Oxygen delivery and consumption in head-injured and multiple trauma patients

Critically ill patients often demonstrate that whole body oxygen consumption (VO2) is dependent on oxygen delivery (DO2). In this retrospective study, the relationship of VO2 to DO2 in patients with isolated head injury (HI, n = 18) was compared to that in patients with multiple trauma (MT, n = 60) without serious head injury. Mean pulmonary capillary wedge pressure, central venous pressure, arterial PCO2, cardiac index, and oxygen delivery were significantly lower in HI, but oxygen consumption was not different in the groups. In both groups, changes in DO2 (delta DO2) within each patient were significantly correlated with changes in VO2 (delta VO2) in that same patient. This relationship was not different between the HI patients, (delta VO2 = (0.20 +/- 0.02) delta DO2), and the MT patients (delta VO2 = (0.17 +/- 0.01) delta DO2). When these groups were further divided into those with high hematocrit (greater than 32%) and low hematocrit (less than 32%), HI patients with a low hematocrit demonstrated a steeper regression slope, with 26 +/- 3% of the DO2 change being reflected in the VO2 change. This was significantly greater than the slope in HI patients with high hematocrit (13 +/- 3%) and the MT patients at high (19 +/- 2%) or low (16 +/- 2%) hematocrits. These data show a correlation between changes in oxygen delivery and consumption that is similar in both head-injury patients and multiple trauma patients without serious head injury. This relationship was greatest in head-injured patients at low hematocrit. This relationship of VO2 and DO2 in both groups suggests an influence of neurohumoral factors rather than local tissue phenomena.(ABSTRACT TRUNCATED AT 250 WORDS)     

Reversal of depressed oxygen consumption accompanying in vivo protamine sulphate-heparin interactions by the prostacyclin analogue, iloprost.

Oxygen consumption (VO2) is known to be depressed 50 to 60% during protamine sulphate reversal of heparin anticoagulation. Accompanying this event are systemic hypotension, pulmonary artery hypertension and thrombocytopaenia. The effect of a pro-stacyclin analogue, iloprost, on protamine-induced changes in VO2 was assessed in this investigation. Three groups of anaesthetised adult mongrel dogs were studied: Group I--control subjects received i.v. normal saline infusions (n = 10); Group II--subjects received low-dose i.v. iloprost infusions (25-50 ng/kg/min) over 30 min (n = 7); and Group III--subjects received high-dose i.v. iloprost infusions (175 ng/kg/min) over 30 min (n = 7). All dogs initially received sodium heparin, 150 IU/kg i.v. Protamine sulphate, 1.5 mg/kg i.v., was subsequently administered over 10 s following the first 20 min of saline or iloprost infusion. Continuous measurements included: mixed venous (SvO2) and arterial (SaO2) oxygen saturation, arterial blood pressure, pulmonary artery pressure, heart rate and carotid artery flow (CaQ). Thermodilution cardiac output (CO) allowed calculation of VO2. Platelet counts were performed before and 3 min after protamine infusion. The VO2 declines in Group II and III subjects compared to Group I controls were markedly less. Maximum VO2 declines in Group I control dogs of -38.2 +/- 26.7% and Group II dogs of -34.1 +/- 36.8% at 75 to 90 s post-reversal contrasted to -2.9 +/- 31.9% in Group III animals at the same time interval. VO2 increases occurred 3 to 10 min after protamine exposure in Group III animals, as did attenuation of systemic hypotensive and pulmonary hypertensive responses in this group.(ABSTRACT TRUNCATED AT 250 WORDS)     

Splanchnic oxygen consumption in septic and hemorrhagic shock

Oxygen consumption (VO2) is dependent on oxygen delivery (DO2) in septic shock. Local hypoxia with later secondary organ failure may develop, however, despite an often hyperdynamic circulation. The splanchnic organs seem to be of vital importance in this context. In experiments performed in pigs we compared total body VO2 and DO2 with oxygen consumption and delivery in the gastrointestinal organs and the liver in two different shock states: (1) septic shock induced by peritonitis (n = 6) and (2) hemorrhagic shock (n = 6). Another group of six animals not in shock served as controls. Total, gastrointestinal, and liver DO2 decreased in a similar pattern in both septic and hemorrhagic shock. Gastrointestinal and liver VO2 increased in sepsis, whereas it was unchanged in hemorrhage. In the later phase of sepsis, liver VO2, but not gastrointestinal VO2, again decreased, because liver oxygen extraction was almost total and liver DO2 decreased further. The development of flow-dependent liver hypoxia was reflected in a decrease in liver lactate turnover (increased liver lactate release) during late sepsis. Early hypoxia in the splanchnic region is suggested as a plausible mechanism behind the development of secondary organ failure, especially in sepsis.     

