Mean Cardiac Output Research Articles

Hemodynamic evaluation in preterm infants using ultrasonic cardiac output monitor (USCOM).

We aimed to establish reference ranges for USCOM parameters in preterm infants, determine factors that affect cardiac output, and evaluate the measurement repeatability. This retro-prospective study was performed at Fondazione IRCCS San Gerardo dei Tintori, Monza, Italy. We included infants below 32weeks of gestational age (GA) and/or 1500g of birth weight (BW). We excluded infants with congenital heart diseases or hemodynamic instability. Measurements were performed at 3 ± 1, 7 ± 2, and 14 ± 2 postnatal days. We analyzed 204 measurements from 92 patients (median GA = 30.57weeks, BW = 1360g). The mean (SD) cardiac output (CO) was 278 (55) ml/min/kg, cardiac index (CI) was 3.1 (0.5) L/min/m2, and systemic vascular resistance (SVRI) was 1292 (294) d*s*cm-5/m2. CO presented a negative correlation with postmenstrual age (PMA), while SVRI presented a positive correlation with PMA. The repeatability coefficient was 31ml/kg/min (12%). Conclusion: This is the first study describing reference values for USCOM parameters in hemodynamically stable preterm infants and factors affecting their variability. Further studies to investigate the usefulness of USCOM for the longitudinal assessment of patients at risk for cardiovascular instability or monitoring the response to therapies arewarranted. What is Known: • The ultrasonic cardiac output monitoring (USCOM) has been widely used on adult and pediatric patients and reference ranges for cardiac output (CO) by USCOM have been established in term infants. What is New: • We established reference values for USCOM parameters in very preterm and very-low-birth-weight infants; the reference ranges for CO by USCOM in the study population were 198-405 ml/kg/min. • CO normalized by body weight presented a significant negative correlation with postmenstrual age (PMA); systemic vascular resistance index presented a significant positive correlation with PMA.

Evaluation of ventricular-vascular coupling with critical care metrics: An in silico approach.

Mean arterial pressure and cardiac output provide insufficient guidance for the management of intraoperative hypotension (IOH). In silico models offer additional insights into acute changes in hemodynamic parameters that may be encountered during IOH. A computational model (CM) generated parameters quantifying ventricular-vascular coupling, and pressure-volume construct across levels of aortic compliance (CA ). We studied how a loss from normal-to-stiff CA impacts critical care metrics of hemodynamics during vascular occlusion. Pulse pressure (PP), end-systolic pressure (Pes ), arterial compliance (Art-ca), arterial elastance (Art-ea), and dynamic arterial elastance (Eadyn), along mechanical efficiency (ME) were measured at five levels of CA . A loss in CA impacted all variables. During steady-state conditions, PP, Pes , and stroke work increased significantly as CA decreased. Art-ca decreased and Art-ea increased similarly; Eadyn increased and ME decreased. During a decrease in preload across all CA levels, arterial dynamics measures remained linear. The CM demonstrated that a loss in CA impacts measures of arterial dynamics during steady-state and transient conditions and the model demonstrates that critical care metrics are sensitive to changes in CA . While Art-ca and Art-ea were sensitive to changes in preload, Eadyn did not change.

Liver-targeted nanoparticles delivering nitric oxide reduce portal hypertension in cirrhotic rats

Nitric oxide (NO) is a small vasodilator playing a key role in the pathogenesis of portal hypertension. Here, we assessed the potential therapeutic effect of a NO donor targeted to the liver by poly(beta-amino ester) nanoparticles (pBAE NPs) in experimental cirrhosis. Retinol-functionalized NO donor pBAE NPs (Ret pBAE NPs) were synthetized with the aim of actively targeting the liver. Administration of Ret pBAE NPs resulted in uptake and transfection by the liver and spleen. NPs were not found in other organs or the systemic circulation. Treatment with NO donor Ret pBAE NPs (30 mg/ kg body weight) significantly decreased aspartate aminotransferase, lactate dehydrogenase and portal pressure (9.75 ± 0.64 mmHg) compared to control NPs (13.4 ± 0.53 mmHg) in cirrhotic rats. There were no effects on mean arterial pressure and cardiac output. Liver-targeted NO donor NPs reduced collagen fibers and steatosis, activation of hepatic stellate cells and mRNA expression of profibrogenic and proinflammatory genes. Finally, Ret pBAE NPs displayed efficient transfection in human liver slices. Overall, liver-specific NO donor NPs effectively target the liver and mitigated inflammation and portal hypertension in cirrhotic rats. The use of Ret pBAE may prove to be an effective therapeutic strategy to treat advanced liver disease.

