In silico parametric analysis of femoro-jugular venovenous ECMO and return cannula dynamics: In silico analysis of femoro-jugular VV ECMO.

BACKGROUND: Increasingly, computational fluid dynamics (CFD) is helping explore the impact of variables like: cannula design/size/position/flow rate and patient physiology on venovenous (VV) extracorporeal membrane oxygenation (ECMO). Here we use a CFD model to determine what role cardiac output (CO) plays and to analyse return cannula dynamics. METHODS: Using a patient-averaged model of the right atrium and venae cava, we virtually inserted a 19Fr return cannula and a 25Fr drainage cannula. Running large eddy simulations, we assessed cardiac output at: 3.5-6.5 L/min and ECMO flow rate at: 2-6 L/min. We analysed recirculation fraction (Rf), time-averaged wall shear stress (TAWSS), pressure, velocity, and turbulent kinetic energy (TKE) and extracorporeal flow fraction (EFF = ECMO flow rate/CO). RESULTS: Increased ECMO flow rate and decreased CO (high EFF) led to increased Rf (R = 0.98, log fit). Negative pressures developed in the venae cavae at low CO and high ECMO flow (high CR). Mean return cannula TAWSS was >10 Pa for all ECMO flow rates, with majority of the flow exiting the tip (94.0-95.8 %). CONCLUSIONS: Our results underpin the strong impact of CO on VV ECMO. A simple metric like EFF, once supported by clinical data, might help predict Rf for a patient at a given ECMO flow rate. The return cannula imparts high shear stresses on the blood, largely a result of the internal diameter.

A multimodal stacked ensemble model for cardiac output prediction utilizing cardiorespiratory interactions during general anesthesia.

This study examined the possibility of estimating cardiac output (CO) using a multimodal stacking model that utilizes cardiopulmonary interactions during general anesthesia and outlined a retrospective application of machine learning regression model to a pre-collected dataset. The data of 469 adult patients (obtained from VitalDB) with normal pulmonary function tests who underwent general anesthesia were analyzed. The hemodynamic data in this study included non-invasive blood pressure, plethysmographic heart rate, and SpO2. CO was recorded using Vigileo and EV1000 (pulse contour technique devices). Respiratory data included mechanical ventilation parameters and end-tidal CO2 levels. A generalized linear regression model was used as the metalearner for the multimodal stacking ensemble method. Random forest, generalized linear regression, gradient boosting machine, and XGBoost were used as base learners. A Bland-Altman plot revealed that the multimodal stacked ensemble model for CO prediction from 327 patients had a bias of - 0.001 L/min and - 0.271% when calculating the percentage of difference using the EV1000 device. Agreement of model CO prediction and measured Vigileo CO in 142 patients reported a bias of - 0.01 and - 0.333%. Overall, this model predicts CO compared to data obtained by the pulse contour technique CO monitors with good agreement.

NButGT Reinforces the Beneficial Effects of Epinephrine on Cardiac Mitochondrial Respiration, Lactatemia and Cardiac Output in Experimental Anaphylactic Shock.

Anaphylactic shock (AS) is the most severe form of acute systemic hypersensitivity reaction. Although epinephrine can restore patients' hemodynamics, it might also be harmful, supporting the need for adjuvant treatment. We therefore investigated whether NButGT, enhancing O-GlcNAcylation and showing beneficial effects in acute heart failure might improve AS therapy. Ovalbumin-sensitized rats were randomly allocated to six groups: control (CON), shock (AS), shock treated with NButGT alone before (AS+pre-Nbut) or after (AS+post-Nbut) AS onset, shock treated with epinephrine alone (AS+EPI) and shock group treated with combination of epinephrine and NButGT (AS+EPI+preNBut). Induction of shock was performed with an intravenous (IV) ovalbumin. Cardiac protein and cycling enzymes O-GlcNAcylation levels, mean arterial pressure (MAP), heart rate, cardiac output (CO), left ventricle shortening fraction (LVSF), mitochondrial respiration, and lactatemia were evaluated using Western blotting experiments, invasive arterial monitoring, echocardiography, mitochondrial oximetry and arterial blood samples. AS decreased MAP (-77%, p < 0.001), CO (-90%, p < 0.001) and LVSF (-30%, p < 0.05). Epinephrine improved these parameters and, in particular, rats did not die in 15 min. But, cardiac mitochondrial respiration remained impaired (complexes I + II -29%, p < 0.05 and II -40%, p < 0.001) with hyperlactatemia. NButGT pretreatment (AS+pre-Nbut) efficiently increased cardiac O-GlcNAcylation level as compared to the AS+post-Nbut group. Compared to epinephrine alone, the adjunction of NButGT significantly improved CO, LVSF and mitochondrial respiration. MAP was not significantly increased but lactatemia decreased more markedly. Pretreatment with NButGT increases O-GlcNAcylation of cardiac proteins and has an additive effect on epinephrine, improving cardiac output and mitochondrial respiration and decreasing blood lactate levels. This new therapy might be useful when the risk of AS cannot be avoided.