Changes in intraoperative total oxygen consumption in patients during liver transplantation

The changes in O2-uptake (VO2) during 110 liver transplantations (LTX) were studied using Fick's principle (O2-uptake = cardiac index x arteriovenous O2-content difference). During each of the three operative periods [a dissecting period before clamping of the hepatic vessels (1), the anhepatic phase (2), and after reperfusion of the new liver (3)], two measurements (A and B) were taken. After removal of the liver (2A) the VO2 decreased about 11.4%, and increased after reperfusion (3A) about 44.0%; these changes were significant (P less than 0.001). To evaluate the influence of the various indications for LTX on the course of intraoperative VO2, the following patient groups were compared: patients with hepatic tumors (n = 17), patients with cirrhosis following hepatitis (n = 14), patients with primary biliary cirrhosis (n = 17), patients with cirrhosis plus tumor (n = 11), and patients in a hepatic coma (n = 20), regardless of the underlying liver disease. Groups with less than ten subjects were not considered. The drop of VO2 in the anhepatic period (1B----2A) was between -26.7% (patients with tumors) and -7.3% (patients with cirrhosis plus tumor). The patients with cirrhosis following hepatitis showed a special feature: their VO2 increased about 13.4% after cross-clamping the hepatic vessels. After revascularization, the VO2 increased in all groups between +37.2% and +69.8%. In all groups the level of VO2 was higher after reperfusion (3A) than in the dissecting period (1B), ranging from +5.3% in patients with tumors to +61.6% in patients with cirrhosis following hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Critical hematocrit in intestinal tissue oxygenation during severe normovolemic hemodilution

BACKGROUND: A critical point in oxygen supply for microvascular oxygenation during normovolemic hemodilution has not been identified. The relation between organ microvascular oxygen partial pressure (microPO2) and organ oxygen consumption (VO2) during a decreasing oxygen delivery (DO2) is not well understood. The present study was designed to determine the systemic hematocrit and organ DO2 values below which organ microPO2 and VO2 cannot be preserved by regulatory mechanisms during normovolemic hemodilution. METHODS: Eighteen male Wistar rats were randomized between an experimental group (n = 12), in which normovolemic hemodilution was performed with pasteurized protein solution (PPS), and a control group (n = 6). Systemic hemodynamic and intestinal oxygenation parameters were monitored. Intestinal microPO2 was measured using the oxygen-dependent quenching of palladium-porphyrin phosphorescence. RESULTS: Baseline values in hemodilution and control group were similar. Hemodilution decreased hematocrit to 6.2 +/- 0.8% (mean +/- SD). Constant central venous pressure measurements suggested maintenance of isovolemia. Despite an increasing mesenteric blood flow, intestinal DO2 decreased immediately. Initially, microPO2 was preserved, whereas mesenteric venous PO2 (P(mv)O2) decreased; below a hematocrit of 15%, microPO2 decreased significantly below P(mv)O2. Critical DO2 was 1.5 +/- 0.5 ml x kg(-1) x min(-1) for VO2, and 1.6 +/- 0.5 ml x kg(-1) x min(-1) for microPO2. Critical hematocrit values for VO2 and microPO2 were 15.8 +/- 4.6% and 16.0 +/- 3.5%, respectively. CONCLUSIONS: Intestinal microPO2 and VO2 were limited by a critical decrease in DO2 and hematocrit at the same time. Beyond these critical points not only shunting of oxygen from the microcirculation could be demonstrated, but also a significant correlation between intestinal microPO2 and VO2.     

Is there occult tissue ischemia in chronic end-stage liver disease?

