Venous Blood Oxygen Saturation Research Articles

Abstract 16357: Application of the H2FPEF-score in Pulmonary Arterial Hypertension: Insights From the Amsterdam UMC PAH-cohort

Introduction: Newly diagnosed idiopathic pulmonary arterial hypertension (PAH) patients increasingly have features of patients with heart failure with preserved ejection fraction (HFpEF). These so-called “atypical” PAH patients can be identified using the H2FPEF-score (Reddy, Circulation 2018). This patient group is often excluded from clinical trials, and it is therefore unclear whether they respond similarly to PAH-specific medication. Aim: To assess baseline characteristics and treatment response of patients diagnosed with PAH stratified by the H2FPEF-score. Methods: A retrospective analysis of 253 treatment naïve PAH-patients who underwent diagnostic right heart catheterization at baseline. Groups were compared with ANOVA, post-hoc pairwise t-tests with Bonferroni correction and multivariate Cox proportional hazards analysis. Results: This cohort included 58 (23%) patients with a low (≤1), 159 (63%) patients with an intermediate (2-5) and 36 (14%) patients with a high (≥6) H2FPEF-score. Patients with a high H2FPEF-score were older and more often male, used more diuretics, had more comorbidities and had more often PAH with severely impaired diffusion capacity compared to patients with a low H2FPEF-score. In addition, patients with a high H2FPEF-score had a significantly lower cardiac index, mixed venous blood gas, oxygen saturation and 6-minute walk distance (6MWD) compared to patients with a low H2FPEF-score. A high H2FPEF-score was associated with worse survival despite correcting for confounders (HR 2.99, 95% CI 1.53-5.84, Fig.1 A). Despite potential survival bias, at 1-year follow-up 6MWD (Fig.1 B) significantly improved in patients with a low and intermediate H2FPEF-score, but did not change in patients with a high H2FPEF-score (interaction p-value< 0.001). Conclusions: A high H2FPEF-score is associated with worse survival in PAH. Also, no improvement in 6MWD was observed in patients with a high H2FPEF-score only.

Abstract 17303: Longitudinal Cerebral Oxygen Metabolism in Congenital Heart Disease

Background: Brain growth differences are apparent between different types of cyanotic congenital heart disease, but the underlying mechanism remains unclear. Here, we explored and characterized longitudinal cerebral hemodynamic and oxygen metabolism profiles and their relationships to brain growth patterns in infants with single ventricle physiologies (SV) and transposition of the great arteries (TGA). We hypothesized that there are marked differences in cerebral oxygen metabolism in those with SV compared with TGA. Methods: Cerebral blood flow (CBF), oxygen delivery (CDO2) and consumption (CVO2) and brain growth were measured in 103 term newborns with SV and TGA using MRI at pre- and post-surgery and at follow-up. We measured whole brain size by segmenting a 3D steady state free precession acquisition. Cerebral blood flow was measured using phase contrast imaging of the neck vessels and cerebral venous blood oxygen saturation was derived from T2 oximetry of the superior sagittal sinus. TGAs were divided into those with and without ventricular septums. Results: CBF profiles were similar between the 3 lesion groups. Cerebral oxygen delivery trends increased but were not significantly different between cardiac groups. We observed that this may be mediated by different mechanisms: an increase in arterial saturation in TGAs, and an increase in hemoglobin concentration in SVs. Cerebral oxygen consumption in SV infants remained low (p = 0.54) while that of TGA increased over time (TGA IVS p < 0.001; TGA VSD p <0.001) (Fig. 1), mediated by an unchanging oxygen extraction fraction in SVs (p = 0.59). The SV cerebral oxygen consumption profile aligned with their declining brain weight z-score trajectory. Conclusions: In conclusion, there are characteristic differences in hemodynamic adaptations between SVs and TGAs. Changes in oxygen metabolism may be facilitating brain growth trajectories. This informs us of possible mechanisms involved during a time of critical brain development.

