Venous Oxygen Saturation In Patients Research Articles

Evaluation of red blood cell transfusion effects in lactate and central venous oxygen saturation in patients with severe sepsis and septic shock

Red blood cell (RBC) transfusion is very often performed in critically ill patients despite its potential complications. Its effects on oxygen delivery and microcirculation are not well known. This study aimed at evaluating RBC effects in blood lactate levels (LAC) and central venous oxygen saturation (SvcO2) in patients with severe sepsis and septic shock.

Skeletal muscle oxygen saturation does not estimate mixed venous oxygen saturation in patients with severe left heart failure and additional severe sepsis or septic shock

IntroductionLow cardiac output states such as left heart failure are characterized by preserved oxygen extraction ratio, which is in contrast to severe sepsis. Near infrared spectroscopy (NIRS) allows noninvasive estimation of skeletal muscle tissue oxygenation (StO2). The aim of the study was to determine the relationship between StO2 and mixed venous oxygen saturation (SvO2) in patients with severe left heart failure with or without additional severe sepsis or septic shock.MethodsSixty-five patients with severe left heart failure due to primary heart disease were divided into two groups: groups A (n = 24) and B (n = 41) included patients without and with additional severe sepsis/septic shock, respectively. Thenar muscle StO2 was measured using NIRS in the patients and in 15 healthy volunteers.ResultsStO2 was lower in group A than in group B and in healthy volunteers (58 ± 13%, 90 ± 7% and 84 ± 4%, respectively; P < 0.001). StO2 was higher in group B than in healthy volunteers (P = 0.02). In group A StO2 correlated with SvO2 (r = 0.689, P = 0.002), although StO2 overestimated SvO2 (bias -2.3%, precision 4.6%). In group A changes in StO2 correlated with changes in SvO2 (r = 0.836, P < 0.001; ΔSvO2 = 0.84 × ΔStO2 - 0.67). In group B important differences between these variables were observed. Plasma lactate concentrations correlated negatively with StO2 values only in group A (r = -0.522, P = 0.009; lactate = -0.104 × StO2 + 10.25).ConclusionSkeletal muscle StO2 does not estimate SvO2 in patients with severe left heart failure and additional severe sepsis or septic shock. However, in patients with severe left heart failure without additional severe sepsis or septic shock, StO2 values could be used to provide rapid, noninvasive estimation of SvO2; furthermore, the trend in StO2 may be considered a surrogate for the trend in SvO2. Trial Registration: NCT00384644

Skeletal muscle oxygen saturation estimates mixed venous oxygen saturation in patients with severe left heart failure

Low cardiac output states, such as left heart failure, are characterized by a preserved oxygen extraction ratio compared with severe sepsis. Near-infrared spectroscopy (NIRS) allows noninvasive estimation of skeletal muscle tissue oxygenation (StO2). The aim of study was to determine relationship between StO2 and mixed venous oxygen saturation (SvO2) in patients with severe left heart failure with or without additional severe sepsis or septic shock.

Comparison of dexmedetomidine or midazolam on haemodynamics and mixed venous oxygen saturation in patients undergoing coronary artery bypass grafting (CABG)

Comparison of dexmedetomidine or midazolam on haemodynamics and mixed venous oxygen saturation in patients undergoing coronary artery bypass grafting (CABG)

EVALUATION OF BLOOD TRANSFUSION EFFECTS ON MIXED VENOUS OXYGEN SATURATION AND LACTATE LEVELS IN PATIENTS WITH SIRS/SEPSIS

