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.     

Comparison of gastric intramucosal pH with measures of oxygen transport and consumption in critically ill patients.

OBJECTIVE: To determine the relationship of tonometrically measured gastric intramucosal pH to clinically accepted indices of systemic oxygenation. DESIGN: Prospective, nonintervention study. SETTING: Medical and surgical ICUs of a university hospital. PATIENTS: Critically ill patients (n = 22) with pulmonary artery catheters in place who also required nasogastric suctioning. MEASUREMENTS AND MAIN RESULTS: Tonometric measurements of gastric intramucosal pH were compared with concurrently obtained systemic indices of tissue oxygenation. These variables included oxygen delivery (DO2), oxygen consumption (VO2), oxygen extraction ratio, arterial lactate concentrations, mixed venous PO2, and mixed venous pH. The study period ranged from the time of insertion of the pulmonary artery catheter to the time of its removal. We classified patients who were alive by the end of the study as survivors and those patients who died with the pulmonary artery catheter in place as nonsurvivors. Both groups had similar levels of DO2 during the study period, but nonsurvivors had greater levels of VO2, oxygen extraction ratio, and serum lactate concentrations than survivors. Gastric intramucosal pH, mixed venous pH, and mixed venous PO2 values were lower in nonsurvivors. Both groups demonstrated the phenomenon of oxygen supply dependency. When the final measurements taken before the removal of the pulmonary artery catheter or death were compared, only gastric intramucosal pH and mixed venous pH showed differences between the groups, being lower in nonsurvivors. All the patients who died, except for one, had final gastric intramucosal pH values of less than 7.32. CONCLUSIONS: In this group of patients, death was associated with increased tissue needs for oxygen that were not adequately satisfied by the available levels of oxygen supply. We also conclude that tonometrically measured gastric intramucosal pH is a useful noninvasive adjunct to current methods of monitoring systemic oxygenation.     

Ventilation/perfusion indices do not correlate with the difference between oxygen consumption measured by the Fick principle and metabolic monitoring systems in critically ill patients.

OBJECTIVE: To determine whether the difference between oxygen consumption (VO2) measured by metabolic gas monitoring systems and by the Fick principle is related to venous admixture, deadspace/tidal volume ratio, or alveolar-arterial oxygen tension gradient in critically ill patients. DESIGN: A prospective study. SETTING: An 11-bed general ICU in a 900-bed teaching hospital. PATIENTS: Twenty critically ill patients admitted to the ICU who required mechanical ventilation, right heart catheterization, and arterial and mixed venous gas measurements for normal clinical management. RESULTS: Thirty-three recordings were analyzed. The mean VO2 measured by the metabolic gas monitoring system was 308 +/- 63.9 (SD) mL/min and was significantly greater than the mean VO2 measured by the Fick principle of 284 +/- 72.0 mL/min. The difference between the two measurements of 24.3 +/- 47.6 mL/min correlated poorly with venous admixture (r2 = .0009), dead-space/tidal volume ratio (r2 = .0064) and alveolar-arterial oxygen tension gradient (r2 = .017). CONCLUSIONS: If the difference in VO2 measured by metabolic gas monitoring systems and the Fick principle is due to intrapulmonary VO2 then in critically ill patients the ventilation/perfusion indices of venous admixture, deadspace/tidal volume ratio and alveolar-arterial oxygen tension gradient correlate poorly with intrapulmonary VO2.     

Central venous and mixed venous oxygen saturation: Comparison during canine open-chest cardiopulmonary resuscitation

Mixed venous oxygen saturation (MVO2) is a valuable parameter in monitoring critically ill patients because it serves as an index of the adequacy of the oxygen delivery system. Mixed venous oxygen saturation as reflected by the easily obtainable central venous oxygen saturation (CVO2) may prove useful during cardiopulmonary resuscitation (CPR) as an indicator of both the adequacy of varying CPR regimens and the efficacy of pharmacological interventions. This study investigates the relationship between CVO2 and MVO2 and its clinical usefulness during CPR. Swan-Ganz and central venous catheters were placed in 20 mongrel dogs. Ventricular fibrillation was then induced and, after predetermined downtimes ranging from 5 to 60 minutes, thoracotomy was performed, and open-chest bimanual cardiac massage was started. Central venous and mixed venous blood-gas samples were drawn every five minutes during a 30-minute period of CPR. The correlation between CVO2 and MVO2 was 0.8719 (P less than 0.001) before arrest but deteriorated at all times during CPR with values ranging from 0.1589 (P = 0.542) to 0.5781 (P = 0.024). Although statistically significant at times, the correlation between CVO2 and MVO2 during CPR is not consistently high enough to enable the routine substitution of CVO2 for MVO2 in assessing the oxygen delivery system.     