Sodium octanoate alleviates cardiac and cerebral injury after traumatic cardiac arrest in a porcine model

IntroductionTraumatic cardiac arrest (TCA) is a severe condition with a high mortality rate, and patients who survive from TCA face a poor prognosis due to post-resuscitation injury, including cardiac and cerebral injury, which remains a serious challenge. Sodium octanoate has shown protective effects against various diseases. The present study aims to investigate sodium octanoate's protective effects against cardiac and cerebral injury after TCA in a porcine model. MethodsThe study included a total of 22 male domestic pigs divided into three groups: Sham group (n = 7), TCA group (n = 7), and sodium octanoate (SO) group (n = 8). Hemorrhage was initiated via the right femoral artery by a blood pump at a rate of 2 ml·kg−1·min−1 to establish TCA model. The Sham group underwent only endotracheal intubation and arteriovenous catheterization, without experiencing the blood loss/cardiac arrest/resuscitation model. At 5 min after resuscitation, the SO group received a continuous sodium octanoate infusion while the TCA group received the same volume of saline. General indicators were monitored, and blood samples were collected at baseline and at different time points after resuscitation. At 24 h after resuscitation, pigs were sacrificed, and heart and brain were obtained for cell apoptosis detection, iron deposition staining, oxidative stress detection, and the expression of ferroptosis-related proteins (ACSL4 and GPX4). ResultsSodium octanoate significantly improved mean arterial pressure, cardiac output and ejection fraction induced by TCA. Serum biomarkers of cardiac and cerebral injury were found to increase at all time points after resuscitation, while sodium octanoate significantly reduced their levels. The apoptosis rates of cardiomyocytes and cerebral cortex cells in the SO group were significantly lower than in the TCA group, along with a reduced area of iron deposition staining. The sodium octanoate also reduced oxidative stress and down-regulated ferroptosis which was indicated by protein level alteration of ACSL4 and GPX4. ConclusionOur study's findings suggest that early infusion of sodium octanoate significantly alleviates post-resuscitation cardiac and cerebral injury in a porcine model of TCA, possibly through inhibition of cell apoptosis and GPX4-mediated ferroptosis. Therefore, sodium octanoate could be a potential therapeutic strategy for patients with TCA.

Valproic Acid Treatment Improves Organ Function, Survival Rate, and Lipid Peroxidation in Fatally Scalded Rats

