重型乙型肝炎患者原位肝移植围手术期全身氧代谢的变化

目的 探讨重型乙型肝炎（乙肝）与其他肝病患者原位肝移植围术期全身氧代谢变化的特点。方法 12例重型乙肝患者为试验组。10例其他肝病患者为对照组。以咪唑安定、异丙酚、芬太尼、维库溴铵诱导全麻，术中吸入异氟醚维持麻醉。维库溴铵维持肌松，行改良背驼式原位肝移植术。左桡动脉穿刺测有创动脉压，右颈内静脉穿刺置入漂浮导管。分别于术前、无肝前10min、无肝期25min、新肝期30min和术毕监测动脉和混合静脉血氧分压（PaO2和Pv^-O2）、动脉和混合静脉血氧含量（CaO2和Pv^-O2）及动-静脉血氧含量差（CA-vO2）、氧供（DO2）、氧供指数（DO2I）、氧消耗（VO2）、氧耗指数（VO2I）、氧摄取指数（O2EI）和氧摄取率（O2ER）。结果 ①试验组：与术前相比，无肝前期Pv^-O2上升，Ca-vO2、O2EI、O2ER下降，DO2和VO2无明显变化；无肝期DO2、DO2I、VO2和VO2I均明显下降，DO2、VO2分别下降43％和21％，O2EI和O2ER均明显上升；新肝期PvO2上升，DO2和DO2I明显上升。VO2和VO2I回升至术前水平；术毕时DO2和DO2I依然高于术前水平。②对照组：无肝前期PvO2上升。DO2和VO2无明显变化，O2EI和O2ER下降；无肝期DO2、DO2I、VO2和VO2I均明显下降，DO2下降25％，VO2则下降12％；新肝期PvO2上升，Ca-vO2下降，DO2、DO2I明显上升，VO2和VO2I回升至术前水平；术毕时DO2和DO2I依然高于术前水平。结论肝移植围术期中，全身DO2变化大于VO2变化；重型乙肝患者的全身DO2和VO2变化较其他肝病患者剧烈。     

高容量血液滤过对脓毒症合并急性呼吸窘迫综合征血流动力学和氧代谢的影响

目的探讨连续性高容量血液滤过(HVHF)对严重脓毒症合并急性呼吸窘迫综合征(ARDS)的呼吸、血流动力学和氧代谢的影响。方法选择由各种病因导致的12例脓毒症并发ARDS患者,全部病例均在呼吸机支持下每日连续给予床边HVHF(置换液流量80ml·kg-1·h-1)治疗12~18h,观察治疗前后患者炎性介质〔肿瘤坏死因子α(TNFα)、白细胞介素6(IL6)、IL8、IL10〕、氧合指数(PaO2/FiO2)、急性生理学与慢性健康状况评分系统(APACHE)评分、多器官功能障碍综合征(MODS)评分和胸腔液体容量(TFC)的变化。通过Swan Ganz导管获得心排血量(CO)、外周循环阻力(SVR)、肺循环阻力(PVR)、平均肺动脉压(MPAP)、肺动脉楔压(PAWP)、动脉血氧含量(CaO2)、混合静脉血氧含量(CvO2)、氧消耗(VO2)、氧输送(DO2)和氧摄取率(O2ER)。结果HVHF48h后的MPAP、PVR和TFC均明显下降(P均<0.05)。HVHF72h后,TNFα、IL6和IL8含量较HVHF前均明显下降(P均<0.05),DO2、O2ER和VO2逐渐稳定,并伴随动脉氧分压(PaO2)、PaO2/FiO2和气道峰压(Ppeak)的改善(P<0.05或P<0.01)。结论连续性HVHF可通过清除部分细胞因子,减少TFC,改善严重脓毒症合并ARDS患者的呼吸、血流动力学和氧代谢。     

Cardiovascular and metabolic response to red blood cell transfusion in critically ill volume-resuscitated nonsurgical patients