To evaluate the effects of red blood cell transfusion in patients with SIRS/sepsis who presented hemoglobin levels under 9.0 g/dL at intensive care unit admission, using two parameters of organ perfusion: mixed venous oxygen saturation and serum lactate levels. All patients admitted to the intensive care unit with SIRS/sepsis, as defined by Consensus Conference in 1992, and hemoglobin levels under 9.0 g/dL were included. Hemoglobin levels, mixed venous oxygen saturation, and lactate levels were collected before red blood cell transfusion (pre-T) and up to 1 hour after transfusion (post-T). These variables were analyzed through a paired t test, and results were considered significant if P < .05. Twenty-nine patients (17 male, 12 female) with ages of 61.9 +/- 15.1 (mean +/- SD) years (range, 21-85 years) and a mean APACHE II score of 12.5 +/- 3.75 (7-21) were transfused with a mean of 1.41 packed red cell units. A significant increase in hemoglobin levels was reached by blood transfusion, from 8.14 +/- 0.64 g/dL (pre-T) to 9.4 +/- 0.33 g/dL (post-T), with P <.001. However, this was not accompanied by a significant change in lactate levels, from 1.87 +/- 1.22 mmol/l (pre-T) to 1.56 +/- 0.28 mmol/l (post-T), with P =.28, or in mixed venous oxygen saturation, from 64.3 +/- 8.52% (pre-T) to 67.4 +/- 6.74% (post-T), with P = .13. The results were similar even in patients with hemoglobin levels under 8.0 g/dL (n = 9). These results suggest that red blood cell transfusions, in spite of leading to a significant increase in hemoglobin levels, are not associated with an improvement in tissue oxygenation in patients with SIRS/sepsis and hemoglobin levels < 9 g/dL.

Analysis of the Factors Related to a Decrease in Jugular Venous Oxygen Saturation in Patients with Diabetes Mellitus During Normothermic Cardiopulmonary Bypass

We sought to examine what factors, including cerebrovascular carbon dioxide (CO(2)) reactivity, are related to a decrease in internal jugular venous oxygen saturation (SjvO(2)) during normothermic cardiopulmonary bypass (CPB) in patients with diabetes mellitus. Twenty-three diabetic patients scheduled to undergo elective coronary artery bypass grafting were studied. As a control, 27 age-matched control patients without diabetes mellitus were also examined. After the induction of anesthesia, a fiberoptic oximetry oxygen saturation catheter was inserted into the right jugular bulb to continuously monitor SjvO(2). Arterial and jugular venous blood gases were measured during CPB. The cerebrovascular CO(2) reactivity was measured after the induction of anesthesia and before the start of surgery using a 2.5-MHz pulsed transcranial Doppler probe. The SjvO(2) values in the diabetic group were lower than those in the control group at the initiation of CPB and at 20, 40, and 60 min after the start of CPB. The values for pre- and post-CO(2) reactivity in the control group did not significantly differ (pre-CPB: 4.8% +/- 2.3% mmHg(-1); post-CPB: 5.9% +/- 4.4% mmHg(-1)). In contrast, the values for CO(2) reactivity were lower post CPB than pre-CPB in the diabetic group (Pre-CPB: 6.3% +/- 2.9% mmHg(-1); post-CPB: 4.7% +/- 2.6% mmHg(-1); P < 0.05). In the diabetic group, glycosylated hemoglobin A1c (HbA1c) is considered to be a factor related to a decrease in SjvO(2) during CPB. Cerebrovascular CO(2) reactivity in diabetic patients decreased after the cessation of CPB but not in the control patients. In addition, HbA1c is also thought to be a factor related to a decrease in SjvO(2) in diabetic patients.

Central venous versus mixed venous oxygen saturation in patients undergoing cardiac surgery

Central venous versus mixed venous oxygen saturation in patients undergoing cardiac surgery

Mixed and central venous oxygen saturation in patients with septic shock: is there a difference?

The mixed venous oxygen saturation (mSVO2) is an important marker of global perfusion in patients with septic shock. There is some evidence that central venous oxygen saturation (cSVO2) can replace mSVO2. However, little is known about where it should be located: the superior vena cava (ccSVO2) or the right atrium (acSVO2). This study aimed at evaluating the differences between mSVO2 and cSVO2 (either from the cava or from the atrium) and the impact of them in patient management.

Monitoring mixed venous oxygen saturation in patients with obstructive shock after massive pulmonary embolism.