Background After hypovolemic shock caused by severe burns, lipid peroxidation is an important factor in tissue edema and multiorgan dysfunction syndrome (MODS). Many studies have shown that valproic acid (VPA) inhibits lipid peroxidation and reduces tissue and organ injury. Objectives This study investigated whether the VPA treatment of scalded rats reduced tissue edema by inhibiting lipid peroxidation, thereby improving organ function and survival rate. Materials and Methods A total of 60 male Sprague-Dawley rats (weighing: 280–300 g) with a 50% total body surface area (TBSA) full-thickness dermal burn were randomly assigned to the following 3 groups (with 20 rats per group): (I) the no infusion resuscitation (NR) group; (II) the sodium lactate Ringer’s solution (LR) group; and (III) the sodium valproate Ringer’s solution (VR) group. After scalding, the following hemodynamic parameters were measured: Copper2+-Zinc2+-superoxide dismutase (Cu2+-Zn2+-SOD) activity, thiobarbituric acid reactive substances (TBARSs), oxidized glutathione (GSSG), reduced glutathione (GSH), and antioxidant enzyme activities. Organ function parameters and water content were also measured. Another 60 male Sprague-Dawley rats were used to observe the 24-h survival rate of the rats using the same scald model and fluid resuscitation. Results VPA significantly increased the mean arterial pressure (MAP) and cardiac output (CO), and significantly decreased the pulmonary vascular permeability index (PVPI) and extravascular lung water index (ELWI). VPA also increased plasma Cu2+-Zn2+-SOD activity and decreased the plasma TBARS level. VPA reduced the TBARS level and GSSG in various tissues and increased the concentration of GSH. VPA decreased glutathione peroxidase (GPx) and catalase (CAT) activity, but significantly increased glutathione reductase (GR) activity in various tissues. VPA significantly improved organ functions and decreased water content. VPA significantly improved the survival rate, and the 24-h survival rate of the VR group was double that of the LR group. Conclusion Resuscitation with VPA reduced tissue edema, protected visceral functions, and improved the survival rate of rats with severe burn shock (BS) by alleviating lipid peroxidation.

Indirect cardiac output assessment in a swine pediatric acute respiratory distress syndrome model

PurposeTo investigate the correlation between volume of carbon dioxide elimination (V̇CO2) and end-tidal carbon dioxide (PETCO2) with cardiac output (CO) in a swine pediatric acute respiratory distress syndrome (ARDS) model. MethodsRespiratory and hemodynamic variables were collected from twenty-six mechanically ventilated juvenile pigs under general anesthesia before and after inducing ARDS, using oleic acid infusion. ResultsPrior to ARDS induction, mean (SD) CO, V̇CO2, PETCO2, and dead space to tidal volume ratio (Vd/Vt) were 4.16 (1.10) L/min, 103.69 (18.06) ml/min, 40.72 (3.88) mmHg and 0.25 (0.09) respectively. Partial correlation coefficients between average CO, V̇CO2, and PETCO2 were 0.44 (95% confidence interval: 0.18–0.69) and 0.50 (0.18–0.74), respectively. After ARDS induction, mean CO, V̇CO2, PETCO2, and Vd/Vt were 3.33 (0.97) L/min, 113.71 (22.97) ml/min, 50.17 (9.73) mmHg and 0.40 (0.08). Partial correlations between CO and V̇CO2 was 0.01 (−0.31 to 0.37) and between CO and PETCO2 was 0.35 (−0.002 to 0.65). ConclusionARDS may limit the utility of volumetric capnography to monitor CO.

Encouraging Regular Aortic Valve Opening for EVAHEART 2 LVAD Support Using Virtual Patient Hemodynamic Speed Modulation Analysis.

This study focuses on investigating the EVAHEART 2 left ventricular assist device (LVAD) toward designing optimal pump speed modulation (PSM) algorithms for encouraging aortic valve (AV) flow. A custom-designed virtual patient hemodynamic model incorporating the EVAHEART 2 pressure-flow curves, cardiac chambers, and the systemic and pulmonary circulations was developed and used in this study. Several PSM waveforms were tested to evaluate their influence on the mean arterial pressure (MAP), cardiac output (CO), and AV flow for representative heart failure patients. Baseline speeds were varied from 1,600 to 2,000 rpm. For each baseline speed, the following parameters were analyzed: 1) PSM ratio (reduced speed/baseline speed), 2) PSM duration (3-7 seconds), 3) native ventricle contractility, and 4) patient MAP of 70 and 80 mm Hg. More than 2,000 rpm virtual patient scenarios were explored. A lower baseline speed (1,600 and 1,700 rpm) produced more opportunities for AV opening and more AV flow. Higher baseline speeds (1,800 and 2,000 rpm) had lower or nonexistent AV flow. When analyzing PSM ratios, a larger reduction in speed (25%) over a longer PSM (5+ seconds) duration produced the most AV flow. Lower patient MAP and increased native ventricle contractility also contributed to improving AV opening frequency and flow. This study of the EVAHEART 2 LVAD is the first to focus on leveraging PSM to enhance pulsatility and encourage AV flow. Increased AV opening frequency can benefit aortic root hemodynamics, thereby improving patient outcomes.