We examined the cardiovascular and metabolic response to RBC transfusion in patients with circulatory shock after volume resuscitation. Data were analyzed from 36 transfusions in 32 patients who were undergoing continuous hemodynamic monitoring. Transfusions were administered for moderate to severe anemia, mean Hgb 8.3 g/dl. The diagnosis were sepsis (19/36), cardiogenic shock (14/36), connective tissue disease (2/36), and severe hypocalcemia (1/36). Benefit from transfusion was defined as an improvement in tissue oxygen utilization (increased oxygen consumption [VO2] or decreased lactate), a decrease in myocardial VO2 (MAP x HR), or a decrease in myocardial work (left ventricular work index). Mean transfusion volume was 577 ml over 4.5 h. Hgb and oxygen delivery (DO2) increased by 27% and 28%, respectively, while pulmonary artery wedge pressure and cardiac index were unchanged. No significant change was noted in VO2, or lactate, after augmentation of red cell mass. An increase occurred in myocardial work indices and MAP x HR. No changes were identified when subgroups were analyzed based on diagnosis, pretransfusion Hgb, lactate, or VO2 levels. We conclude that selective increase in DO2 by augmentation of RBC mass and oxygen-carrying capacity did not improve the shock state in these volume-resuscitated patients, regardless of the etiology of the shock.     

Oxygen transport in adult respiratory distress syndrome and other acute circulatory problems: relationship of oxygen delivery and oxygen consumption

OBJECTIVE: To evaluate the evidence that oxygen consumption (VO2) is pathologically dependent on oxygen delivery (DO2). DATA SOURCES: Studies published since 1972 with their relevant bibliographies and computerized search of MEDLINE. STUDY SELECTION: All clinical papers reporting the relationship of: VO2 to DO2 in the adult respiratory distress syndrome (ARDS), sepsis, other critically ill patients, and normal individuals; cardiac output determined by measured VO2 to calculated VO2 from the arterial-mixed venous oxygen difference; blood lactate to DO2; and selected basic science studies. DATA EXTRACTION: Study quality was assessed and all pertinent data were summarized. RESULTS OF DATA EXTRACTION: Normal individuals display physiologic dependence of VO2 at very low levels of DO2 (330 mL/min.m2). Pathologic dependence of VO2 on DO2 entails two concepts: a) VO2 varies directly with DO2 over a wide range of DO2 and b) of particular import, tissue oxygen extraction is compromised. This pathologic supply dependence was initially identified in patients with ARDS; subsequently, it has been demonstrated in patients with sepsis and in a variety of other critically ill individuals. There are substantial, but not uniform, data documenting this dependence of VO2 on DO2 in ARDS. In some studies, this relationship correlates best with increased lactate concentrations. However, increased blood lactate concentrations do not accurately track other evidence of tissue hypoxia. Some researchers have attributed the finding of this supply dependency to artifact, when VO2 is determined by the arterial-mixed venous oxygen difference. However, when these methods are compared, the correlation is excellent. Others have raised the concern that appreciable changes in VO2, even over short periods of time, may result in physiologic increases in DO2. However, when "control" groups have been contemporaneously compared with patients with ARDS using the same methodology, they have not shown supply dependency. Interwoven throughout the studies reviewed is overwhelming and uniform evidence that both mixed venous oxygen tension (PVO2) and mixed venous oxygen content (CVO2) correlate poorly with cardiac output, DO2, or VO2. The inconsistencies in identifying pathologic DO2 dependency may well reflect the unknown variables that exist in patients with ARDS, perhaps better labeled, multiple organ system failure. CONCLUSIONS: Pathologic dependence of VO2 on DO2, especially the inability to increase tissue oxygen extraction, is present in most patients with ARDS and many other critically ill individuals. PVO2 and CVO2 are both unreliable indicators of cardiac output, DO2, or VO2.     

