Venous Oxygen Tension Research Articles

Mixed venous oxygen tension is a crucial prognostic factor in pulmonary hypertension: a retrospective cohort study

BackgroundThe prognostic value of mixed venous oxygen tension (PvO2) at pulmonary hypertension diagnosis treated with selective pulmonary vasodilators remains unclear. This study sought to investigate the association of PvO2 with long-term prognosis in pulmonary arterial hypertension (PAH) and medically treated chronic thromboembolic pulmonary hypertension (CTEPH) and to identify the distinct mechanisms influencing tissue hypoxia in patients with CTEPH or PAH.MethodsWe retrospectively analyzed data from 138 (age: 50.2 ± 16.6 years, 81.9% women) and 268 (age: 57.4 ± 13.1 years, 72.8% women) patients with PAH and CTEPH, respectively, diagnosed at our institution from 1983 to 2018. We analyzed the survival rates of patients with/without tissue hypoxia (PvO2 < 35 mmHg) and identified their prognostic factors based on the pulmonary hypertension risk stratification guidelines.ResultsSurvival was significantly poorer in patients with tissue hypoxia than in those without it for PAH (P = 0.001) and CTEPH (P = 0.017) treated with selective pulmonary vasodilators. In patients with PAH, PvO2 more strongly correlated with prognosis than other hemodynamic prognostic factors regardless of selective pulmonary vasodilators usage. PvO2 was the only significant prognostic factor in patients with CTEPH treated with pulmonary hypertension medication. Patients with CTEPH experiencing tissue hypoxia exhibited significantly poorer survival than those in the intervention group (P < 0.001). PvO2 more strongly correlated with the cardiac index (CI) than the alveolar-arterial oxygen gradient (A-aDO2) in PAH; whereas in CTEPH, PvO2 was more strongly correlated with A-aDO2 than with CI.ConclusionsPvO2 may represent a crucial prognostic factor for pulmonary hypertension. The prognostic impact of tissue hypoxia affects different aspects of PAH and CTEPH, thereby reflecting their distinct pathogenesis.

The physiological basis of pulmonary arterial hypertension.

Pulmonary arterial hypertension (PAH) is a rare dyspnoea-fatigue syndrome caused by a progressive increase in pulmonary vascular resistance and eventual right ventricular (RV) failure. In spite of extensive pulmonary vascular remodelling, lung function in PAH is generally well preserved, with hyperventilation and increased physiological dead space, but minimal changes in lung mechanics and only mild to moderate hypoxaemia and hypocapnia. Hypoxaemia is mainly caused by a low mixed venous oxygen tension from a decreased cardiac output. Hypocapnia is mainly caused by an increased chemosensitivity. Exercise limitation in PAH is cardiovascular rather than ventilatory or muscular. The extent of pulmonary vascular disease in PAH is defined by multipoint pulmonary vascular pressure–flow relationships with a correction for haematocrit. Pulsatile pulmonary vascular pressure–flow relationships in PAH allow for the assessment of RV hydraulic load. This analysis is possible either in the frequency domain or in the time domain. The RV in PAH adapts to increased afterload by an increased contractility to preserve its coupling to the pulmonary circulation. When this homeometric mechanism is exhausted, the RV dilates to preserve flow output by an additional heterometric mechanism. Right heart failure is then diagnosed by imaging of increased right heart dimensions and clinical systemic congestion signs and symptoms. The coupling of the RV to the pulmonary circulation is assessed by the ratio of end-systolic to arterial elastances, but these measurements are difficult. Simplified estimates of RV–pulmonary artery coupling can be obtained by magnetic resonance or echocardiographic imaging of ejection fraction.

Central venous–arterial CO2 pressure difference in correlation to dynamic changes of serum lactate level in patients with polytrauma

Background and aim of work Early diagnosis, rapid intervention, and correction of tissue hypoperfusion are the major aims in the management of polytraumatized patients. The venous-to-arterial carbon dioxide tension difference is a marker of the adequacy of cardiac output to global metabolic demand, and so, its detection is a helpful method to determine patients who stay under resuscitation way. Regarding this, its monitoring could help the physicians to make the decision to give treatment targeting at improving cardiac output. Patients and methods This is a prospective single-center observational study done on 40 patients with polytrauma admitted to Assiut University Hospital resuscitation room and followed for the first 12 h of ICU stay. At the start of resuscitation, central venous and arterial blood samples were obtained to estimate the mixed venous-to-arterial carbon dioxide tension difference from the baseline values. All consecutive paired blood samples were collected for each studied patient within the following first hour, after the sixth hour, and after the 12th hour. Other data collection Hourly urine output during the early 12 h, kidney function, and hemodynamics of arterial carbon dioxide tension, arterial oxygen tension, central venous carbon dioxide tension, and central venous oxygen tension were assessed. Arterial oxygen saturation and mixed venous oxygen saturation, arterial and central venous lactate, hemoglobin concentration, and ICU stay were examined as well. Results The differences between arterial tenson and oxygen tension showed insignificant differences. There were changes in the mixed venous-to-arterial carbon dioxide tension difference over time period. Comparison between basal value and the follow-up results showed insignificant difference as well. There was significant difference between baseline lactate level and its corresponding measure at the 12th hour after resuscitation reflecting to somewhat optimal resuscitation. The hemodynamic changes (increases) over time included mean arterial blood pressure and central venous pressure. There were significant changes during the whole follow-up period in comparison with the baseline values. Urine output showed significant increases over time when compared with the second hour urine volume. There is significant correlation between blood lactate level and the difference between venous and arterial oxygen after 6 h of resuscitation; this was a strong positive correlation. The difference between blood lactate level and the difference between venous and arterial carbon dioxide is statistically significant at the baseline of resuscitation there is a moderate positive correlation. Conclusion Central venous–arterial carbon dioxide pressure difference in correlation to dynamic changes of serum lactate could be used as an indicator of tissue perfusion in patients with polytrauma.