An interactive simulator to deepen the understanding of Guyton's venous return curve.

Mean circulatory filling pressure, venous return curve, and Guyton's graphical analysis are basic concepts in cardiovascular physiology. However, some medical students may not know how to view and interpret or understand them adequately. To deepen students' understanding of the graphical analysis, in place of having to perform live animal experiments, we developed an interactive cardiovascular simulator, as a self-learning tool, as a web application. The minimum closed-loop model consisted of a ventricle, an artery, resistance, and a vein, excluding venous resistance. The simulator consists of three modules: setting (parameters and simulation modes), calculation, and presentation. In the setting module, the user can interactively customize model parameters, compliances, resistance, Emax of the ventricular contractility, total blood volume, and unstressed volume. The hemodynamics are calculated in three phases: filling (late diastole), ejection (systole), and flow (early diastole). In response to the user's settings, the simulator graphically presents the hemodynamics: the pressure-volume relations of the artery, vein, and ventricle, the venous return curves, and the stroke volume curves. The mean filling pressure is calculated at approximately 7 mmHg at the initial setting. The venous return curves, linear and concave, are dependent on the venous compliance. The hemodynamic equilibrium point is marked on the crossing point of venous return curve and the stroke volume curve. Users can interactively do discovery learning, and try and confirm their interests and get their questions answered about hemodynamic concepts by using the simulator.

Advanced maternal age alters cardiac functional and structural adaptations to pregnancy in rats.

A significant number of pregnancies occur at advanced maternal age (>35 yr), which is a risk factor for pregnancy complications. Healthy pregnancies require massive hemodynamic adaptations, including an increased blood volume and cardiac output. There is growing evidence that these cardiovascular adaptations are impaired with age, however, little is known about maternal cardiac function with advanced age. We hypothesized that cardiac adaptations to pregnancy are impaired with advanced maternal age. Younger (4 mo; ∼early reproductive maturity in humans) and aged (9 mo; ∼35 yr in humans) pregnant Sprague-Dawley rats were assessed and compared with age-matched nonpregnant controls. Two-dimensional echocardiographic images were obtained (ultrasound biomicroscopy; under anesthesia) on gestational day 19 (term = 22 days) and compared with age-matched nonpregnant rats (n = 7-9/group). Left ventricular structure and function were assessed using short-axis images and transmitral Doppler signals. During systole, left ventricular anterior wall thickness increased with age in the nonpregnant rats, but there was no age-related difference between the pregnant groups. There were no significant pregnancy-associated differences in left ventricular wall thickness. Calculated left ventricular mass increased with age in nonpregnant rats and increased with pregnancy only in young rats. Compared with young pregnant rats, the aortic ejection time of aged pregnant rats was greater and Tei index was lower. Overall, the greater aortic ejection time and lower Tei index with age in pregnant rats suggest mildly altered cardiac adaptations to pregnancy with advanced maternal age, which may contribute to adverse outcomes in advanced maternal age pregnancies.NEW & NOTEWORTHY We demonstrated that even before the age of reproductive senescence, rats show signs of age-related alterations in cardiac structure that suggests increased cardiac work. Our data also demonstrate, using an in vivo echocardiographic approach, that advanced maternal age in a rat model is associated with altered cardiac function and structure relative to younger pregnant controls.

Effect of lower body negative pressure on cardiac and cerebral function in postural orthostatic tachycardia syndrome: A pilot MRI assessment.