重症急性胰腺炎血流动力学和氧代谢变化的实验研究

目的 观察重症急性胰腺炎(SAP)猪的血流动力学和氧代谢变化特点,为临床治疗提供理论依据。方法 通过向主胰管逆行注入含质量分数为4％牛磺胆酸钠和质量分数为1％胰蛋白酶的生理盐水溶液(1 ml／kg)诱导猪SAP模型(n=8);通过Swan-Ganz导管和心电监护仪,连续监测心率(HR)、中心静脉压(CVP)、平均动脉压(MAP)、肺动脉楔压(PAWP)、平均肺动脉压(MPAP)和心排血量,计算心脏指数(CI);通过对制模前(0 h)和制模后6、12、24及36 h的动脉及混和静脉血的血气分析,计算出相应的全身氧输送(DO2)、氧耗(VO2)和氧摄取率(O2ext),分析上述各指标的变化。结果 制模12 h MAP和CI与0 h比较显著下降(P均<0.05)。动脉氧分压(PaO2)和DO2都有下降的趋势。与0 h比较,PaO2在制模后6 h以后下降显著,DO2在制模后24 h下降最显著(P均<0.05)。VO2和O2ext的走势一致,都在制模后6 h上升至最高水平(P均<0.05),然后一直下降,制模后24 h较6 h差异具有显著性(P均<0.05)。结论SAP时不仅有血流动力学紊乱,而且有氧代谢障碍。SAP导致多器官功能障碍综合征(MODS)的因素可能与VO2和O2ext下降有关。     

Effect of blood transfusion on oxygen consumption in pediatric septic shock

Treatment plans for pediatric septic shock advocate increasing oxygen consumption (VO2). Recent studies in septic shock indicate that improving oxygen delivery (DO2) by increasing blood flow will increase VO2. We prospectively examined the effect on VO2 of improving DO2 by increasing oxygen content (CO2) with blood transfusion in eight hemodynamically stable septic shock patients. Transfusion consisted of 8 to 10 ml/kg of packed RBC over 1 to 2 h. Hemodynamic and oxygen transport measurements were obtained before and after blood transfusion. Transfusion significantly (p less than .05) increased Hgb and Hct from 10.2 +/- 0.8 g/dl and 30 +/- 2% to 13.2 +/- 1.4 g/dl and 39 +/- 4%, respectively (mean +/- SD). DO2 significantly (p less than .05) increased after transfusion (599 +/- 65 to 818 +/- 189 ml/min.m2), but VO2 did not change (166 +/- 68 to 176 +/- 74 ml/min.m2; NS). In pediatric septic shock patients, increasing CO2 by blood transfusion may not increase VO2.     

Blood transfusion and oxygen consumption in surgical sepsis

OBJECTIVE: To evaluate the use of serum lactic acid values to predict flow-dependent increases in oxygen consumption (VO2) in response to increasing oxygen delivery (DO2) after blood transfusion in surgical sepsis. DESIGN: Prospective study. SETTING: Tertiary care, trauma center. PATIENTS: Twenty-one patients, postsurgical or posttrauma, judged septic by defined criteria. INTERVENTIONS: Serum lactic acid concentrations, DO2, and VO2 were measured before and after transfusion therapy. MEASUREMENTS AND MAIN RESULTS: Overall, the DO2 increased from 532 +/- 146 to 634 +/- 225 (SD) mL/min.m2 (p less than .001), and the VO2 increased from 145 +/- 39 to 160 +/- 56 mL/min.m2 (p = .02). These changes occurred with an Hgb increase from 9.3 +/- 1.1 to 10.7 +/- 1.5 g/dL (p less than .001). The patients were grouped by their pretransfusion serum lactic acid values. In those patients with normal (less than 1.6 mmol/dL) serum lactic acid (n = 10), DO2 increased from 560 +/- 113 to 676 +/- 178 mL/min.m2 (p less than .02), and VO2 increased from 150 +/- 25 to 183 +/- 46 mL/min.m2 (p less than .02). However, in the increased serum lactic acid group (n = 17), VO2 was not significantly changed after transfusion (143 +/- 46 to 146 +/- 58 mL/min.m2) despite increased DO2 (515 +/- 163 to 609 +/- 251 mL/min.m2, p less than .01). CONCLUSIONS: Blood transfusion can be used to augment DO2 and VO2 in septic surgical patients. Increased serum lactic acid values do not predict patients who will respond. The absence of lactic acidosis should not be used in this patient population to justify withholding blood transfusions to improve flow-dependent VO2. Patients who have increased lactate concentrations may have a peripheral oxygen utilization defect that prevents improvement in VO2 with increasing DO2.     

