A prospective randomized trial comparing oxygen delivery versus transcutaneous pressure of oxygen values as resuscitative goals

Transcutaneous pressure of oxygen (PtcO2) correlates with arterial pressure of oxygen (PaO2) in nonshock states, but in shock states, PtcO2 approximates cardiac output with no response to increasing fraction of inspired oxygen (FiO2) and PaO2. An incremental change of more than 21 mmHg in PtcO2 in response to an FiO2 of 1.0 (identified as the oxygen challenge test [OCT]) implies adequate tissue perfusion, and lack of response has been associated with mortality. Patients with severe sepsis and septic shock requiring pulmonary artery catheters were randomized to two groups: the oxygen delivery (DO2) group was treated to a DO2 and mixed venous oxygen saturation goals, and the PtcO2 group was treated to achieve an OCT value of 40 mmHg or more. The DO2 (n = 30) and PtcO2 (n = 39) groups were similar in baseline characteristics. Mortality rate was 12 (40%) of 39 for the DO2 group and 5 (13%) of 39 for the PtcO2 group (P = 0.02). Logistic regression analysis of the statistically significant variables between survivors and nonsurvivors demonstrated that inability to reach the PtcO2 goal at 24 h after resuscitation (T24) and a positive cardiac history are associated with mortality (P < 0.001). The area under the receiver operating curve was 0.824 for the OCT at T24. The best OCT value was 25 mmHg at T24 with positive and negative predictive values of 87% and 90%, respectively. Treating patients with severe sepsis/septic shock to an OCT value of 25 mmHg or more may provide a specific end point of resuscitation that may be associated with better survival than resuscitating to the central hemodynamic parameters of DO2 and mixed venous oxygen saturation.     

Lung fluid dynamics and supply dependency of oxygen uptake during experimental endotoxic shock and volume resuscitation

BACKGROUND AND METHODS: We studied the effect of volume resuscitation on lung fluid balance and systemic oxygen extraction during septic shock in eight anesthetized dogs. Sepsis was induced using a 2-hr continuous infusion of Escherichia coli endotoxin at 0.25 micrograms/min.kg. Relationships between oxygen uptake (VO2) and oxygen supply (DO2) were performed acutely during stepwise controlled decrements in cardiac output by progressive inflation of an intracardiac balloon. At each stage, DO2 and corresponding VO2 were measured independently and the individual critical DO2 level was referred to as the point below which the relationship held. The slope of such a constructed relationship was defined as the maximal oxygen extraction ratio. Lung fluid balance was assessed by measurements of extravascular lung water. All values were studied at baseline, after endotoxin insult, and after reversing hypotension by a 10% dextran infusion. RESULTS: Endotoxin infusion led to a shock state that associated hypotension (from 135 to 63 mm Hg) with increases in blood lactate (from 0.53 to 3.9 mmol/L). The mean critical DO2 and maximal oxygen extraction ratio were significantly altered from 7.9 to 17.8 mL/min.kg and from 0.81 to 0.38, respectively. After reversing hypotension by 28 mL/kg colloid infusion, the critical DO2 (11.4 mL/min.kg) and maximal oxygen extraction ratio (0.48) were significantly improved. However, restoration of normal values required a state of fluid overload by further dextran infusion (8 mL/kg). At the end of the fluid challenge, extravascular lung water significantly increased from 6.4 to 17.4 mL/kg. CONCLUSIONS: These data suggest that volume loading may reverse endotoxin-induced peripheral perfusion abnormalities. However, substantial pulmonary edema may occur, possibly jeopardizing the beneficial effects of fluid expansion.     

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.     

Transcutaneous and liver surface PO2 during hemorrhagic hypotension and treatment with phenylephrine

Transcutaneous PO2 (PtcO2) and liver surface PO2 (PIO2) were measured in six mongrel dogs during hemorrhagic shock, normotensive shock, and volume resuscitation. Normotension was produced during extreme hypovolemia by an infusion of phenylephrine. PtcO2 and PlO2 were compared to each other and to hemodynamic and oxygen transport variables. PtcO2 and PlO2 correlated well with cardiac index (CI) r = .71 and .86, respectively; n = 60) and with each other (r = .79; n = 60). Heart rate, mean arterial pressure (MAP), and PaO2) correlated less with PtcO2 or PlO2. During the normotensive shock period, PtcO2, PIO2, CI, oxygen delivery (DO2), and oxygen consumption (VO2) were all severely decreased, while PaO2 and MAP were normal and lactic acid concentrations were elevated. It was concluded that PtcO2 follows changes in PlO2 during hypotensive and normotensive low cardiac output shock in mongrel dogs. Low PtcO2 values are associated with low values of PlO2, DO2, VO2, and rising lactic acid concentrations in dogs. These animal data imply that low PtcO2 values encountered in clinical monitoring during anesthesia and surgery may correspond to decreased blood volume, blood flow, and PlO2.     