How Do We Monitor Oxygenation during the Management of PPHN? Alveolar, Arterial, Mixed Venous Oxygen Tension or Peripheral Saturation?

Oxygen is a pulmonary vasodilator and plays an important role in mediating circulatory transition from fetal to postnatal period. Oxygen tension (PO2) in the alveolus (PAO2) and pulmonary artery (PaO2) are the main factors that influence hypoxic pulmonary vasoconstriction (HPV). Inability to achieve adequate pulmonary vasodilation at birth leads to persistent pulmonary hypertension of the newborn (PPHN). Supplemental oxygen therapy is the mainstay of PPHN management. However, optimal monitoring and targeting of oxygenation to achieve low pulmonary vascular resistance (PVR) and optimizing oxygen delivery to vital organs remains unknown. Noninvasive pulse oximetry measures peripheral saturations (SpO2) and a target range of 91–95% are recommended during acute PPHN management. However, for a given SpO2, there is wide variability in arterial PaO2, especially with variations in hemoglobin type (HbF or HbA due to transfusions), pH and body temperature. This review evaluates the role of alveolar, preductal, postductal, mixed venous PO2, and SpO2 in the management of PPHN. Translational and clinical studies suggest maintaining a PaO2 of 50–80 mmHg decreases PVR and augments pulmonary vasodilator management. Nevertheless, there are no randomized clinical trials evaluating outcomes in PPHN targeting SpO2 or PO2. Also, most critically ill patients have umbilical arterial catheters and postductal PaO2 may not be an accurate assessment of oxygen delivery to vital organs or factors influencing HPV. The mixed venous oxygen tension from umbilical venous catheter blood gas may assess pulmonary arterial PO2 and potentially predict HPV. It is crucial to conduct randomized controlled studies with different PO2/SpO2 target ranges for the management of PPHN and compare outcomes.

Efficacy of Almitrine in the Treatment of Hypoxemia in Sars-Cov-2 Acute Respiratory Distress Syndrome

Efficacy of Almitrine in the Treatment of Hypoxemia in Sars-Cov-2 Acute Respiratory Distress Syndrome

Brain Hypoxia Secondary to Diffusion Limitation in Hypoxic Ischemic Brain Injury Postcardiac Arrest.

We sought to characterize 1) the difference in the diffusion gradient of cellular oxygen delivery and 2) the presence of diffusion limitation physiology in hypoxic-ischemic brain injury patients with brain hypoxia, as defined by parenchymal brain tissue oxygen tension less than 20 mm Hg versus normoxia (brain tissue oxygen tension > 20 mm Hg). Post hoc subanalysis of a prospective study in hypoxic-ischemic brain injury patients dichotomized into those with brain hypoxia versus normoxia. Quaternary ICU. Fourteen adult hypoxic-ischemic brain injury patients after cardiac arrest. Patients underwent monitoring with brain oxygen tension, intracranial pressure, cerebral perfusion pressure, mean arterial pressure, and jugular venous bulb oxygen saturation. Data were recorded in real time at 300Hz into the ICM+ monitoring software (Cambridge University Enterprises, Cambridge, United Kingdom). Simultaneous arterial and jugular venous bulb blood gas samples were recorded prospectively. Both the normoxia and hypoxia groups consisted of seven patients. In the normoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen tension, and cerebral perfusion pressure were 29 mm Hg (SD, 9), 45 mm Hg (SD, 9), and 80 mm Hg (SD, 7), respectively. In the hypoxia group, the mean brain tissue oxygen tension, jugular venous bulb oxygen to brain tissue oxygen tension gradient, and cerebral perfusion pressure were 14 mm Hg (SD, 4), 53 mm Hg (SD, 8), and 72 mm Hg (SD, 6), respectively. There were significant differences in the jugular venous bulb oxygen tension-brain oxygen tension gradient (16 mm Hg [sd, 6] vs 39 mm Hg SD, 11]; p < 0.001) and in the relationship of jugular venous bulb oxygen tension-brain oxygen tension gradient to cerebral perfusion pressure (p = 0.004) when comparing normoxia to hypoxia. Each 1 mm Hg increase in cerebral perfusion pressure led to a decrease in the jugular venous bulb oxygen tension-brain oxygen tension gradient by 0.36 mm Hg (95% CI, -0.54 to 0.18; p < 0.001) in the normoxia group, but no such relation was demonstrable in the hypoxia group. In hypoxic-ischemic brain injury patients with brain hypoxia, there is an elevation in the jugular venous bulb oxygen tension-brain oxygen tension gradient, which is not modulated by changes in cerebral perfusion pressure.