环境低温对非麻醉猪失血性休克血流动力学及氧代谢的影响

目的 探讨环境低温对非麻醉猪失血性休克血流动力学及氧代谢的影响.方法 沈阳军区总医院动物中心提供的巴马香猪16头随机(随机数字法)分为:室温休克组和低温休克组,每组8头.按30 mL/kg放血建立失血性休克模型,记录建模前及建模后4h内不同时点的核心体温、心率、平均动脉压、中心静脉压、心输出量、混合静脉血氧饱和度及血气等变化,并计算氧摄取率、氧供指数和氧耗指数.采用SPSS11.0软件包行计量资料的成组t检验.结果 模型建立后室温组动物的核心体温略有下降,环境低温使核心体温下降更加明显.低温组动物的病死率较室温组明显增加(P＜0.05).休克导致氧供和氧耗明显下降.室温组和低温组的血流动力学指标、氧供和氧耗的差异无统计学意义,但两者在pH值、乳酸和氧提取率上差异具有统计学意义(P＜0.05).结论 环境低温加重了失血性休克后的氧代谢紊乱,使预后进一步恶化.     

Comparison of systemic oxygen delivery and uptake with NIR spectroscopy of brain during normovolemic hemodilution in the rabbit.

Incremental hyperoxic normovolemic hemodilution was utilized to progressively decrease oxygen delivery (DO2) in anesthetized rabbits. At decreasing DO2, we compared systemic responses related to the adequacy of DO2, i.e. mixed venous oxygen saturation (SvO2), oxygen consumption (VO2), and arterial lactate concentrations, to near infrared spectroscopy (NIRS) of the brain, a regional measure of intracellular oxygen availability. We sought concomitantly to define critical SvO2 and DO2, beyond which whole body VO2 begins to decline and arterial lactate concentrations increase. NIR Spectroscopy provided the means to test the hypothesis that systemic indicators of inadequate DO2 would not accurately reflect the oxygenation of a critical organ such as the brain. In thirteen rabbits anesthetized with fentanyl, paralyzed and artificially ventilated at an FIO2 of 0.60, hemodilution produced an early decrease in mixed venous oxygen saturation. When mixed venous oxygen saturation decreased below approximately 50%, arterial lactate concentrations began to increase significantly. Further decreases in oxygen delivery precipitated a decline in systemic VO2. Finally, NIRS revealed an increase in the reduction level of brain cytochrome a,a3 after systemic parameters of oxygen delivery had been altered. Analysis of the data indicated that falling SvO2 predicted inadequate DO2 to tissue during early hemodilution under narcotic/relaxant anesthesia and that the brain showed evidence of intracellular hypoxia only after systemic parameters such as SvO2 were affected markedly.     

Cardiorespiratory responses to fluid administration in peritonitis

Intravascular volume expansion was studied in 59 critically ill patients with a wide variety of sepsis and in a small group of 12 patients with peritonitis; either 500 ml of 5% albumin solution or 2 units of packed red blood cells were given over a 60-min period. During the 2-h period after volume loading, significant increases in mean arterial pressure (MAP), pulmonary capillary wedge pressure (WP), central venous pressure (CVP), and oxygen consumption (VO2) were observed. One hour after fluid administration MAP had risen from 72 +/- 16 (SD) at baseline to 78 +/- 17 mm Hg (p less than .01), WP from 9 +/- 5 to 16 +/- 7 mm Hg (p less than .05), CVP from 7 +/- 4 to 9 +/- 4 mm Hg (p less than .05) and VO2 from 132 +/- 19 to 148 +/- 31 ml/min X m2 (p less than .01). Improvement in VO2 after volume loading is consistent with the concept that circulatory problems in sepsis result in less VO2 than is needed and that intravascular volume expansion in normovolemic septic patients may improve peripheral perfusion as measured by oxygen uptake.     

