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Background: We previously demonstrated the involvement of the Ca2+-independent protein kinase C-delta (PKC-delta) isoform in sevoflurane-induced cardioprotection against ischaemia and reperfusion (I/R) injury. Since sevoflurane is known to modulate myocardial Ca2+-handling directly, in this study we investigated the role of the Ca2+-dependent PKC-alpha isoform in sevoflurane-induced cardioprotective signalling in relation to reactive oxygen species (ROS), adenosine triphosphate-sensitive mitochondrial K+ (mitoK+(ATP)) channels, and PKC-delta.Methods: Preconditioned (15 min 3.8 vol% sevoflurane) isolated rat right ventricular trabeculae were subjected to I/R, consisting of 40 min superfusion with hypoxic, glucose-free buffer, followed by normoxic glucose-containing buffer for 60 min. After reperfusion, contractile recovery was expressed as percentage of force development before I/R. The role of PKC-alpha, ROS, mitoK+(ATP) channels, and PKC-delta was established using the following pharmacological inhibitors: Go6976 (GO; 50 nM), n-(2-mercaptopropionyl)-glycine (MPG; 300 microM), 5-hydroxydecanoic acid sodium (5HD; 100 microM), and rottlerin (ROT; 1 microM).Results: Preconditioning of trabeculae with sevoflurane improved contractile recovery after I/R [65 (3)% (I/R + SEVO) vs 47 (3)% (I/R); n = 8; P < 0.05]. This cardioprotective effect was attenuated in trabeculae treated with GO [42 (4)% (I/R + SEVO + GO); P > 0.05 vs (I/R)]. In sevoflurane-treated trabeculae, PKC-alpha translocated towards mitochondria, as shown by immunofluorescent co-localization analysis. GO and MPG, but not 5HD or ROT, abolished this translocation.Conclusions: Sevoflurane improves post-ischaemic contractile recovery via activation of PKC-alpha. ROS production, but not opening of mitoK+(ATP) channels, precedes PKC-alpha translocation towards mitochondria. This study shows the involvement of Ca2+-dependent PKC-alpha in addition to the well-established role of Ca2+-independent PKC isoforms in sevoflurane-induced cardioprotection. [ABSTRACT FROM AUTHOR]

Background: Prehospital management of severe traumatic brain injury (TBI) focuses on preventing secondary brain injury. Therefore, hypotension should be prevented, or if present, should be promptly treated in order to maintain optimal cerebral perfusion pressure. Fluid resuscitation is a traditional mainstay in the prehospital treatment of hypotension, however, the choice of fluid type that is to be administered in the prehospital setting is the subject of an on-going debate. This systematic review and meta-analysis was therefore performed to assess the effect of different fluid types on outcome in patients with severe TBI., Methods: PubMed, Embase and Web of Science were searched for articles up to March 2020. Studies comparing two or more prehospital administered fluid types with suspected or confirmed severe TBI were deemed eligible for inclusion. Studied outcomes were mortality and (extended) Glasgow Outcome Scale (GOS). The meta-analysis tested for differences in survival between hypertonic saline (HTS) and normotonic crystalloids (i.e. normal saline or Lactated Ringer's) and between hypertonic saline with dextran (HSD) and normotonic crystalloids. The systematic review is registered in the PROSPERO register with number CRD42020140423., Results: This literature search yielded a total of 519 articles, of which 12 were included in the systematic review and 6 were included in the meta-analysis. Eleven studies found no statistically significant difference in survival between patients treated with different fluid types (e.g. normal saline and hypertonic saline). All studies assessing neurological outcome, measured through (extended) GOS, found no statistically significant difference between different fluid types. Meta-analysis showed no better survival for patients treated with HSD, when compared to normotonic crystalloids (overall RR 0.99, 95% CI 0.93-1.06). Moreover, HTS compared to normotonic crystalloids does not result in a better survival (overall RR 1.04, 95% CI 0.97-1.12)., Conclusions: This systematic review and meta-analysis did not demonstrate a survival or neurological benefit for one specific fluid type administered in the prehospital setting., Competing Interests: Declaration of Competing Interest The authors report no conflict of interest., (Copyright © 2020. Published by Elsevier Ltd.)