Patients with massive pulmonary embolism and obstructive shock usually require hemodynamic stabilization and thrombolysis. Little is known about the optimal and proper use of volume infusion and vasoactive drugs, or about the titration of thrombolytic agents in patients with relative contraindication for such treatment. The aim of the study was to find the most rapidly changing hemodynamic variable to monitor and optimize the treatment of patients with obstructive shock following massive pulmonary embolism. Ten consecutive patients hospitalized in the medical intensive care unit in the community General Hospital with obstructive shock following massive pulmonary embolism were included in the prospective observational study. Heart rate, systolic arterial pressure, central venous pressure, mean pulmonary-artery pressure, cardiac index, total pulmonary vascular-resistance index, mixed venous oxygen saturation, and urine output were measured on admission and at 1, 2, 3, 4, 8, 12, and 16 hours. Patients were treated with urokinase through the distal port of a pulmonary-artery catheter. At 1 hour, mixed venous oxygen saturation, systolic arterial pressure and cardiac index were higher than their admission values (31+/-10 vs. 49+/-12%, p<0.0001; 86+/-12 vs. 105+/-17 mmHg, p<0.01; 1.5+/-0.4 vs. 1.9+/-0.7 L/min/m2, p<0.05; respectively), whereas heart rate, central venous pressure, mean pulmonary-artery pressure and urine output remained unchanged. Total pulmonary vascular-resistance index was lower than at admission (29+/-10 vs. 21+/-12 mmHg/L/min/m2, p<0.05). The relative change of mixed venous oxygen saturation at hour 1 was higher than the relative changes of all other studied variables (p<0.05). Serum lactate on admission and at 12 hours correlated to mixed venous oxygen saturation (r=-0.855, p<0.001). In obstructive shock after massive pulmonary embolism, mixed venous oxygen saturation changes more rapidly than other standard hemodynamic variables.

Increasing mean arterial pressure improves jugular venous oxygen saturation in patients with and without preexisting stroke during normothermic cardiopulmonary bypass

Study objective To examine whether increasing mean arterial pressure (MAP) with the administration of phenylephrine would improve internal jugular venous oxygen saturation (SjvO2) during normothermic cardiopulmonary bypass (CPB) in patients with preexisting stroke. Design Prospective, controlled study. Setting Cardiovascular center and university hospital. Patients 17 patients with preexisting stroke who were scheduled for elective coronary artery bypass graft (CABG) surgery, and a control group of 17 age-matched patients without preexisting stroke. Interventions After the induction of anesthesia, a fiberoptic oximetry catheter was inserted into the right jugular bulb to monitor SjvO 2. After measuring the baseline partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values immediately before the start of the study protocol, MAP was increased by the repeated administration of a 10 μg bolus of phenylephrine, until it reached 200% of baseline values. Measurements Partial pressure of the arterial and jugular venous blood gases and cardiovascular hemodynamic values before and after the treatment were recorded. Main results There was no significant difference between the groups in SjvO 2 values at baseline (Mann-Whitney U test: p = 0.22). SjvO 2 values in both groups were increased after the administration of phenylephrine (SjvO 2 values in the control group: 60 ± 5%, SjvO 2 values in the stroke group: 57 ± 5%). There was no significant difference between the stroke and control groups in SjvO 2 values after the administration of phenylephrine (Mann-Whitney U test: p = 0.08). Conclusions Increasing MAP improves SjvO 2 in patients with or without preexisting stroke during normothermic CPB.

Guiding heart failure care by invasive hemodynamic measurements: Possible or useful?