Validity of Peripheral Capillary Oxygen Saturation and Normal Mixed Venous Oxygen Tension in Measurement of O2 Content

Background The change in venous oxygen saturation occurs earlier, and even its reduction is faster than arterial oxygen saturation. The aim of this study was to validate SvO2 and PvO2 for O2 content measurement in children hospitalized with respiratory distress. Materials and Methods In this cross-sectional study, 80 children who were admitted with respiratory distress were included in the study according to the study inclusion and exclusion criteria. Baseline characteristics such as age and gender were recorded in the data collection form, designed by the researcher. In order to determine the amount of SaO2 and PaO2 the arterial blood sample was prepared, venous blood sample was prepared to determine the amount of hemoglobin, SvO2 and PvO2. The gold standard for the determination of O2 content was the arterial blood sample. All samples were examined by a blood gas analyzer and then calculated using the formula of O2 content values. For SvO2 and PvO2 validation, we used diagnostic analysis methods including sensitivity, specificity, positive and negative predictive values. Cut-point value for SvO2 and PvO2 were 76.50 and 44.30, respectively. Results In this study, the patients’ mean age was 5.15 ± 4.20 years. 62.5% (n=50) were male and 38.5% (n=30) were female. The values ​​of arterial and venous O2 content were 14.13 ± 3.05 and 11.95 ± 3.04 from a total of 80 patients. SvO2 and PvO2 for measuring O2 content had a sensitivity of 80.5 and 71.80%, respectively, and specificity of 80.5 and 78%, respectively. Conclusion SvO2 and PvO2 have good validity for evaluating O2 content in patients admitted to PICU. So that SvO2 had a sensitivity and specificity of over 80%, and PvO2 had a sensitivity and specificity of over 70%.

Pulmonary hypertension with a low cardiac index requires a higher PaO2 level to avoid tissue hypoxia.

The optimal oxygen supplementation needed to avoid tissue hypoxia in patients with pulmonary hypertension (PH) remains unclear. This study aimed to identify the arterial oxygen tension (PaO2 ) level needed to avoid tissue hypoxia which results in a poor prognosis in patients with PH. We retrospectively analysed the data for 1571 right heart catheterizations in patients suspected of having PH between 1983 and 2017 at our institution. Examinations were classified according to mean pulmonary arterial pressure (mPAP), cardiac index (CI) and the presence of lung disease, pulmonary arterial hypertension (PAH) or chronic thromboembolic PH (CTEPH). The PaO2 levels needed to avoid tissue hypoxia were compared in each subgroup. The estimated PaO2 equivalent to a mixed venous oxygen tension (PvO2 ) of 35 mm Hg (tissue hypoxia) was 63.2 mm Hg in all patients, 77.0 mm Hg in those with decreased CI (<2.5 L/min/m2 ) and 57.0 mm Hg in those with preserved CI. Multivariate regression analysis identified mPAP, CI and PaO2 to be independent predictors of extremely low PvO2 . Similar results were observed regardless of the severity of PH or the presence of lung disease, PAH or CTEPH. The PaO2 level needed to avoid tissue hypoxia was higher in patients with mild PH and decreased CI than in those with severe PH and preserved CI (70.2 vs 61.5 mm Hg). These findings indicate that a decreased CI rather than increased mPAP induces tissue hypoxia in PH. Patients with PH and decreased CI may need adjustment of oxygen therapy at higher PaO2 levels compared with patients with preserved CI.

