Hepatic perfusion and splanchnic oxygen consumption in patients postinjury

Hepatic dysfunction following injury is felt to be due to hepatic ischemia. To test this hypothesis we measured hepatic blood flow (HBF) and splanchnic oxygen delivery and consumption in nine multiply injured patients. HBF, measured by indocyanine green clearance, was 0.4 +/- 0.1 L/min/m2 12 hours after injury. It steadily increased to 1.3 +/- 0.1 L/min/m2 by 1 week after injury. Changes in cardiac output were similar and were due largely to changes in HBF. Hepatic hypoperfusion was correlated with subsequent increases in serum bilirubin. High oxygen consumption was associated with high HBF and oxygen delivery, and splanchnic oxygen consumption became a large fraction (range, 21-67%) of total body oxygen consumption. Although splanchnic oxygen delivery was diminished with low HBF, splanchnic oxygen consumption remained normal (37 +/- 2 ml/min/m2) due to increased oxygen extraction. We conclude that hepatic blood flow is markedly reduced after injury. Reduced HBF is correlated with liver dysfunction although normal splanchnic oxygen consumption is maintained.     

Evaluation de l'hématose dans l'insuffisance respiratoire aiguë: Mesure de la différence alvéolo-artérielle d'oxygène ou calcul du shunt ?

Information provided by computation of shunt and alveolar arterial oxygen differences have been compared in 58 épisodes of acute respiratory failure. In order to demonstrate the role of hemodynamic factors on pulmonary gas exchange, we compared blood gas measurements made in 29 patients with a high cardiac output and a reduced arteriovenous oxygen difference {C(a - v?)O₂ < 3.5 ml}, with 33 measurements corresponding to a low cardiac output and a widened C(a - v?)O₂ (> 6.5 ml). When the data was pooled together, the same P(A - a)O₂ corresponded to many different shunt values, depending on the level of mixed venous oxygenation (Pv?O₂). Q?s/Q?tot and P(A - a)O₂ were quasi linearly correlated only when they corresponded to patients with the same C(a - v?)O₂. For the same value of shunt, the PaO₂ was always raised when the Pv?O₂ was raised. As far as pulmonary gas exchange is concerned, shunt calculation in acute respiratory failure is preferable to P(A - a)O₂, especially when some hemodynamic disturbance is present.     

Optimal temperature for the management of severe traumatic brain injury: effect of hypothermia on intracranial pressure,systemic and intracranial hemodynamics,and metabolism

OBJECTIVE: We studied the effect of hypothermia on intracranial pressure, systemic and intracranial hemodynamics, and metabolism in patients with severe traumatic brain injury to clarify the optimal temperature for hypothermia, with a view toward establishing the proper management techniques for such patients. METHODS: The study was performed in 31 patients with severe head injury (Glasgow Coma Scale score as high as 5). All patients were sedated, paralyzed, ventilated, and cooled to 33 degrees C. Brain temperature, core temperature, intracranial pressure, cerebral perfusion pressure, jugular venous oxygen saturation, mixed venous oxygen saturation, cardiac output, oxygen delivery, oxygen consumption, and resting energy expenditure were monitored continuously. RESULTS: Intracranial pressure decreased significantly at brain temperatures below 37 degrees C and decreased more sharply at temperatures 35 to 36 degrees C, but no differences were observed at temperatures below 35 degrees C. Cerebral perfusion pressure peaked at 35.0 to 35.9 degrees C and decreased with further decreases in temperature. Jugular venous oxygen saturation and mixed venous oxygen saturation remained in the normal range during hypothermia. Resting energy expenditure and cardiac output decreased progressively with hypothermia. Oxygen delivery and oxygen consumption decreased to abnormally low levels at rectal temperatures below 35 degrees C, and the correlation between them became less significant at less than 35 degrees C than that when temperatures were 35 degrees C or higher. Brain temperature was consistently higher than rectal temperature by 0.5 +/- 0.3 degrees C. CONCLUSION: These results suggest that, after traumatic brain injury, decreasing body temperature to 35 to 35.5 degrees C can reduce intracranial hypertension while maintaining sufficient cerebral perfusion pressure without cardiac dysfunction or oxygen debt. Thus, 35 to 35.5 degrees C seems to be the optimal temperature at which to treat patients with severe traumatic brain injury.     