Background: Hypovolaemia is generally believed to induce centralization of blood volume. Therefore, we evaluated whether induced hypo- and hypervolaemia result in changes in central blood volumes (pulmonary blood volume (PBV), intrathoracic blood volume (ITBV)) and we explored the effects on the distribution between these central blood volumes and circulating blood volume (Vd circ)., Methods: Six anaesthetized, spontaneously breathing Foxhound dogs underwent random blood volume alterations in steps of 150 ml (mild) to 450 ml (moderate), either by haemorrhage, retransfusion of blood, or colloid infusion. PBV, ITBV and Vd circ were measured using (transpulmonary) dye dilution. The PBV/Vd circ ratio and the ITBV/Vd circ ratio were used as an assessment of blood volume distribution., Results: 68 blood volume alterations resulted in changes in Vdcirc ranging from -33 to +31%. PBV and ITBV decreased during mild and moderate haemorrhage, while during retransfusion, PBV and ITBV increased during moderate hypervolaemia only. The PBV/Vd circ ratio remained constant during all stages of hypo- and hypervolaemia (mean values between 0.20-0.22). This was also true for the ITBV/Vd circ ratio, which remained between 0.31 and 0.32, except for moderate hypervolaemia, where it increased slightly to 0.33 (0.02), P<0.05., Conclusions: Mild to moderate blood volume alterations result in changes of Vd circ, PBV and ITBV. The ratio between the central blood volumes and Vd circ generally remained unaltered. Therefore, it could be suggested that in anaesthetized spontaneously breathing dogs, the cardiovascular system maintains the distribution of blood between central and circulating blood volume., (© The Author 2015. Published by Oxford University Press on behalf of the British Journal of Anaesthesia. All rights reserved. For Permissions, please email: journals.permissions@oup.com.)

Background: Current cardiopulmonary resuscitation (CPR)-guidelines recommend an increased chest compression depth and rate compared to previous guidelines, and the use of automatic feedback devices is encouraged. However, it is unclear whether this compression depth can be maintained at an increased frequency. Moreover, the underlying surface may influence accuracy of feedback devices. We investigated compression depths over time and evaluated the accuracy of a feedback device on different surfaces., Methods: Twenty-four volunteers performed four two-minute blocks of CPR targeting at current guideline recommendations on different surfaces (floor, mattress, 2 backboards) on a patient simulator. Participants rested for 2 minutes between blocks. Influences of time and different surfaces on chest compression depth (ANOVA, mean [95% CI]) and accuracy of a feedback device to determine compression depth (Bland-Altman) were assessed., Results: Mean compression depth did not reach recommended depth and decreased over time during all blocks (first block: from 42 mm [39-46 mm] to 39 mm [37-42 mm]). A two-minute resting period was insufficient to restore compression depth to baseline. No differences in compression depth were observed on different surfaces. The feedback device slightly underestimated compression depth on the floor (bias -3.9 mm), but markedly overestimated on the mattress (bias +12.6 mm). This overestimation was eliminated after correcting compression depth by a second sensor between manikin and mattress., Conclusion: Strategies are needed to improve chest compression depth, and more than two providers should alternate with chest compressions. The underlying surface does not necessarily adversely affect CPR performance but influences accuracy of feedback devices. Accuracy is improved by a second, posterior, sensor.

Epidural anesthesia is associated with the risk of unintended dural perforation and concomitant leakage of cerebrospinal fluid (CSF) from the subarachnoidal space. This may remain asymptomatic or trigger post-dural puncture headache (PDPH). Cerebral nerve lesions after attempted epidural anesthesia are very rare. Here we report a case of unilateral paresis of the cranial nerve VI (N. abducens) after attempted thoracic epidural anesthesia. Herein, diagnosis of N. abducens paresis was probably delayed because the optical symptoms, such as blurred and double vision, were attributed to optical hallucinations caused by a concomitant (S)-ketamine infusion. In all patients with optical symptoms such as blurred or double vision a paresis of the abducens nerve should be considered.