Improved U-Net Model to Estimate Cardiac Output Based on Photoplethysmography and Arterial Pressure Waveform.

We aimed to estimate cardiac output (CO) from photoplethysmography (PPG) and the arterial pressure waveform (ART) using a deep learning approach, which is minimally invasive, does not require patient demographic information, and is operator-independent, eliminating the need to artificially extract a feature of the waveform by implementing a traditional formula. We aimed to present an alternative to measuring cardiac output with greater accuracy for a wider range of patients. Using a publicly available dataset, we selected 543 eligible patients and divided them into test and training sets after preprocessing. The data consisted of PPG and ART waveforms containing 2048 points with the corresponding CO. We achieved an improvement based on the U-Net modeling framework and built a two-channel deep learning model to automatically extract the waveform features to estimate the CO in the dataset as the reference, acquired using the EV1000, a commercially available instrument. The model demonstrated strong consistency with the reference values on the test dataset. The mean CO was 5.01 ± 1.60 L/min and 4.98 ± 1.59 L/min for the reference value and the predicted value, respectively. The average bias was -0.04 L/min with a -1.025 and 0.944 L/min 95% limit of agreement (LOA). The bias was 0.79% with a 95% LOA between -20.4% and 18.8% when calculating the percentage of the difference from the reference. The normalized root-mean-squared error (RMSNE) was 10.0%. The Pearson correlation coefficient (r) was 0.951. The percentage error (PE) was 19.5%, being below 30%. These results surpassed the performance of traditional formula-based calculation methods, meeting clinical acceptability standards. We propose a dual-channel, improved U-Net deep learning model for estimating cardiac output, demonstrating excellent and consistent results. This method offers a superior reference method for assessing cardiac output in cases where it is unnecessary to employ specialized cardiac output measurement devices or when patients are not suitable for pulmonary-artery-catheter-based measurements, providing a viable alternative solution.

Association between speckle tracking echocardiography and pressure-volume loop derived parameters at increasing levels of myocardial damage in a porcine model of acute cardiogenic shock

Abstract Background Echocardiography is a diagnostic cornerstone in acute cardiovascular care. However, the relationship between speckle tracking assessed global longitudinal strain (LS) and Doppler-based echocardiography with basic physiological markers of cardiac function derived from pressure-volume loops remains poorly elucidated, especially with increasing levels of myocardial damage. Objectives We aimed to describe the association between LS and Doppler-based echocardiography and direct measurements of central hemodynamic parameters from conductance catheter-based pressure-volume loops in an animal model with increasing left ventricular (LV) dysfunction. Methods Twelve Danish landrace pigs weighing 75-80 kg were used. All instrumentations were performed percutaneously, including placement of a conductance catheter in the LV. Progressive LV dysfunction was induced by stepwise embolization trough the left main coronary artery every three minutes until a 50% reduction in cardiac output or mixed venous saturation, compared to baseline, or a mixed venous saturation <30%. Echocardiography was performed through a subxiphoid midline incision, and was done at baseline and 90 seconds after each injection. Results With progressive LV dysfunction, mean cardiac output decreased from 5.6 l/min (SD: 0.9) to 2.1 l/min (SD: 0.9) and mean mixed venous saturation deteriorated from 61.1%(SD: 7.9) to 35.3% (SD: 6.1). Mean LS and LV outflow tract velocity time integral (LVOT VTI) declined from -13.8% (SD 3.0) to -6.1% (SD: 2.0) and 16.9 cm (SD: 2.6) to 7.8 cm (SD: 1.8), respectively (Figure 1). LS and LVOT VTI showed the strongest correlation to stroke work in unadjusted univariate regression (r2=0.53 and r2=0.49, respectively. p<0.01 for both). LS correlated significantly, but modest, with stroke volume (r2=0.46, p<0.01), end-systolic elastance (r2=0.32, p<0.01), systolic blood pressure (r2=0.37, p<0.01), ventriculo-arterial coupling(r2=0.34, p<0.01), and arterial elastance (r2=0.23, p<0.01) (Figure 2). In a multivariate regression analysis, LS showed significant correlation with stroke work, systolic blood pressure, and end-diastolic wall stress (r2=0.60, p<0.01). Conclusion In an animal model of acute progressive LV dysfunction, echocardiographic and conductance catheter-based measurements changed significantly. LS and LVOT VTI displayed the earliest and the largest alterations with increased myocardial damage and LS showed moderate correlations with contractility, arterial elastance and ventriculo-arterial coupling. This indicates that LS is a marker of overall ventricular performance.Echocardiographic changes from baselineScatter plot of LS and hemodynamics