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.     

Sequential physiologic interactions in pediatric cardiogenic and septic shock

We report that the pediatric cardiogenic shock and septic shock populations show similar hemodynamic and oxygen utilization physiologic relationships during aggressive intensive care therapy. We examined the mathematical relationships between vascular tone and flow, and oxygen utilization and oxygen delivery (DO2) in the early and middle stages of cardiogenic and septic shock. The fitted curves between cardiac index and systemic vascular resistance, and oxygen consumption (VO2) and DO2 were clinically and statistically similar in both shock populations. We found no evidence for decreased oxygen extraction in sepsis as compared to the cardiogenic shock population. In addition, it appears that the major determinant of VO2 in these populations is DO2, not oxygen extraction. We suggest that patients with cardiogenic or septic shock can be treated according to similar physiologic principles.     

Transcutaneous pressure of oxygen: a noninvasive and early detector of peripheral shock and outcome

A noninvasive tool to recognize early shock would improve outcome by providing prompt recognition of tissue ischemia and precise resuscitation endpoint. The skin is the first tissue bed to vasoconstrict in shock states. Studies have demonstrated that transcutaneous partial pressure of oxygen (PtCO2) increases with higher FiO2 in nonshock states as arterial pressure of oxygen (PaO2) increases, but in shock situations, PtCO2 mirrors changes in cardiac output and oxygen delivery with minimum response to increasing FiO2 and PaO2. This study examined the relationship of hemodynamic variables and the degree of PtCO2 response to FiO2 of 1.0 (identified as the "oxygen challenge test") to mortality and organ failure. This prospective observational study examined 38 patients requiring at least 24 h of cardiac output monitoring for shock resuscitation in the Surgical Intensive Care Unit. Patients were resuscitated to the standard protocol of blood pressure, urine output, oxygen delivery (DO2), and mixed venous O2 (SvO2). Seventy-nine percent of the patients (30/38) with a mean age of 59 +/- 21 years had septic shock or severe sepsis with a 26% mortality (10/38). Measurements included hemodynamic variables, PtCO2, and outcome (mortality and organ failure). In this study, the ability of PtCO2 value to increase by 21 mmHg on a FiO2 of 1.0, at 24 h of resuscitation, divided survivors from nonsurvivors, P <.001. The PtCO2 response to FiO2 may provide an additional noninvasive method of detecting early shock as well as a specific endpoint of resuscitation.     

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.     

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.     

Thenar oxygen saturation and invasive oxygen delivery measurements in critically ill patients in early septic shock

This prospective study was aimed to test the hypothesis that tissue hemoglobin oxygen saturation (StO?) measured noninvasively using near-infrared spectroscopy is a reliable indicator of global oxygen delivery (DO?) measured invasively using a pulmonary artery catheter (PAC) in patients with septic shock. The study setting was a 26-bed medical-surgical intensive care unit at a university hospital. Subjects were adult patients in septic shock who required PAC hemodynamic monitoring for resuscitation. Interventions included transient ischemic challenge on the forearm. After blood pressure normalization, hemodynamic and oximetric PAC variables and, simultaneously, steady-state StO? and its changes from ischemic challenge (deoxygenation and reoxygenation rates) were measured. Fifteen patients were studied. All the patients had a mean arterial pressure above 65 mmHg. The DO? index (iDO?) range in the studied population was 215 to 674 mL O?/min per m. The mean mixed venous oxygen saturation value was 61% ± 10%, mean cardiac index was 3.4 ± 0.9 L/min per m, and blood lactate level was 4.6 ± 2.7 mmol/L. Steady-state StO? significantly correlated with iDO?, arterial and venous O? content, and O? extraction ratio. A StO? cutoff value of 75% predicted iDO? below 450, with a sensitivity of 0.9 and a specificity of 0.9. In patients in septic shock and normalized MAP, low StO? reflects extremely low iDO?. Steady-state StO? does not correlate with moderately low iDO?, indicating poor sensitivity of StO? to rule out hypoperfusion.     

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.     