Study of multimodal monitoring in neurocritical care patients

To explore the significance of multimodal monitoring in the monitoring and treatment of neurocritical care patients. 104 neurocritical care patients admitted to the department of Critical Care Medicine of Fujian Provincial Hospital from March 2019 to January 2020 were enrolled. Patients were randomly assigned into two groups, with 52 in each group. In the routine monitoring treatment group, heart rate, blood pressure, respiratory rate and the changes in consciousness and pupils were monitored after operation. The patients were treated with routine medicine to reduce intracranial pressure (ICP), maintain proper cerebral perfusion pressure (CPP), balance fluid intake and output, and maintain the airway clear. Patients in the multimodal monitoring treatment group were treated with invasive ICP monitoring, ultrasound to assess brain structure, ultrasound to measure optic nerve sheath diameter (ONSD), transcranial color doppler (TCCD), internal jugular venous blood oxygen saturation monitoring, near-infrared spectroscopy (NIRS), non-invasive cerebral blood oxygen saturation monitoring and quantitative electroencephalogram monitoring. According to the monitoring results, the patients were given targeted treatment with the goal of controlling ICP and improving brain metabolism. The length of intensive care unit (ICU) stay, the incidences of neurological complications (secondary cerebral infarction, cerebral hemorrhage, high intracranial pressure, etc.), and the incidences of poor prognosis [6 months after the onset of Glasgow outcome score (GOS) 1 to 3] were compared between the two groups. Spearman rank correlation analysis of the correlation between invasive ICP and the ICP value which was calculated by TCCD. The receiver operating characteristic (ROC) curve of invasive ICP and pulsatility index of middle cerebral artery (PIMCA) were used to predict poor prognosis. The length of ICU stay in the multimodal monitoring treatment group was significantly shorter than that of the routine monitoring treatment group (days: 6.27±3.81 vs. 9.61±5.09, P < 0.01), and the incidence of neurological complications was significantly lower than that in the routine monitoring treatment group (9.62% vs. 25.00%, P < 0.05). In the multimodal monitoring treatment group, 37 cases had a good prognosis and 15 cases had a poor prognosis, while the routine monitoring treatment group had a good prognosis in 27 cases and a poor prognosis in 25 cases. The incidence of poor prognosis in the multimodal monitoring treatment group was lower than that of the routine monitoring treatment group (28.85% vs. 48.08%, P < 0.05). In the multimodal monitoring treatment group, the invasive ICP and PIMCA of patients with good prognosis were significantly lower than those of patients with poor prognosis [invasive ICP (mmHg, 1 mmHg = 0.133 kPa): 16 (12, 17) vs. 22 (20, 24), PIMCA: 0.90±0.33 vs. 1.39±0.58, both P < 0.01]. There was no significant difference in resistance index of the middle cerebral artery (RIMCA) between the good prognosis group and the poor prognosis group (0.63±0.12 vs. 0.66±0.15, P > 0.05). There was a positive correlation between the invasive ICP and the ICP value which was calculated by TCCD (r = 0.767, P < 0.001). ROC curve analysis showed that the area under ROC curve (AUC) of invasive ICP for poor prognosis prediction was 0.906, the best cut-off value was ≥ 18 mmHg, the sensitivity was 86.49%, and the specificity was 86.67%. The AUC of PIMCA for poor prognosis prediction was 0.759, the best cut-off value was ≥ 1.12, the sensitivity was 81.08%, and the specificity was 60.00%. The AUC of invasive ICP was greater than PIMCA (Z = 2.279, P = 0.023). Comprehensive analysis of multimodal monitoring indicators for neurocritical care patients to guide clinical treatment can reduce the length of hospital stay, and reduce the risk of neurosurgery complications and disability; invasive ICP can predict poor prognosis of neurocritical care patients.

P1061ACID-BASE MODELLING AND TREND IN CENTRAL VENOUS OXYGEN SATURATION IN HEMODIALYSIS

Abstract Background and Aims Central venous oxygen saturation (sO2cv) is commonly used as a proxy of cardiac output in non-uremic populations. Recently, the decrease in sO2cv commonly observed in many hemodialysis (HD) sessions was correlated with ultrafiltration volume (UFV) and was suspected to be linked with a treatment-induced decrease in cardiac output (Zhang et al, NDT 2018). High variability in sO2cv has also been associated with all-cause mortality in this group of patients (Zhang et al, Blood Purif 2019). We adapted a comprehensive mathematical model of whole body oxygen (O2) and carbon dioxide (CO2) biochemistry, storage and transport and applied it to simulate the changes in sO2cv during bicarbonate hemodialysis to test their connection with changes in CO. Method The original model of biochemistry and transport of base excess, CO2 and O2 was originally developed by Rees and Andreassen (Crit Rev Biomed Eng 2005), and describes in detail the chemical and respiratory mechanisms that regulate the biochemical status in different physiological compartments of the patients’ body (venous blood, arterial blood, tissue cells, interstitial fluid). The model was modified to include the effect of the HD treatment on these systems, allowing to calculate the variations in venous and arterial sO2. Treatment perturbations included the removal via ultrafiltration of interstitial fluid and plasma volume (and consequent hemoconcentration), and infusion of bicarbonate. Simulation experiments of 4h HD sessions were carried out with bicarbonate dialysate concentration = 35 mmol/L and dialysance = 198 mL/min, and various ultrafiltration volumes (UFV); CO was assumed to decrease by 2% for each 1% change in blood volume. The initial biochemical status of the patient was defined assuming 20 mEq/L bicarbonate concentration, 7.4 pH, and 97% oxygen saturation in the arterial compartment, resulting in initial sO2cv equal to 66.6%. Both artero-venous and veno-venous access were simulated. Results The model predicted a negative linear trend for sO2cv with variable slope depending on UFV, as shown in the table: The trend in sO2cv was directly proportional to the decrease in CO during HD and inversely proportional to UFV. In case of constant CO, the simulated sO2cv would actually increase during the session. Although the type of vascular access determined changes in other simulated quantities, partial pressures of CO2 and O2 and oxygen saturation in both arterial and venous blood were practically unchanged. Conclusion Our model confirmed the correlation between the trend in sO2cv and UFV already highlighted in previous works. Moreover, it showed that the decrease in cardiac output is a major determinant of the decrease in sO2cv during the HD session. The developed mathematical model may provide physiological insights in the development of new technologies to monitor changes in cardiac performance during HD.

Establishment of a Linear Correlation Model of Central Venous Blood Oxygen Saturation and Lactate in Sepsis

Introduction: Studies have shown that there is a complex relationship between lactate and ScvO2. Methods: A retrospective study was carried out in 37 intensive care patients with sepsis or septic shock. The relationship between lactate and ScvO2 was explored with correlation analysis and simple linear modelling. Results: Lactate and ScvO2 were significantly correlated in patients with septic shock (r2 = 0.46, p = 0.001; y = -4.11x+ 82.62), but not in sepsis. y Significant correlation between these parameters was also found in the group of patients who went on to die (r2 = 0.67, p &lt; 0.01; y = -3.70x + 78.61), but not in patients who survived. Conclusions: In sepsis, the correlation between ScvO2 and lactate is not constant over the sepsis course and may be dynamic. In the resuscitation of sepsis and/or septic shock, changes in ScvO2 requires further study.