Haemodynamic changes in patients with severe head injury

Summary Haemodynamic studies were carried out in 12 patients who had sustained severe head injury. Radial artery pressure (AP), pulmonary artery pressure (PAP), central venous pressure (CVP), and pulmonary wedge pressure (PAWP) were directly measured. Heart rate was monitored from the ECG, and cardiac output (CO) was measured intermittently by the thermodilution technique. Arterial and mixed venous blood samples were withdrawn simultaneously for measurement of PH, PCO₂, PO₂, and oxygen saturation. Additional cardiovascular data were calculated from standard formulae. The haemodynamic pattern in these head-injured patients was characterized by high cardiac index, low systemic vascular resistance, moderately high systemic pressure and heart rate, high pulmonary artery pressure and wedge pressure, and normal stroke index. These findings may be the result of autonomic or adrenergic stimulation by the injured brain.     

Does general anesthesia with inhalation anesthetics worsen hypoxemia in patients with end-stage liver disease and an intrapulmonary shunt?

Hepatopulmonary syndrome (HPS) is common among patients with end-stage liver disease (ESLD); however, the effects of general anesthesia on oxygenation capacity have not been studied in these patients. The aim of this study was to evaluate the effects of general anesthesia with inhalation anesthetics on oxygenation parameters according to intrapulmonary shunt grade in patients undergoing liver transplantation. Fifty-eight liver transplant recipients were divided into 2 groups according to the intrapulmonary shunt grade as determined using preoperative echocardiography using the microbubble-syringe technique. Patients in the ‘no shunt’ group (n = 44) had either no detectable or a mild shunt, whereas those in the “shunt” group (n = 14) displayed moderate to severe changes. Arterial blood gas analysis was performed twice for each patient: preoperatively and 30 minutes after induction of general anesthesia. We calculated arterial oxygen partial pressure-to-FiO₂ ratio (PaO₂/FiO₂), alveolar-arterial oxygen difference (A-aDO₂), age-corrected A-aDO₂, A-aDO₂-to-inspiratory oxygen fraction ratio (AaDO₂/FiO₂), and alveolar oxygen partial pressure-to-PaO₂ ratio (PAO₂/PaO₂). In the preoperative period, the PaO₂ was lower in the shunt compared with the no shunt group (77.8 ± 24.3 vs 92.9 ± 14.5, respectively; P = .016), as was the PaO₂/FiO₂. A-aDO₂, age-corrected A-aDO₂, A-aDO₂/FiO₂, and PAO₂/PaO₂ were all greater in the shunt group preoperatively. After induction of general anesthesia, all parameters increased in both groups, but the differences between the 2 groups were no longer significant. Patients with ESLD who underwent liver transplantation with a moderate to severe intrapulmonary shunt showed lower preoperative oxygenation capacities than those without a shunt or with a mild shunt. General anesthesia decreased oxygenation capacity in all patients, but the differences between the 2 groups were no longer significant after induction.     