The quest to discover effective methodologies to monitor the course of disease and response to therapeutic agents in patients with chronic heart failure continues. The relentless progression of underlying left ventricular dysfunction and periodic, severe symptomatic decompensation often requiring hospitalization remain essential features of the heart failure syndrome despite significant therapeutic advances. Clinical trials of specific therapeutic agents have shown efficacy in large groups of patients. But outcome, even with the most effective agents, is recognized to be heterogeneous for largely unexplained reasons. The idea that treatment of individual patients with heart failure could be guided by serial measurements of surrogate end points for mortality and morbidity remains attractive to clinicians. Several assumptions underlie the concept that sequential physiologic measurements such as hemodynamics can be used to guide therapy: (1) measurements indicative of clinical response during heart failure can be ascertained, albeit with varying degrees of difficulty; (2) serial determinations of these measurements, such as left ventricular dysfunction, neurohormonal activation, and central hemodynamics, will predict clinical responses to general measures and pharmacologic therapy; (3) these measurements are not sufficiently risky, expensive, or cumbersome to preclude their being obtained as a part of routine clinical practice; (4) these measurements are sufficiently reproducible to provide the basis for making therapeutic changes in individual patients; (5) continuous measurements rather than serial snapshots of, for example, hemodynamics are likely best; (6) adjustment of currently available treatment strategies will favorably effect the measures that are monitored; (7) the frequency of therapeutic adjustments and subsequent follow-up study prompted by serial measurements is feasible for most patients; and (8) monitoring physiologic aspects of the disease process will provide more benefit than expending similar resources on changes in the process of delivery of care, ie, measurements of right heart hemodynamics with medication adjustment versus patient management via a heart failure program. Magalski et al in this issue of Journal of Cardiac Failure describe one strategy for monitoring the course of chronic heart failure that begins early work to address some of these issues.

Effects of isoflurane, sevoflurane and propofol anaesthesia on jugular venous oxygen saturation in patients undergoing coronary artery bypass surgery

We investigated the effect of sevoflurane, isoflurane and propofol on jugular venous bulb oxygen saturation (SjO2) in 21 patients undergoing coronary artery bypass graft surgery (CABG) during and after normothermic cardiopulmonary bypass (CPB). Patients received a standardized anaesthetic consisting of fentanyl, midazolam and were then randomly allocated to receive either isoflurane, sevoflurane or propofol for maintenance. SjO2 values were significantly lower than baseline 1 h after CPB in the propofol but not the isoflurane or the sevoflurane groups. Furthermore, SjO2 values were significantly higher during CPB in the isoflurane group (P = 0.0081) and significantly lower 6 h after CPB in the sevoflurane group (P = 0.0447) when compared to the propofol group. We conclude that jugular venous desaturation during and after normothermic CPB is more likely during propofol anaesthesia.

The Effect of Hyperventilation and Hyperoxia on Cerebral Venous Oxygen Saturation in Patients with Traumatic Brain Injury

The Effect of Hyperventilation and Hyperoxia on Cerebral Venous Oxygen Saturation in Patients with Traumatic Brain Injury

The Effect of Hyperventilation and Hyperoxia on Cerebral Venous Oxygen Saturation in Patients with Traumatic Brain Injury

Eighteen head-injured patients undergoing hyperventilation were studied for changes in jugular venous oxygen saturation (SjvO2) and arteriovenous oxygen content difference (AVDO2) in response to changes in PaO2 and PaCO2. SjvO2 decreased significantly from 66% +/- 3% to 56% +/- 3% (mean +/- SD) when PaCO2 decreased from 30 to 25 mm Hg at a PaO2 of 100-150 mm Hg. SjvO (2) values returned to baseline (66% +/- 2%) when PaCO2 was restored to 30 mm Hg. Repetition of the study at a PaO2 of 200-250 mm Hg produced a similar pattern. However, SjvO2 values were significantly greater with PaO2 within the range of 200-250 mm Hg (77% +/- 4% and 64% +/- 3%) than SjvO2 measured at a PaO2 of 100-150 mm Hg at PaCO2 values of both 30 and 25 mm Hg. AVDO2 also improved with a PaO2 of 200-250 mm Hg at each PaCO2 (P < 0.001). In conclusion, decreases in SjvO2 associated with decreases in PaCO2 may be offset by increasing PaO2. Implications: The adequacy of cerebral oxygenation can be estimated in head-injured patients by monitoring jugular bulb oxygen saturation and the arteriovenous oxygenation content difference. Increasing the partial pressure of arterial oxygen above normal offset deleterious effects of hyperventilation on jugular bulb oxygen saturation and arteriovenous oxygenation content difference in head-injured patients. (Anesth Analg 1998;87:850-3)

The effect of hyperventilation and hyperoxia on cerebral venous oxygen saturation in patients with traumatic brain injury.