Lower Oxygen Saturation in the Internal Cerebral Vein of Patients with Sickle Cell Disease Revealed By Qsm-MRI

Introduction: Imaging of brain oxygenation can be a powerful tool to assess the risk of stroke in patients with sickle cell disease (SCD), and may potentially aid in stroke prevention. Currently, there is disagreement in oxygen extraction fraction estimated by techniques that measure tissue oxygenation from deep brain structures, and techniques that measure blood oxygenation in the sagittal sinus. Quantitative susceptibility mapping (QSM) is an MRI technique that can noninvasively measure venous blood oxygen saturation (SvO2) in deep cerebral structures based on the magnetic susceptibility shift of venous blood caused by deoxyhemoglobin. In this study, our goal was to compare venous oxygen saturation measured by QSM in the internal cerebral vein (ICV) to venous oxygenation in the sagittal sinus (SS) in SCD patients, anemia subjects with normal hemoglobin and healthy controls. Methods: 16 SCD patients, 7 non-sickle anemia patients and 11 healthy controls participated in the study(Table 1). All subjects provided written consent to a protocol approved by the Committee on Clinical Investigation (CCI#11-00083). Images were acquired on a clinical 3 T Philips system with a 32-channel RF coil. The 3D gradient echo sequence had parameters: TR = 30 ms, α = 25°, 2 echoes: TE1 = 4.94 ms, ΔTE = 5.2 ms, FOV = 210 x 190 x 120 mm, spatial resolution: 0.6 x 0.6 x 1.3 mm, SENSE acceleration rate = 2 in the phase-encoding direction, BW = 289 Hz/pix and total acquisition time = 6 mins 50 seconds. Flow-compensation was added in the readout direction only, which was the anterior-posterior (AP) direction. For each subject, phase images were fitted to generate a B0 field map. Brain extraction and phase unwrapping was performed using FSL. Background field was removed using PDF. Unreliable phase voxels were identified and removed from the brain mask for subsequent processing. L1-regularized field-to-susceptibility inversion was performed to derive the susceptibility map (lambda = 4*10-4). Venous oxygen saturation was computed based on: χ = (1 - SvO2)χd-oHct + χo-wHct [1] where χ is the susceptibility measurement of the ICV, χd-o is the susceptibility shift per unit hematocrit between fully oxygenated and fully deoxygenated erythrocytes, and χo-w is the susceptibility shift between oxygenated blood cells and water. Values of 0.27 ppm (c.g.s unit) and -0.03 ppm were used for χd-o and χo-w. The ROI mask of the ICV was manually selected based on the susceptibility map that was threshold at 0.1 ppm to avoid partial-volume effect. Only the segment that had an angle below 30 degree with respect to the AP axis was included. The purpose was to exclude regions that were susceptible to flow artifact. Intra-ROI average venous oxygen saturation were computed. Group difference of venous oxygen saturation was tested using Student t-test. Results: Figure 2a shows ICV magnetic susceptibility increases linearly with hematocrit as predicted by Eq [1]. Mean ICV venous oxygen saturation in the three groups was 73.9% in CTL, 73.6% in ACTL, compared with SCD 69.3%, p&amp;lt;0.05 by analysis of variance. Figure 3 compares the ICV and SS oxygen saturation as a function of hemoglobin concentration. At normal hemoglobin values, SS saturation was lower than in the ICV, but this difference disappeared with increasing anemia severity. After controlling for hemoglobin value, there were no patient group differences in oxygen saturation in either location. Discussion: In non-anemic subjects, SS oxygen saturation was lower than in the ICV, potentially reflecting increased oxygen demand of the cerebral cortex compared with deep brain structures. ICV is one of the major deep cortical veins, and oxygen saturation of this vein can indicate the oxygenation of deep structures of the cerebral hemispheres, including the basal ganglia, corpus callosum and thalamus. With progressive anemia, brain blood flow increases to preserve cerebral oxygen delivery (not shown), but favors grey matter perfusion at the expense of deep white matter structures. This could explain the decline in venous saturation with hemoglobin seen in the ICV compared with the rise in venous saturation observed in the SS. Alternatively, global increases in flow may homogenize and shorten microvascular transit times, equalizing the oxygen extraction across brain vascular territories. Disclosures Coates: celgene: Consultancy, Honoraria, Other: steering committee of clinical study; agios pharma: Consultancy, Honoraria; vifor: Consultancy, Honoraria; apo pharma: Consultancy, Honoraria, Speakers Bureau. Wood:Apopharma: Consultancy; BiomedInformatics: Consultancy; National Institutes of Health: Research Funding; Imago Biosciences: Consultancy; WorldcareClinical: Consultancy; Philips Healthcare: Research Funding; BluebirdBio: Consultancy; Celgene: Consultancy.

Resuscitative effect of aortic balloon occlusion on traumatic cardiac arrest in swine