Postural orthostatic tachycardia syndrome (POTS) is characterized by an excessive heart rate (HR) response upon standing and symptoms indicative of inadequate cerebral perfusion. We tested the hypothesis that during lower body negative pressure (LBNP), individuals with POTS would have larger decreases in cardiac and cerebrovascular function measured using magnetic resonance (MR) imaging. Eleven patients with POTS and 10 healthy controls were studied at rest and during 20 min of -25 mmHg LBNP. Biventricular volumes, stroke volume (SV), cardiac output (Qc), and HR were determined by cardiac MR. Cerebral oxygen uptake (VO2 ) in the superior sagittal sinus was calculated from cerebral blood flow (CBF; MR phase contrast), venous O2 saturation (SvO2 ; susceptometry-based oximetry), and arterial O2 saturation (pulse oximeter). Regional cerebral perfusion was determined using arterial spin labelling. HR increased in response to LBNP (p < 0.001) with no group differences (HC: +9 ± 8 bpm; POTS: +13 ± 11 bpm; p = 0.35). Biventricular volumes, SV, and Qc decreased during LBNP (p < 0.001). CBF and SvO2 decreased with LBNP (p = 0.01 and 0.03, respectively) but not cerebral VO2 (effect of LBNP: p = 0.28; HC: -0.2 ± 3.7 mL/min; POTS: +1.1 ± 2.0 mL/min; p = 0.33 between groups). Regional cerebral perfusion decreased during LBNP (p < 0.001) but was not different between groups. These data suggest patients with POTS have preserved cardiac and cerebrovascular function.

Pulmonary CT perfusion robustly measures cardiac output in the context of multilevel pulmonary occlusion: a porcine study.

BACKGROUND: To validate pulmonary computed tomography (CT) perfusion in a porcine model by invasive monitoring of cardiac output (CO) using thermodilution method. METHODS: Animals were studied at a single center, using a Swan-Ganz catheter for invasive CO monitoring as a reference. Fifteen pigs were included. Contrast-enhanced CT perfusion of the descending aorta and right and left pulmonary artery was performed. For variation purposes, a balloon catheter was inserted to block the contralateral pulmonary vascular bed; additionally, two increased CO settings were created by intravenous administration of catecholamines. Finally, stepwise capillary occlusion was performed by intrapulmonary arterial injection of 75-µm microspheres in four stages. A semiautomatic selection of AFs and a recirculation-aware tracer-kinetics model to extract the first-pass of AFs, estimating blood flow with the Stewart-Hamilton method, was implemented. Linear mixed models (LMM) were developed to calibrate blood flow calculations accounting with individual- and cohort-level effects. RESULTS: Nine of 15 pigs had complete datasets. Strong correlations were observed between calibrated pulmonary (0.73, 95% confidence interval [CI] 0.6-0.82) and aortic blood flow measurements (0.82, 95% CI, 0.73-0.88) and the reference as well as agreements (± 2.24 L/min and ± 1.86 L/min, respectively) comparable to the state of the art, on a relatively wide range of right ventricle-CO measurements. CONCLUSIONS: CT perfusion validly measures CO using LMMs at both individual and cohort levels, as demonstrated by referencing the invasive CO. RELEVANCE STATEMENT: Possible clinical applications of CT perfusion for measuring CO could be in acute pulmonary thromboembolism or to assess right ventricular function to show impairment or mismatch to the left ventricle. KEY POINTS: • CT perfusion measures flow in vessels. • CT perfusion measures cumulative cardiac output in the aorta and pulmonary vessels. • CT perfusion validly measures CO using LMMs at both individual and cohort levels, as demonstrated by using the invasive CO as a reference standard.

Lactate infusion elevates cardiac output through increased heart rate and decreased vascular resistance: a randomised, blinded, crossover trial in a healthy porcine model.