Effect of increasing oxygen delivery postburn on oxygen consumption and oxidant-induced lipid peroxidation in the adult sheep

We studied the relationship between oxygen delivery (DO2) and oxygen consumption (VO2) in the early post-burn period. Unanesthetized sheep with a 15% total body surface (TBS) third-degree burn were resuscitated back to baseline VO2 and vascular pressures. DO2 was adjusted further by infusion and removal of whole blood. The response was compared to the same maneuver in nonburned sheep. We found that increasing DO2 after burns resulted in a 32% increase in VO2, while the same maneuver in controls produced no change in VO2. We then determined whether the increase in VO2, caused by volume loading, resulted in a further increase in postburn oxidant release and lipid peroxidation measured as conjugated dienes. Plasma conjugated dienes increased significantly and equally by 30% in burns maintained at baseline VO2 vs. the increased VO2. Therefore, the increased oxygen used is not simply resulting in further oxidant damage. VO2 was maintained equally in both burned animals and controls with a decrease in DO2 by increased oxygen extraction from Hgb. We conclude that standard burn resuscitation does not restore adequate DO2 for oxygen demands. The 30% increase in VO2 achieved by increasing DO2 does not lead to a further release of oxidants from burn tissue and is therefore potentially beneficial for cell function.     

Cardiorespiratory and metabolic effects of dopamine and dobutamine infusions in dogs

The effects of iv dobutamine and dopamine infusions were studied at six incremental doses (range 5 to 160 micrograms/kg.min) in two groups of five dogs. Dobutamine decreased the systemic vascular resistance (SVR), without significant changes in mean arterial pressure (MAP), or pulmonary vascular resistance (PVR). Dopamine increased MAP, SVR, and PVR, except for a decrease at 10 micrograms/kg.min. Both drugs produced dose-related increases in cardiac output and venous admixture; however, with dopamine the dose-response curve reached a plateau at doses greater than 40 micrograms/kg.min. While the oxygen consumption (VO2) increased progressively in both groups, the oxygen availability ratio (DO2/VO2) and arteriovenous oxygen content difference (CaO2 - CvO2) were maintained mainly by increased cardiac output in the dobutamine group and hemoglobin concentration in the dopamine group. Thirty minutes after termination of drug infusions, the DO2/VO2 dropped, and CaO2 - CvO2 increased significantly in both groups. These changes were mainly due to sustained high VO2; however, in the dopamine group, a larger imbalance resulted from further decreases in cardiac output to levels below the control value.     

Alterations in tissue oxygen consumption and extraction after trauma and hemorrhagic shock

OBJECTIVES: Although trauma and hemorrhage are associated with tissue hypoperfusion and hypoxemia, changes in oxygen delivery (DO2), oxygen consumption VO2), and oxygen extraction at the organ level in a small animal (such as the rat) model of trauma and hemorrhage have not been examined. Therefore, the objectives of this study were to determine whether blood flow, DO2, VO2, and oxygen extraction ratio in various organs are differentially altered after trauma-hemorrhagic shock and acute resuscitation in the rat. DESIGN: Prospective, randomized animal study. SETTING: A university research laboratory. SUBJECTS: Male Sprague-Dawley rats (n = 6-7 animals/group) weighing 275-325 g. INTERVENTIONS: Male rats underwent laparotomy (i.e., soft tissue trauma) and were bled to and maintained at a blood pressure of 40 mm Hg until 40% of shed blood volume was returned in the form of lactated Ringer's solution. They were then resuscitated with four times the volume of shed blood with lactated Ringer's solution for 60 mins. At 1.5 hrs postresuscitation, cardiac output and blood flow were determined by using strontium-85 microspheres. Blood samples (0.15 mL each) were collected from the femoral artery and vein and the hepatic, portal, and renal veins to determine total hemoglobin and oxygen content. Systemic and regional DO2, VO2, and oxygen extraction ratio were then calculated. MEASUREMENTS AND MAIN RESULTS: Both the systemic hemoglobin and systemic arterial oxygen content in hemorrhaged animals at 1.5 hrs postresuscitation were >50% lower as compared with sham-operated controls. Cardiac output and blood flow in the liver, small intestine, and kidneys decreased significantly, but blood flow in the brain and heart remained unaltered after hemorrhage and resuscitation. Systemic DO2 and VO2 were 73% and 54% lower, respectively, than controls at 1.5 hrs after resuscitation. Similarly, regional DO2 and VO2 in the liver, small intestine, and kidneys decreased significantly under such conditions. In addition, the liver had the most severe reduction in VO2 (76%) among the tested organs. However, the oxygen extraction ratio in the liver of sham animals was the highest (72%) and remained unchanged after hemorrhage and resuscitation. CONCLUSION: Because the liver experienced the most severe reduction in VO2 associated with an unchanged oxygen extraction capacity, this organ appears to be more vulnerable to hypoxic insult after hemorrhagic shock.     