Objective To investigate the resuscitation effect of aortic balloon occlusion (ABO) on the traumatic cardiac arrest (TCA) in swine. Methods Twenty-seven male domestic swine weighing (32.7±3.8)kg were utilized. After 40% of estimated blood volume was removed within 20 minutes, the animals were subjected to 5 minutes of untreated ventricular fibrillation and then 5 minutes of cardiopulmonary resuscitation. Additionally, fluid resuscitation was initiated coincident with the beginning of cardiopulmonary resuscitation. The animals were randomly divided into model group (n=12) and ABO group (n=15). Once cardiopulmonary resuscitation was implemented, aortic balloon was concurrently inflated to stop the blood flow of descending thoracic aorta at the level of the diaphragm in the ABO group. In the model group, aortic balloon was placed in the same position without inflation. During cardiopulmonary resuscitation, the changes of coronary perfusion pressure (CPP), forehead's regional cerebral oxygen saturation (rSO2) and pressure of end-tidal CO2 (PETCO2) were continuously monitored, and the rate of return of spontaneous circulation (ROSC), duration of cardiopulmonary resuscitation, number of shocks and dose of epinephrine were recorded. At 5 minutes after successful resuscitation, the levels of arterial blood gas, lactate and jugular venous blood oxygen saturation (SjvO2) were measured. Results Compared with the model group, the values of CPP, rSO2 and PETCO2 during cardiopulmonary resuscitation were significantly increased in the ABO group [CPP: (33.5±5.6)mmHg vs. (23.1±5.2)mmHg at 1 minute, (35.3±6.0)mmHg vs. (26.8±7.4)mmHg at 2 minutes, (36.3±6.3)mmHg vs. (28.2±6.3)mmHg at 3 minutes, (40.1±7.1)mmHg vs. (30.5±6.2)mmHg at 4 minutes, (38.1±7.5)mmHg vs. (29.8±5.3)mmHg at 5 minutes; rSO2: (45.4±5.2)% vs. (39.2±5.1)% at 1 minute, (47.2±3.6)% vs. (42.0±6.4)% at 2 minutes, (47.7±3.0)% vs. (41.5±5.4)% at 3 minutes, (47.0±2.5)% vs. (42.1±5.9)% at 4 minutes, (47.1±2.0)% vs. (41.5±7.4)% at 5 minutes; PETCO2: (17.0±3.5)mmHg vs. (12.7±4.2)mmHg at 1 minute, (18.5±3.7)mmHg vs. (14.5±2.7)mmHg at 2 minutes, (20.7±5.3)mmHg vs. (15.5±3.2)mmHg at 3 minutes, (18.7±4.5)mmHg vs. (14.9±3.5)mmHg at 4 minutes, (18.2±3.2)mmHg vs. (14.5±4.2)mmHg at 5 minutes] (all P<0.05). The rate of ROSC was significantly higher in the ABO group than in the model group[100%(15/15) vs. 75%(9/12)] (P<0.05). Additionally, shorter duration of cardiopulmonary resuscitation, less number of shocks and lower doses of epinephrine were observed in the ABO group when compared with the model group[duration of cardiopulmonary resuscitation: 5(5, 5)minutes vs. 5(5, 12.5)minutes, number of shocks: 1(1, 1)times vs. 1(1, 4)times, dose of epinephrine: 0.62(0.62, 0.74)mg vs. 0.64(0.59, 2.59)mg] (all P<0.05). At 5 minutes after resuscitation, the level of arterial lactate was significantly decreased and the value of SjvO2 was significantly increased in the ABO group compared with the model group[Lactate: (9.6±0.8)mmol/L vs. (10.8±1.4)mmol/L; SjvO2: (50.0±8.6)% vs. (37.9±16.3)%] (both P<0.05). Conclusions In a swine model of TCA, ABO can increase cardiac and cerebral perfusion during cardiopulmonary resuscitation and improve the efficacy of cardiopulmonary resuscitation. It might provide a novel and effective method for the resuscitation of TCA in the clinical setting. Key words: Heart arrest; Cardiopulmonary resuscitation; Aortic balloon occlusion

Correlation Between External Jugular Venous and Central Venous Blood Oxygen Saturation in Patient Under General Anesthesia

Correlation Between External Jugular Venous and Central Venous Blood Oxygen Saturation in Patient Under General Anesthesia

Clinical value of early liquid resuscitation guided by passive leg-raising test combined with transthoracic echocardiography in patients with septic shock

To explore the clinical value of early fluid resuscitation guided by passive leg-raising test (PLR) combined with transthoracic echocardiography (TTE) in patients with septic shock. A prospective randomized controlled trial (RCT) was conducted. Seventy-four patients with septic shock admitted to China-Japan Friendship Hospital from January 2017 to October 2018 were enrolled. The patients were randomly divided into control group and experimental group with 37 patients in each group. Both groups of patients were treated with broad-spectrum antibiotics empirically, while received fluid resuscitation via the subclavian vein catheter. The patients of control group were given rapid fluid replacement, and those of experimental group received fluid replacement according to result of PLR combined with TTE. The stroke volume (SV) was measured by TTE before and after PLR, volumetric response of patients was judged by stroke volume variation (SVV). If the SVV ≥ 15%, it was considered that there was a volume responsiveness, and fluid loading was given. If SVV < 15%, it was considered that there was no volume shortage, and the restrictive fluid replacement was given. The goal of fluid resuscitation in both groups were to simultaneously meet the central venous pressure (CVP) of 8-12 mmHg (1 mmHg = 0.133 kPa), mean arterial pressure (MAP) ≥ 65 mmHg, urine volume ≥ 0.5 mL×kg-1×h-1, and central venous blood oxygen saturation (ScvO2) ≥ 0.70 within 6 hours. Vasoactive drugs were used when the patients could not achieve the treatment goals. The MAP, lactic acid (Lac), oxygenation index (PaO2/FiO2) and ScvO2 of the patients were determined at 6 hours of treatment, and serum C-reactive protein (CRP) and chest CT were reviewed at 48 hours of treatment, and compared with those before treatment. The total hospital stay and the mortality were recorded. There was no significant difference in gender, age, body weight and etiological structure between the two groups, which indicated that the baseline data were generally balanced. There was no statistical difference in MAP, Lac, PaO2/FiO2, ScvO2 and CRP before infusion between the two groups. After 6 hours of treatment, the MAP, Lac, PaO2/FiO2 and ScvO2 of the two groups were all better than those before infusion. Except for the difference in MAP between the experimental group and the control group (mmHg: 78.76±5.22 vs. 76.35±6.66, P > 0.05), the other three parameters in the experimental group were significantly better than those in the control group [Lac (mmol/L): 2.52±1.15 vs. 3.89±1.42, PaO2/FiO2 (mmHg): 338.14±27.47 vs. 303.35±22.52, ScvO2: 0.70±0.04 vs. 0.63±0.05, all P < 0.01]. After 48 hours of treatment, CRP levels of both groups were lower than those before infusion, and the experimental group was better than the control group (mg/L: 110.12±39.80 vs. 137.98±31.23, P < 0.01). Chest CT showed that the incidence of pulmonary edema in the experimental group was significantly lower than that in the control group [13.5% (5/37) vs. 37.8% (14/37), P < 0.01]. The hospital stay of the experimental group was shorter than that of the control group (days: 21.47±5.58 vs. 28.33±4.93, P < 0.01), but no significant difference in mortality was found between the two groups [18.9% (7/37) vs. 18.9% (7/37), P > 0.05]. Compared with the traditional rapid fluid replacement, early fluid resuscitation treatment strategies guided by the PLR combined with TTE, could better improve perfusion and oxygenation level of tissues and organs, avoid pulmonary edema caused by rapid fluid replacement, shorten the hospital stay in patients with septic shock, but had no significant effect on hospital mortality.