Cardiovascular and metabolic responses to severe head injury

The cardiovascular and metabolic responses to severe head injury were studied in the acute phase after severe head injury with the object of determining if a common response was present and, if so, its significance in the management of the patients' intracranial and systemic physiological states. The cardiovascular response to head injury was studied by measurement of cardiac output, pulmonary capillary wedge pressure, arterial blood pressure, arterial and mixed venous blood gases and arterial and mixed venous epinephrine and norepinephrine serially in 15 patients during the first three days after injury. A hyperdynamic state was found characterized by increased cardiac output and cardiac work, moderate hypertension, tachycardia, decreased or normal systemic and pulmonary vascular resistance, increased pulmonary shunting and increased oxygen delivery and utilisation. Arterial E and NE levels correlated well with the cardiac output, cardiac work, blood pressure, heart rate, oxygen delivery, and oxygen utilization but not with vascular resistance or pulmonary shunt. The magnitude of the hyperdynamic state did not correlate with intracranial pressure, Glasgow Coma Score, or findings on CT scan.The metabolic response to head injury was studied by measurement of resting metabolic expenditure (RME) in 14 comatose head-injured patients in the first nine days after injury. During this period patients were fed with a continuous parenteral infusion of a formula containing 2 Kcal/cc and 10 mg nitrogen/liter. Indirect calorimetry was carried out for 102 patient-days. The mean resting metabolic expenditure (RME) for nonsedated, nonparalysed patients was 138 ± 37% of that expected for a non-injured resting person of equivalent age, sex, and body surface area. Nitrogen excretion was measured for 109 patient-days. The mean excretion was 20.2 ± 6.4 mg/day. The mean protein caloric contribution was 23.9 ± 6.7% and was greater than 25% for six patients, compared to normal values of 10–15%. Despite hyperalimentation, positive nitrogen balance for any 3-day period was achieved in only seven patients, and required replacement of 161% to 240% of RME with the parenterally administered formula. Head-injured patients had a metabolic response similar to that reported for patients with burns of 20–40% of the body surface.     

Total body oxygen supply-demand balance in burned patients under enflurane anesthesia

The effects of enflurane anesthesia on the oxygen supply-demand balance have been studied in nine hypermetabolic-hyperdynamic burned patients undergoing debridement and skin-grafting procedures. Mean burn size was 55% of total body surface area. The patients were without cardiac, lung, hepatic, and kidney dysfunction and were not septic. Anesthesia was induced with sodium pentothal and maintained with enflurane and nitrous oxide in oxygen. Ventilation was controlled to maintain PaCO2 within normal limits. Crystalloid solutions and blood were administered to maintain adequate heart filling pressures. Serial measurements of cardiac output, arterial and mixed venous blood gases, and oxygen content were made before, during, and after anesthesia. Following induction of anesthesia and enflurane administration, cardiac output, oxygen delivery, and oxygen consumption decreased in a parallel fashion to approximately 60% of control. These variables did not change significantly throughout the procedure and returned to control values when enflurane was discontinued. Arteriovenous oxygen content difference did not increase and metabolic acidosis did not develop, suggesting that tissue perfusion remained adequate. Under anesthesia, oxygen consumption in burned patients was similar to that observed in normal subjects, indicating that enflurane blunts the hypermetabolic effects of thermal injury. It is concluded that in burned patients enflurane decreases metabolic rate and cardiac output, and maintains an adequate oxygen supply-demand balance.     

Effects of traumatic hypovolemic shock on renal function

Renal and systemic hemodynamic evaluations were made in 16 patients within 12- to 72-hr after injury in an effort to determine the effects of severe traumatic hypovolemic shock on renal function. Eleven patients were again studied in the convalescent period. All patients had stable vital signs at time of renal evaluation and no patient received vasopressors or diuretics within 24 hr of study.The early postresuscitative period was associated with a significant reduction in effective renal plasma flow, true renal plasma flow, true renal blood flow, renal oxygen consumption, and the percentage of renal blood flow compared to the total cardiac output; renal vascular resistance, osmolar clearance, and sodium clearance were increased at this time. The glomerular filtration rate, extracellular fluid space, cardiac output, and total peripheral resistance remained normal.All abnormal renal parameters returned to normal with convalescence except in those patients who developed nonoliguric renal failure which was associated with a persistant decrease in glomerular filtration rate and effective renal plasma flow during convalescence.The clinical significance of these findings including the roles of loop diuretics and vasodilators are discussed.     

Myocardial function following cardiopulmonary bypass.