Correlating the severity of paraquat poisoning with specific hemodynamic and oxygen metabolism variables

OBJECTIVE: To investigate the hemodynamics and oxygen metabolism of patients with varying degrees of severity of paraquat poisoning. DESIGN: Prospective, observational, clinical study. SETTING: Intensive care unit in a university hospital. PATIENTS: Forty-three consecutive patients with paraquat and/or diquat poisoning were classified into three groups by the severity index of paraquat poisoning (SIPP; hr/mg/L). INTERVENTIONS: Standard treatments included specific respiratory management, fluid resuscitation, and aggressive circulatory support. MEASUREMENTS AND MAIN RESULTS: Serum paraquat and diquat levels were measured at arrival, and SIPP was calculated. The cardiac index (CI), left ventricular stroke work index (LVSWI), systemic vascular resistance index (SVRI), oxygen delivery index (DO2I), oxygen consumption index (VO2I), and oxygen extraction ratio (O2ER) were measured at 6, 12, 24, 36, 48, 72, and 96 hrs postadmission. A significant inverse correlation between SIPP and survival time was found in 31 fatal cases (r = .85; p < .001). In the SIPP 10-50 group, CI, DO2I, VO2I, and O2ER were maintained at higher levels than in the SIPP group of <10 (p < .05), whereas SVRI decreased significantly (p < .05). In the SIPP group of >50, CI, LVSWI, SVRI, DO2I, and VO2I decreased, whereas O2ER had a tendency to increase progressively. There was a significant correlation between SVRI and SIPP, O2ER and SIPP, and O2ER and SVRI 24 hrs after admission, respectively (p < .001). CONCLUSIONS: Paraquat poisoning is characterized by high oxygen consumption with high oxygen extraction, with the degree of derangement based on the severity index. The development of a marked imbalance between increased oxygen demand and decreased oxygen supply because of myocardial depression might be a possible cause of death in circulatory failure.     

液体复苏对初进高海拔地区重度失血性休克犬氧合功能的影响

目的 探讨液体复苏对初进高海拔地区重度失血性休克犬氧合功能的影响.方法 13只成年杂种犬由海拔1 510 m地区用1 d时间被运至3 780 m的高海拔地区,随机分为3组.每只犬麻醉后经颈静脉放置漂浮导管进行氧合功能监测,经股动脉放血使平均动脉压(MAP)维持在(35±5)mm Hg(1 mm Hg=0.133 kPa).建立重度失血性休克模型.对照组:制模后不进行液体复苏;乳酸林格液(LR)组:制模1 h输1.5倍失血茸的LR;羟乙基淀粉(HES)组:制模后1 h输入等失血量的6%HES 贺斯);然后B组模型犬均输以5 ml·kg-1·h1LR作为维持量,在不同时间点观察氧合功能的变化.结果 对照组犬在制模后2 h全部死亡.休克1 h,两个液体复苏组氧消耗(VO2)、氧输送(DO2)、氧摄取率(O2ER)、动脉血氧饱和度(SaO2)均较放血前明显降低,而静脉血氧饱和度(SvO2)、肺泡一动脉血氧分压差(A-aDO2)较休克前明显升高(p均<0.05).复苏2 h,LR组VO2、DO2、O2ER、SaO2均较休克1 h显著升高,而A-aDO2则显著降低(P均<0.05);HES组VO:、DO2、O2ER均较休克1 h显著升高.而SvO2显著降低(P均<0.05).结论 对初进高海拔地区的重度失血性休克犬如果不进行有效的液体复苏,死亡率达100%;输入1.5倍失血量的LR后2 h氧合功能达到了预期的复苏指标;而输入等失血量的6%HES后2 h氧合功能没有达到预期的复苏指标.     