Effects of sevoflurane and propofol on hemodynamics, cerebral oxygen metabolism and analgesia during maintenance of paediatric anaesthesia

Purpose: To investigate the effects of sevoflurane and propofol on hemodynamics, cerebral oxygen metabolism and analgesia during maintenance of paediatric anaesthesia.Methods: A total of 134 paediatric patients undergoing surgical anaesthesia in the General Surgery Department of Children’s Hospital of Nanjing Medical University from July 2016 to July 2017 were anesthetised with propofol (control group, n = 67) or sevoflurane (study group, n = 67). The hemodynamics, cerebral oxygen metabolism index, analgesic effect and adverse reaction were determined in both groups and compared.Results: Heart rate (HR) differed significantly between the two groups in the A3 stage (p &lt; 0.05). Systolic and diastolic blood pressures (SBP and DBP) were statistically different between the two groups in the A2 stage (p &lt; 0.05). In the A2 and A3 stages, jugular venous blood oxygen saturation (SjvO2) was higher in the study group, and the differential between arterial oxygen and jugular venous blood oxygen saturation (Da-jvO2) and cerebral oxygen extraction rate (CERO2) were lower than corresponding values in the control group (p &lt; 0.05). In both groups of patients, SjvO2 in A3 stage was lower than that in A2 stage (p &lt; 0.05), and Da-jvO2 and CERO2 were higher in A3 stage than those in A2 stage (p &lt; 0.05).Conclusion: Sevoflurane and propofol maintain balance in cerebral oxygen metabolism and hemodynamic stability when used as paediatric anaesthesia. However, sevoflurane is superior to propofol in protecting the brain tissue of children from damage.Keywords: Propofol, Sevoflurane, Hemodynamics, Cerebral oxygen metabolism, Analgesic

Mapping hepatic blood oxygenation by quantitative BOLD (qBOLD) MRI.

Abnormalities in hepatic oxygen delivery and oxygen consumption may serve as a significant indicator of hepatic cellular dysfunction and may predict treatment response. However, conventional and oxygen-enhanced hepatic BOLD MRI can only provide semiquantitative assessment of hepatic oxygenation. A hepatic quantitative BOLD (qBOLD) model was proposed for noninvasive mapping of hepatic venous blood oxygen saturation (Yv ) and deoxygenated blood volume (DBV) in human subjects. The validity and the estimation bias of the proposed model were evaluated by Monte Carlo simulations. Eight healthy subjects were scanned after written consent with institutional review board approval. Monte Carlo simulations demonstrated that the proposed single-compartment hepatic qBOLD model leads to significant deviation of the predicted T2* decay profile from the simulated signal due to high hepatic blood volume fraction. Small relative estimation bias for hepatic Yv and significant overestimation for hepatic DBV were observed, which can be corrected by applying the calibration curves established from simulations. After correction, the mean hepatic Yv in human subjects was 56.8 ± 6.8%, and the mean hepatic DBV was 0.190 ± 0.035, consistent with measurements from other invasive approaches. Except in regions with significant vascular contamination, the maps for hepatic Yv and DBV were relatively homogenous. With estimation bias correction, the hepatic qBOLD approach enables noninvasive mapping of hepatic blood volume and oxygenation in human subjects. The established protocol may be used to quantitatively assess hepatic tissue hypoxia in multiple liver diseases.

Exercise desaturation as a marker of disease severity in pulmonary arterial hypertension

Introduction Pulmonary hypertension patients develop hemodynamic changes that contribute to the symptoms, especially during exertion. The inability of the heart to increase cardiac output and the ventilation/perfusion mismatch, may explain the presence of exercise oxygen desaturation. Rationale The rational is to study the relation of exercise oxygen desaturation with the severity of pulmonary arterial hypertension (PAH) group I. Patients and methods Thirty-nine patients diagnosed as having PAH group I were included in the study; 30 (76.9%) female patients and nine (23.1%) male patients. Six-minute walk distance (6MWD) was performed as a marker for the risk of mortality. The degree of desaturation was calculated. The disease severity is assessed in terms of right atrial pressure (RAP), oxygen saturation of the mixed venous blood, cardiac output, mean pulmonary artery pressure, and peripheral vascular resistance. Results The mean age was 37.74±10.58; the patients were presented within functional classes II and III. The mean 6MWD (264.95±87.32), RAP (10.87±6.22), and oxygen saturation of the mixed venous blood (58.67±8.13) denote moderate risk of mortality in 1 year of 5–10%. The mean degree of desaturation is 3.72%, and the basal oxygen saturation is 94.44%. There was a statistically significant negative correlation between the 6MWD and RAP, and positive correlation between 6MWD and arterial oxygen saturation, as well as between the mean pulmonary artery pressure and degree of desaturation. Conclusion Exercise desaturation is an important factor in the development and deterioration of PAH, yet it has no significant correlation with the parameters of the disease severity used.