Twenty-one patients have been studied in the 48 h after valve replacement to determine the possible contribution of abnormalities of left ventricular myocardial blood flow and oxygen consumption to the impaired cardiac performance which is sometimes evident in such patients. In the 14 patients making an uneventful recovery (Group A) the mean values for blood flow and oxygen consumption were both higher than in resting man, while the arterio-coronary sinus oxygen content difference was narrowed, with a high coronary sinus oxygen tension. Five patients had a low cardiac output (Group B) and had similar levels of blood flow and oxygen consumption to Group A, while the coronary sinus oxygen content and tension were reduced. When the heart rate was increased by pacing (Group C) myocardial oxygen consumption increased but coronary blood flow failed to rise, while the arterio-coronary sinus oxygen content difference widened slightly. It is concluded that the low postoperative cardiac output is not due to low coronary blood flow or myocardial oxygen supply, but these patients have a limited ability to increase their already high coronary blood flow. Therefore any increase in oxygen demand may be met by the potentially detrimental mechanism of widening the arterio-coronary sinus difference, with lower coronary sinus and tissue oxygen tension.     

Beta-blocker use is associated with improved outcomes in adult trauma patients

BACKGROUND: Beta-adrenoreceptor blocker (beta-blocker) therapy may improve outcomes in surgical patients by decreasing cardiac oxygen consumption and hypermetabolism. Because beta-blockers can lower the systemic blood pressure and cerebral perfusion pressure, there is concern regarding their use in patients with head injury. However, beta-blockers may protect beta-receptor rich brain cells by attenuating cerebral oxygen consumption and metabolism. We hypothesized that beta-blockers are safe in trauma patients, even if they have suffered a significant head injury. METHODS: Using pharmacy and trauma registry data of a Level I trauma center, we identified a cohort of trauma patients who received beta-blockers during their hospital stay (beta-cohort). Trauma admissions who did not receive beta-blockers were in the control cohort. beta-blocker status, in combination with other variables associated with mortality, were placed in a stepwise multivariate logistic regression to identify independent predictors of fatal outcome. RESULTS: In all, 303 (7%) of 4,117 trauma patients received beta-blockers. In the beta-cohort, 45% of patients were on beta-blockers preinjury. The most common reason to initiate beta-blocker therapy was blood pressure (60%) and heart rate (20%) control. The overall mortality rate was 5.6% and head injury was considered to be the major cause of death. After adjusting for age, Injury Severity Scale score, blood pressure, Glasgow Coma Scale score, respiratory status, and mechanism of injury, the odds ratio for fatal outcome was 0.3 (p < 0.001) for beta-cohort as compared with control. Decreased risk of fatal outcome was more pronounced in patients with a significant head injury. CONCLUSIONS: beta-blocker therapy is safe and may be beneficial in selected trauma patients with or without head injury. Further studies looking at beta-blocker therapy in trauma patients and their effect on cerebral metabolism are warranted.     

Effects of intravenous anesthesia on VA/Q distribution: a study performed during ventilation with air and with 50% oxygen, supine and in the lateral position

Distribution of ventilation and perfusion in relation to ventilation-perfusion ratio (VA/Q) were studied in 14 patients, with a mean age of 59 yr, before elective lung surgery, in the supine position when awake, during intravenous anesthesia and mechanical ventilation with air, after increasing the fraction of inspired oxygen (FIO2) to 0.5, and in the lateral position. Before anesthesia, small inert gas shunts and perfusion of low VA/Q regions, indicating some degree of VA/Q mismatch, were observed in several patients. After induction, FIO2 = 0.21, the major changes were a significant decrease in cardiac output and an increase in log SD for perfusion from 0.77 +/- 0.45 (SD) to 1.13 +/- 0.50 (SD), while the shunt remained low at 1% of cardiac output and arterial oxygen tension (PaO2) was unchanged. An increase to FIO2 = 0.5 induced only small changes with a shunt of 2.5% of cardiac output. In the lateral position, the shunt was 4.0% and increases in ventilation to high VA/Q regions were observed. The lack of marked changes in the VA/Q distribution after induction either could be a result of only minor alterations in the distribution of ventilation and perfusion or an effective vascular response to alveolar hypoxia (hypoxic pulmonary vasoconstriction, HPV).     