Whether pathological oxygen supply dependency exists in patients with chronic end-stage liver disease (CESLD) is unknown, although the frequently occurring multiorgan dysfunction seen in these patients may be the result of occult tissue ischemia. In this study, 15 adult patients with CESLD were evaluated for the presence of pathological oxygen supply dependency and, thus, occult tissue ischemia before undergoing orthotopic liver transplantation. Whole-body oxygen consumption (VO2) was measured using indirect calorimetry at baseline, at reduced oxygen delivery (DO2) using positive end-expiratory pressure, and at increased DO2 using volume infusion. As a group, no significant increase or decrease in VO2 was observed with changes in DO2. However, 4 patients showed increases in VO2 of 14%, 10.8%, 9.6%, and 8.2% when DO2 was increased. The study results suggest that pathological oxygen supply dependency is present in a subset of patients with CESLD, and the existence of occult tissue ischemia is speculated.     

异氟醚控制性降压对颅内动脉瘤夹闭术病人血液动力学及组织氧合的影响

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Oxygen kinetics in experimental sepsis.

Systemic oxygen delivery (DO2) is normally four to five times higher than oxygen consumption (VO2), and VO2 is independent of DO2. If DO2 is decreased to less than twice VO2, a state of anaerobic metabolism and supply dependency occurs. Some authors have reported that this biphasic relationship is altered in the adult respiratory distress syndrome or sepsis to a condition of continuous supply dependency. If that were true, it would affect both our understanding and management of metabolism during sepsis. Therefore we measured VO2 and DO2 in a dog peritonitis model. DO2 was regulated with controlled pericardial tamponade. During sepsis VO2 increased 28% from a mean baseline of 5.6 to 7.3 cc O2/kg/min (p less than 0.005). As progressive cardiac tamponade was applied during sepsis, the DO2/VO2 ratio fell. When the DO2/VO2 ratio was greater than 2.4, VO2 remained independent of DO2. At DO2/VO2 ratios less than 2.4, VO2 was dependent on the level of DO2, and it diminished rapidly as DO2 decreased. Oxygen saturation in mixed venous blood (SvO2) consistently reflected the DO2/VO2 ratio in a fashion similar to that in normal dogs. A ratio of DO2/VO2 of 2.4 corresponded with an SvO2 of 42% +/- 12%, which was identified as a statistically significant critical SvO2 that marked onset of VO2 supply dependence. In this dog septic model, VO2 is independent of DO2 when DO2 is adequate. A state of continuous supply dependency does not exist. SvO2 reflects the status of the DO2/VO2 relationship in the septic state.     

急性等容血液稀释对组织氧供氧耗的影响

目的：通过观察急性等容血液稀释（ＡＮＨＤ）时组织ＤＯ２、ＶＯ２的变化，寻找ＡＮＨＤ的生理极限。方法：１０只健康成年杂种犬，用戊巴比妥钠、维库溴铵静脉麻醉后行气管内插管，控制呼吸。每只犬进行三个水平即中度（ＨＤ１）、深度（ＨＤ２）、极深度（ＨＤ３）ＡＮＨＤ，然后回输自家血，测定血流动力学指标，动脉及混合静脉血气，动脉血乳酸等，以观察ＡＮＨＤ时ＤＯ２、ＶＯ２的变化。结果：ＨＤ１（ＨＣＴ＝１９．４３％±１．９７％），ＨＤ２（ＨＣＴ＝１４．７３％±０．９９％）时，ＤＯ２分别降低４２％和５２％，ＥＲＯ２分别升高４０％和８８％，ＣＩ升高４１％和４８％，而ＶＯ２只降低４．８％和５．２％，动脉血乳酸末升高。ＨＤ３（ＨＣＴ＝９．５０％±０．８８％）时，ＤＯ２降低７３％，ＥＲＯ２升高２００％，ＣＩ降低，ＶＯ２降低３５％，动脉血乳酸显著增加。回输自家血后，ＤＯ２、ＶＯ２及血乳酸均恢复。结论：中、深度ＨＤ时，ＤＯ２减少，ＶＯ２可通过增加ＥＲＯ２和ＣＩ代偿；极深度ＨＤ时ＶＯ２降低显著，出现无氧代谢，ＨＤ达极限。     

Dobutamine increases oxygen consumption during constant flow cardiopulmonary bypass

We have studied the effects of flow and dobutamine on systemic haemodynamic variables, oxygen delivery (DO2) and oxygen consumption (VO2) in 20 patients during cardiopulmonary bypass (CPB) with mild hypothermia (34 degrees C). In a subgroup of seven patients, we also studied the effects on gastric microcirculatory blood flow (MCF) using laser Doppler flowmetry. During CPB, measurements were made before and after two interventions: the first consisted of increasing flow from 2.4 to 3.0 litre min-1 m-2 for 10 min; the second consisted of an infusion of dobutamine at a rate of 6 micrograms kg-1 min-1 for 10 min during constant flow CPB. There were no significant differences in DO2, VO2 or haemodynamic variables between the two baseline measurements. The increase in flow raised DO2 (27%, P < 0.001), mean arterial pressure (P < 0.01) and MCF (P < 0.01), but failed to increase VO2. In contrast, dobutamine infusion increased VO2 (11%, P < 0.001) during constant flow CPB without significant changes in DO2, systemic haemodynamic variables or MCF. These results indicate that increases in VO2 during dobutamine may be flow-independent.      