Hemodynamic monitoring and adequate volume-therapy, as well as the treatment with positive inotropic drugs and vasopressors are the basic principles of the postoperative intensive care treatment of patient after cardiothoracic surgery. The goal of these S3 guidelines is to evaluate the recommendations in regard to evidence based medicine and to define therapy goals for monitoring and therapy. In context with the clinical situation the evaluation of the different hemodynamic parameters allows the development of a therapeutic concept and the definition of goal criteria to evaluate the effect of treatment. Up to now there are only guidelines for subareas of postoperative treatment of cardiothoracic surgical patients, like the use of a pulmonary artery catheter or the transesophageal echocardiography. The German Society for Thoracic and Cardiovascular Surgery (Deutsche Gesellschaft für Thorax-, Herz- und Gefässchirurgie, DGTHG) and the German Society for Anaesthesiology and Intensive Care Medicine (Deutsche Gesellschaft für Anästhesiologie und lntensivmedizin, DGAI) made an approach to ensure and improve the quality of the postoperative intensive care medicine after cardiothoracic surgery by the development of S3 consensus-based treatment guidelines. Goal of this guideline is to assess the available monitoring methods with regard to indication, procedures, predication, limits, contraindications and risks for use. The differentiated therapy of volume-replacement, positive inotropic support and vasoactive drugs, the therapy with vasodilatators, inodilatators and calcium sensitizers and the use of intra-aortic balloon pumps will also be addressed. The guideline has been developed following the recommendations for the development of guidelines by the Association of the Scientific Medical Societies in Germany (AWMF). The presented key messages of the guidelines were approved after two consensus meetings under the moderation of the Association of the Scientific Medical Societies in Germany (AWMF).

The international Brain Trauma Foundation guidelines recommend prehospital endotracheal intubation in all patients with traumatic brain injury (TBI) and a Glasgow Coma Scale (GCS)< or =8. Close adherence to these guidelines is associated with improved outcome, but not all severely injured TBI patients receive adequate prehospital airway support. Here we hypothesized that guideline adherence varies when skills are involved that rely on training and expertise, such as endotracheal intubation. We retrospectively studied the medical records of CT-confirmed TBI patients with a GCS< or =8 who were referred to a level 1 trauma centre in Amsterdam (n=127). Records were analyzed for demographic parameters, prehospital treatment modalities, involvement of an emergency medical service (EMS) and respiratory and metabolic parameters upon arrival at the hospital. Patients were mostly male, aged 45+/-21 years with a median injury severity score (ISS) of 26. Of all patients for whom guidelines recommend endotracheal intubation, only 56% were intubated. In 21 out of 106 severe cases an EMS was not called for, suggesting low guideline adherence. Especially those TBI patients treated by paramedics tended to develop higher levels of stress markers like glucose and lactate. We observed a low degree of adherence to intubation guidelines in a Dutch urban area. Main reasons for low adherence were the unavailability of specialized care, scoop and run strategies and absence of a specialist physician in cases where intubation was recommended. The discrepancy between guidelines and reality warrants changing practice to improve guideline compliance and optimize outcome in TBI patients.

Background: We previously demonstrated the involvement of the Ca2+-independent protein kinase C-delta (PKC-delta) isoform in sevoflurane-induced cardioprotection against ischaemia and reperfusion (I/R) injury. Since sevoflurane is known to modulate myocardial Ca2+-handling directly, in this study we investigated the role of the Ca2+-dependent PKC-alpha isoform in sevoflurane-induced cardioprotective signalling in relation to reactive oxygen species (ROS), adenosine triphosphate-sensitive mitochondrial K+ (mitoK+(ATP)) channels, and PKC-delta., Methods: Preconditioned (15 min 3.8 vol% sevoflurane) isolated rat right ventricular trabeculae were subjected to I/R, consisting of 40 min superfusion with hypoxic, glucose-free buffer, followed by normoxic glucose-containing buffer for 60 min. After reperfusion, contractile recovery was expressed as percentage of force development before I/R. The role of PKC-alpha, ROS, mitoK+(ATP) channels, and PKC-delta was established using the following pharmacological inhibitors: Go6976 (GO; 50 nM), n-(2-mercaptopropionyl)-glycine (MPG; 300 microM), 5-hydroxydecanoic acid sodium (5HD; 100 microM), and rottlerin (ROT; 1 microM)., Results: Preconditioning of trabeculae with sevoflurane improved contractile recovery after I/R [65 (3)% (I/R + SEVO) vs 47 (3)% (I/R); n = 8; P < 0.05]. This cardioprotective effect was attenuated in trabeculae treated with GO [42 (4)% (I/R + SEVO + GO); P > 0.05 vs (I/R)]. In sevoflurane-treated trabeculae, PKC-alpha translocated towards mitochondria, as shown by immunofluorescent co-localization analysis. GO and MPG, but not 5HD or ROT, abolished this translocation., Conclusions: Sevoflurane improves post-ischaemic contractile recovery via activation of PKC-alpha. ROS production, but not opening of mitoK+(ATP) channels, precedes PKC-alpha translocation towards mitochondria. This study shows the involvement of Ca2+-dependent PKC-alpha in addition to the well-established role of Ca2+-independent PKC isoforms in sevoflurane-induced cardioprotection.