Central Haemodynamics and Oxygen Transport With and Without Continuous Positive Pressure Ventilation After Open-heart Surgery

Twelve patients, subjected 20 h earlier to coronary artery bypass surgery, were studied on discontinuation of the postoperative mechanical ventilation employing PEEP+5 cmH₂O (CMV + PEEP). Compared to the values obtained during CMV + PEEP, cardiac index and mixed venous blood oxygen tension increased with the change to spontaneous ventilation at ambient pressure, employing a 28% O² Ventimask® for the intubated patient. There was a slight decrease in both the arterial oxygen content and oxygen tension, but the increase in cardiac output compensated well for the lowering in the arterial oxygen content, and consequently the systemic oxygen transport was statistically unaltered. Oxygen consumption, pulmonary shunt fraction and arteriovenous oxygen content difference also remained unaltered. The observations suggest that after open-heart surgery, CMV using a PEEP as low as+ 5 cmH₂O may exert, in comparison to controlled oxygen therapy during spontaneous breathing, a significant lowering effect on the already compromised cardiac performance. This necessitates continuous weighing of the beneficial effects obtained by employing postoperative CMV + PEEP, against the adverse haemodynamic effects, although the alterations in cardiac output may partly ensue from the changes in metabolism, muscular effort and oxygen consumption during the two modes of ventilation, although there was no significant increase in oxygen consumption.     

The reason for cardiac output reduction after aortic cross-clamping

The hypothesis that a decrease in cardiac output during infrarenal aortic cross-clamping is related to a decrease in oxygen consumption in the perfused tissues (cross-clamp-adapted oxygen consumption) rather than to deterioration of myocardial performance has been tested. Twenty-two patients undergoing excision of an aortic abdominal aneurysm were randomly divided into two groups of equal number. During aortic cross-clamping, Group 1 patients received nitroglycerin infusion, 1 to 2 micrograms.kg-1.min-1, whereas Group 2 patients did not receive a nitroglycerin infusion. During aortic cross-clamping, cross-clamp-adapted body oxygen consumption decreased equally in both groups by 40 to 42 percent of baseline values, whereas cardiac output decreased by 17 percent in Group 2 but did not change significantly in Group 1. Mixed venous oxygen content increased significantly after induction of anesthesia and prior to aortic cross-clamping in both groups. During cross-clamping, the values of mixed venous oxygen content remained increased in Group 2 and increased further in Group 1. The data support our hypothesis since a decrease in cardiac output was not associated with an increase in filling pressures during aortic cross-clamping, but was instead associated with an increase in mixed venous oxygen content and a decrease in the arteriovenous oxygen content difference. Nitroglycerin infusion was associated with a further increase in mixed venous oxygen content during aortic cross-clamping and a decrease in the arteriovenous oxygen content difference, without a concomitant increase in oxygen utilization.     

Temperature regulation as possible prognostic indicator in patients with acute intracranial lesions

Summary 24 patients, 16 after severe head injury and 8 after spontaneous intracranial haematoma, were investigated by external cold load in order to determine their thermoregulatory capabilities.Tympanic temperature, several skin temperatures and oxygen consumption were measured. The patients where examined for SSEP and AEP. The cold induced thermoregulatory threshold temperature was determined by calculating the mean body temperature and by determining mean body temperature at which oxygen consumption increased due to the external cold load.In all patients core temperature and mean body temperature were significantly elevated by 1 °C compared to controls. There was no difference of the course of the various body temperatures during cold load in the patient groups. In the trauma group 8 patients were able to increase oxygen use (VO₂) during cold exposure, the other 8 patients showed no physiological thermoregulatory reaction. The heatproduction threshold temperature was increased by 1 °C in the patient groups compared to controls. There was no significant correlation of AEP and SSEP findings to a preserved or disturbed thermoregulatory reaction. In the trauma patients, who were able to respond to a cold load, the outcome was significantly better (GOS=3–5), than in those patients, who did not show a physiological increase of VO₂ due to the cold load (GOS=1–2).In conclusion, measurement of body temperatures alone is not sufficient to determine termoregulatory capacities. An examination using thermophysiological methods however provides more information about the function and structure damaged after severe head injury. An intact thermoregulatory systems seems to be correlated with a better prognosis after head injury.Dedicated to Prof. Dr. K. Brück, Former Head of the Institute of Physiology of the University of Giessen, Federal Republic of Germany.     

