Mixed Venous Oxygen Content Research Articles

Cardiopulmonary Effects of Positive Pressure Ventilation During Acute Lung Injury

To assess the gas exchange and hemodynamic effects of pressure-limited ventilation (PLV) strategies in acute lung injury (ALI). We hypothesized that in ALI, the reduction of plateau airway pressure (Paw) would be associated with less alveolar overdistention and thus have better hemodynamic and gas exchange characteristics than larger tidal volume (Vr) ventilation. Laboratory. Prospective time-controlled sequential animal study. Right atrial, pulmonary artery, left atrial, arterial, lateral pleural (Ppl), and pericardial (Ppc) pressures, Paw, ventricular stroke volume, mean expired CO2, and arterial and mixed venous oxygen contents. Airway resistance and static lung compliance were also measured. Intermittent positive pressure ventilation (IPPV) given before (control) and after induction of ALI by oleic acid infusion (0.1 mL/kg). IPPV at FIO2 of 1, VT of 12 mL/kg, and frequency adjusted to maintain normocarbia. ALI PLV was given during ALI and defined as that VT which gave a similar plateau Paw to that of control IPPV. High-frequency jet ventilation (HFJV) and ALI HFJV were also given and defined as frequency within 10% of heart rate and mean Paw similar to that during control IPPV. After ALI, static lung compliance, PaO2, and pH decreased, whereas airway resistance and PaCO2 increased. For a constant lung volume, Ppl and Ppc were not different between control and ALI. Both absolute dead space (VD) and intrapulmonary shunt fraction increased after ALI, but absolute VD was lower with ALI PLV and ALI HFJV when compared with ALI IPPV. Ventilation did not alter hemodynamics during ALI. Changes in lung volume determine Ppc and Ppl. PLV strategies do not alter hemodynamics but result in less of an increase in VD/VT than would be predicted from the obligatory decrease in VT.

Continuous thermodilution cardiac output: Agreement with fick and bolus thermodilution methods

Cardiac outputs were determined with continuous thermodilution, bolus thermodilution, and the Fick method during pharmacologically varied hemodynamics. Prospective comparison of techniques. University animal laboratory. Swine. Swine were anesthetized, tracheally intubated, and instrumented to measure continuous (QTDC) and bolus (QTDB) thermodilution cardiac outputs and sample arterial and mixed venous blood. Continuous thermodilution of blood was facilitated by computer modulation of a thermal filament wrapped around the portion of the pulmonary artery catheter residing in the right atrium and ventricle. QTDC was computed from the thermodilution curve monitored by the thermistor. Bolus thermodilution was performed in triplicate by injecting 10 mL of 5% dextrose in water (0 to 4 degrees C). Oxygen consumption (VO2) was calculated as the averaged minute rate of disappearance of spirometer oxygen over a 6-minute steady state. Cardiac output was determined with the direct Fick method (QF) by dividing VO2 by the difference in arterial and mixed venous oxygen content. Basal QTDC was increased and decreased with an intravenous infusion of dobutamine or labetalol, respectively. Data are summarized as mean +/- SD or 95% confidence interval (CI 95%). Agreement between methods of determining cardiac output was assessed by calculating bias, percent bias, and percent coefficient of determination (100 r2). Eighteen swine (38.9 +/- 1.2 kg) exhibited a range of QTDC from 2.2 to 14.8 L/min. Mean measurement variance of VO2, CaO2, CvO2, and QTDB was 1.5%, 1.5%, 2.0%, and 11.8%, respectively. Mean bias, percent bias, and 100 r2 was 0.004 +/- 1.05 L/min (CI 95%: 0.18 to 0.19 L/min), -0.37 +/- 13.8% (CI 95%: -2.75 to 2.01), and 89% between QTDC and QF, respectively. Bias, percent bias, and 100 r2 was 0.05 +/- 1.09 L/min (CI 95%: -0.14 to 0.23 L/min, 1.21 +/- 13.06% (CI 95%: -1.03 to 3.46%), and 91% between QTDC and QTDB, respectively. Bias, percent bias, and 100 r2 (Fig 6) was -0.04 +/- 0.69 L/min (CI 95%: -0.16 to -.08 L/min), -1.23 +/- 9.17% (CI 95%: -2.8 to 0.35%), and 94% between QTDB and QF, respectively. Automatic cardiac output computed with continuous thermodilution appears accurate and reliable. Also, good agreement was confirmed between cardiac output derived by continuous and bolus thermodilution methods and bolus thermodilution and Fick methods.