Hemodynamic monitoring and adequate volume-therapy, as well as the treatment with positive inotropic drugs and vasopressors, are the basic principles of the postoperative intensive care treatment of patient after cardiothoracic surgery. The goal of these S3 guidelines is to evaluate the recommendations in regard to evidence based medicine and to define therapy goals for monitoring and therapy. In context with the clinical situation the evaluation of the different hemodynamic parameters allows the development of a therapeutic concept and the definition of goal criteria to evaluate the effect of treatment. Up to now there are only guidelines for subareas of postoperative treatment of cardiothoracic surgical patients, like the use of a pulmonary artery catheter or the transesophageal echocardiography. The German Society for Thoracic and Cardiovascular Surgery and the German Society for Anaesthesiology and Intensive Care Medicine made an approach to ensure and improve the quality of the postoperative intensive care medicine after cardiothoracic surgery by the development of S3 consensus-based treatment guidelines. Goal of this guideline is to assess available monitoring methods and their risks as well as the differentiated therapy of volume-replacement, positive inotropic support and vasoactive drugs, the therapy with vasodilators, inodilators and calcium-sensitizers and the use of intra-aortic balloon pumps. The guideline has been developed according to the recommendations for the development of guidelines by the Association of the Scientific Medical Societies in Germany (AWMF). The presented key messages of the guidelines were approved after two consensus meetings under the moderation of the Association of the Scientific Medical Societies in Germany (AWMF).

Carbon monoxide arises during incomplete combustion of organic material, is incorporated into the circulation via the lungs and displaces oxygen from hemoglobin. Consecutively, symptoms of intoxication such as headache, vertigo, nausea, seizures and coma may result in a dose dependent fashion. Carbon monoxide is however also generated endogenously during heme degradation catalysed by heme oxgenase enzymes. The isoform hemeoxygenase-1 is inducible by oxidative stress and may mediate cytoprotection mainly attributable to endogenously produced carbon monoxide. Exogenous applied carbon monoxide has also been shown to confer protection in experimental studies. Meanwhile, in addition to the toxicological properties, antiinflammatory and cytoprotective effects of carbon monoxide have moved into the focus of scientific interest.

Background and Objectives: During partial liquid ventilation perfluorocarbons are instilled into the airways from where they subsequently evaporate via the bronchial system. This process is influenced by multiple factors, such as the vapour pressure of the perfluorocarbons, the instilled volume, intrapulmonary perfluorocarbon distribution, postural positioning and ventilatory settings. In our study we compared the effects of open and closed breathing systems, a heat-and-moisture-exchanger and a sodalime absorber on perfluorocarbon evaporation during partial liquid ventilation., Methods: Isolated rat lungs were suspended from a force transducer. After intratracheal perfluorocarbon instillation (10 mL kg(-1)) the lungs were either ventilated with an open breathing system (n = 6), a closed breathing system (n = 6), an open breathing system with an integrated heat-and-moisture-exchanger (n = 6), an open breathing system with an integrated sodalime absorber (n = 6), or a closed breathing system with an integrated heat-and-moisture-exchanger and a sodalime absorber (n = 6). Evaporative perfluorocarbon elimination was determined gravimetrically., Results: When compared to the elimination half-life in an open breathing system (1.2 +/- 0.07 h), elimination half-life was longer with a closed system (6.4 +/- 0.9 h, P 0.05) when compared to a closed system., Conclusions: Evaporative perfluorocarbon loss can be reduced effectively with closed breathing systems, followed by the use of sodalime absorbers and heat-and-moisture-exchangers.