Dobutamine and Nitroglycerin Versus Milrinone for Perioperative Management of Pulmonary Hypertension in Mitral Valve Surgery. A Randomized Controlled Study

To compare the effects of dobutamine and nitroglycerin to milrinone in young patients with severe pulmonary hypertension undergoing mitral valve replacement. A prospective randomized, double-blinded, controlled study. Single university hospital. Forty patients had systolic pulmonary arterial pressure ≥60 mmHg and were scheduled for elective mitral valve replacement. The patients were divided randomly into 2 equal groups according to the drugs given during the study. The patients in group I received 5 to 20 µg/kg/min of dobutamine and 0.5 to 3 µg/kg/min of nitroglycerin, and patients in group II received a loading dose of milrinone, 50 µg/kg over 10 minutes, followed by a maintenance dose of 0.25 to 0.75 µg/kg/min. The primary outcome was the effects of interventional drugs on mean pulmonary artery pressure. The secondary outcomes were the effects of interventional drugs on systemic and pulmonary hemodynamic parameters measured from induction of anesthesia until the first 12 hours in the intensive care unit stay. There was a more significant decrease in mean pulmonary artery pressure, pulmonary capillary wedge pressure, and central venous pressure in group II than group I at all time points after cardiopulmonary bypass. There were more significant increases in heart rate, mean arterial pressure, cardiac output, and mixed venous oxygen tension in group I than group II, which became more obvious in time. In both groups, there was a significant decrease in systemic vascular resistance and pulmonary vascular resistance at all times. Milrinone provides adequate cardiac performance, causing a greater reduction in pulmonary artery pressure and pulmonary capillary wedge pressure.

Comparison of different methods to calculate venous admixture in anaesthetized horses

ObjectiveThe aim of this study was to compare different methods to determine venous admixture (Q˙s/Q˙t) in anaesthetized horses. The first objective was to estimate Q˙s/Q˙t using jugular venous blood oxygen content (Q˙s/Q˙t jugular), and a fixed value for the oxygen extraction (F-shunt). The second objective was to assess the influence of blood pressure and positioning on oxygen extraction. The third objective was to perform regression analysis between jugular and mixed venous blood oxygen tensions. Study designProspective, experimental trial. AnimalsThe study was performed with seven warmblood horses that were anaesthetized with detomidine, butorphanol, ketamine, diazepam and isoflurane in oxygen. MethodsMultiple simultaneous arterial, jugular venous and pulmonary arterial blood samples were taken under normotensive and hypotensive conditions in lateral and dorsal recumbency. Arterial, mixed venous, and end-capillary oxygen content were calculated. ResultsA significant correlation between Q˙s/Q˙t and Q˙s/Q˙t jugular was found [intraclass correlation coefficient (ICC) = 0.68, p < 0.001], and Bland–Altman analysis showed a bias of –11.5% and wide limits of agreement (–27.7% to 4.6%). F-shunt significantly correlated with Q˙s/Q˙t (ICC = 0.88, p < 0.001), and Bland–Altman analysis showed a lower bias (–1.97) and narrower limits of agreement (–13.8% to 9.9%). Positioning and blood pressure significantly influenced oxygen extraction. The regression formula was Y = 0.80X + 2.61 (where Y is the calculated mixed venous oxygen tension and X is the jugular venous oxygen tension) when outliers were excluded (ICC=0.82, p < 0.001). Conclusions and clinical relevanceThis study shows that F-shunt provides reasonable estimates of Q˙s/Q˙t but can possibly be improved by using simple algorithms without the need for pulmonary arterial catheterization. These algorithms use blood pressure- and positioning-dependent oxygen extraction and regression analysis between jugular venous and pulmonary arterial oxygen tension. Although promising, the validity of these algorithms needs to be determined in future studies.

Differential Effects of Low-Dose Erythropoietin in Rat Model of Diabetic Nephropathy

Background. Previous reports on the renoprotective effect of erythropoietin (EPO) in the setting of chronic kidney disease (CKD) have yielded conflicting results. The aim of this study is to clarify the effect of low, non-hematopoietic dose of EPO on the evolution of diabetic nephropathy (DN) in rat model. Methods. Low dose of recombinant human EPO (150 U/kg, s.c. three times/week) was given to streptozotocin (STZ)-induced diabetic rats in two schedules; in the first one, EPO was given from day 2 after STZ injection till the end of the study (28 weeks) as prophylactic treatment; and in the other schedule EPO was given after development of DN (last 8 weeks) as therapeutic treatment. Albuminuria, blood pressure, creatinine clearance, renal venous oxygen tension (vPO2), plasma EPO, hematocrit and renal histopathology were assessed. Results. Unexpectedly, 28 weeks administration of EPO to diabetic rats led to aggravation of albuminuria and worsening of histopathological damage in spite of partial correction of renal hypoxia. Contrary to this, terminal 8 weeks EPO therapy of DN reduced albuminuria and demonstrated some favorable effects on biochemical changes and histologic picture. Conclusion. Low dose EPO exerted differential effects in rat model of DN according to treatment duration. In addition, findings of the present study warrants further investigations of the exact renoprotective role of EPO in diabetic patients with CKD who receive EPO therapy for long periods.

Effects of Changes in Arterial Carbon Dioxide and Oxygen Partial Pressures on Cerebral Oximeter Performance.