Application of dexmedetomidine in intracranial arterial stenting and its influence on the serum myocardial enzyme, cTnI and LVEF

Objective To analyze the application of dexmedetomidine in intracranial arterial stenting and its influence on the serum myocardial enzyme, cardiac troponin I(cTnI) and left ventricular ejection fraction(LVEF). Methods From March 2015 to March 2017, 94 cases with intracranial arterial stenting in the People's Hospital of Lishui were divided into control group and observation group by the random number table method, with 47 cases in each group.The control group was treated with conventional anesthesia, the observation group was treated with dexmedetomidine.The enzyme creatine phosphate kinase isoenzyme(CK-MB), creatine phosphate kinase(CK), cTnI, LVEF, inflammatory factor, neural function, brain oxygen metabolism and complications in the two groups were compared. Results After surgery, the CK-MB, CK, cTnI levels of the observation group were lower than those of the control group[(35.27±4.41)U/L, (488.30±61.03)U/L, (3.85±0.49)μg/L vs.(46.40±5.79)U/L, (611.21±76.40)U/L, (4.72±0.59)μg/L], the LVEF of the observation group was higher than that of the control group[(45.60±5.72)% vs.(43.12±5.39)%], the differences were statistically significant(t=10.484, 8.619, 7.777, 2.163, all P<0.05). The interleukin-6(IL-6) and interleukin-8(IL-8), tumor necrosis factor-α(TNF-α), S-100β, specificity enolization enzyme(NSE), cerebral metabolic rate of oxygen(ERO2), arterial blood oxygen saturation(PaO2), carotid venous blood oxygen saturation(SjvO2) of the observation group were better than those of the control group(t=5.794, 6.177, 15.065, 6.964, 5.606, 3.147, 2.116, 2.807, all P<0.05). The incidence rate of complication of the observation group was lower than that of the control group(χ2=17.091, P<0.05). Conclusion Application of dexmedetomidine in intracranial arterial stenting can protect myocardium, inhibit the serum levels of myocardial enzyme, cTnI rise, and is conducive to the recovery of LVEF. Key words: Intracranial arterial diseares; Stents; Myocardial enzymes; Cardiac troponin I; Cardiac output; Dexmedetomidine

Defining the optimal duration for normothermic regional perfusion in the kidney donor: A porcine preclinical study.

Kidneys from donation after circulatory death (DCD) are highly sensitive to ischemia-reperfusion injury and thus require careful reconditioning, such as normothermic regional perfusion (NRP). However, the optimal NRP protocol remains to be characterized. NRP was modeled in a DCD porcine model (30minutes of cardiac arrest) for 2, 4, or 6hours compared to a control group (No-NRP); kidneys were machine-preserved and allotransplanted. NRP appeared to permit recovery from warm ischemia, possibly due to an increased expression of HIF1α-dependent survival pathway. At 2hours, blood levels of ischemic injury biomarkers increased: creatinine, lactate/pyruvate ratio, LDH, AST, NGAL, KIM-1, CD40 ligand, and soluble-tissue-factor. All these markers then decreased with time; however, AST, NGAL, and KIM-1 increased again at 6hours. Hemoglobin and platelets decreased at 6hours, after which the procedure became difficult to maintain. Regarding inflammation, active tissue-factor, cleaved PAR-2 and MCP-1 increased by 4-6hours, but not TNF-α and iNOS. Compared to No-NRP, NRP kidneys showed lower resistance during hypothermic machine perfusion (HMP), likely associated with pe-NRP eNOS activation. Kidneys transplanted after 4 and 6hours of NRP showed better function and outcome, compared to No-NRP. In conclusion, our results confirm the mechanistic benefits of NRP and highlight 4hours as its optimal duration, after which injury markers appear.

Dose and timing of normal saline resuscitation on endothelial glycocalyx in early septic shock