BACKGROUND: Lactate is traditionally recognized as a by-product of anaerobic metabolism. However, lactate is a preferred oxidative substrate for stressed myocardium. Exogenous lactate infusion increases cardiac output (CO). The exact mechanism underlying this mechanism has yet to be elucidated. The aim of this study was to investigate the cardiovascular mechanisms underlying the acute haemodynamic effects of exogenous lactate infusion in an experimental model of human-sized pigs. METHODS: In this randomised, blinded crossover study in eight 60-kg-pigs, the pigs received infusions with one molar sodium lactate and a control infusion of tonicity matched hypertonic saline in random order. We measured CO and pulmonary pressures using a pulmonary artery catheter. A pressure-volume admittance catheter in the left ventricle was used to measure contractility, afterload, preload and work-related parameters. RESULTS: Lactate infusion increased circulating lactate levels by 9.9 mmol/L (95% confidence interval (CI) 9.1 to 11.0) and CO by 2.0 L/min (95% CI 1.2 to 2.7). Afterload decreased as arterial elastance fell by  -1.0 mmHg/ml (95% CI  -2.0 to  -0.1) and systemic vascular resistance decreased by  -548 dynes/s/cm5 (95% CI  -261 to  -835). Mixed venous saturation increased by 11 percentage points (95% CI 6 to 16), whereas ejection fraction increased by 16.0 percentage points (95% CI 1.1 to 32.0) and heart rate by 21 bpm (95% CI 8 to 33). No significant changes in contractility nor preload were observed. CONCLUSION: Lactate infusion increased cardiac output by increasing heart rate and lowering afterload. No differences were observed in left ventricular contractility or preload. Lactate holds potential as a treatment in situations with lowered CO and should be investigated in future clinical studies.

Prediction of preload dependency using phenylephrine-induced peripheral perfusion index during general anaesthesia: a prospective observational study.

BACKGROUND: Tracking preload dependency non-invasively to maintain adequate tissue perfusion in the perioperative period can be challenging.The effect of phenylephrine on stroke volume is dependent upon preload. Changes in stroke volume induced by phenylephrine administration can be used to predict preload dependency. The change in the peripheral perfusion index derived from photoplethysmography signals reportedly corresponds with changes in stroke volume in situations such as body position changes in the operating room. Thus, the peripheral perfusion index can be used as a non-invasive potential alternative to stroke volume to predict preload dependency. Herein, we aimed to determine whether changes in perfusion index induced by the administration of phenylephrine could be used to predict preload dependency. METHODS: We conducted a prospective single-centre observational study. The haemodynamic parameters and perfusion index were recorded before and 1 and 2 min after administering 0.1 mg of phenylephrine during post-induction hypotension in patients scheduled to undergo surgery. Preload dependency was defined as a stroke volume variation of ≥ 12% before phenylephrine administration at a mean arterial pressure of < 65 mmHg. Patients were divided into four groups according to total peripheral resistance and preload dependency. RESULTS: Forty-two patients were included in this study. The stroke volume in patients with preload dependency (n = 23) increased after phenylephrine administration. However, phenylephrine administration did not impact the stroke volume in patients without preload dependency (n = 19). The perfusion index decreased regardless of preload dependency. The changes in the perfusion index after phenylephrine administration exhibited low accuracy for predicting preload dependency. Based on subgroup analysis, patients with high total peripheral resistance tended to exhibit increased stroke volume following phenylephrine administration, which was particularly prominent in patients with high total peripheral resistance and preload dependency. CONCLUSION: The findings of the current study revealed that changes in the perfusion index induced by administering 0.1 mg of phenylephrine could not predict preload dependency. This may be attributed to the different phenylephrine-induced stroke volume patterns observed in patients according to the degree of total peripheral resistance and preload dependency. TRIAL REGISTRATION: University Hospital Medical Information Network (UMIN000049994 on 9/01/2023).

Easy method to determine fluid responsiveness in septic shock patients: end-tidal CO2 - a prospective observational study.