Hemodynamic responses of horses to anesthesia and surgery, before and after administration of a low dose of endotoxin.

Seven horses, which were part of an investigation of the effect of endotoxin administration on vascular reactivity, were anesthetized on two separate occasions for surgical excision of 4-cm sections of palmar digital artery and vein. On the first occasion, the horses were given an infusion of 1 L 0.9% NaCl solution intravenously (i.v.) just before induction of anesthesia (control); on the second occasion, the horses received an infusion of 1 L 0.9% NaCl containing Escherichia coli endotoxin, 0.1 microgram/kg (endotoxin). On both occasions, anesthesia was induced with xylazine, guaifenesin, and ketamine, and maintained with halothane in oxygen. Hemodynamic measurements were made with the horses under anesthesia immediately before beginning surgery (period 1), during skin incision (period 2), during dissection and excision of the vessels (period 3), during skin suturing (period 4), and after completion of surgery during bandaging (period 5). Hemoglobin concentration and mixed venous oxygen content were greater at all periods in horses that received endotoxin. Otherwise, there were no significant differences in hemodynamic parameters between control horses and horses administered endotoxin before beginning surgery (period 1). During surgery and bandaging, horses administered endotoxin had significantly higher heart rate (periods 3, 4, and 5), cardiac index (periods 3, 4, and 5), and oxygen delivery (periods 2, 3, 4, and 5) than did control horses, and mean arterial blood pressure (period 2) and systemic vascular resistance (periods 2, 3, 4, and 5) were less than in control horses. Compared with period 1, surgical stimulation in control horses was associated with increased mean arterial blood pressure and systemic vascular resistance (periods 2, 3, 4, and 5), but cardiac index and oxygen delivery were decreased (periods 3, 4, and 5).(ABSTRACT TRUNCATED AT 250 WORDS)

Estimation of cardiac index by means of the arterial and the mixed venous oxygen content and pulmonary oxygen uptake determination in the early post-operative period following surgery of congenital heart disease

To assess the reliability of estimation of cardiac index based on the mixed venous oxygen saturation and methods of improving the estimation of cardiac index. PICU in an university hospital. In the post-operative period following complete repair of congenital heart disease we carried out 55 measurements of blood gases in 25 infants and children (mean age 16.1 months, mean body surface 0.43 m2) from a systemic artery (arterial) and the pulmonary artery (mixed venous). We also determined the pulmonary oxygen uptake and calculated the cardiac index (CI) using Fick's principle. In the analysis we compared the CI with the mixed venous oxygen saturation (SvO2) and with the quotient of the arterial oxygen content (CaO2) and the oxygen extraction (Ca-vDO2). This quotient is equal to arterial oxygen delivery (DO2) divided by the oxygen consumption (VO2). Pearson's correlation coefficient was 0.77 when SvO2 was compared to CI in a linear regression model. Assuming an inverse relationship between SvO2 and CI the correlation was much better (r = 0.90). However, the best estimation of CI provides the quotient CaO2/Ca-vDO2 (r = 0.93). CaO2/Ca-vDO2 correlates much better with CI than the SvO2, therefore CI could be better estimated based on CaO2/Ca-vDO2. Furthermore CaO2/Ca-vDO2 provides good information about the oxygen supply situation of the body.

Oxygen delivery and consumption in critically ill pregnant patients: Association with ophthalmic artery diastolic velocity