During partial liquid ventilation perfluorocarbons are eliminated mainly by evaporation via the airways. The effects of intrapulmonary perfluorocarbon volume, respiratory rate, tidal volume, as well as the level of end-expiratory pressure on perfluorocarbon elimination from isolated lungs, were studied. Nonperfused rabbit lungs underwent partial liquid ventilation (2-15 mL x kg(-1) perfluorocarbon) with variable levels of end-expiratory pressure (0-10 cmH2O), respiratory rates (15-60 breaths x min(-1)) and tidal volumes (3.3-10.0 mL x kg(-1)). Evaporative loss of perfluorocarbon was determined gravimetrically as rate of change in lung weight. At constant respiratory settings, intrapulmonary liquid volume determined evaporative loss in a nonlinear fashion. Mean evaporation at a liquid volume of 5 mL x kg(-1) was 13% lower compared to evaporation at a liquid volume of 15 mL x kg(-1). Any increase in end-expiratory pressure reduced perfluorocarbon evaporation, e.g. by approximately 50% when end-expiratory pressure was increased from 0 to 10 cmH2O. At constant end-expiratory pressure and perfluorocarbon filling evaporation increased in a linear fashion with increasing respiratory rate and tidal volume. In summary, the experiments suggested that evaporative loss of perfluorocarbons during partial liquid ventilation of isolated lungs is increased with increasing intrapulmonary liquid volume, respiratory rate and tidal volume and is reduced in a level-dependent fashion by the application of positive end-expiratory pressure.

Objective: Partial liquid ventilation with perfluorocarbons may increase alveolar hydrostatic transmural pressure and may result in a redistribution of pulmonary blood flow from dependent to nondependent lung regions. To test this hypothesis under controlled study conditions, we determined intrapulmonary blood flow distributions during gas and perfluorocarbon ventilation in isolated rabbit lungs., Design: Controlled animal study with an ex vivo isolated lung preparation., Setting: Research laboratory for Experimental Anesthesiology at the Heinrich-Heine-University of Düsseldorf., Subjects: New Zealand White rabbits., Interventions: The lungs were perfused with autologous blood at constant flow (150 mL/min) and ventilated with 5% C(O2) in air (positive end-expiratory pressure, 2 cm H2O; tidal volume, 10 mL/kg body weight; respiratory rate, 30 breaths/ min) without and with perfluorocarbon administered intratracheally (15 mL/kg)., Measurements and Main Results: Regional lung perfusion was measured with colored microspheres in apical, central, peripheral, and basal samples before and after bronchial instillation of perfluorocarbons. Compared with gas ventilation, intrapulmonary blood flow during perfluorocarbon ventilation was higher in apical samples (49.4+/-8.6 mL/min/g vs. 38.3+/-6.8 mL/min/g dry weight; p = .03) and lower in basal samples (22.2+/-5.1 mL/min/g vs. 39.9+/-8.2 mL/min/g; p = .04)., Conclusions: Our findings suggest that during partial liquid ventilation, intrapulmonary blood flow is redistributed toward less-dependent lung regions. (Crit Care Med 2000; 28:1522-1525)