Oxygen consumption and delivery relationship in brain-dead organ donors

The oxygen delivery (DO2) and consumption (VO2) relationship in brain- dead organ donors is unknown. Therefore, in a prospective study, we determined the DO2/VO2 relationship in 21 consecutive brain-dead patients. Patients were allocated to one of two groups, according to plasma lactate concentration: normal (group NL, n = 11) or high (> 2.5 mmol litre-1) (group HL, n = 10). VO2 was measured independently, using indirect calorimetry, under control conditions, during low DO2 challenge with PEEP administration, and high DO2 challenge with inflation of medical antishock trousers and volume expansion or blood transfusion, as required. Under control conditions, there were no significant differences between groups NL and HL in haemodynamic or oxygenation variables, both groups having a low VO2 (mean 114 (SD 21) ml min-1 m-2). In group HL there was a different DO2/VO2 relationship pattern, with a dependent VO2 only. The mean slope of the DO2/VO2 relationship was significantly higher in group HL than in group NL (0.12 (0.09) vs 0.04 (0.07), P < 0.05). We conclude that brain death was associated with a low VO2, and patients in group HL exhibited DO2/VO2 dependency which was not observed in patients in group NL.      

Mild hypothermia has minimal effects on the tolerance to severe progressive normovolemic anemia in Swine

BACKGROUND: The benefits of hypothermia during acute severe anemia are not entirely settled. The authors hypothesized that cooling would improve tolerance to anemia. METHODS: Eight normothermic (38.0 +/- 0.5 degrees C) and eight hypothermic (32.0 +/- 0.5 degrees C) pigs anesthetized with midazolam-fentanyl-vecuronium-isoflurane (0.5% inspired concentration) were subjected to stepwise normovolemic hemodilution (hematocrit, 15%, 10%, 7%, 5%, 3%). Critical hemoglobin concentration (Hgb(CRIT)) and critical oxygen delivery (DO(2CRIT)), i.e., the hemoglobin concentration (Hgb) and oxygen delivery (DO2) at which oxygen consumption (VO2, independently measured by indirect calorimetry) was no longer sustained, and Hgb at the moment of death, defined prospectively as the point when VO2, decreased below 40 ml/min, were used to assess the tolerance of the two groups to progressive isovolemic anemia. RESULTS: At hematocrits of 15% and 10% (Hgb, 47 and 31 g/l), VO2 was maintained in both groups by an increase (P < 0.001) in cardiac output (CO) and extraction ratio (ER; P< 0.001) with unchanged mean arterial lactate concentration (L(art)). At hematocrit of 7% (Hgb, 22 g/l), all normothermic but no hypothermic animals had DO2-dependent VO2. No normothermic and three hypothermic animals survived to 5% hematocrit (Hgb, 15 g/l), and none survived to 3%. Hgb(CRIT) was 23 +/- 2 g/l and 19 +/- 6 g/l (mean +/- SD) in normothermic and hypothermic animals, respectively (P = 0.053). Hgb at death was 19 +/- 3 g/l versus 14 +/- 4 g/l (P = 0.015), and DO(2CRIT) was 8.7 +/- 1.7 versus 4.6 +/- 0.8 ml x kg(-1) x min(-1) (P < 0.001). CONCLUSION: During progressive normovolemic hemodilution in pigs, hypothermia did not significantly change Hgb(CRIT), but it decreased the Hgb at death, i.e., short-term survival was prolonged.     