Abstract 11895: Efficacy of Maintaining Mean Aortic Pressure by Percutaneous Left Ventricular Assist Device for Hemodynamic Support in Ventricular Tachycardia Ablation - Relation to Cycle Length

Introduction: Percutaneous left ventricular assist device (pLVAD) has been used to maintain mean aortic pressure (MAP) during ventricular tachycardia (VT) ablation (ABL) and is a class II recommendation. We sought to assess the ability of pLVAD to maintain MAP and its relationship to VT cycle length (CL). Methods: All patients who underwent CA for VT with pLVAD support within a 3-year period were included. Type of pLVAD was determined by operator. Insertion of device was performed under fluoroscopy via femoral arterial sheath. Acute ablation success was defined as absence of inducible VT at end of procedure. Results: A total of 9 patients were included. Most patients had ischemic cardiomyopathy (Table 1); pLVAD was inserted prophylactically in 66.67% of patients and for refractory VT/VF storm in 22.2%. One patient was had critical AS and underwent balloon valvuloplasty prior to VT ablation. Impella CP was used in 78%, and Impella 2.5 in 22%, mean cardiac output was 2.9 + 0.5 L at mean P flow rate 7.3 + 1.3. CARTO was used in 89% and ESI Navx in 11% for electroanatomic/activation mapping. There were no instances of electromagnetic interference, despite the use of magnetic mapping system in all cases (CARTO in 8, Stereotaxis in 1). Mean PCWP was 17.88 + 10.12 pre-ablation vs 23.57 + 8.30 post-ablation (p=ns). There were 24 VTs, 42% were sustained, with a mean CL 342 + 80 msec, ranging from 223 to 558 msec. Mean MAP pre-ablation was 67.44 + 12.85 mmHg vs 61.86 + 13.27 post-ablation with absent negative correlation to VT CL (p=ns). There was no difference in MAP between VT Cl > 300 msec vs < 300 msec: 66 + 11 vs 59 + 14 mm Hg, (p=ns). Mean dose of phenylephrine was 452 mcg. pLVAD was removed at the end of procedure, there were no femoral site complications. Conclusions: pLVAD utilization maintains stable MAP even with faster VT cycle length in patients undergoing VT ABL under general anesthesia obviating need for high dose pressor support.

Abstract 15822: Cardiac Effects of EDG-7500, a Novel Cardiac Sarcomere Regulator: In vitro and in vivo Evidence for Slowing Isovolumic Contraction and Improved Ventricular Compliance

