarch to their individual critical Hct (onset of myocardial ischaemia; significant ECG changes). At the critical Hct, hyperoxic ventilation was initiated. In nine complete datasets, global O(2) delivery and consumption, local tissue O(2) partial pressure (tpO(2)) (MDO-Electrode, Eschweiler, Kiel, Germany) and organ blood flow (microsphere method) in skeletal muscle were analyzed at baseline, after haemodilution to the critical Hct and after 15 min of hyperoxic ventilation., Results: At the critical Hct (7.2+/-1.2%), tpO(2) was reduced from 23+/-3 to 10+/-2 Torr with 50% of all values in the hypoxic range (<10 Torr, all P<0.05). During hyperoxic ventilation, contribution of physically dissolved O(2) to the O(2) delivery and O(2) consumption increased by 400 and 563% (P<0.05) and instantly restored tpO(2) to 18+/-2 Torr, (hypoxic values 25%, P<0.05)., Conclusion: Hyperoxic ventilation reversed tissue hypoxia at the critical Hct due to preferential utilization of plasma O(2) and allowed temporary preservation of tissue oxygenation. During haemodilution, hyperoxic ventilation might offer an effective bridge until red cells are ready for transfusion.

As an alternative to transfusion of red blood cells, intravenously (iv) administered artificial oxygen (O(2)) carriers are intended to increase the reduced O(2) carrying capacity of blood in the case of acute severe anemia, i.e. hemorrhagic shock or extreme normovolemic hemodilution (ANH). Actually, two groups of artificial O(2) carriers are investigated: ultrapurified, stroma-free hemoglobin solutions (SFH) of human or bovine origin and synthetically produced perfluorocarbons (PFC). SFH may be administered in large amounts and are suitable for 1:1 replacement of blood losses in case of hemorrhage as well as for isovolemic exchange of blood during ANH. In both situations SFH solutions effectively restore (hemorrhagic shock) and maintain (extreme ANH) tissue oxygenation despite extremely low hematocrit values. The vasopressor property of the isolated Hb molecule leads to a species-dependent (rodent>pig>human) increase in systemic and pulmonary vascular resistance, but leaves overall distribution of cardiac output uninfluenced. Due to the particulate nature of PFC emulsions, iv administration has to be restricted to small doses (3-4.5 ml/kg body weight for the actually investigated 60% w/v perflubron emulsion) in order to avoid overload of the reticuloendothelial system. Thus PFC emulsions are unsuitable for isovolemic blood replacement in hemorrhagic shock or ANH. Low-dose iv PFC administration in already hemodiluted subjects, however, creates an additional margin of safety to guarantee adequate tissue oxygenation which allows for further, extreme ANH, without risking tissue hypoxia.

Background: Intravenously administered perfluorocarbon (PFC) emulsions increase oxygen solubility in plasma. PFC might therefore temporarily replace red cells (RBCs) lost during intraoperative hemorrhage. In patients who have undergone hemodilution, the return of autologous blood may be delayed by the administration of PFC, and autologous RBCs may be saved for transfusion after surgical bleeding is stopped and PFC is cleared by the reticuloendothelial system., Study Design and Methods: In 22 anesthetized, hemodiluted dogs (hemoglobin [Hb] 7 g/dL) breathing 100-percent O2, an intraoperative volume-compensated blood loss was simulated. The efficacy of three therapeutic regimens in maintaining tissue oxygenation was compared: 1) RBC group (n = 7): maintenance of a Hb > 7 g per dL by transfusion of autologous RBCs; 2) PFC group (n = 7): bolus application of a second-generation PFC emulsion (60% wt/vol perflubron) and further acute normovolemic hemodilution (ANH) to a Hb of 3 g per dL; and 3) control group (n = 7): further ANH alone to a Hb of 3 g per dL. Systemic and myocardial oxygenation status and tissue oxygenation were assessed., Results: Autologous RBCs transfused to maintain a Hb of 7 g per dL preserved hemodynamics and tissue oxygenation during blood loss. In the PFC and control groups, heart rate and cardiac index increased significantly in response to further ANH. Tissue oxygenation was not different in the PFC and the RBC groups. Direct comparison of the PFC and control groups revealed better tissue oxygenation in the PFC group, as reflected by significantly higher mixed venous, coronary venous, and local tissue pO2 on liver and skeletal muscle., Conclusion: Bolus intravenous administration of 60-percent (wt/vol) perflubron emulsion and further hemodilution from a Hb of 7 g per dL to one of 3 g per dL were as effective as autologous RBC transfusion in maintaining tissue oxygenation during volume-compensated blood loss designed to mimic surgical bleeding.

Adequate organ function requires adequate provision of cells with oxygen (O2). The driving force for O2-diffusion from ambient air to its site of consumption in cell mitochondria is the oxygen partial pressure (pO2) gradient along this pathway. After uptake in the lungs, O2 transport in blood is achieved (1) through binding to haemoglobin and (2) through physical dissolution in plasma. While the sum of O2 in these two transport states defines total oxygen content of blood, the delivery of O2 to different organs is determined by cardiac output and arterial O2 content, being the product of both parameters. In the case of anaemia, intravascular volume and cardiac compensatory mechanisms determine the degree of O2 content reduction allowable prior tissue hypoxia and lactacidosis occur. When intravascular volume is preserved (e.g. normovolemic dilutional anaemia), reductions in O2 content are tolerated to a much higher degree than in hypovolemic anaemia (e.g. haemorrhagic shock).

Background Changes in heart rate variability (HRV) during anaesthesia depend on multiple influences such as hypnosis, analgesia, surgical stress, and interacting drugs. Several recent studies have aimed to establish HRV-based monitoring tools to measure perioperative stress or anaesthetic depth. Although hyperoxic ventilation (HV) is known to alter autonomic cardiovascular regulation, there have been no studies investigating its influence on time- and frequency-domain analysis during general anaesthesia. Therefore, we have examined the effects of HV on cardiovascular neuroregulation of anaesthetized patients and conscious volunteers by analysis of relevant HRV parameters. Methods Fourteen healthy volunteers and 14 anaesthetized, ventilated ASA I patients sequentially breathed room air ( 0.21), pure oxygen ( 1.0), and then room air. During each episode, standardized HRV parameters were calculated from 5 min ECG recordings. Results HV significantly reduced HR and increased the standard deviation of RR interval values, the root mean square of successive RR interval differences, and the high-frequency (HF) power of the spectral components, whereas the low-frequency (LF) power and the LF/HF ratio of HRV were reduced in both groups. All changes were reversible after was reduced to normoxia. Conclusions In both healthy volunteers and anaesthetized patients, HV resulted in comparable and reversible changes of established HRV parameters. These changes might be relevant enough to bias HRV-based analgesia and anaesthesia monitoring and could result in a clinically relevant misinterpretation of HRV parameters as indicators of anaesthetic depth during HV. [ABSTRACT FROM PUBLISHER]