Objectives: We aimed to investigate the relation between orbital vessel flow velocity and (i)xygen delivery, oxygen consumption, cardiac index, and systemic vascular resistance index in critically ill pregnant patients.Study Design: Eighteen pregnant or early postpartum patients requiring invasive monitoring were prospectively studied with Doppler ultrasonography. The blood flow velocity and resistance index from the central retinal and ophthalmic arteries were plotted against the oxygen delivery index, oxygen consumption index, cardiac index, and systemic vascular resistance index. Linear and polynomial regression analysis. and receiver-operator characteristic curves were used to examine the data.Results: The ophthalmic artery resistance index correlated with oxygen consumption, oxygen delivery index, and cardiac index. Only the cardiac index was independently related to the the ophthalmic artery resistance index. The ophthalmic artery diastolic velocity correlated with oxygen consumption index, oxygen delivery index, and cardiac index. The ophthalmic artery diastolic velocity correlated independently with mixed venous oxygen content and arteriovenous oxygen content difference. The central retinal artery Doppler index did not correlate with any of the invasively measured parameters. An ophthalmic artery diastolic velocity of > 7.12 ern/sec identified 75% of patients with an oxygen consumption index of < 140 ml/min per square meter and 91% of patients with an oxygen delivery index of < 600 ml/min per square meter.Conclusions: These data suggest that the ophthalmic artery flow velocity is correlated with systemic oxygen delivery and consumption. This relationship may have potential research applications in the noninvasive assessment of oxygen delivery index and oxygen consumption index in critically ill pregnant patients.

Cardiopulmonary effects of halothane in hypovolemic dogs

Summary Cardiopulmonary effects of halothane administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. Halothane was delivered by face mask, dogs were intubated, then halothane end-tidal concentration of 1.13 ± 0.02% was maintained, and cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to halothane administration, systemic vascular resistance index, oxygen extraction, and base deficit increased. Compared with baseline values, these variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, pulmonary arterial occlusion pressure, cardiac index, oxygen delivery index, oxygen consumption index, mixed venous oxygen tension, mixed venous oxygen content, venous admixture, arterial bicarbonate concentration, and mixed venous pH. At all times after intubation, arterial and venous oxygen tensions and mixed venous carbon dioxide tensions were increased. Three minutes after intubation, base deficit and mixed venous carbon dioxide tension increased, and mean arterial pressure and arterial and venous pH decreased, compared with values measured immediately prior to halothane administration. Fifteen minutes after intubation, systemic vascular resistance index decreased and, at 15 and 30 minutes, mean arterial pressure and arterial and venous pH remained decreased. At 60 minutes, mean pulmonary arterial pressure and pulmonary arterial occlusion pressure were increased and mixed venous pH was decreased, compared with values measured before halothane administration. Results of this study indicated that induction of anesthesia with halothane and maintenance at an end-tidal halothane concentration of 1.13% induced significant changes in blood pressure, with minimal effects on cardiac output and pulmonary function, when administered to hypovolemic dogs.

Uremic Myopathy Limits Aerobic Capacity in Hemodialysis Patients

Eleven end-stage renal disease patients trained by stationary cycling during their hemodialysis treatments. After a 6-week control period, 12 weeks of training began and was increased to 30 to 60 minutes at > or = 70% of peak heart rate. Baseline, pretraining and, posttraining exercise tests were performed. Workload (WL), oxygen uptake (VO2peak), cardiac output (Q), heart rate (HR), and arterial oxygen content (CaO2) were measured. Stroke volume (SV), arteriovenous oxygen difference ((a-v)O2), and mixed-venous oxygen content (CvO2) were calculated. Rectus femoris biopsies were obtained pretraining and posttraining. At peak exercise, WL increased from 60 +/- 4 to 70 +/- 6 W (P < 0.05), VO2peak showed an upward trend from 14.8 +/- 0.9 to 16.8 +/- 1.3 mL/kg/min (P < 0.1), and Q, HR, SV, CaO2, CvO2, and (a-v)O2 were unchanged. Ten of the 11 patients increased WL, but only six increased VO2peak (five of 11 patients decreased VO2peak). The difference between groups (P < 0.02) was attributable to (a-v)O2, which increased in those who increased VO2peak (P < 0.02). There was an upward trend for succinate dehydrogenase activity (P < 0.06), and phosphofructokinase activity increased (P < 0.05). However, the rectus femoris capillary to fiber ratio, type I and II fiber areas, and fiber area variability were unchanged, and neither histomorphologic nor enzymatic activity changes were related to change in VO2peak. We conclude that not all dialysis patients increase VO2peak after training, but most can improve exercise capacity. Patients who improved VO2peak widened their (a-v)O2 difference, increasing oxygen extraction and showing that oxygen delivery is not always the limiting factor. Thus, the limitation of VO2peak in dialysis patients is a complex interaction of central and peripheral factors. Muscle therapies, such as exercise training, are needed in addition to increased oxygen delivery in rehabilitation of dialysis patients.