Background: Hypertrophic Cardiomyopathy (HCM) is a disease where excess acto-myosin crossbridge formation results in hyperdynamic contraction, LV hypertrophy, and diastolic dysfunction due to increased myocardial stiffness. Conventional negative inotropes alleviate, to some degree, the systolic alteration in HCM, but do not improve LV filling. EDG-7500 is a small molecule that preferentially decreases diastolic tension and slows the velocity of myocardial force generation by regulating, but not inhibiting, cardiac myosin. This study assessed pharmacodynamic responses to EDG-7500. Methods: Myofilament biomechanics and sarcomere structure were evaluated on LV permeabilized pig fibers. In vivo, dogs were instrumented for arterial pressure and LV pressure-volume recordings. Data were obtained with vehicle, EDG-7500 (n = 5; 0.3 mg/kg IV), or metoprolol (2-4 mg/kg IV, n = 3); systemic and LV hemodynamics and load-independent function were examined. *:P<0.05 for EDG-7500 vs. vehicle Results: X-ray diffraction studies showed EDG-7500 preserved the myosin head population competent to form crossbridges as well as the recruitment of reserve myosin-heads during calcium activation. EDG-7500 (1μM) slowed crossbridge formation, with a limited reduction in maximal force (-6±2%) and decreased diastolic tension. At 0.3 mg/kg, EDG-7500 slowed early contraction (PEP: +10±1%*) and reduced the peak rate of LV pressure development (+dP/dtmax: -8 ± 1%*) with minimal reductions in peak end systolic elastance (Emax: -4±1%*). Systemic mean arterial pressure and cardiac output were unchanged. EDG-7500 increased LV end-diastolic volume (+5 ± 1%*) and preserved LV end-diastolic pressure (EDP: -8 ± 3%, 9 ± 1 to 8 ± 1 mmHg). A downward and rightward shift of the pressure-volume relationship indicated improved LV compliance. β-AR blockade did not elicit this pro-compliant effect (EDP: +26 ± 12%). Conclusions: Cardiac sarcomere regulation with EDG-7500 has a unique cardiovascular profile characterized by the overall preservation of the myosin motor-head population and a slowing of early cardiac contraction and improved LV distensibility. This cardiovascular profile could have salutary effects in patients with HCM or patients with impaired diastolic function.

Using a Mock Circulatory Loop as a Regulatory Science Tool to Simulate Different Heart Failure Conditions.

Mechanical circulatory support (MCS) device therapy is one of the primary treatment options for end-stage heart failure (HF), whereby a mechanical pump is integrated with the failing heart to maintain adequate tissue perfusion. The ISO 14708-5:2020 standard prescribes generic guidelines for nonclinical device evaluation and system performance testing of MCS devices using a mock circulatory loop (MCL). However, the utility of MCLs in premarket regulatory submissions of MCS devices is ambiguous, and the specific disease states that the device is intended to treat are not usually simulated. Hence, we aim to outline the potential of MCLs as a valuable regulatory science tool for characterizing MCS device systems by adequately representing target clinical-use HF conditions on the bench. Target pathophysiologic hemodynamics of HF conditions (i.e., cardiogenic shock (CS), left ventricular (LV) hypertrophy secondary to hypertension, and coronary artery disease), along with a healthy adult at rest and a healthy adult during exercise are provided as recommended test conditions. The conditions are characterized based on LV, aorta, and left atrium pressures using recommended cardiac hemodynamic indices such as systolic, diastolic, and mean arterial pressure, mean cardiac output (CO), cardiac cycle time, and systemic vascular resistance. This study is a first step toward standardizing MCLs to generate well-defined target HF conditions used to evaluate MCS devices.

Role of right heart catheterization in diagnosis of pulmonary arterial hypertension

Abstract Background Pulmonary hypertension (PH) presumably has an impact on 1% or less of the world’s population. Right Heart Catheterization (RHC) is essential for determining PH problems. RHC determines prognosis and offers helpful information on the degree of hemodynamic impairment. Therefore, this comparative study was carried out to determine the diagnostic role, pitfalls associated, and complications encountered during RHC in suspected cases of PAH and chronic thromboembolic pulmonary hypertension (CTEPH). Methods The observational cohort study was conducted on 75 patients with clinical suspicion of PH and CTEPH. All patients were subjected to full history taking, ECG, Echocardiography, and radiological investigations including Chest radiography (CXR), high-resolution computed tomography (HRCT), and computed tomography (CT) pulmonary angiography. Results The mean pulmonary artery mean pressure (PAMP) was 46.05 ± 9.631 mmHg, the mean Pulmonary artery dilatation (PAD) was 30.04 ± 1.082 mm the mean ejection fraction (EF%) was 63.87%, the mean right ventricular diameter was 45.83 ± 0.444 mm. The mean pulmonary artery wedge pressure (PAWP) was 10.91 ± 2.303 mmHg, and the mean cardiac output (CO) was 4.00 ± 0.773 L/min mean cardiac index (CI) was 1.94 ± 0.416 L/min/m2. Doppler echocardiographic estimated pulmonary artery systolic pressure (DE-ePASP) and estimated pulmonary, artery, end-diastolic pressure (ePADP) significantly positively correlated with RHC-PASP (P < 0.001) and mean DE-ePAP significantly positively Correlated with mean RHC-PAP (P < 0.001). Conclusions RHC is still the only method that can completely and accurately diagnose PAH. however, the combination between right cardiac catheterization and echocardiography provides a more accurate diagnosis of the diseases and their complications.