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.     

The relationship between oxygen delivery and oxygen consumption during fluid resuscitation of burn-related shock

Although burn-related shock resuscitation based on invasive hemodynamic monitoring has been reported at an increased rate, little is known about appropriate hemodynamic end points. Shock resuscitation based on oxygen transport criteria has been widely used for patients with trauma and patients who undergo surgery, and supranormal values of oxygen delivery (DO2) have been reported in association with an improved survival rate. This improved survival rate has been attributed to a shifting of the critical threshold of DO2 to higher values in these patients. In patients with thermal injuries, the effects of the manipulation of hemodynamics to optimize oxygen transport have not been proven. It is still unclear whether these patients exhibit delivery-dependent oxygen consumption (VO2) during the shock phase. The goal of this study was to evaluate the existence of oxygen supply dependency and to determine critical levels of DO2 in patients with burns. In a prospective study that included 16 patients with serious thermal injuries, we studied the effects of volume loading on DO2 and VO2. A transpulmonary double dilution technique was used for hemodynamic monitoring, and resuscitation end points included a normalization of preload and cardiac output parameters within 24 hours of the thermal injury. Fluid loading with crystalloids and colloids, according to our resuscitation protocol, was used to augment cardiac output and DO2. Of the 16 patients with a mean of 46% total body surface area burned (range, 22%-80%), 8 patients survived and 8 patients died. With the use of progressive fluid loading, cardiac index was restored within 24 hours of admission in all of the patients. Successful resuscitation was associated with increased levels of DO2 and VO2 and with declining serum lactate levels. VO2 appeared to be dependent on DO2 during the resuscitation period (r = 0.596), and the correlation was significantly stronger in the patients who survived (r = 0.744) than in the patients who died (r = 0.368; P < .05). A critical threshold of oxygen supply could not be identified. We concluded that increasing DO2 by fluid resuscitation increases VO2 during hypovolemic shock after a severe burn injury.     

Relationship of oxygen delivery and mixed venous oxygenation to lactic acidosis in patients with sepsis and acute myocardial infarction

Critical decreases in oxygen delivery (DO2) and mixed venous oxygen saturation (SvO2) are associated with anaerobic metabolism and, therefore, lactic acidosis. We studied 50 consecutive patients with sepsis and 50 consecutive patients with acute myocardial infarction (AMI) in whom the arterial blood lactate was greater than 1 mmol/L in order to determine critical thresholds of DO2 and SvO2. In both groups, critical values of DO2 or SvO2 associated with lactic acidosis could not be identified. The DO2 ranged from 136 to 811 ml/min.m2 and SvO2 ranged from 28% to 73% in the patients with sepsis. The DO2 ranged from 115 to 434 ml/min.m2 and SvO2 from 17% to 72% in patients with AMI. The absence of threshold values for DO2 and SvO2 probably reflects the influence of distributive flow abnormalities as well as differences in metabolic requirements in these critically ill patients.     

Hemodynamic and oxygen transport effects of dobutamine in critically ill general surgical patients

The effects of dobutamine on hemodynamic and oxygen transport were evaluated in 43 studies on 34 critically ill general (noncardiac) surgical patients. Dobutamine, beginning at a low dose (2.5 micrograms/kg X min) significantly increased cardiac index (CI), oxygen delivery (DO2), and oxygen consumption (VO2), while decreasing mean arterial pressure, pulmonary artery and wedge pressures, and systemic and pulmonary vascular resistances; blood gases, pH, and pulmonary shunt were not significantly changed. These effects were seen in postoperative and septic patients, as well as in patients with normal, low, and high control CI. These responses were poor in terminally ill and hypovolemic patients; however, when the latter were given additional fluids, their responses were markedly improved. The hemodynamic effects of dobutamine are well known, but the DO2 and VO2 effects, which suggest improved tissue perfusion, have not been appreciated.     