Experience with phenylephrine as a component of the pharmacologic support of septic shock

OBJECTIVE: To evaluate the use of the selective alpha 1-adrenergic receptor agonist phenylephrine in the hemodynamic support of patients with septic shock. DESIGN: Retrospective analysis of clinical use of phenylephrine. SETTING: Surgical ICU in a university hospital. PATIENTS: Thirteen patients with septic shock (diagnosed by defined criteria) requiring pharmacologic support for the treatment of hypotension. INTERVENTIONS AND MAIN RESULTS: All patients underwent invasive hemodynamic monitoring followed by volume resuscitation and inotropic support to reverse flow-dependent oxygen consumption and lactic acidosis. Patients with persistent hypotension (mean arterial pressure [MAP] less than 65 mm Hg) and vasodilation (systemic vascular resistance index [SVRI] less than 1500 dyne.sec/cm5.m2 received phenylephrine at iv infusion rates of 0.5 to 9 micrograms/kg.min to maintain MAP greater than 70 mm Hg. MAP, SVRI, left ventricular stroke work index, and stroke volume index were significantly (p less than .05) increased after phenylephrine administration and at the time of highest oxygen consumption (VO2). Cardiac index was unchanged initially but increased at the time of highest VO2 (p less than .05). Pulmonary artery occlusion pressure and heart rate were unchanged. Average baseline VO2 increased from 145 to 200 mL/min.m2 and oxygen delivery (DO2) increased from 447 to 597 mL/min.m2 during phenylephrine treatment (p less than .05). Blood lactate concentrations decreased and urine output increased significantly (p less than .05), while serum creatinine concentrations remained unchanged during phenylephrine therapy. CONCLUSIONS: Treatment with phenylephrine was associated with beneficial hemodynamic effects when used to maintain perfusion, while increasing DO2 and VO2 in patients with septic shock.     

Effect of Ibuprofen on interleukin-1beta-induced abnormalities in hemodynamics and oxygen metabolism in rabbits

We showed previously that the administration of interleukin (IL)-1beta induces circulatory shock and impairs the oxygen consumption (VO2)/oxygen delivery (DO2) relation by increasing the slope of the supply-independent line in rabbits. We tested the effect of ibuprofen, a specific inhibitor of the development of shock in this model, on the VO2/DO2 abnormality. Eighteen rabbits were divided randomly into three groups (n = 6 each) and intravenously given 10 microg/kg of IL-1beta alone or 10 microg/kg of IL-1beta followed by 10 mg/kg of ibuprofen or saline (control). All rabbits were subjected to stepwise cardiac tamponade by inflation of a handmade balloon placed into the pericardial sac to reduce DO2. The VO2/DO2 relation was then analyzed by the dual line method. The IL-1beta group had a significantly lower mean arterial pressure than that of the other groups before cardiac tamponade, and this reduction in mean arterial pressure was suppressed completely by treatment with ibuprofen. The cardiac index did not differ between groups. The slope of the supply-independent line was increased significantly by administration of IL-1beta, and this increase was attenuated significantly by treatment with ibuprofen (IL-1beta only: y = 0.14x + 6.1, ibuprofen: y = 0.06x + 8.5, control: y = 0.01x + 9.0). We conclude that ibuprofen reversed the IL-1beta-induced shock by restoring the systemic vascular resistance to normal and thereby normalized the VO2/DO2 relation in the supply-independent range of DO2.     

Systemic and muscle oxygen uptake/delivery after dopexamine infusion in endotoxic dogs.

BACKGROUND AND METHODS: This study was designed to test whether dopexamine, a dopaminergic and beta 2-adrenergic agonist, would a) increase systemic oxygen delivery (DO2) in endotoxic dogs, and b) interfere with the ability of resting skeletal muscle to extract oxygen. There were three treatment groups (n = 6 in each group): control, endotoxin alone (E) 4 mg/kg iv, and endotoxin + dopexamine (E + D) 12 micrograms/kg.min. Data were analyzed between and within groups by split-plot analysis of variance with significance of identified differences tested post hoc by Duncan's multiple range test. Donor RBC and dextran were used after endotoxin to maintain adequate perfusion pressures, with Hct kept near 40%. Blood flow to left hindlimb muscles was decreased in controlled steps of 15 min each after stabilization. RESULTS: In E group, cardiac output (Qt), mean arterial pressure (MAP), systemic DO2, and oxygen uptake (VO2) decreased despite blood volume expansion. In E + D group with similar volume expansion, dopexamine maintained Qt, systemic DO2, and VO2 near the control levels, although MAP and systemic vascular resistance were reduced. In comparison with control subjects, endotoxin increased critical DO2 in the isolated limb muscles from 4.6 to 7. mL/kg.min and decreased critical oxygen extraction from 81% to 68%. The pressure/flow relationship in the limb became flattened, indicating loss of vascular reactivity. In the E + D group, there was no further change in the pressure/flow curve nor in the critical oxygen extraction level. CONCLUSIONS: Dopexamine provided hemodynamic support for endotoxic dogs, thereby increasing total DO2 and VO2, while not altering oxygen extraction in the muscle.     