Critical oxygen delivery in conscious humans is less than 7.3 ml O2 x kg(-1) x min(-1)

BACKGROUND: The "critical" level of oxygen delivery (DO2) is the value below which DO2 fails to satisfy the metabolic need for oxygen. No prospective data in healthy, conscious humans define this value. The authors reduced DO2 in healthy volunteers in an attempt to determine the critical DO2. METHODS: With Institutional Review Board approval and informed consent, the authors studied eight healthy, conscious volunteers, aged 19-25 yr. Hemodynamic measurements were obtained at steady state before and after profound acute isovolemic hemodilution with 5% albumin and autologous plasma, and again at the reduced hemoglobin concentration after additional reduction of DO2 by an infusion of a beta-adrenergic antagonist, esmolol. RESULTS: Reduction of hemoglobin from 12.5+/-0.8 g/dl to 4.8+/-0.2 g/dl (mean +/- SD) increased heart rate, stroke volume index, and cardiac index, and reduced DO2 (14.0+/-2.9 to 9.9+/-20 ml O2 x kg(-1) x min(-1); all P<0.001). Oxygen consumption (VO2; 3.0+/-0.5 to 3.4+/-0.6 ml O2 x kg(-1) x min(-1); P<0.05) and plasma lactate concentration (0.50+/-0.10 to 0.62+/-0.16 mM; P<0.05; n = 7) increased slightly. Esmolol decreased heart rate, stroke volume index, and cardiac index, and further decreased DO2 (to 7.3+/-1.4 ml O2 x kg(-1) x min(-1); all P<0.01 vs. before esmolol). VO2 (3.2+/-0.6 ml O2 x kg(-1) x min(-1); P>0.05) and plasma lactate (0.66+/-0.14 mM; P>0.05) did not change further. No value of plasma lactate exceeded the normal range. CONCLUSIONS: A decrease in DO2 to 7.3+/-1.4 ml O2 x kg(-1) min(-1) in resting, healthy, conscious humans does not produce evidence of inadequate systemic oxygenation. The critical DO2 in healthy, resting, conscious humans appears to be less than this value.     

Adrenergic support during anesthesia in experimental endotoxin shock: norepinephrine versus dobutamine

The effects of norepinephrine and dobutamine were compared during endotoxin shock in dogs anesthetized either with enflurane (E: 1.5%, N = 12) or with i.v. ketamine (K: 5 mg.kg-1 + 0.2 mg.kg-1.min-1, N = 12). An i.v. bolus of 1.5 mg.kg-1 E. coli endotoxin was followed by saline infusion to restore left-sided filling pressures at baseline. With E, heart rate, mean arterial pressure and stroke index decreased (P less than 0.01). The decrease in oxygen delivery (DO2) and in oxygen consumption (VO2) was associated with an increase in blood lactate. In contrast, K anesthesia was associated with remarkable hemodynamic stability. DO2 was well maintained, VO2 decreased (P less than 0.01) and blood lactate did not change. Under E anesthesia, mean arterial pressure increased more with norepinephrine and heart rate increased more with dobutamine. Under K anesthesia, cardiac index, stroke index and left ventricular stroke work index increased similarly with both agents. In both groups DO2 and VO2 increased markedly. The amount of fluid infused was higher with dobutamine than with norepinephrine. Thus, enflurane but not ketamine had depressant cardiovascular effects at the doses used in this model. With both anesthetics, norepinephrine and dobutamine could effectively improve cardiac function. Dobutamine could therefore represent a valuable alternative to norepinephrine for cardiovascular support during anesthesia in septic shock.     

Mild Hypothermia Has Minimal Effects on the Tolerance to Severe Progressive Normovolemic Anemia in Swine

Background: The benefits of hypothermia during acute severe anemia are not entirely settled. The authors hypothesized that cooling would improve tolerance to anemia.

Methods: Eight normothermic (38.0 +/- 0.5[degrees]C) and eight hypothermic (32.0 +/- 0.5[degrees]C) pigs anesthetized with midazolam-fentanyl-vecuronium-isoflurane (0.5% inspired concentration) were subjected to stepwise normovolemic hemodilution (hematocrit, 15%, 10%, 7%, 5%, 3%). Critical hemoglobin concentration (HgbCRIT) and critical oxygen delivery (DO2CRIT), i.e., the hemoglobin concentration (Hgb) and oxygen delivery (DO2) at which oxygen consumption (VO2, independently measured by indirect calorimetry) was no longer sustained, and Hgb at the moment of death, defined prospectively as the point when VO2 decreased below 40 ml/min, were used to assess the tolerance of the two groups to progressive isovolemic anemia.