Muscle perfusion and oxygen consumption by near-infrared spectroscopy in septic-shock and non-septic-shock patients

OBJECTIVE: To measure muscle blood flow (Qtis) and oxygen consumption (VO(2)tis) in septic and non-septic critically ill patients by near-infrared spectroscopy (NIRS). SETTING: Surgical intensive care unit of a university hospital. PATIENTS AND PARTICIPANTS: Four patients with septic shock, eight post-surgical critically ill patients and ten healthy volunteers. MEASUREMENTS AND RESULTS: Oxyhaemoglobin (HbO(2)) and deoxyhaemoglobin (HbH) variations after venous occlusion were measured by NIRS in the brachioradialis muscle. We calculated Qtis by the rate of HbO(2) and HbH increase in the first 30 s of venous occlusion divided by haemoglobin blood concentration. VO(2)tis was calculated by subtraction of the arterial HbH from the initial increase of HbH after venous occlusion extrapolated to 1 min. Tissue oxygenation index [TOI = HbO(2)/(HbO(2)+HbH)] was also measured before venous occlusion. Two measurements in patients with septic shock, and one measurement in non-septic-shock patients and healthy subjects, were obtained. Of the measurements, 35% were repeated because of low-quality NIRS signal. VO(2)tis and Qtis were two times larger ( P<0.05) in patients with septic shock than in patients without and in healthy subjects. The TOI was very similar among the three groups. CONCLUSION: In septic-shock patients the increase in VO(2)tis was associated with an equivalent increase in Qtis. Therefore, tissue O(2) supply does not seem to be a limiting factor for muscle O(2) consumption. NIRS combined with venous occlusion allows a rapid, non-invasive and simultaneous assessment of regional perfusion and oxygen consumption. In case of microcirculatory shunt occurrence, the TOI should be cautiously used to assess tissue oxygenation state.     

Respiratory index/pulmonary shunt relationship: quantification of severity and prognosis in the post-traumatic adult respiratory distress syndrome

The relationship between the respiratory index (RI = alveolar-arterial oxygen gradient [P(A-a)O2] normalized by PaO2) and the pulmonary shunt (Qsp/Qt) has been examined in 929 studies from 240 critically ill post-traumatic patients. Of these, 88 patients (443 studies) were individuals who developed post-traumatic adult respiratory distress syndrome (ARDS) and 152 were patients (486 studies) who did not develop ARDS. This study demonstrates that the RI to Qsp/Qt [RI/(Qsp/Qt)] relationship was significantly (p less than .0001) increased in patients who developed fatal ARDS compared with those who did not develop ARDS, or with those whose ARDS resolved. Because of the increased oxygen consumption (VO2) in ARDS patients in association with their severe limitations in gas exchange (RI) and increased Qsp/Qt, surviving ARDS patients had a significant increase in the cardiac index which resulted in a higher oxygen delivery to VO2 ratio. ARDS patients showed significant (p less than .0001) evidence of increased pulmonary vascular tone, correlated with the increase in the RI/(Qsp/Qt) relationship. In addition, those patients with high RI/(Qsp/Qt) also had increased right ventricular (RVSW) to left ventricular work (LVSW) ratios which were shown to be a direct function of the rise in RI. This increase in both RVSW/LVSW and RI/(Qsp/Qt) ratios was significantly (p less than .0001) correlated with an increased mortality. Thus, the RI/(Qsp/Qt) relationship, which can be obtained from arterial and mixed venous blood gases and saturations only, can be used to predict the severity of the ARDS process as well as important pulmonary vascular and right ventricular overload consequences.     