Cerebral oximetry (cerebral oxygen saturation; ScO2) is used to noninvasively monitor cerebral oxygenation. ScO2 readings are based on the fraction of reduced and oxidized hemoglobin as an indirect estimate of brain tissue oxygenation and assume a static ratio of arterial to venous intracranial blood. Conditions that alter cerebral blood flow, such as acute changes in PaCO2, may decrease accuracy. We assessed the performance of two commercial cerebral oximeters across a range of oxygen concentrations during normocapnia and hypocapnia. Casmed FORE-SIGHT Elite (CAS Medical Systems, Inc., USA) and Covidien INVOS 5100C (Covidien, USA) oximeter sensors were placed on 12 healthy volunteers. The fractional inspired oxygen tension was varied to achieve seven steady-state levels including hypoxic and hyperoxic PaO2 values. ScO2 and simultaneous arterial and jugular venous blood gas measurements were obtained with both normocapnia and hypocapnia. Oximeter bias was calculated as the difference between the ScO2 and reference saturation using manufacturer-specified weighting ratios from the arterial and venous samples. FORE-SIGHT Elite bias was greater during hypocapnia as compared with normocapnia (4 ± 9% vs. 0 ± 6%; P < 0.001). The INVOS 5100C bias was also lower during normocapnia (5 ± 15% vs. 3 ± 12%; P = 0.01). Hypocapnia resulted in a significant decrease in mixed venous oxygen saturation and mixed venous oxygen tension, as well as increased oxygen extraction across fractional inspired oxygen tension levels (P < 0.0001). Bias increased significantly with increasing oxygen extraction (P < 0.0001). Changes in PaCO2 affect cerebral oximeter accuracy, and increased bias occurs with hypocapnia. Decreased accuracy may represent an incorrect assumption of a static arterial-venous blood fraction. Understanding cerebral oximetry limitations is especially important in patients at risk for hypoxia-induced brain injury, where PaCO2 may be purposefully altered.

Effect of Acute Transfusion on Cerebral Oxygenation in Patients with Sickle Cell Disease

Introduction : The molecular abnormality in sickle hemoglobin (HbS) produces a unique cellular pathology characterized by fragile and rigid red blood cells which block the microcirculation, which, in concert with large vessel vasculopathy and the anemia of sickle cell disease (SCD), compromises oxygen delivery to the brain and other organs. Long-term, periodic transfusions are commonly used to prevent and ameliorate neurologic complications related to vasculopathy, particularly stroke. Despite widespread use of transfusions, little is known about the physiological effects on cerebral O2 delivery, which represents an integration of multiple, potentially opposing processes. While increased hematocrit improves O2 carrying capacity, the consequent elevation of blood viscosity has the potential to impede blood flow to cerebral tissue. Also, 2,3-BPG levels in stored blood are depleted, temporarily impairing O2 delivery. Advances in cerebral oximetry (using near infrared spectroscopy) provide an opportunity to address these issues directly to study cerebral oxygenation following transfusions in SCD. The FORE-SIGHT© cerebral oximeter (CAS Medical Systems) measures cerebral tissue hemoglobin saturation (SCTO2), a mixture of arterial and venous oxygen saturation (30:70) in a voxel of tissue near the gray-white junction in the frontal lobes. Using measured arterial Hb saturation (SaO2) by peripheral pulse oximetry and SCTO2 by cerebral oximetry, cerebral venous Hb saturation (SvO2) can be derived. Additionally, using a measured HbO2 affinity curve derived at the time of SCTO2 determination, SvO2 can be converted to venous oxygen tension, PvO2. PvO2 is in dynamic equilibrium with tissue oxygen tension and represents the best estimate of tissue oxygenation. The primary objective of this study was to use cerebral oximetry to assess and monitor cerebral tissue oxygenation following an elective pre-operative RBC transfusion.Methods : This pilot prospective cohort study enrolled 12 patients with sickle cell anemia (SS, Sb0 thalassemia) in steady-state, who had elective, pre-operative transfusions. Patients who had received transfusion within 3 months or had known cerebral vasculopathy were excluded. Nine patients completed the planned 3 months of study follow up. Two patients were taken off study within a week of enrollment because of difficulties with cerebral oximetry measurements. One did not follow-up after 2 months of participation. Each patient had measurements of SCTO2 prior to the initiation of transfusion, continuously during transfusion, and at predetermined times points post-transfusion, for up to 3 months. Other parameters related to cerebral Hb oxygenation were also measured, including Hb, HbA, HbF, HbS, P50 and 2,3-BPG. The relationship between cerebral oxygenation with age and other predictors of oxygenation was assessed using linear mixed models. The first two post-transfusion measurements (within 96 hours) were compared against pre-transfusion measurements using Wilcoxon signed-rank tests.Results : SCTO2 was significantly associated with age (p=0.02), Hb (p=0.01) and HbA % (p=0.03 (Table 1). Immediately post-transfusion, SCTO2, increased from median values of 58% to 68.5%, p 0.004 (Table 2). Arterial saturation (SaO2) was unchanged post-transfusion, thus the increase in SCTO2 resulted in an increased (calculated) venous saturation (SvO2). P50 fell post transfusion, as expected, and despite increased SvO2, PvO2 remained unchanged. Arterial and venous oxygen content (CaO2, CvO2) increased post transfusion as expected because Hb and SvO2 increased. However, the difference in arterial and venous oxygen content (CdO2 = CaO2 - CvO2) remained unchanged after transfusion. Similar trends in these parameters were observed in second measurements made up to 96 hours after transfusion (Table 2). Since oxygen delivery equals CdO2 × blood flow, cerebral oxygen delivery would only increase if blood flow were increased by transfusion, contrary to reports {Neurology. 1989 Mar;39(3):344-8; Stroke 25:2153-8, 1994}.Conclusion: Although cerebral hemoglobin oxygen saturation (SCTO2) increased after acute transfusion, calculated tissue oxygen tension (PvO2) and apparent oxygen delivery (CdO2) remained unchanged, providing no evidence for acute improvement in cerebral oxygenation after transfusion in SCD. [Display omitted] DisclosuresQuinn:Global Blood Therapeutics: Research Funding.