Blood pressure management during aortic surgery: urapidil compared to isosorbide dinitrate

The efficacy and hemodynamic effects of urapidil, an arteriolar vasodilator, and isosorbide dinitrate, a venodilator, were compared, when used for blood pressure control during abdominal aortic surgery. Urapidil is an α-adrenergic receptor antagonist with serotonin-1A receptor-agonist activity in the central nervous system. Hemodynamic profiles were recorded before and after the administration of the study drug (±10 minutes before aortic clamping), 3 and 10 minutes following aortic clamping, and before and 3 and 10 minutes following the removal of the aortic clamp. Arterial and mixed venous oxygen contents were compared. Both groups of 18 patients were similar with respect to demographic profiles, anesthetic technique, and perioperative fluid therapy. Identical heart rate and blood pressure profiles were obtained. In contrast to isosorbide dinitrate, urapidil produced a 17% ( P < 0.05) increase in cardiac index as a result of a 30% ( P < 0.001) decrease in systemic vascular resistance before placement of the aortic clamp. In patients treated with urapidil, cardiac index was higher ( P < 0.05) 10 minutes after aortic clamping, before removal of the clamp, and 10 minutes later. The arterio-venous oxygen content difference decreased from 3.2 ± 0.8 mL O 2/dL to 2.4 ± 1.0 mL O 2/dL ( P < 0.01) following urapidil, but did not change during the administration of isosorbide dinitrate. It is concluded that urapidil is an effective and safe drug for the prevention of the hemodynamic consequences of aortic clamping. Compared to a venodilator (isosorbide dinitrate), urapidil offers the advantage of improving cardiac output and oxygen delivery.

Respiratory dysfunction following cardiopulmonary bypass: verification of a non-invasive technique to measure shunt fraction

Respiratory dysfunction is a well recognized complication of cardiopulmonary bypass. The size of the pulmonary shunt fraction is the best indicator of respiratory dysfunction but its measurement conventionally requires use of a pulmonary artery catheter to measure mixed venous oxygen content. We compared pulmonary shunt fraction, based on a non-invasive technique using a previously described mathematical model, with shunt fraction measured invasively using a pulmonary artery catheter in 22 patients undergoing elective coronary artery surgery. The mean shunt fraction measured by the invasive technique was 19·6 ± 2·0 (18·8–20·4)% of cardiac output at 24 h (± 1 sd and 90% confidence intervals) and 20·9 ± 2·9 (19·8–22·0)% of cardiac output at 44 h post-surgery. There was good agreement between the two methods of measurement. The mean difference was 0·21 percentage points with 95% confidence interval −0·01 to 0·43. The limits of agreement (−1·17 to 1·59) are small enough to be confident that the non-invasive method can be used to give the same result as that obtained using a pulmonary artery catheter. The values for shunt fractions obtained by the non-invasive technique were 19·7 ± 2·3 (18·8–20·6)% of cardiac output at 24 h and 20·7 ± 2·5 (19·7–21·6)% of cardiac output at 44 h. The non-invasive measurement of the shunt fraction provided us with a simple, practical method for following a further ten patients over an extended period of time where prolonged catheterization is impractical.

Oxygen kinetics during liver transplantation: The relationship between delivery and consumption