BACKGROUND: In critically ill patients, especially those with septic shock, fluid management can be a challenging aspect of clinical care. One of the primary steps in treating patients with hemodynamic instability is optimizing intravascular volume. The Passive Leg Raising (PLR) maneuver is a reliable test for assessing fluid responsiveness, as demonstrated by numerous studies and meta-analyses. However, its use requires the measurement of cardiac output, which is often complex and may necessitate clinician experience and specialized equipment. End-Tidal Carbon Dioxide (ETCO2) measurement is relatively easy and is generally stable under steady metabolic conditions. It depends on the body's CO2 production, diffusion of CO2 from the lungs into the bloodstream, and cardiac output. If the other two parameters (metabolic conditions and minute ventilation) are constant, ETCO2 can provide information about cardiac output. The aim of the present study is to investigate the sensitivity of ETCO2 measurement in demonstrating fluid responsiveness. METHODS: All patients diagnosed with septic shock and meeting the inclusion criteria were subjected to a passive leg raising test, and cardiac outputs were measured by echocardiography. An increase in cardiac output of 15% or more was considered indicative of the fluid responder group, while patients with an increase below 15% or no increase were classified as the non-responder group. Patients' intensive care unit admission diagnoses, initial laboratory parameters, tidal volume, minute volume before and after the PLR maneuver, mean and systolic blood pressure, heart rate, Pulse Pressure Variation (PPV) values, and ETCO2 values were recorded. RESULTS: Before and after the ETCO2 test, there was no statistically significant difference between the two groups. However, the change in ETCO2 (ΔETCO2) was significantly higher in the responder group. In the non-responder group, ΔETCO2 was 2.57% (0.81), whereas it was 5.71% (2.83) in the responder group (p<0.001). Receiver Operating Characteristic (ROC) analysis was performed for ΔETCO2, baseline Stroke Volume Variation (SVV), ΔSVV, baseline Heart Rate (HR), ΔHR, baseline PPV, and ΔPPV to predict fluid responsiveness. ΔETCO2 predicted fluid responsiveness with a sensitivity of 85% and a specificity of 86% when it was 4% or higher. When ΔETCO2 was 5% or higher, it predicted fluid responsiveness with a specificity of 99.3% and a sensitivity of 75.5%, with an Area Under the Curve (AUC) of 0.89 (95% confidence interval, 0.828-0.961). CONCLUSION: This study demonstrates that in septic patients, ETCO2 during the PLR test can indicate fluid responsiveness with high sensitivity and specificity and can be used as an alternative to cardiac output measurement.

Validation of a noninvasive cardiac output monitor in maternal cardiac disease: comparison of NICOM and transthoracic echocardiogram.

BACKGROUND: The physiological changes to the cardiovascular system during pregnancy are considerable and are more pronounced in those with cardiac disease. In the general population, noninvasive hemodynamic monitoring is a valid alternative to pulmonary artery catheterization, which poses risk in the pregnant population. There is limited data on noninvasive cardiac output monitoring in pregnancy as an alternative to pulmonary artery catheterization. OBJECTIVE: We sought to compare transthoracic echocardiography with a noninvasive cardiac output monitor (NICOM, Cheetah Medical) in pregnant patients with and without cardiac disease. STUDY DESIGN: This was a prospective, open-label validation study that compared 2-dimensional transthoracic echocardiography with NICOM estimations of cardiac output in each trimester of pregnancy and the postpartum period. Participants with and without cardiac disease with a singleton gestation were included. NICOM estimations of cardiac output were derived from thoracic bioreactance and compared with 2-dimensional transthoracic echocardiography for both precision and accuracy. A mean percentage difference of ±30% between the 2 devices was considered acceptable agreement between the 2 measurement techniques. RESULTS: A total of 58 subjects were enrolled; 36 did not have cardiac disease and 22 had cardiac disease. Heart rate measurements between the 2 devices were strongly correlated in both groups, whereas stroke volume and cardiac output measurements showed weak correlation. When comparing the techniques, the NICOM device overestimated cardiac output in the control group in all trimesters and the postpartum period (mean percentage differences were 50.3%, 52.7%, 48.1%, and 51.0% in the first, second, and third trimesters and the postpartum period, respectively). In the group with cardiac disease, the mean percentage differences were 31.9%, 29.7%, 19.6%, and 35.2% for the respective timepoints. CONCLUSION: The NICOM device consistently overestimated cardiac output when compared with 2-dimensional transthoracic echocardiography at all timepoints in the control group and in the first trimester and postpartum period for the cardiovascular disease group. The physiological changes of pregnancy, specifically the mean chest circumference and total body water, may alter the accuracy of the cardiac output measurement by the NICOM device as they are currently estimated. Although NICOM has been validated for use in the critical care setting, there is insufficient data to support its use in pregnancy.

Exercise induced plasma volume expansion lowers cardiovascular strain during 15-km cycling time-trial in acute normobaric hypoxia.