A randomised comparison of bolus phenylephrine and ephedrine for the management of spinal hypotension in patients with severe preeclampsia and fetal compromise

BackgroundStudies in healthy patients undergoing elective caesarean delivery show that, compared with phenylephrine, ephedrine used to treat spinal hypotension is associated with increased fetal acidosis. This has not been investigated prospectively in women with severe preeclampsia. MethodsPatients with preeclampsia requiring caesarean delivery for a non-reassuring fetal heart tracing were randomised to receive either bolus ephedrine (7.5–15mg) or phenylephrine (50–100µg), to treat spinal hypotension. The primary outcome was umbilical arterial base excess. Secondary outcomes were umbilical arterial and venous pH and lactate concentration, venous base excess, and Apgar scores. ResultsAmong 133 women, 64 who required vasopressor treatment were randomised into groups of 32 with similar patient characteristics. Pre-delivery blood pressure changes were similar. There was no difference in mean [standard deviation] umbilical artery base excess (−4.9 [3.7] vs −6.0 [4.6] mmol/L for ephedrine and phenylephrine respectively; P=0.29). Mean umbilical arterial and venous pH and lactate concentrations did not significantly differ between groups (7.25 [0.08] vs 7.22 [0.10], 7.28 [0.07] vs 7.27 [0.10], and 3.41 [2.18] vs 3.28 [2.44] mmol/L respectively). Umbilical venous oxygen tension was higher in the ephedrine group (2.8 [0.7] vs 2.4 [0.62]) kPa, P=0.02). There was no difference in 1- or 5-min Apgar scores, numbers of neonates with 1-min Apgar scores <7 or with a pH <7.2. ConclusionsIn patients with severe preeclampsia and fetal compromise, fetal acid-base status is independent of the use of bolus ephedrine versus phenylephrine to treat spinal hypotension.

Microvascular Perfusion Heterogeneity Impairs Oxygenation and Contributes to Peripheral Vascular Disease in Metabolic Syndrome

Development of the metabolic syndrome in obese Zucker rats (OZR) is associated with impaired fatigue‐resistance of in situ skeletal muscle paralleling a blunted functional hyperemia. However, recent studies suggest that reduced bulk oxygen delivery to skeletal muscle with elevated metabolic demand may not explain the compromised muscle performance. Using novel experimental data and recent insight into altered microvascular perfusion in OZR, we developed a simulation for tissue oxygenation with increasing metabolic demand in lean (LZR) and OZR skeletal muscle using physiologically‐realistic data and relationships. With elevated metabolic demand, blood flow to, and oxygen uptake by, in situ skeletal muscle increased in both strains, although the response was blunted in OZR. However, venous blood oxygen tension (PvO2) draining the muscle of OZR was elevated versus LZR across metabolic demands; a paradoxical response given assumptions of increased microvascular residency time in OZR. Using a microvascular network model of multiple Krogh cylinders supplied by a network with homogeneous flow distribution at bifurcations (γ=0.5), we were unable to simulate tissue oxygenation and PvO2 differences between LZR and OZR. However, with introduction of increasing perfusion asymmetry (γ&gt;0.5), changes to microvascular hematocrit and increased plasma skimming throughout the network, our ability to simulate the experimental results was much improved. As a result, our data suggest that increased perfusion asymmetry (γ) within the muscle microcirculation is not only a defining characteristic of metabolic syndrome, it is required to effectively model and understand alterations in blood‐tissue oxygen exchange in this highly translationally relevant model of human disease risk.Support or Funding InformationNational Institutes of Health and American Heart Association

Cardiac oxygen limitation during an acute thermal challenge in the European perch: effects of chronic environmental warming and experimental hyperoxia