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。     

Cell metabolism in patients undergoing major valvular heart surgery: relationship with intra and postoperative hemodynamics, oxygen transport, and oxygen utilization patterns

The relationships between cell metabolism and both hemodynamics and oxygen transport/utilization (VO2/DO2) pattern were evaluated intra and postoperatively in eight patients undergoing major valvular heart surgery with the aid of moderately hypothermic cardiopulmonary bypass (CPB). Quadriceps femoris specimens were obtained by the needle biopsy technique for muscle ATP, ADP, AMP, phosphocreatine (PCr), creatine and lactate determination at anesthesia induction, after CPB, as well as in the ICU 18 h after surgery. Moreover, hemodynamic variables, oxygen transport and utilization indices, and plasma lactate were measured at the same intervals and throughout the CPB period. After CPB, muscle ATP and PCr contents were reduced (p less than .05) as compared to those of both pre-CPB patients and healthy control subjects; muscle and plasma lactate levels were increased (p less than .05). Mean VO2 and DO2 values measured during CPB significantly decreased (p less than .05), but VO2 reduction was proportionally greater than that of DO2 (-62% vs. -41%). No correlation was found between VO2 and DO2 at that time, but a significant relationship (p less than .05) was found at the end of CPB. A further decrease in muscle ATP and PCr levels was measured in the ICU, as muscle and plasma lactate levels were still elevated. At that time, VO2 and DO2 were not significantly different from pre-CPB values, but were significantly (p less than .05) correlated with each other.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

Whole body oxygen consumption and critical oxygen delivery in response to prolonged and severe carbon monoxide poisoning

BACKGROUND: Carbon monoxide (CO) poisoning remains the leading cause of death by poisoning in the world. One of the major proposed mechanisms for CO toxicity is the binding of CO to cytochrome oxidase and interference with cellular oxygen utilization but evidence for this is inconclusive. AIM OF STUDY: This study examined the effects of prolonged CO exposure on the dynamics of whole body oxygen consumption (VO(2)) and oxygen delivery (DO(2)) in an attempt to observe if CO exposure results in a defect of oxygen utilization defect as determined by a reduction in VO(2) during the course of poisoning prior to reaching the point where VO(2) is directly dependent on DO(2). This critical level of DO(2) (DO(2)crit) produced by CO poisoning was compared to historical values produced by other insults, which decrease global body DO(2). METHODS: Five small dogs were ventilated for 2 h with 0.25% CO and room air followed by 0.5% CO until death. Cardiac index (Q), DO(2), VO(2), oxygen extraction ratio (OER), and systemic lactate were measured every 15 min until death. RESULTS: Carboxyhemoglobin (COHb) levels increased linearly over 2.5 h to values above 80% until death. VO(2) remained constant and not significantly different from baseline below a COHb of 80%. At COHb levels above 80%, VO(2) precipitously dropped. Similarly lactate levels were not significantly elevated from baseline until VO(2) dropped. DO(2) decreased by 78% (from 23+/-6 ml/kg/min to 5+/-4 ml/kg/min) over time despite an increase in Q by 58% until levels of COHb were above 80%. OER increased from 19+/-5% to 50+/-11% until death. The calculated DO(2)crit was 10.7+/-4 ml/min/kg, which is not significantly different from values ranging from 7 to 13 ml/min/kg reported in the literature due to other insults, which reduce DO(2). CONCLUSION: In this canine model of prolonged CO exposure, no gradual reduction in VO(2) or increase in systemic lactate prior to reaching DO(2)crit was noted. In addition, CO exposure does not appear to change the DO(2)crit. The combination of these findings does not support the theory that CO produces a whole body intracellular defect in oxygen utilization.     

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。     

Hepatic and splanchnic oxygen consumption during acute hypoxemic hypoxia in anesthetized pigs