The purpose of our study was to assess the influence of a single high-intensity interval exercise (HIIE) bout in normoxia on plasma volume (PV) and consequent cycling performance in normobaric hypoxia (0.15 FiO2, simulating ~2,500 m). Eight males (VO2peak: 48.8 ± 3.4 mL/kg/min, 24.0 ± 1.6 years) completed a hypoxic 15 km cycling time trial (TT), followed by a crossover intervention of either HIIE (8x4 min cycling bouts at 85% of VO2peak) or CON (matched kJ production from HIIE at 50% of VO2peak). 48 hours post intervention, an identical TT was performed. Cardiovascular parameters were measured via impedance cardiography during each TT. Changes in PV was measured 24 and 48 hours post HIIE and CON. HIIE increased PV at 24 (4.1 ± 3.9%, P = 0.031) and 48 (6.7 ± 1.7, P = 0.006) hours post, while no difference was observed following the CON (1.3 ± 1.1% and 0.3 ± 2.8%). The higher PV led to an increased stroke volume (P = 0.03) and cardiac output (P = 0.02) during the hypoxic TT, while heart rate was not changed (P = 0.49). We observed no changes in time to completion (-0.63 ± 0.57 min, P = 0.054) and power output (7.37 ± 7.98 W, P = 0.078) between TTs. In the absence of environmental stress, a single bout of HIIE was an effective strategy to increase PV and reduce the cardiovascular strain during a cycling TT at moderate simulated altitude but did not impact hypoxic exercise performance. Trial registration: Clinical Trials ID: NCT05800808.

Fetal hemodynamic changes and mitochondrial dysfunction in myocardium and brain tissues in response to anemia: a lesson from hemoglobin Bart's disease.

OBJECTIVE: Whether or not the effects of anemia in the early phase, while the fetuses attempts to increase cardiac output to meet oxygen requirement in peripheral organs, is detrimental to the fetal developing vital organs is little-known. The objective of this is to compare prenatal cardiovascular changes and post-abortal cellular damages in the myocardium as a pumping organ and the brain as a perfused organ between anemic fetuses (using fetal Hb Bart's disease as a study model) in pre-hydropic phase and non-anemic fetuses. METHODS: Fetuses affected by Hb Bart's disease and non-anemic fetuses at 16-22 weeks were recruited to undergo comprehensive fetal echocardiography. Cord blood analysis was used to confirm the definite diagnosis of fetal Hb Bart's disease and normal fetuses. Fetal cardiac and brain tissues were collected shortly after pregnancy termination for the determination of oxidative stress and mitochondrial function, including mitochondrial ROS production and mitochondrial membrane changes. RESULTS: A total of 18 fetuses affected by Hb Bart's disease and 13 non-anemic fetuses were recruited. The clinical characteristics of both groups were comparable. The affected fetuses showed a significant increase in cardiac dimensions, cardiac function, cardiac output and brain circulation without deteriorating cardiac contractility and preload. However, in the affected fetuses, mitochondrial dysfunction was clearly demonstrated in brain tissues and in the myocardium, as indicated by a significant increase in the membrane potential change (p-value < 0.001), and a significant increase in ROS production in brain tissues, with a trend to increase in myocardium. The findings indicated cellular damage in spite of good clinical compensation. CONCLUSION: The new insight is that, in response to fetal anemia, fetal heart increases in size (dilatation) and function to increase cardiac output and blood flow velocity to provide adequate tissue perfusion, especially brain circulation. However, the myocardium and brain showed a significant increase in mitochondrial dysfunction, suggesting cellular damage secondary to anemic hypoxia. The compensatory increase in circulation could not completely prevent subtle brain and heart damage.

Use of the USCOM® noninvasive cardiac output measurement system to predict the development of pre-eclampsia in hypertensive pregnancies.