Results: At hematocrits of 15% and 10% (Hgb, 47 and 31 g/l), VO2 was maintained in both groups by an increase (P < 0.001) in cardiac output (CO) and extraction ratio (ER;P < 0.001) with unchanged mean arterial lactate concentration (Lart). At hematocrit of 7% (Hgb, 22 g/l), all normothermic but no hypothermic animals had DO2-dependent VO2. No normothermic and three hypothermic animals survived to 5% hematocrit (Hgb, 15 g/l), and none survived to 3%. HgbCRIT was 23 +/- 2 g/l and 19 +/- 6 g/l (mean +/- SD) in normothermic and hypothermic animals, respectively (P = 0.053). Hgb at death was 19 +/- 3 g/l versus 14 +/- 4 g/l (P = 0.015), and DO2CRIT was 8.7 +/- 1.7 versus 4.6 +/- 0.8 ml [middle dot] kg-1 [middle dot] min-1 (P < 0.001).     

Differential alterations in systemic and regional oxygen delivery and consumption during the early and late stages of sepsis.

BACKGROUND: Studies have indicated that regional changes in oxygen utilization during sepsis cannot be predicted from the changes in the whole body oxygen delivery (DO2) and consumption (VO2). The aim of this study, therefore, was to determine whether differential alterations in systemic and regional DO2 and VO2 occur during the early and late stages of sepsis. METHODS: Adult male Sprague-Dawley rats were subjected to sepsis by cecal ligation and puncture (CLP). At 5 hours (i.e., the early, hyperdynamic phase of sepsis) or 20 hours (i.e., the late, hypodynamic phase) after CLP, cardiac output, and organ blood flow were measured by radioactive microspheres. Systemic and regional DO2 and VO2 were determined and plasma levels of lactate were measured. RESULTS: Cardiac output and blood flow to the liver, small intestine, and kidneys increased at 5 hours and decreased at 20 hours after CLP. Although both systemic DO2 and VO2 increased at 5 hours after CLP, systemic DO2 but not VO2 decreased at 20 hours. At 5 hours after CLP, intestinal and renal DO2 increased. However, DO2 in all the tested organs decreased at 20 hours after CLP. VO2 increased in the liver, small intestine, and kidneys at 5 hours after CLP but decreased only in the liver and small intestine at 20 hours after the onset of sepsis. Moreover, plasma lactate levels increased at the late stage of sepsis. CONCLUSION: Because hepatic and intestinal VO2 but not systemic and renal VO2 decreased at 20 hours after CLP, the liver and small intestine seem to be more vulnerable to the hypoxic insult during the hypodynamic stage of polymicrobial sepsis.     

重症先天性心脏病围术期氧供量和氧耗量的变化

目的了解重症先天性心脏病围术期的氧合状态.方法测定了22例心脏复跳后连续应用多巴酚丁胺或米力农情况下体外循环中、停体外循环后30min、手术结束、术后2h、术后16h的心脏指数(CI)、氧输送量(DO2)、氧耗量(VO2)和氧摄取率(ERO2).结果(1)体外循环中和体外循环结束DO2和VO2有高度正相关性(P＜0.01),相关系数分别为0.861,0.811;(2)体外循环中与体外循环后30min各数据比较CI、DO2、VO2前者明显低于后者(P＜0.05或0.01),ERO2无显著性差异;(3)体外循环结束后各点数据比较,CI能维持在3L@min-1@m-2以上,DO2能维持在550ml@min-1@m-2以上(术后16h最高,明显高于手术结束,P＜0.05),VO2能维持在120ml@min-1@m-2以上术后16h最低,术后2h最高,且明显高于体外循环后30min和术后16h(P＜0.05).结论(1)重症先天性心脏病围术期存在病理性氧供依赖;(2)心脏复跳后应用多巴酚丁胺能改善组织对氧的摄取和利用;(3)体外循环后连续应用多巴酚丁胺或米力农很难进行DO2、VO2、CI的超正常值维护,但CI高于ShoemakerWC提出的在治疗心源性休克所需维护的水平,即应不小于3L@min-1@m-2;(4)手术后16h循环功能尚未完全恢复,仍需继续加强正性肌力药的治疗.     