Objectives: The density of perfluorocarbons is almost twice that of blood. Therefore, we hypothesized that partial liquid ventilation with these fluids markedly affects pulmonary hemodynamics and filtration coefficients. To test these hypotheses we studied pressure-flow relationships, vascular compliances, capillary pressures, and filtration coefficients in normal and perfluorocarbon-ventilated rabbit lungs., Design: Controlled animal study with an ex-vivo isolated lung preparation., Setting: Research laboratory for experimental anesthesiology at the Heinrich-Heine-University of Düsseldorf., Subjects: Fourteen New Zealand White rabbits., Interventions: The lungs were perfused under zone 3 flow conditions with autologous blood at various flow rates (50 to 250 mL/min, closed circuit, roller pump, 37 degrees C) and ventilated with 5% CO2 in air (positive end-expiratory pressure: 2 cm H2O, tidal volume: 10 mL/kg, respiratory rate: 30 breaths/min) without (control group, n=7) and with (n=7) perfluorocarbon administered intratracheally (15 mL/kg)., Measurements and Main Results: Pulmonary arterial, left atrial, and airway pressures, as well as blood reservoir volume (reflecting changes in pulmonary blood volume) and lung weight, were measured continuously. Inconsistent with our hypothesis, we found no significant differences between both groups in the slopes and intercepts of the pressure-flow relationships. There were no significant differences in capillary pressures determined by double occlusion (6.7+/-1.2 vs. 6.3+/-1.3 cm H2O for control group, p=.53), vascular compliances (0.51+/-0.10 vs. 0.47+/-0.09 mL/cm H2O for control group, p=.38), and filtration coefficients (0.33+/-0.06 vs. 0.37+/-0.07 mL/min/mm Hg/100 g wet weight for control group, p=.80, Mann-Whitney)., Conclusions: Partial liquid ventilation with perfluorocarbons has no relevant effects on pulmonary filtration coefficients and global hemodynamic variables of isolated zone 3 lungs. These findings suggest that right ventricular afterload is not changed with partial liquid ventilation. It is likely, however, that intrapulmonary blood flow is redistributed toward less-dependent regions, although relevant global hemodynamic changes are absent during partial liquid ventilation.

The pulmonary capillaries are in such close proximity to the terminal airways that changes in capillary blood temperature should also cause changes in bronchial wall temperature. Therefore, we hypothesized that injection of cold solutions into the pulmonary artery would yield bronchial temperature-time curves similar to those in the pulmonary artery and left atrium. These bronchial curves should mainly represent the capillary bed. Isolated rabbit lungs (n=8) were ventilated (5% CO2 in air) and perfused (autologous blood, 37 degrees C) at various flow rates (50-200 mL x min[-1]). Thermistor probes (diameter 0.46 mm) registered temperature changes in the pulmonary artery, at the bronchial wall (wedge position) and in the left atrium after injection of 0.8 mL Ringer's lactate (0 degrees C) into the pulmonary artery. Bronchial temperature-time curves were found to resemble "dilution" curves located between pulmonary arterial and left atrial curves. Independent of flow rate, their appearance times, peaks and calculated mean transit times were between those from the pulmonary artery and the left atrium. We conclude that bronchial temperature-time curves reflect transcapillary heat transport and that this approach might be useful in gaining further information about vascular transport processes in the interior of the lung.

Quantitative information about the effects of pulmonary blood volume (Qp) on pulmonary haemodynamics is lacking since Qp changes inevitably with flow. To separate flow-dependent from volume-dependent changes in intravascular pressures we imposed changes in Qp (measured continuously) by altering outflow pressure in seven isolated, blood-perfused rabbit lungs and studied the effects of Qp on the relations between arteriovenous pressure gradient (DeltaP) and blood flow (Q.) under two conditions: flow-dependent volume changes were either permitted or compensated. In the latter circumstances, DeltaP changed more for a given change in Q.. The DeltaP/Q. relations were shifted to smaller DeltaP when Qp was increased. Hence, the calculated flow resistance (R = DeltaP/Q.) decreased with increasing Qp at a given Q.. Assuming constant viscosity, changes in R can be predicted from changes in vessel geometry and thus Qp. We found that R increased less than expected (by a factor of 3-7.5 instead of 9) when Qp was reduced to one-third. This discrepancy may be explained by a change in blood distribution within the lung despite constant Qp and by a change in apparent blood viscosity with Q.. Regardless of these speculations we have shown that Qp determines DeltaP at each flow and thus flow resistance.