Oxygen supply to the heart has been hypothesized to limit cardiac performance and whole animal acute thermal tolerance (CTmax) in fish. We tested these hypotheses by continuously measuring venous oxygen tension (Pvo2) and cardiovascular variables in vivo during acute warming in European perch (Perca fluviatilis) from a reference area during summer (18°C) and a chronically heated area (Biotest enclosure) that receives warm effluent water from a nuclear power plant and is normally 5-10°C above ambient (24°C at the time of experiments). While CTmax was 2.2°C higher in Biotest compared with reference perch, the peaks in cardiac output and heart rate prior to CTmax occurred at statistically similar Pvo2 values (2.3-4.0 kPa), suggesting that cardiac failure occurred at a common critical Pvo2 threshold. Environmental hyperoxia (200% air saturation) increased Pvo2 across temperatures in reference fish, but heart rate still declined at a similar temperature. CTmax of reference fish increased slightly (by 0.9°C) in hyperoxia, but remained significantly lower than in Biotest fish despite an improved cardiac output due to an elevated stroke volume. Thus, while cardiac oxygen supply appears critical to elevate stroke volume at high temperatures, oxygen limitation may not explain the bradycardia and arrhythmia that occur prior to CTmax Acute thermal tolerance and its thermal plasticity can, therefore, only be partially attributed to cardiac failure from myocardial oxygen limitations, and likely involves limiting factors on multiple organizational levels.

Central venous saturation in septic shock: co-oximetry vs gasometry

ObjectivesCentral venous oxygen saturation calculated by gasometry (Gaso-Scvo2) is more available than central venous oxygen saturation measured by co-oximetry (Co-oxy-Scvo2) in environments with less resources and underdeveloped countries. Therefore, we aimed to determine the agreement between Co-oxy-Scvo2 and Gaso-Scvo2 and between central venous oxygen tension measured by gasometry (Gaso-Pcvo2) and Co-oxy-Scvo2, respectively. Design and settingsThis is a prospective study in a university hospital’s intensive care unit. PatientsSixteen patients were studied during the first 48 hours after diagnosis of septic shock. All patients were intubated, connected to mechanical ventilation, and resuscitated according to the standards of care. Measurements and resultsOne hundred eleven pairs of central venous blood measurements were analyzed both by conventional gasometry and co-oximetry. Bland and Altman analysis between Co-oxy-Scvo2 and Gaso-Scvo2 showed lack of agreement (1.7 [−10.7, +14.2]). A Gaso-Scvo2 less than 70% had a positive predictive value of 63% in relation to Co-oxy-Scvo2, and its negative predictive value was 90% with 20% false-positives and 5% false-negatives. The area under the receiver operator characteristic curve of Gaso-Pcvo2 to discriminate a Co-oxy-Scvo2 greater than or equal to 70% was 0.87 (confidence interval, 0.80-0.93), and the best cut-off point was a Gaso-Pcvo2 more than 40 mm Hg, (sensitivity, 75%; specificity, 93%). ConclusionsThe reliability of Gaso-Scvo2 determination during the resuscitation phase of septic shock is not acceptable. There is a good agreement between a Gaso-Pcvo2 more than 40 mm Hg and a Co-oxy-Scvo2 greater than or equal to 70%. Our results suggest that given these limitations, Gaso-Scvo2 results should be interpreted with caution, helped by Gaso-Pcvo2 measurements and in context with other perfusion parameters.

Monitoring the effects of propofol and sevoflurane on cerebral oxygen supply-demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery

Background Increasing awareness of neurologic abnormalities associated with congenital heart surgical intervention has heightened investigations for prevention of neurologic injury during the perioperative period. This study investigated the effects of propofol and sevoflurane on cerebral oxygen supply demand balance using transcranial Doppler sonography and jugular bulb saturation in pediatric open heart surgery. Methods After obtaining institutional approval and a written consent from parents, 60 children who were admitted for elective open cardiac surgery for correction of congenital heart disease using CPB were included in this study. Children were randomized into two groups; group (P) and group (S). Induction of Anesthesia was achieved by 5 μg/Kg I.V. fentanyl, propofol 2- 2.5 mg/Kg (in propofol or P group) or sevoflurane 2-3 MAC (in sevoflurane or S group). Anesthesia was maintained by propofol infusion between 75-100 μg/kg/min in P group or sevoflurane 2 MAC in S group. Calculated parameters from the blood gas variables included cerebral metabolic rate of oxygen (CMRO 2 ), cerebral extraction of oxygen (CeO 2 ) and cerebral blood flow equivalent (CBF). Arterial blood gases (ABG) and velocities of flow were monitored by Trancranial Doppler at 5 time points : before the surgery, before CPB, during CPB (after establishment of full flow), after CPB and after recovery. Neurological examination and CT scan were done before surgery and 2 days after that. Results There is no significant difference between the two groups in demographic data. Children in propofol group showed lower heart rate values after induction and after CPB than those in sevoflurane group. Mean arterial pressure was statistically higher in sevoflurane group compared with propofol group after induction. Children in sevoflurane group showed significantly higher; velocity maximum, velocity mean and pulsatile index, in the after induction and after bypass periods than those in propofol group. Velocity minimum showed no difference between the two groups. SjvO 2 , CMRO 2 , CeO 2 and CBF was significantly different after induction in sevoflurane group compared with propofol group. Perioperative blood gases showed no difference between the studied groups. Conclusion Compared with propofol anesthesia, sevoflurane anesthesia provides a wider margin of safety against impaired cerebral oxygenation and better preservation of systemic hemodynamics. Moreover, cerebral oxygen saturation may not reflect changes in cerebral oxygenation as monitored by jugular venous oxygen tension measurement in children undergoing CPB.