Prognostic value of hemodynamic indices in patients with sepsis after fluid resuscitation

BACKGROUNDSepsis usually causes hemodynamic abnormalities. Hemodynamic index is one of the factors to identify the severity of sepsis and an important parameter to guide the procedure of fluid resuscitation. The present study investigated whether the assessment of hemodynamic indices can predict the outcomes of septic patients undergoing resuscitation therapy.AIMTo evaluate the prognostic value of hemodynamic indices in patients with sepsis after fluid resuscitation.METHODSA retrospective study was conducted in 120 patients with sepsis at Hainan General Hospital/Hainan Affiliated Hospital of Hainan Medical University between October 2016 and October 2019. All patients were treated with sodium chloride combined with dextran glucose injection for fluid resuscitation. Patients’ hemodynamic parameters were monitored, including heart rate (HR), cardiac index (CI), systemic vascular resistance index (SVRI), mean arterial pressure (MAP), central venous pressure (CVP), and central venous oxygen saturation. The prognostic value of hemodynamic indices was determined based on the prognosis status.RESULTSDuring fluid resuscitation, 86 patients developed septic shock and 34 did not. Ninety-nine patients survived and 21 patients died at 28 d after the treatment. Heart rate, CI, mean arterial pressure, SVRI, and CVP were higher in patients with septic shock and patients who died from septic shock than in non-shock patients and patients who survived, and central venous oxygen saturation was lower in patients with shock and patients who died than in non-shock patients and the survivors (P < 0.05). When prognosis was considered as a dependent variable and hemodynamic parameters was considered as independent variables, the results of a logistic regression analysis showed that CI, SVRI, and CVP were independent risk factors for septic shock, and CI was an independent risk factor for 28-d mortality (P < 0.05).CONCLUSIONHemodynamic indices can be used to evaluate the prognosis of septic patients after fluid resuscitation.     

创伤失血性休克早期液体复苏策略及氧代谢监测的临床观察

目的:观察创伤失血性休克限制性液体复苏及充分液体复苏的临床疗效及对氧代谢的影响。方法:将218例创伤失血性休克患者随机分为治疗组(n=110)及对照组(n=108),分别进行限制性液体复苏及充分液体复苏。比较两组输液量、病死率及并发症(ARDS、MODS、脓毒血症)发生率,复苏2 h后氧输送(DO-2)、氧消耗(VO2)、混合静脉血氧饱和度(SVO2)情况及24 h乳酸恢复情况。结果:治疗组输液量显著少于对照组(P0.01),治疗组死亡率、并发症发生率明显低于对照组(P0.05);治疗组DO_2、VO_2、SVO_2及24 h乳酸恢复正常例数均明显高于对照组(P0.05)。结论:与充分液体复苏比较,对创伤失血性休克进行限制性液体复苏能减少输液量,降低病死率及并发症发生率,且在组织供氧及纠正乳酸酸中毒方面有明显优势。     

Early hemodynamic correlates of survival in patients with septic shock

In this retrospective study, we attempted to identify early in the course of septic shock hemodynamic variables that differ between survivors and nonsurvivors. We examined the records of 78 patients with septic shock from our medical ICU (40 survivors and 38 nonsurvivors). Significant differences were found in cardiac index (CI) (4.07 +/- 0.25 vs. 2.98 +/- 0.25 L/min.m2) and oxygen delivery (DO2) (15.6 +/- 0.7 vs. 12.7 +/- 0.8 ml/min.kg) at 48 h between surviving and nonsurviving patients. Furthermore, an analysis of the relationship between DO2 and VO2 suggests a critical level of DO2 to be 15 ml/min.kg. Although no difference could be detected in initial arterial lactate concentrations, levels at 48 h were significantly different between survivors and nonsurvivors (2.6 +/- 0.2 vs. 4.1 +/- 0.5 mEq/L, respectively).     

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.