OBJECTIVE: To compare the hepatosplanchnic oxygen consumption (VO2) with the hepatic and splanchnic VO2 and to calculate the critical oxygen delivery (DO2crit) below which VO2 decreases in the hepatic, splanchnic, and hepatosplanchnic regions in a model of hypoxemic hypoxia. DESIGN: Prospective animal study. SETTING: University research laboratory. SUBJECTS: Anesthetized and ventilated pigs (n = 7). INTERVENTIONS: The right carotid artery was cannulated to measure mean arterial pressure. A pulmonary artery catheter was inserted to measure mean pulmonary arterial pressure and cardiac output. After a midline abdominal incision, two flow probes were positioned around the portal vein and the hepatic artery to measure portal vein blood flow and hepatic artery blood flow. Oxygen and lactate contents in the carotid artery, the portal vein, and the hepatic vein were measured in blood samples obtained from the appropriate catheters. MEASUREMENTS AND MAIN RESULTS: After a 2-hr stabilization period, hemodynamic and biological variables were recorded during acute hypoxemic hypoxia (FIO2 = 0.5, 0.4, 0.3, 0.21, 0.15, 0.10, and 0.07). VO2, DO2, and DO2crit were determined in the hepatic, splanchnic, and hepatosplanchnic regions. The hepatosplanchnic VO2 was 48 +/- 5 mL/min at high FIO2 (40% for the liver and 60% for the splanchnic organs) and decreased below FIO2 of 0.15. Lactate uptake in the whole hepatosplanchnic region remained steady at FIO2 values of 0.5 to 0.15 and then switched to a lactate release at low FIO2. However, the splanchnic region released lactate, whereas lactate was taken up by the liver. DO2crit in the hepatic, splanchnic, and hepatosplanchnic regions was 24 +/- 3, 38 +/- 2, and 49 +/- 4 mL/min, but the systemic DO2crit, below which regional VO2 became oxygen supply dependent, did not differ in the liver, splanchnic, and hepatosplanchnic regions. CONCLUSIONS: The variables of oxygenation and lactate flux measured in the hepatosplanchnic region summarize the metabolic changes of various organs that may vary in different ways during hypoxemic hypoxia.     

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.     

Persistence of supply dependency of oxygen uptake at high levels of delivery in adult respiratory distress syndrome

OBJECTIVE: To identify any plateau in oxygen consumption (VO2) when oxygen delivery (DO2) is increased in patients with the adult respiratory distress syndrome (ARDS). DESIGN: Clinical prospective study; multiple regression analysis was done to assess the relationship between VO2 and DO2 for pooled data and for each individual patient. SETTING: University hospital ICU. PATIENTS: Twenty consecutive patients aged 18 to 78 yrs (mean 43.5) in whom ARDS was present during their ICU stay. INTERVENTIONS: Multiple measurements were obtained in individual patients (mean number of measurements 40, range 20 to 83) and mathematical models were fitted to both pooled and individual patient data. DO2 ranged from 212 to 1550 mL/min.m2 with a maximum of 758 to 1550 mL/min.m2 (mean 1136). Because of the large variations between patients, it was not justifiable to describe a relationship for the pooled data and each case was analyzed individually. MEASUREMENTS AND MAIN RESULTS: We found the optimal regression model to be linear in 13 patients, cubic in four, and either cubic or linear in one. Two patients demonstrated no significant relationship. The relationship for the group was determined from each patient's data and was best described by linear regression. CONCLUSIONS: In no patient was there evidence of a plateau, despite high levels of DO2 being achieved in all patients.     

Comparison of oxygen consumption measurements: indirect calorimetry versus the reversed Fick method

OBJECTIVE: To compare measurement of oxygen consumption (VO2) by spirometry and the reversed Fick method. DESIGN: Within-patient comparison using simultaneous measurements by the two methods, one previously calibrated on a metabolic simulator. PATIENTS: Twenty sets of observations on eight patients (57 to 83 yrs) requiring mechanical ventilation in a critical care unit. INTERVENTIONS: None during or immediately before the measurements. MEASUREMENTS AND MAIN RESULTS: Duplicate pairs of measurements of VO2 were made with a previously validated spirometric technique and the reversed Fick method (Qt[CaO2 - CVO2]), where Qt is cardiac output, CaO2 is arterial oxygen content, and CVO2 is mixed venous oxygen content. The coefficient of variation of the difference between duplicate measurements by the former technique was only 2.53% compared with 10.4% for the latter. The mean VO2 measurement by the spirometric method was 285.7 +/- 40.7 (SD) mL/min standard temperature and pressure, dry (STPD) and for the reversed Fick method, the mean VO2 measurement was 249.3 +/- 38.5 mL/min STPD. The mean difference was 36.4 +/- 28.5 mL/min STPD (p less than .001). CONCLUSIONS: The repeatability of the spirometric method was four times better than the reversed Fick method. The latter gave a significantly lower value that probably, in part, reflects the VO2 of the lung, which is included in the spirometric method but not in the reversed Fick measurement.