Oxygen metabolism during and after cardiac surgery: role of CPB

BACKGROUND: Cardiopulmonary bypass (CPB) has been reported to increase oxygen metabolism and to influence the relation between oxygen consumption (VO(2)) and delivery (DO(2)) in the early hours after cardiac surgery. To investigate the role of CPB, we studied oxygen metabolism in coronary artery bypass procedures performed on-pump (CABG) and off-pump (OPCAB). METHODS: Twenty-five patients were randomized to undergo CABG (n = 14) or OPCAB (n = 11). All patients received the same anesthetic management. Oxygen metabolism variables were assessed before induction of anesthesia and up to 18-hours after surgery. RESULTS: At baseline, before induction of anesthesia, there were no differences between CABG and OPCAB in oxygen consumption (VO(2)), delivery (DO(2)), or extraction (ExO(2)). After surgery VO(2) and ExO(2) increased in both groups, while DO(2) decreased. No significant differences between CABG and OPCAB were detected in postoperative VO(2), DO(2), and ExO(2) levels. The relation between VO(2) and DO(2) was very similar in CABG and OPCAB patients throughout the study, and no significant differences were detected in slopes and intercepts of the regression lines between CABG and OPCAB at all time points. There was, however, a significant effect of time on the relation between VO(2) and DO(2): this relation was stronger in the postoperative period, and the slope of this relation increased over time as well. CONCLUSIONS: A hypermetabolic state and progressive and significant increases in the strength of the relationship between VO(2) and DO(2) and in the slope of this relationship occur after both CABG and OPCAB. Cardiopulmonary bypass is not responsible for these changes in oxygen metabolism.     

Low oxygen delivery produced by anemia, hypoxia, and low cardiac output.

In pentobarbital-anesthetized dogs, oxygen delivery (DO2) was measured by thermodilution cardiac output and cooximeter determined oxygen content, while oxygen consumption (VO2) was measured independently by spirometry. Oxygen delivery was decreased by isovolemic dilutional anemia, breathing hypoxic gas mixtures, or cardiac tamponade to reduce cardiac output. Baseline VO2 (cc/kg/min) for the three groups was 5.9 +/- 0.7 (anemia), 5.4 +/- 0.4 (hypoxia), and 5.6 +/- 0.1 (low C.O.) (NS). A critical level of oxygen delivery (DO2crit) was found at 9-10 cc/kg/min (anemia), 10-11 cc/kg/min (hypoxia), and 9-10 cc/kg/min (low C.O.) (NS.). Below this level, VO2 fell (became supply dependent) and lactic acidosis occurred, regardless of the mechanism of impaired oxygen delivery.     

Comparison of parameters for detection of splanchnic hypoxia in children undergoing cardiopulmonary bypass with pulsatile versus nonpulsatile normothermia or hypothermia during congenital heart surgeries

The aim of this study is to evaluate gastric mucosal oxygenation together with whole-body oxygen changes in infants undergoing congenital heart surgery with cardiopulmonary bypass (CPB) procedure and the use of either pulsatile or nonpulsatile mode of perfusion with normothermia and pulsatile or nonpulsatile moderate hypothermia. Sixty infants undergoing congenital cardiac surgery were randomized into four groups as: nonpulsatile normothermia CPB (NNCPB, n = 15), pulsatile normothermia CPB (PNCPB, n = 15), nonpulsatile moderate hypothermia CPB (NHCPB, n = 15), and pulsatile moderate hypothermia CPB (PHCPB, n = 15) groups. In NNCPB and PNCPB groups, mild hypothermia was used (35°C), whereas in NHCPB and PHCPB groups, moderate hypothermia (28°C) was used. Gastric intramucosal pH (pHi), whole-body oxygen delivery (DO(2)) and consumption (VO(2)), and whole-body oxygen extraction fraction were measured at sequential time points intraoperatively and up to 2 h postoperatively. The measurement of continuous tonometry data was collected at desired intervals. The values of DO(2), VO(2), and whole-body oxygen extraction fraction were not different between groups before CPB and during CPB, whereas the PNCPB group showed higher values of DO(2), VO(2), and whole-body oxygen extraction fraction compared to the other groups at the measurement levels of 20 and 60 min after aortic cross clamp, end of CPB, and 2 h after CPB (P < 0.0001). Between groups, no difference was observed for pHi, lactate, and cardiac index values (P > 0.05). This study shows that the use of normothermic pulsatile perfusion (35°C) provides better gastric mucosal oxygenation as compared to other perfusion strategies in neonates and infants undergoing congenital heart surgery with CPB procedures.