To observe the effect of different doses and timing of normal saline (NS) resuscitation combined with norepinephrine (NE) on endothelial glycocalyx in rabbits with early septic shock. Thirty New Zealand male rabbits were randomly divided into sham group, model group, 30 mL and 60 mL timely resuscitation groups (30 mL and 60 mL timely group), and 30 mL delayed resuscitation group (30 mL delayed group) with 6 rabbits in each group. The rabbit model of septic shock was reproduced by cecal ligation and puncture (CLP). The rabbits in sham group were only received abdominal cavity open without cecal and ligation. The rabbits in 30 mL and 60 mL timely groups and 30 mL delayed group were intravenous infused with 30 mL/kg or 60 mL/kg NS immediately or 1 hour after model reproduction for 1 hour, and the mean arterial pressure (MAP) was maintained over 75 mmHg (1 mmHg = 0.133 kPa) compared with intravenous pumping of 0.02-0.05 μg×kg-1×min-1 NE followed by 5 mL/h NS infusion till the end of the experiment. The rabbits in sham and model groups were only given 5 mL/h NS. The changes in arterial blood gas before and immediately after resuscitation were observed in three fluid resuscitation groups. The internal jugular vein blood was collected at 0, 3, 6 hours after model reproduction. The levels of syndecan-1 (polysaccharide envelope marker) in plasma were determined by enzyme linked immunosorbent assay (ELISA). The rabbits were sacrificed at 6 hours after model reproduction, and the lung tissue was harvested. Western Blot was used to determine the protein expressions of intercellular adhesion molecule-1 (ICAM-1), matrix metalloproteinase 2 (MMP-2) and syndecan-1. The positive expression of syndecan-1 in lung tissue was observed by immunohistochemical method. (1) Blood gas analysis: compared with the results before resuscitation, the levels of lactic acid (Lac) after resuscitation in three fluid resuscitation groups were significantly decreased, especially in 30 mL timely group; the central venous blood oxygen saturation (ScvO2) was significantly increased, especially in 30 mL delayed group. Oxygenation index (PaO2/FiO2) was improved in 30 mL timely and 30 mL delayed resuscitation groups, which was decreased in 60 mL delayed group. (2) Plasma marker: compared with sham group, plasma syndecan-1 level in model group was significantly increased with a time-dependent manner. Plasma syndecan-1 levels at 3 hours in 30 mL timely and 30 mL delayed groups were significantly decreased as compared with those of model group (ng/L: 138.0±2.4, 139.7±15.7 vs. 161.5±4.1, both P < 0.05), but it was significantly increased at 6 hours in 30 mL delayed group (ng/L: 213.1±19.4 vs. 206.4±15.5, P < 0.05). The plasma syndecan-1 levels at 3 hours and 6 hours in 60 mL timely group were significantly higher than those in model group (ng/L: 233.0±28.9 vs. 161.5±4.1, 252.3±27.2 vs. 206.4±15.5, both P < 0.05). (3) Protein expression in lung tissue: compared with sham group, the protein expressions of ICAM-1 and MMP-2 in lung tissue of model group were significantly increased, and syndecan-1 protein expression was significantly decreased. After 30 mL timely or 30 mL delayed resuscitation, the protein expressions of ICAM-1 and MMP-2 in lung tissue were significantly decreased, and syndecan-1 protein expression was significantly increased, especially in 30 mL timely group, which showed statistical differences as compared with those of model group (ICAM-1 protein: 0.56±0.09 vs. 1.04±0.05, MMP-2 protein: 0.83±0.15 vs. 1.06±0.06, syndecan-1 protein: 2.09±0.08 vs. 0.99±0.03, all P < 0.05). The change tendency of protein expressions in 60 mL timely group was opposite to the other two resuscitation groups. (4) Immunohistochemistry: the positive expression of syndecan-1 in lung tissues was significant in the sham group, and it was lowered in model group. The positive expression of syndecan-1 was increased after 30 mL timely or 30 mL delayed resuscitation, but further weakened in 60 mL timely group. The dose and timing of resuscitation with NS in septic shock can affect pulmonary vascular endothelial glycocalyx function. The timely resuscitation with 30 mL NS in combination with NE plays a protective effect on endothelial cell and glycocalyx. However, NS resuscitation which was not timely or excessive infusion can make the glycocalyx degradation more obvious, resulting in increased endothelial permeability, microcirculation damaged, thus aggravate lung injury.

Correction of Anemia and Evaluation of Efficacy of Red Blood Cell Transfusion in Patients with Oncohematological Diseases

Aim. To study the quality of life (QL) of patients with oncohematological diseases and anemia with respect to hemoglobin level and to evaluate the efficacy of red blood cell transfusion (RBCT). Materials &amp; Methods. QL of patients (n = 326) was studied using FACT-An questionnaire. RBCT efficacy was evaluated in two groups. The first group included patients (n = 28; 13 men and 15 women) with oncohematological diseases and chronic anemia aged 23-80 (median 65) years, the second (control) group included patients (n = 12; 11 men and 1 woman) after severe blood loss after injury (acute anemia) aged 25-43 (median 36) years. The baseline levels of hemoglobin (Hb) and hematocrit (Ht) were &lt; 80 g/L and &lt; 25 % in all patients, respectively. The target levels of Hb and Ht were &gt; 80 g/L and &gt; 25 %, respectively. Results. The association between the severity of anemia and QL was shown. The lowest QL was observed in patients with grade III-IV anemia (Hb &lt; 80 g/L). Each patient in both groups received 1-8 units of blood cells (median 2) during the hospital stay. After RBCT the levels of Hb and Ht increased from 64.1 ± 2.7 g/L to 90.2 ± 1.7 g/L and from 20.1 ± 0.8 % to 28.9 ± 0.7 %, respectively. The levels of Hb and Ht in the second (control) group increased from 65.9 ± 3.0 g/L to 88.3 ± 3.2 g/L and from 19.6 ± 0.9 % to 26.7 ± 1.4 %, respectively. Venous blood oxygen saturation (SvO&lt;sub&gt;2&lt;/sub&gt;) increased in the first group from 42.0 ± 3.3 % to 57.6 ± 4.1 %, and in the second group from 51.3 ± 1.9 % to 69.0 ± 1.3 %. However, after RBCT the SvO&lt;sub&gt;2&lt;/sub&gt; level reached &gt; 60 % only in 67.9 % of patients in the first group and in all the patients (100 %) in the second group. In 32.1 % of patients with various forms of hematologic cancer and chronic anemia tissue hypoxia was still observed after RBCT despite increased Hb &gt; 80 g/L and Ht &gt; 25 %. Therefore, it was proposed to raise the target Hb and Ht threshold levels for patients with low SvO&lt;sub&gt;2&lt;/sub&gt;. Conclusion. The effect of the severity of anemia on QL was demonstrated. The patients with Hb &lt; 80 g/L were shown to have low quality of life.