Oxygen delivery-dependent oxygen consumption in acute respiratory failure

OBJECTIVE: To investigate whether oxygen consumption (VO2) is dependent on oxygen delivery (DO2) in adult respiratory distress syndrome (ARDS) and non-ARDS acute respiratory failure. DESIGN: Intervention study of a consecutive sample of patients admitted to the ICU with the diagnosis of acute respiratory failure. SETTING: Tertiary care center. PATIENTS: Thirteen consecutive patients with a diagnosis of ARDS and 11 with a diagnosis of respiratory failure not due to ARDS. Patients were monitored with an oximetric pulmonary artery catheter and mechanically ventilated. INTERVENTIONS: DO2 was decreased by the application of positive end-expiratory pressure (PEEP) (20 cm H2O), and subsequently increased by an iv infusion of dobutamine (10 micrograms/kg.min). RESULTS: After the application of PEEP, DO2 decreased significantly in both groups. However, VO2 decreased significantly (p less than .01) only in the ARDS group. When dobutamine was infused, DO2 increased significantly (p less than .01) in both groups, but VO2 increased only in ARDS patients. DO2 correlated significantly with VO2 both in ARDS (r2 = .81, p less than .01) and in non-ARDS (r2 = .38, p less than .05) patients. The correlation coefficient was significantly higher for ARDS than for non-ARDS patients. Comparing the slopes of the regression lines, a stronger dependency of VO2 on DO2 was found in ARDS than in non-ARDS respiratory failure (p less than .001). The oxygen extraction ratio correlated with DO2 in non-ARDS patients (r2 = .49, p less than .05), but not in ARDS patients. CONCLUSIONS: VO2 is dependent on DO2 over a wide range of DO2 values in acute respiratory failure. This dependency phenomenon is much stronger in ARDS than in respiratory failure due to other causes. Due to the abnormal dependency of VO2 on DO2, changes in the oxygenation status may not be reflected by changes in mixed venous oxygen saturation in ARDS.     

'Multi-associations': predisposed to misinterpretation of peripheral tissue oxygenation and circulation in neonates

Interpretation of peripheral circulation in ill neonates is crucial but difficult. The aim was to analyse parameters potentially influencing peripheral oxygenation and circulation. In a prospective observational cohort study in 116 cardio-circulatory stable neonates, peripheral muscle near-infrared spectroscopy (NIRS) with venous occlusion was performed. Tissue oxygenation index (TOI), mixed venous oxygenation (SvO(2)), fractional oxygen extraction (FOE), fractional tissue oxygen extraction (FTOE), haemoglobin flow (Hbflow), oxygen delivery (DO(2)), oxygen consumption (VO(2)), and vascular resistance (VR) were assessed. Correlation coefficients between NIRS parameters and demographic parameters (gestational age, birth weight, age, actual weight, diameter of calf, subcutaneous adipose tissue), monitoring parameters (heart rate, arterial oxygen saturation (SaO(2)), mean blood pressure (MAP), core/peripheral temperature, central/peripheral capillary refill time) and laboratory parameters (haemoglobin concentration (Hb-blood), pCO(2)) were calculated. All demographic parameters except for Hbflow and DO(2) correlated with NIRS parameters. Heart rate correlated with TOI, SvO(2), VO(2) and VR. SaO(2) correlated with FOE/FTOE. MAP correlated with Hbflow, DO(2), VO(2) and VR. Core temperature correlated with FTOE. Peripheral temperature correlated with all NIRS parameters except VO(2). Hb-blood correlated with FOE and VR. pCO(2) levels correlated with TOI and SvO(2). The presence of multiple interdependent factors associated with peripheral oxygenation and circulation highlights the difficulty in interpreting NIRS data. Nevertheless, these findings have to be taken into account when analysing peripheral oxygenation and circulation data.     