In anesthetized humans, oxygen consumption is independent of oxygen delivery above a critical threshold. Below this critical level, lactic acid is a marker of anaerobic metabolism and tissue oxygen debt, and heralds a supply dependency of oxygen consumption. The goal of this study was to determine whether a threshold value for oxygen delivery below which oxygen consumption becomes supply dependent can be identified in patients with normal, impaired, or absent liver function. Measurements were made in 34 surviving patients (group 1) and in 16 nonsurvivors with sepsis and postoperative liver graft failure (group 2). Hemodynamic measurements and blood samples were taken 10 minutes after introduction of anesthesia, 10 minutes after cross-clamping, and 10 minutes after reperfusion of the new liver. At these time points, we measured blood lactate, cardiac output, and arterial and mixed venous oxygen contents in order to calculate oxygen consumption and oxygen delivery. In both groups, cardiac output, oxygen delivery, and oxygen consumption decreased during the anhepatic phase and increased after unclamping of the inferior vena cave. Lactate increased in both groups during surgery, but was significantly higher in nonsurvivors (6.6 ± 0.4 mmol/L) than in survivors (4.6 ± 0.1 mmol/L) ( P <.05). With similar changes for oxygen delivery and oxygen consumption during increased lactate levels we could not identify a clear supply dependency of oxygen consumption in survivors and nonsurvivors during liver transplantation. We conclude that the interpretation of blood lactate levels during circulatory shock can be biased due to a reduced lactate clearance in patients with impaired liver function, unrelated to the status of the relationship between oxygen delivery and consumption. Moreover, elevated blood lactate after liver transplantation predicts postoperative complications and death.

Determinants of VO2peak in patients with end-stage renal disease: on and off dialysis.

Peak oxygen uptake (VO2peak) of patients on maintenance hemodialysis is very low. Exercise training performed during, or "on" dialysis, and at other times, "off" dialysis, both improve VO2peak. Equivalence of these approaches has not been shown, nor have the physiologic factors limiting VO2peak been clarified in these patients. We hypothesized that hemodialysis does not acutely alter the cardiovascular response to peak exercise, and further that anemia and a low peak heart rate limit VO2peak. Ten patients with end-stage renal disease (ESRD) performed cycle ergometry to peak exercise. Peak oxygen uptake measured immediately prior to dialysis was compared with predicted values, and with measurements obtained during the second 30 min of dialysis. The determinants of VO2peak were compared with previously reported norms. "Off" dialysis, VO2peak for nine of 10 patients was below the 95% confidence limit for normals. Their cardiovascular response to peak exercise was unchanged by 30-60 min of hemodialysis. Stroke volume was similar to that of normals; however, peak heart rate was 77% of predicted, and hematocrit was 27% (at rest). Peak exercise mixed-venous oxygen content was 3.6 ml O2 ml.dl-1 blood, similar to values reported for athletes. These findings show that up to 1 h of dialysis minimally effects VO2peak, and imply that low oxygen delivery limited VO2peak in these patients.

Effect of beta-adrenergic receptor antagonism on chloralose-induced hemodynamic changes in newborn lambs.

alpha-Chloralose is an anesthetic commonly used in cardiovascular research. Using a chronically instrumented neonatal lamb model, we previously determined that chloralose has important effects on basal hemodynamics and arterial oxygen tension as compared with those of paired conscious control lambs. We wished to determine whether beta-adrenergic receptor stimulation accounted for chloralose-induced hemodynamic effects and to investigate the influence of chloralose and beta-adrenergic receptor antagonism on oxygen metabolism. In paired studies, five lambs were given chloralose intravenously (30 mg/kg i.v.) after propranolol (1 mg/kg i.v.) or saline control. The group pretreated with propranolol had reduced heart rate (HR 206 +/- 12 vs. 244 +/- 10 beats/min, p = 0.04) and cardiac output (CO 253 +/- 29 vs. 302 +/- 40 ml/min/kg, p = 0.005) 30 min after chloralose as compared with control; pretreatment with propranolol also attenuated the systemic hypertensive response to chloralose (77 +/- 8 vs. 89 +/- 5 mm Hg, p = 0.055). No difference in the response of stroke volume (SV), atrial or pulmonary arterial pressures, or pulmonary and systemic vascular resistances (PVR, SVR) were observed between treatment groups. No differences between propranolol and saline treatment groups were observed in arterial and mixed venous oxygen contents, arteriovenous (A-V) oxygen difference, oxygen extraction, or oxygen consumption; a reduction in oxygen delivery observed after propranolol as compared with saline was not altered by chloralose. We conclude that tachycardia and increase in CO induced by chloralose in lambs probably are mediated by beta-adrenergic receptor stimulation, which may be direct or indirect.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiovascular and respiratory effects of propofol administration in hypovolemic dogs