Imaging putative foetal cerebral blood oxygenation using susceptibility weighted imaging (SWI).

To evaluate the magnetic susceptibility, ∆χ v , as a surrogate marker of venous blood oxygen saturation, S v O 2, in second- and third-trimester normal human foetuses. Thirty-six pregnant women, having a mean gestational age (GA) of 31 2/7 weeks, underwent magnetic resonance imaging (MRI). Susceptibility-weighted imaging (SWI) data from the foetal brain were acquired. ∆χ v of the superior sagittal sinus (SSS) was quantified using MR susceptometry from the intra-vascular phase measurements. Assuming the magnetic property of foetal blood, ∆χ do , is the same as that of adult blood, S v O 2 was derived from the measured Δχ v . The variation of ∆χ v and S v O 2, as a function of GA, was statistically evaluated. The mean ∆χ v in the SSS in the second-trimester (n = 8) and third-trimester foetuses (n = 28) was found to be 0.34± 0.06 ppm and 0.49 ±0.05 ppm, respectively. Correspondingly, the derived S v O 2 values were 69.4% ±3.27% and 62.6% ±3.25%. Although not statistically significant, an increasing trend (p = 0.08) in Δχ v and a decreasing trend (p = 0.22) in S v O 2 with respect to advancing gestation was observed. We report cerebral venous blood magnetic susceptibility and putative oxygen saturation in healthy human foetuses. Cerebral oxygen saturation in healthy human foetuses, despite a slight decreasing trend, does not change significantly with advancing gestation. • Cerebral venous magnetic susceptibility and oxygenation in human foetuses can be quantified. • Cerebral venous oxygenation was not different between second- and third-trimester foetuses. • Foetal cerebral venous oxygenation does not change significantly with advancing gestation.

Hemodynamics and tissue oxygenation effects after increased in positive end-expiratory pressure in coronary artery bypass surgery

BackgroundCardiac surgery is widely used in the treatment of cardiovascular diseases. However, several complications can be observed during the postoperative period. Positive end expiratory pressure (PEEP) improves gas exchange, but it might be related to decreased cardiac output and possible impairment of tissue oxygenation. The aim of this study was to investigate the hemodynamic effects and oxygen saturation of central venous blood (ScvO2) after increasing PEEP in hypoxemic patients after coronary artery bypass (CAB) surgery.MethodsSeventy post-cardiac surgery patients (CAB), 61 ± 7 years, without ventricular dysfunction (left ventricular ejection fraction 57 ± 2%), with hypoxemia (PaO2/FiO2 ratio <200) were enrolled. Heart rate, mean arterial pressure, arterial and venous blood samples were measured at intensive care unit and PEEP was increased to 12 cmH2O for 30 min.ResultsAs expected, PEEP12 improved arterial oxygenation and PaO2/FiO2 ratio (p < 0.0001). Reduction in ScvO2 was observed between PEEP5 (63 ± 2%) and PEEP12 (57 ± 1%; p = 0.01) with higher values of blood lactate in PEEP12 (p < 0.01). No hemodynamic effects (heart rate, mean arterial pressure, SpO2; p > 0.05) were related.ConclusionIncreased PEEP after cardiac surgery decreased ScvO2 and increased blood lactate, even with higher O2 delivery. PEEP did not interfere in hemodynamics status in CAB patients, suggesting that peripheral parameters must be controlled and measured during procedures involving increased PEEP in post-cardiac surgery patients in the intensive care unit.

Simulation of oxygen saturation measurement in a single blood vein.

The value of oxygen saturation in venous blood, SvO2, has important clinical significance since it is related to the tissue oxygen utilization, which is related to the blood flow to the tissue and to its metabolism rate. However, existing pulse oximetry techniques are not suitable for blood in veins. In the current study we examine the feasibility of difference oximetry to assess SvO2 by using two near-infrared wavelengths and collecting the backscattered light from two photodetectors located at different distances from the light source.

Low Blood Arterial Oxygenation During Venovenous Extracorporeal Membrane Oxygenation: Proposal for a Rational Algorithm-Based Management.

Venovenous extracorporeal membrane oxygenation (VV-ECMO) is a therapeutic option in the management of the most severe forms of acute respiratory distress syndrome. Oxygenation during VV-ECMO depends on many parameters, and its management is complex. The management of ECMO is still not completely codified. The aim of this study was to rationalize the management of hypoxemia during VV-ECMO. To build a comprehensive flow diagram for management of hypoxemia during VV-ECMO, we considered (1) relationship between O2 arterial saturation and its determinants; (2) analysis of physiopathology of oxygenation under VV-ECMO; and (3) main guidelines and recommendations recapitulated in troubleshooting charts. We propose a stepwise approach that could guide specific intervention to improve oxygenation during VV-ECMO. The first step is to obtain adequate pump flow, the main determinant of oxygenation, by eliminating a mechanical problem or inadequate venous drainage. Second, if hypoxemia persists, algorithm considers multiple reasons for inadequate oxygenation, namely: (1) excessive recirculation, (2) excessive cardiac output (decrease of ratio pump flow/cardiac output), (3) decrease in SvO2 (oxygen saturation in mixed venous blood), (4) malfunction of oxygenator, and (5) deterioration of residual lung function. Finally, for each modification of oxygenation parameters, specific measures are proposed to restore an adequate oxygenation by extracorporeal membrane oxygenation. If hypoxemia occurs during VV-ECMO, collecting oxygenation parameters and a clear step-by-step algorithm could guide specific intervention to improve oxygenation. This flow diagram is in accordance with current recommendations recapitulated in guidelines or troubleshooting chart but more accurate and complete. Although rational and appealing, it remains to be tested together with a number of still unsolved issues.