延迟复苏对失血性休克犬循环氧动力学指标的影响

【目的】研究延迟补液对致死性失血性休克循环氧动力学指标的影响。【方法】Beagle犬14只,先期无菌手术行颈动、静脉置管,24h后从颈动脉放血造成失血性休克,总失血量为全身血容量的40％。随机分为延迟补液组（DR,n=8）和立即补液组（IR,n =6）。失血后第1个24小时DR组无治疗,IR组静脉输入3倍失血量的葡萄糖电解质溶液。失血后24h起两组犬均实施静脉补液。测定犬失血前和失血后2、4、8、24、48和72h非麻醉状态下的平均动脉压（MAP）,抽取动脉和混合静脉血测定动脉、混合静脉氧分压（PaO2、PcvO2）及血氧含量、计算氧供量（DO2）和氧耗量（VO2）,并统计失血后72h病死率。【结果】DR组MAP伤后4h降至最低,仅为失血前的38．4％。IR组MAP伤后4h起各时间点均显著高于DR组（P〈0．05）,并于失血后6h恢复至失血前水平。DR组72h死亡率为62．5％（5／8）,而IR组无一死亡。两组失血后PaO2、pH、DO2和VO2较失血前均显著降低,动脉二氧化碳分压（PaCO2）显著升高（均P〈0．05）。立即补液组上述指标迅速恢复,失血后4h起PaO2、PH、DO2和VO2显著高于延迟补液组,PaCO2低于延迟补液组（均P〈0．05）。失血后7Zh立即补液组除DO2和VO2外,PaO2、PaCO2和pH均恢复至失血前水平;而延迟补液组上述指标仍显著低于或高于0h水平（均P〈0．05）。【结论】失血性休克后延迟补液显著加重循环氧动力学障碍,增加休克动物的病死率。     

Pulmonary oxygen consumption: a hypothesis to explain the increase in oxygen consumption of low birth weight infants with lung disease

OBJECTIVE: We determined pulmonary oxygen consumption (VO2lung) in low-birthweight infants with acute lung disease to help explain the greater whole-body oxygen consumption (VO2wb) in these infants with than in those without lung disease. METHODS AND MATERIALS: Eleven infants (birth weight 1,076+/-364 g; gestational age 28+/-3 weeks) undergoing mechanical ventilation for respiratory distress syndrome were studied in their first week of life. We measured VO2wb by indirect calorimetry and simultaneously determined systemic oxygen uptake (VO2Fick) as the product of cardiac output (echocardiography) and the arterial-mixed venous oxygen content difference (cooximetry) assuming that VO2wb-VO2Fick accounts for VO2lung. Right atrial blood samples were used to determine mixed venous oxygenation, and infants were excluded if samples returned saturations greater than 89%. RESULTS: VO2lung was 1.92+/-1.74 ml x kg(-1) x min(-1), representing 25% of their VO2wb (7.58+/-1.48 ml x kg(-1) x min(-1)). VO2lung was not correlated with clinical measures of acute disease severity. However, infants with the most severe changes on follow-up radiography (Edwards score 5 as assessed by radiologist blinded for VO2 data) all had a VO2lung level greater than 2.0 ml x kg(-1) x min(-1). CONCLUSION: VO2lung can account for the elevated metabolic rate in low-birthweight infants with lung injury. We speculate that this reflects in part inflammatory pulmonary processes and may herald chronic lung disease.