Background: The amount of oxygen consumed by the lung itself is difficult to measure because it is included in whole-body gas exchange. It may be increased markedly under pathological conditions such as lung infection or adult respiratory distress syndrome. To estimate normal oxygen consumption of the human lung as a basis for further studies, respiratory gas analysis during total cardiopulmonary bypass may be a simple approach because the pulmonary circulation is separated from systemic blood flow during this period., Methods: Lung oxygen consumption was determined in 16 patients undergoing cardiac surgery. During total cardiopulmonary bypass their lungs were ventilated with low minute volumes (tidal volume, 150 ml; rate, 6 min-1; inspiratory oxygen fraction, 0.5; positive end-expiratory pressure, 3 mmHg). All expiratory gas was collected and analyzed by indirect calorimetry. As a reference value also, whole-body oxygen consumption of these patients was determined before total cardiopulmonary bypass. In a pilot study of eight additional patients (same ventilatory pattern), the contribution of systemic (bronchial) blood flow to pulmonary gas exchange during cardiopulmonary bypass was assessed. For this purpose, the amount of enflurance diffusing from the systemic blood into the bronchial system was measured., Results: The human lung consumes about 5-6 ml oxygen per minute at an esophageal temperature of 28 degrees C. Prebypass whole-body oxygen consumption measured at nearly normothermic conditions was 198 +/- 28 ml/min. Mean lung and whole-body respiratory quotients were similar (0.84 and 0.77, respectively). Extrapolating lung oxygen consumption to 36 degrees C suggests that the lung consumes about 11 ml/min or about 5% of total body oxygen consumption. Because the amount of enflurane diffused from the systemic circulation into the bronchial system during cardiopulmonary bypass was less than 0.1%, the contribution of bronchial blood flow to lung gas exchange can be assumed to be negligible., Conclusions: The lung consumes about 5% of whole-body oxygen uptake.

Background: Inhalational anesthetics inhibit hypoxic pulmonary vasoconstriction (HPV) in vivo and in vitro with a half-maximum inhibiting effect (ED50) within concentrations applied for general anesthesia. Because it is unknown whether desflurane acts likewise, we studied its effect on HPV in isolated blood-perfused rabbit lungs and compared its ED50 with that of halothane., Methods: Isolated blood-perfused rabbit lungs were randomly allocated to treatment with either desflurane (n = 6) or halothane (n = 6). HPV, defined as an increase in pulmonary arterial pressure (PAP) at constant flow, was elicited by decreasing inspiratory oxygen concentration from 20% to 3% for 4 min. This effect was determined without (control HPV) and with increasing concentrations of the anesthetics (fraction of inspired carbon dioxide kept constant at 4.8 +/- 0.2%, perfusate temperature at 37 degrees C, and blood flow at 100 ml.min-1)., Results: Before exposure to the anesthetics, PAP increased by 8.6 +/- 1.9 cmH2O for all lungs within 4 min of hypoxia (control PAP for all lungs 19.6 +/- 2.5 cmH2O). Desflurane decreased this effect in a concentration-dependent fashion with an ED50 of 14.5%, compared with that of halothane, with an ED50 of 1.7%., Conclusions: Assuming that 1 minimum alveolar concentration (MAC) values of desflurane and halothane for rabbits are 8.9% and 1.39%, respectively, this study yields ED50 values for the inhibition of HPV of approximately 1.6 MAC for desflurane and 1.2 MAC for halothane (P not statistically significant).

The combination of two rare complications in intensive care caused an acute life-threatening situation. Following puncture of the left subclavian vein a pneumothorax developed over the course of a couple of days. The inserted thoracic drain dislocated into the subcutaneous tissue. During the induction of anaesthesia and controlled ventilation a tension pneumothorax developed. A decrease in oxygen saturation and an increase in the ventilation pressure led first to the diagnosis "malposition of the double lumen endotracheal tube", but its correct position could be confirmed by bronchoscopy. Finally, the tension pneumothorax was diagnosed by x-ray of the chest. This life-threatening situation could be treated by the insertion of a thoracic drain. The operation could be performed without any problems.

Necrotizing fasciitis and myositis due to Lancefield group A beta-haemolytic streptococcal infection is a medical emergency. Survival depends on aggressive early wound management as well as high-dose intravenous antibiotics. We report about a 28-year-old man with fulminant necrotizing fasciitis and myositis of his right arm, in whom many features of the toxic shock syndrome were present, including profound hypotension and renal failure. After extensive surgical debridement with amputation of his arm in combination with high-dose intravenous penicillin G the patient recovered from this serious infection.