Summary Cardiopulmonary effects of propofol were studied in hypovolemic dogs from completion of, until 1 hour after administration. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. After stabilization at this pressure for 1 hour, 6 mg of propofol/kg of body weight was administered iv to 7 dogs, and cardiopulmonary effects were measured. After blood withdrawal and prior to propofol administration, oxygen utilization ratio increased, whereas mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary capillary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, and mixed venous oxygen content decreased from baseline. Three minutes after propofol administration, mean pulmonary arterial pressure, pulmonary vascular resistance, oxygen utilization ratio, venous admixture, and arterial and mixed venous carbon dioxide tensions increased, whereas mean arterial pressure, arterial oxygen tension, mixed venous oxygen content, arterial and mixed venous pH decreased from values measured prior to propofol administration. Fifteen minutes after propofol administration, mixed venous carbon dioxide tension was still increased; however by 30 minutes after propofol administration, all measurements had returned to values similar to those measured prior to propofol administration.

Carbon monoxide and pulmonary circulation in an ovine model.

The direct pulmonary vasoconstrictive effects of inhaled carbon monoxide were evaluated in chronically instrumented and anesthetized sheep (1.7% halothane in air) (n = 8). The response to carbon monoxide (2%), which was applied for 8 minutes through a double-lumen tube alternately to the left or right lung of each animal, was compared with baseline values. The induced carboxyhemoglobin level (65%) led to increases in cardiac output, pulmonary arterial pressure, stroke volume index, and heart rate. Systemic vascular resistance decreased, and pulmonary vascular resistance and mean arterial pressure were unchanged. The changes in pressure and flow were equivalent no matter which lung was exposed to carbon monoxide. No diversion of blood from one lung to the other was observed during the test period. We conclude that carbon monoxide does not have a direct pulmonary vasoconstrictive effect. The increase in pulmonary arterial pressure is a result of the decrease in mixed venous oxygen content (stimulus for hypoxic pulmonary vasoconstriction) and the increase in cardiac output.

Cardiopulmonary effects of etomidate in hypovolemic dogs

Summary Cardiopulmonary effects of etomidate administration were studied in hypovolemic dogs. Baseline cardiopulmonary data were recorded from conscious dogs after instrumentation. Hypovolemia was induced by withdrawal of blood from dogs until mean arterial pressure of 60 mm of Hg was achieved. Blood pressure was maintained at 60 mm of Hg for 1 hour, by further removal or replacement of blood. One milligram of etomidate/kg of body weight was then administered iv to 7 dogs, and the cardiopulmonary effects were measured 3, 15, 30, and 60 minutes later. After blood withdrawal and prior to etomidate administration, heart rate, arterial oxygen tension, and oxygen utilization ratio increased. Compared with baseline values, the following variables were decreased: mean arterial pressure, mean pulmonary arterial pressure, central venous pressure, pulmonary wedge pressure, cardiac index, oxygen delivery, mixed venous oxygen tension, mixed venous oxygen content, and arterial carbon dioxide tension. Three minutes after etomidate administration, central venous pressure, mixed venous and arterial carbon dioxide tension, and venous admixture increased, and heart rate, arterial and venous pH, and arterial oxygen tension decreased, compared with values measured immediately prior to etomidate administration. Fifteen minutes after etomidate injection, arterial pH and heart rate remained decreased. At 30 minutes, only heart rate was decreased, and at 60 minutes, mean arterial pressure was increased, compared with values measured before etomidate administration. Results of this study indicate that etomidate induces minimal changes in cardiopulmonary function when administered to hypovolemic dogs.

Adult Respiratory Distress Syndrome: Sequence and Importance of Development of Multiple Organ Failure