Mechanical Support for Postcardiotomy Heart Failure

Cardiac failure remains a life-threatening complication for certain patients undergoing intracardiac repair. Despite improvements in surgical techniques, methods of myocardial protection, and postoperative care, patients are frequently at risk to develop postoperative low output syndrome. Approximately 1% of cardiac surgical patients cannot be weaned from extracorporeal circulation in spite of adequate volume loading, the use of inotropic support, and initiation of intraaortic balloon pumping. In these cases, ventricular assist devices (VAD) can mechanically aid the failing heart and reverse the low output state. The concept of mechanical support for the failing left ventricle was first proposed by Clauss et al. in 1961. By 1968, Kantrowitz and associates had developed and refined the first intraaortic balloon pump (IABP). Through the efforts of Moulopolous and others, this device evolved into the present-day intraaortic balloon pump (IABP). Clinical evidence for the efficacy of left ventricular assist devices (LVAD) remained questionable until 1980, when the National Heart, Blood and Lung Institute evaluated short-term LVADs by comparing various types of mechanical aids. This report focused attention primarily on the failing left ventricle (LV). As the use of inotropic support, intraaortic balloon pumping, and LVADs improved, a small group of patients emerged who could not be separated from extracorporeal circulation due to a failing right ventricle. The failing right ventricle emerged as a unique clinical entity similar to postcardiotomy left ventricular failure that also benefited from mechanical cardiac assistance. Current therapy at major centers incorporating mechanical assist devices is based on the premise that the low output state will allow the failing heart to recover from a reversible injury. The frequent occurrence of postcardiotomy ischemia may be due to several factors such as poor myocardial protection, overdistension of the LV, emboli, coronary spasm or technical problems. Whatever the etiology, the end product of cardiac failure is a demand for oxygen consumption that cannot be met, thus leading to cardiac demise.     

Effects of Nitroglycerin on Central Haemodynamics and V.A/Q. Distribution During Ventilation with F102 = 1.0 in Patients After Coronary Bypass Surgery

The effects of nitroglycerin (TNG) infusion during ventilation with FIO2 = 1.0 on central haemodynamics and the distribution of ventilation-perfusion (VA/Q) were studied with the multiple inert gas elimination technique in eight patients after coronary bypass surgery. Administration of TNG resulted in a significant decrease in mean arterial pressure, and an increase in heart rate while cardiac output remained unchanged. Mean right atrial, pulmonary arterial and pulmonary wedge pressures all decreased. There was a significant reduction in PaO2 from 50.5 to 32.7 kPa, while Pao2 remained unchanged in a control group of eight patients. This was mainly due to an increase in shunt from 9.3 to 16.5% of cardiac output during TNG-infusion. In the control group there was also an increase in shunt from 9.7 to 12.1% of cardiac output with a simultaneous decrease of the same magnitude in perfusion of regions with low VA/Q (0.005-0.1). This was not evident in the group receiving TNG. Twenty min after termination of TNG-infusion the effects on central haemodynamics and gas exchange were not fully reversed. The mechanism behind the increase in inert gas shunt observed with infusion of TNG during oxygen breathing is probably a selective effect on vessels with remaining high vasomotor tone despite high alveolar oxygen tension.     

Oxygen utilization during surface-induced deep hypothermia

Oxygen utilization during surface-induced deep hypothermia under ether anesthesia and respiratory alkalosis, with and without 30 minutes of circulatory arrest, was studied in 12 dogs. Oxygen consumption and saturation, hemoglobin, hematocrit, Po₂, Pco₂, and pH of arterial and mixed venous blood were measured, and oxygen content, arteriovenous oxygen differences, and cardiac output were calculated.There were slightly decreased but persistent arteriovenous oxygen differences during cooling until low cardiac output developed around 18°C., which would suggest continued unloading of oxygen from hemoglobin despite the presence of severe alkalosis. The oxygen debt developed during total circulatory occlusion or from low cardiac output was repaid in the early rewarming period when circulation was reestablished. Venous Po₂ became progressively lower below 25°C. Tissue oxygen uptake is presumably accomplished by lowering tissue oxygen tension, but this drop apparently does not grossly impair tissue function since all dogs tolerated the procedure well and are long-term survivors.     