Sex differences in hemodynamic response to high-intensity interval exercise.

Sex differences in the cardiorespiratory and hemodynamic response to exercise exist due to differences in heart size, blood volume, and hemoglobin mass, eliciting higher maximal oxygen uptake (VO2max ) in men versus women. Data are equivocal whether sex differences in training responsiveness occur. This study investigated potential sex differences in the hemodynamic response (stroke volume (SV) and cardiac output (CO)) to high-intensity interval exercise (HIIE). Habitually active men (n = 15) and women (n = 13) underwent VO2max testing, followed by three HIIE sessions consisting of the 4 × 4, 10 × 1, and reduced exertion high-intensity training (REHIT), whose order was randomized. During exercise, oxygen uptake (VO2 ) and hemodynamic responses were determined. Results showed no sex difference in peak relative VO2 (p = 0.263), CO (p = 0.277), or SV (p = 0.116), although absolute values were higher in men (p < 0.05). Peak absolute (127.3 ± 20.6 vs. 115.2 ± 16.6 mL/beat, p = 0.004, d = 0.66) and relative SV (111.0 ± 15.5 vs. 100.7 ± 11.1% max, p = 0.005, d = 0.78) were higher with REHIT versus 4 × 4. No sex differences in mean relative VO2 , CO, or SV occurred (p > 0.05). Data showed lower mean VO2 during REHIT versus 4 × 4 (59.3 ± 6.8 vs. 65.8 ± 5.8 %VO2max , p < 0.001, d = 1.05) and 10 × 1 (59.3 ± 6.8 vs. 69.1 ± 7.4 %VO2max , p < 0.001, d = 1.4). Mean CO was lower in REHIT than 10 × 1 (79.8 ± 8.6 vs. 84.0 ± 7.4% max, p = 0.012, d = 0.53). Previously reported differences in VO2max response to HIIE may not be due to unique hemodynamic responses.

Hemodynamic impact of ephedrine on hypotension during general anesthesia: a prospective cohort study on middle-aged and older patients

BackgroundEphedrine is a mixed α- and β-agonist vasopressor that is frequently used for the correction of hypotension during general anesthesia. β-responsiveness has been shown to decrease with age; therefore, this study aimed to determine whether aging would reduce the pressor effect of ephedrine on hypotension during general anesthesia.MethodsSeventy-five patients aged ≥ 45 years were included in this study, with 25 patients allocated to each of the three age groups: 45–64 years, 65–74 years, and ≥ 75 years. All patients received propofol, remifentanil, and rocuronium for the induction of general anesthesia, followed by desflurane and remifentanil. Cardiac output (CO) was estimated using esCCO technology. Ephedrine (0.1 mg/kg) was administered for the correction of hypotension. The primary and secondary outcome measures were changes in the mean arterial pressure (MAP) and CO, respectively, at 5 min after the administration of ephedrine. ResultsThe administration of ephedrine significantly increased MAP (p < 0.001, mean difference: 8.34 [95% confidence interval (CI), 5.95–10.75] mmHg) and CO (p < 0.001, mean difference: 7.43 [95% CI, 5.20–9.65] %) across all groups. However, analysis of variance revealed that the degree of elevation of MAP (F [2, 72] = 0.546, p = 0.581, η2 = 0.015 [95% CI, 0.000–0.089]) and CO (F [2, 72] = 2.023, p = 0.140, η2 = 0.053 [95% CI, 0.000–0.162]) did not differ significantly among the groups. Similarly, Spearman’s rank correlation and multiple regression analysis revealed no significant relation between age and the changes in MAP or CO after the administration of ephedrine.ConclusionThe administration of ephedrine significantly increased MAP and CO; however, no significant correlation with age was observed in patients aged > 45 years. These findings suggest that ephedrine is effective for the correction of hypotension during general anesthesia, even in elderly patients.Trial registrationUMIN-CTR (UMIN000045038; 02/08/2021).