Cardiopulmonary effects of intravenous fentanyl infusion in dogs during isoflurane anesthesia and with concurrent acepromazine or dexmedetomidine administration during anesthetic recovery

To evaluate the cardiopulmonary effects of IV fentanyl administration in dogs during isoflurane anesthesia and during anesthetic recovery with or without dexmedetomidine or acepromazine. 7 sexually intact male purpose-bred hound-type dogs aged 11 to 12 months. Dogs received a loading dose of fentanyl (5 μg/kg, IV) followed by an IV infusion (5 μg/kg/h) for 120 minutes while anesthetized with isoflurane and for an additional 60 minutes after anesthesia was discontinued. Dogs were randomly assigned in a crossover design to receive dexmedetomidine (2.5 μg/kg), acepromazine (0.05 mg/kg), or saline (0.9% NaCl) solution (1 mL) IV after anesthesia ceased. Cardiopulmonary data were obtained during anesthesia and for 90 minutes after treatment administration during anesthetic recovery. Concurrent administration of fentanyl and isoflurane resulted in significant decreases in mean arterial blood pressure, heart rate, and cardiac index and a significant increase in Paco2. All but Paco2 returned to pretreatment values before isoflurane anesthesia was discontinued. During recovery, dexmedetomidine administration resulted in significant decreases in heart rate, cardiac index, and mixed venous oxygen tension and a significant increase in arterial blood pressure, compared with values for saline solution and acepromazine treatments. Acepromazine administration resulted in significantly lower blood pressure and higher cardiac index and Po2 in mixed venous blood than did the other treatments. Dexmedetomidine treatment resulted in significantly lower values for Pao2 and arterial pH and higher Paco2 values than both other treatments. Fentanyl resulted in transient pronounced cardiorespiratory effects when administered during isoflurane anesthesia. During anesthetic recovery, when administered concurrently with an IV fentanyl infusion, dexmedetomidine resulted in evidence of cardiopulmonary compromise and acepromazine transiently improved cardiopulmonary performance.

Use of near‐infrared spectroscopy to identify trends in regional cerebral oxygen saturation in horses

Alterations in cerebral haemodynamics may contribute to perianaesthetic complications in horses. Near-infrared spectroscopy (NIRS) is frequently used intraoperatively in man to provide information regarding cerebral perfusion. To determine whether NIRS can identify trends in regional cerebral oxygen saturation (rSO2) in horses and whether there is a correlation between rSO2 and venous oxygen tensions. A cerebral oximeter sensor recorded rSO2 from the dorsal sagittal sinus of 6 healthy horses. Values for rSO2, arterial and venous oxygen and carbon dioxide tensions (PaO2, PvO2, PaCO2 and PvCO2 respectively), along with arteriovenous oxygen saturations (SavO2) were recorded in unsedated (recording period [RP] 1), sedated (RP2) and anaesthetised horses (RP3-5) and during recovery (RP6-8). During anaesthesia, horses were ventilated to achieve states of normo- (RP3), hyper- (RP4) and hypocapnoea (RP5). Data were evaluated descriptively and analysed using linear mixed-effects models and Pearson's correlation coefficient. Overall mean ± s.d. values for rSO2, PaO2, PvO2, PaCO2, SavO2 and mean arterial pressure varied significantly by RP (P<0.001). Significant decreases in rSO2 were identified between RP1 and the post anaesthetic periods (P<0.001). No significant differences in rSO2 values were identified between RP1 and the intra-anaesthesia periods or between RP3, RP4 and RP5. Significant correlations were identified between rSO2 and PaO2 (r = 0.448, P<0.001), rSO2 and PvO2 (r = 0.512, P<0.001) and rSO2 and SavO2 (r = 0.469, P<0.001). This is the first study to identify trends in rSO2 in horses using NIRS. A positive correlation was identified between rSO2 and PvO2, suggesting that alterations in cerebral oxygenation may be reflected in PvO2 . Near-infrared spectroscopy may be used to monitor trends in rSO2 during equine anaesthesia. Decreasing rSO2 values may act as an early warning signal, alerting clinicians to potential cerebral desaturation events and indicating a need for intervention.