Splanchnic blood flow and oxygen consumption: effects of enteral nutrition and dopexamine in the elderly cardiac surgery patient

BACKGROUND: After cardiac surgery, patients are at risk of organ dysfunction because of decreased perfusion. Different measures have been used to increase the splanchnic blood flow. We compared the effects of enteral nutrition and dopexamine on the cardiac output, splanchnic blood flow and oxygen consumption. METHODS: Sixteen patients undergoing cardiac surgery were included. Indocyanine green extraction and thermodilution were used for repeated measurements of the splanchnic blood flow and cardiac output. On the first post-operative day, indocyanine green infusion was started. Patients were randomized to start with dopexamine (Dpx group) or enteral nutrition (EN group). After 180 min, both groups received a combination of dopexamine and enteral nutrition. Blood gases from the hepatic vein and pulmonary and radial arteries were analysed repeatedly. RESULTS: In the Dpx group, the cardiac index increased with dopexamine infusion, but not when enteral nutrition was added. In the EN group, enteral nutrition alone did not increase the cardiac index, but dopexamine addition increased the cardiac index in this group. The splanchnic blood flow increased initially in the Dpx group, but then returned to baseline and remained constant on addition of enteral nutrition. In the EN group, the splanchnic blood flow initially remained at baseline, but increased after dopexamine addition. There was no difference between the groups with regard to systemic or splanchnic oxygen consumption or the oxygen extraction ratio. In the Dpx group, lactate increased from baseline with no further increase on addition of enteral nutrition. Lactate was unchanged in the EN group. CONCLUSIONS: Dopexamine and enteral nutrition caused no adverse effects on oxygen consumption or the oxygen extraction ratio. Enteral nutrition did not increase the splanchnic blood flow or cardiac index. Dopexamine increased the systemic blood flow with only a transient effect on the splanchnic blood flow. Dopexamine increased the lactate concentration, possibly indicating a more ischaemic condition.     

Effects of the Level of CPAP on Central Haemodynamics and Oxygen Transport

The effects of different levels of continuous positive airway pressure (CPAP) on central haemodynamics and oxygen transport were studied in ten spontaneously breathing male patients who had undergone aortocoronary bypass graft operation 18 h earlier. With increasing CPAP levels ranging from 5 cm H₂O (0.49 kPa) (CPAP 5) to 15 cmH₂O (1.47 kPa) (CPAP 15), the cardiac index was found to decrease significantly, while the intraluminal pulmonary capillary wedge and right atrial pressures increased simultaneously. The mean systemic arterial pressure remained unaltered, while the mean pulmonary arterial pressure increased with increasing CPAP. Systemic oxygen transport changed concomitantly with the changes in cardiac output, since arterial blood oxygen content was not altered. The mixed venous blood oxygen tension decreased with increasing CPAP, as did the cardiac output. No changes in the total oxygen consumption or in the arteriovenous oxygen content difference were found at the various CPAP levels. Pulmonary vascular resistance was significantly higher during CPAP 0 than during CPAP 5, possibly indicating development of local pulmonary vasoconstriction following hypoxia caused by closure of the small airways as a consequence of a reduction in the functional residual capacity during CPAP 0. Thus, low level CPAP might be beneficial in maintaining proper lung volume in an intubated patient after aortocoronary bypass surgery. The observations also suggest that, in these patients, CPAP levels exceeding 10 cmH₂O bring about cardiac depression leading to an undesirable reduction in systemic oxygen transport. Mixed venous blood oxygen tension may offer information useful in the adjustment of the level of CPAP.