OBJECTIVES: To assess the ability of the USCOM® (USCOM), using measurements of cardiac output (CO) and systemic vascular resistance (SVR), to predict the development of pre-eclampsia (PE) and severe PE in hypertensive pregnancies. STUDY DESIGN: Prospective cohort study of women in the second or third trimester recruited at a tertiary center in Sydney, Australia. Demographic data and hemodynamic measurements using the USCOM were taken for all study participants at recruitment. Pregnancy outcome, including development of PE and severe PE, was tracked. Data were analyzed using ANOVA testing, pair-wise comparison testing, and Student's t-testing. RESULTS: Recruitment included 65 normotensive controls, 34 women with chronic hypertension (CH), 51 with gestational hypertension (GH), and 21 with PE. Significantly higher weight, body surface area, and blood pressure measurements were found in the hypertensive, compared with the normotensive control and pregnancies. There were no observed differences in USCOM-measured CO, cardiac index, SVR, or systemic vascular resistance index between hypertensive women who did versus did not develop PE or severe PE in later pregnancy. Analysis of the CH and GH subgroups, as well as only unmedicated hypertensive women (n = 24), also showed no significant difference in hemodynamic parameters between those who did or did not develop PE or severe PE. CONCLUSIONS: Our group was unable to successfully predict the onset of PE or severe PE based on hemodynamic parameters measured with the USCOM. It is possible this relates to the high proportion of women on antihypertensive medication at recruitment.

Comparison of noninvasive cardiac output and stroke volume measurements using electrical impedance tomography with invasive methods in a swine model.

Pulmonary artery catheterization (PAC) has been used as a clinical standard for cardiac output (CO) measurements on humans. On animals, however, an ultrasonic flow sensor (UFS) placed around the ascending aorta or pulmonary artery can measure CO and stroke volume (SV) more accurately. The objective of this paper is to compare CO and SV measurements using a noninvasive electrical impedance tomography (EIT) device and three invasive devices using UFS, PAC-CCO (continuous CO) and arterial pressure-based CO (APCO). Thirty-two pigs were anesthetized and mechanically ventilated. A UFS was placed around the pulmonary artery through thoracotomy in 11 of them, while the EIT, PAC-CCO and APCO devices were used on all of them. Afterload and contractility were changed pharmacologically, while preload was changed through bleeding and injection of fluid or blood. Twenty-three pigs completed the experiment. Among 23, the UFS was used on 7 pigs around the pulmonary artery. The percentage error (PE) between COUFS and COEIT was 26.1%, and the 10-min concordance was 92.5%. Between SVUFS and SVEIT, the PE was 24.8%, and the 10-min concordance was 94.2%. On analyzing the data from all 23 pigs, the PE between time-delay-adjusted COPAC-CCO and COEIT was 34.6%, and the 10-min concordance was 81.1%. Our results suggest that the performance of the EIT device in measuring dynamic changes of CO and SV on mechanically-ventilated pigs under different cardiac preload, afterload and contractility conditions is at least comparable to that of the PAC-CCO device. Clinical studies are needed to evaluate the utility of the EIT device as a noninvasive hemodynamic monitoring tool.

Carbon dioxide and cardiac output as major contributors to cerebral oxygenation during apnoeic oxygenation.

Apnoeic oxygenation has experienced a resurgence in interest in critical care and perioperative medicine. However, its effect on cerebral oxygenation and factors influencing it, have not yet been investigated in detail. By using near-infrared spectroscopy, we intended to provide further evidence for the safety of apnoeic oxygenation and to increase our understanding of the association between cerebral perfusion, haemodynamic, respiratory and demographic factors. In this secondary analysis of a prospective randomized controlled noninferiority trial, we recruited 125 patients, who underwent surgery under general anaesthesia with neuromuscular blockade. Arterial blood samples were taken every 2 min for a total of 15 min under apnoeic oxygenation with 100% oxygen. Near-infrared spectroscopy and cardiac output were continuously measured. Statistical analysis was performed using uni- and multivariable statistics. Ninety-one complete data sets were analysed. In six patients the SpO2 fell below 92% (predefined study termination criterion). The significant average increase of cerebral oxygenation was 0.5%/min and 2.1 mmHg/min for the arterial pressure of carbon dioxide (paCO2). The median cardiac output increased significantly from 5.0 l/min (IQR 4.5-6.0) to 6.5 l/min (IQR 5.7-7.5). The most significant effect on cerebral oxygenation was exhibited by the variable paCO2 and non-specific patient factors, followed by cardiac output and paO2. Apnoeic oxygenation proves to have a high safety profile while significantly increasing cerebral oxygenation, paCO2 and cardiac output. In reverse, NIRS might act as a reliable clinical surrogate of paCO2 and cardiac output during stable arterial oxygenation.