Eighteen head-injured patients undergoing hyperventilation were studied for changes in jugular venous oxygen saturation (SjvO2) and arteriovenous oxygen content difference (AVDO2) in response to changes in PaO2 and PaCO2. SjvO2 decreased significantly from 66% +/- 3% to 56% +/- 3% (mean +/- SD) when PaCO2 decreased from 30 to 25 mm Hg at a PaO2 of 100-150 mm Hg. SjvO2 values returned to baseline (66% +/- 2%) when PaCO2 was restored to 30 mm Hg. Repetition of the study at a PaO2 of 200-250 mm Hg produced a similar pattern. However, SjvO2 values were significantly greater with PaO2 within the range of 200-250 mm Hg (77% +/- 4% and 64% +/- 3%) than SjvO2 measured at a PaO2 of 100-150 mm Hg at PaCO2 values of both 30 and 25 mm Hg. AVDO2 also improved with a PaO2 of 200-250 mm Hg at each PaCO2 (P < 0.001). In conclusion, decreases in SjvO2 associated with decreases in PaCO2 may be offset by increasing PaO2. The adequacy of cerebral oxygenation can be estimated in head-injured patients by monitoring jugular bulb oxygen saturation and the arteriovenous oxygenation content difference. Increasing the partial pressure of arterial oxygen above normal offset deleterious effects of hyperventilation on jugular bulb oxygen saturation and arteriovenous oxygenation content difference in head-injured patients.

Continuous Monitoring of Mixed Venous Oxygen Saturation in Patients with Acute Myocardial Infarction

Continuous measurement of mixed venous oxygen saturation (SvO2) has been suggested as an adjunct in monitoring critically ill patients. We evaluated SvO2 monitoring in 24 patients suffering from complicated myocardial infarctions. Cardiac output and arterial lactate levels were measured when there were persistent 5 percent changes in SvO2, and otherwise, every 12 hours or as indicated clinically. Increases in SvO2 by 5 and 10 percent corresponded with an increase in cardiac index in 78.5 percent and 75 percent of measurements, respectively. Decreases in SvO2 by 5 and 10 percent corresponded with decreases in cardiac index in 45.5 percent and 61 percent of measurements. Twenty percent changes in cardiac index showed dissimilar directional changes with SvO2 in 62 percent of cases. Arterial blood lactate levels correlated poorly with SvO2. Survivors had significantly higher mean SvO2 and cardiac indices than nonsurvivors (p less than 0.01). The clinical management of patients with myocardial infarction may not be altered in view of the limitations of SvO2 in reflecting tissue hypoxia. We conclude that continuous monitoring of SvO2 may not be a sensitive measure of cardiac output after acute myocardial infarction.

Measurement of central venous oxygen saturation in patients with myocarial infarction.

Central venous oxygen saturation (CVSO 2 ) was measured in 31 patients with myocardial infarction. CVSO 2 correlated well with the patients' clinical course. In those patients not in heart failure, mean ± sem for CVSO 2 was 70 ± 1%. When heart failure was present, CVSO 2 averaged 56 ± 1%. When both heart failure and shock were present, CVSO 2 averaged 43 ± 1%. In nine patients, serial determinations of arterial oxygen saturation and CVSO 2 were made. In 22 of 26 instances, either a fall in CVSO 2 was accompanied by an increase in the arteriovenous oxygen saturation difference or an increase in CVSO 2 was accompanied by a decrease in arteriovenous oxygen saturation difference. Serial measurements of CVSO 2 appear to be a useful method of monitoring changes in myocardial function in patients with myocardial infarction.