To determine the epidemiology of multiple organ failure (MOF) in patients with the adult respiratory distress syndrome.We followed up 50 patients with serial determinations of respiratory and nonrespiratory organ function for seven days after diagnosis.Data were stratified between patients who died and those who survived (defined as hospital discharge).Values that did not differ at any time between the two groups of patients included oxygen availability, oxygen consumption, oxygen extraction, PaCO2, respiratory rate, heart rate, systolic blood pressure, cardiac output, stroke index, systemic vascular resistance, and temperature. Patients who died had greater defects in oxygenation (from day 1 through day 7). They also exhibited decreased arterial oxygen content (from day 1 to day 4), decreased mixed venous oxygen content (day 1), increased peak inspiratory pressure (present on day 2, persisted to day 5, reappeared on day 7), decreased diastolic blood pressure (seen on days 1 through 3, reappeared on day 7), and increased mean pulmonary artery pressure (seen on days 2 and 3). Nonsurvivors also exhibited greater degrees of thrombocytopenia (from day 1 to day 4). Decreases in pH (seen on day 1, reappeared from days 4 to 7), abnormalities in liver function (seen only on day 1), and increases in serum creatinine levels (appeared on day 7) were also observed.Multiorgan dysfunction (MOD) was frequently observed in both groups of patients. Alterations in organ function and the pattern of abnormalities were often subtle and would not be characterized as significant organ dysfunction by most available organ scoring systems. Adult respiratory distress syndrome is a manifestation of systemic disease produced by widespread increases in endothelial permeability; lung dysfunction dominates the early clinical course. When respiratory function is supported, it becomes evident that alterations occur in other organs. Multiorgan failure is really a misnomer; the term emphasizes end-stage changes. Multiorgan dysfunction is common and often resolves without progressing to MOF. Alternatively, MOD can progress to MOF.

Initial evaluation of an intracorporeal oxygenation device.

We describe a recently developed intracorporeal gas transfer device, its potential applications and hazards. To date, patients with potentially reversible respiratory failure have been treated with controlled oxygen therapy and positive pressure ventilation, but this treatment may itself contribute to lung parenchymal damage from barotrauma and oxygen toxicity. Total or partial extracorporeal gas exchange can be used to reduce these risks, but this treatment is complex and has significant morbidity and mortality. This gas exchange device has been designed to provide partial gas transfer with simplicity of insertion and use. The oxygenator lies in the vena cava to provide prepulmonary gas exchange. In preliminary studies with three calves we have shown that the device increases both mean mixed venous and arterial oxygen content and reduces mean arterial carbon dioxide tension.

Comparison of oxygen consumption measurements

To compare measurement of oxygen consumption (VO2) by spirometry and the reversed Fick method. Within-patient comparison using simultaneous measurements by the two methods, one previously calibrated on a metabolic simulator. Twenty sets of observations on eight patients (57 to 83 yrs) requiring mechanical ventilation in a critical care unit. None during or immediately before the measurements. 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). 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.

Induction of a reduction in haemoglobin concentration by enalapril in stable, moderate heart failure: a double blind study.

To study the long term effects (12 weeks) of enalapril on central haemodynamic function and on arterial oxygen content and its determinants--haemoglobin concentration and oxygen saturation--in patients with stable moderate heart failure. Double blind placebo controlled randomised study. 17 patients with stable moderate heart failure caused by dilated cardiomyopathy which was treated with diuretics and digoxin. Central haemodynamic function, arterial oxygen content, arterial haemoglobin concentration, and arterial oxygen saturation were measured at rest and during submaximal exercise. Plasma volume and total body haemoglobin were determined at rest. With enalapril treatment heart rate, pulmonary capillary wedge pressure, mean arterial pressure, and systemic vascular resistance decreased significantly both at rest and during submaximal exercise. Cardiac output did not change at rest but tended to increase (p = 0.06) during submaximal exercise. Arterial oxygen saturation remained unchanged while haemoglobin concentration and arterial oxygen content were significantly reduced. Total body haemoglobin was significantly reduced but the plasma volume remained unchanged. At rest, the reduction in arterial oxygen content resulted in a significantly reduced mixed venous oxygen content. However, during submaximal exercise the increase in cardiac output fully compensated for the reduction in arterial oxygen content and this effect was indicated by the unaltered mixed venous oxygen content. No changes were found in the placebo group after twelve weeks. Enalapril unloads the heart and reduces haemoglobin concentration. During submaximal exercise, the improvement in systemic blood flow was counterbalanced by this negative effect on the oxygen carrying capacity and systemic oxygen delivery was unchanged.

Oxygen transport in adult respiratory distress syndrome and other acute circulatory problems

To evaluate the evidence that oxygen consumption (VO2) is pathologically dependent on oxygen delivery (DO2). Studies published since 1972 with their relevant bibliographies and computerized search of MEDLINE. 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. 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. 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.