Cerebral blood flow autoregulation assessment by correlation analysis between mean arterial blood pressure and transcranial doppler sonography or near infrared spectroscopy is different: A pilot study.

Recently, cerebral autoregulation indices based on moving correlation indices between mean arterial pressure (MAP) and cerebral oximetry (NIRS, ORx) or transcranial Doppler (TCD)-derived middle cerebral artery flow velocity (Mx) have been introduced to clinical practice. In a pilot study, we aimed to evaluate the validity of these indices using incremental lower body negative pressure (LBNP) until presyncope representing beginning cerebral hypoperfusion as well as lower body positive pressure (LBPP) with added mild hypoxia to induce cerebral hyperperfusion in healthy subjects. Five male subjects received continuous hemodynamic, TCD and NIRS monitoring. Decreasing levels of LBNP were applied in 5-minute steps until subjects reached presyncope. Increasing levels of LBPP were applied stepwise up to 20 or 25 mmHg. Normobaric hypoxia was added until an oxygen saturation of 84% was reached. This was continued for 10 minutes. ORx and Mx indices were calculated using previously described methods. Both Indices showed an increase > 0.3 indicating impaired cerebral autoregulation during presyncope. However, there was no significant difference in Mx at presyncope compared to baseline (p = 0.168). Mean arterial pressure and cardiac output decreased only in presyncope, while stroke volume was decreased at the last pressure level. Neither Mx nor ORx showed significant changes during LBPP or hypoxia. Agreement between Mx and ORx was poor during the LBNP and LBPP experiments (R2 = 0.001, p = 0.3339). Mx and ORx represent impaired cerebral autoregulation, but in Mx this may not be distinguished sufficiently from baseline. LBPP and hypoxia are insufficient to reach the upper limit of cerebral autoregulation as indicated by Mx and ORx.

Comparison of the effectiveness of USCOM and echocardiography in assessing cardiac output on pediatric patients with shock

BackgroundShock is a circulatory failure, and its clinical manifestations result in decreased cardiac output. Hemodynamic monitoring is important in shock patients to determine further management. Demand for noninvasive examination methods, such as ultrasound cardiac output monitoring (USCOM) and echocardiography, is increasing because of their practicality and lower risks. ObjectivesThe aim of this study is to compare cardiac output determined using USCOM and echocardiography in pediatric patients with shock. MethodsThis prospective observational study used a cross-sectional data collection approach. It collected data on 48 pediatric shock patients in the Pediatric Intensive Care Unit at Kandou General Hospital (Manado, Indonesia) between March and June 2022. The instruments used were USCOM and echocardiography. The regression analysis results are presented as odds ratios (ORs) with 95 % confidence intervals and p < 0.05. ResultsThe mean cardiac output of pediatric patients with shock was 2.50 (standard deviation [SD] = 2.28) with USCOM and 2.45 (SD = 0.77) with echocardiography. Echocardiographic and USCOM cardiac output values were significantly correlated, with a coefficient of determination (R2) of 0.832 (83.2 %), indicating a near-perfect linear correlation. ConclusionThis study's results show that USCOM is as effective as echocardiography in assessing cardiac output in children with shock.

Impact of TAVR on coronary artery hemodynamics using clinical measurements and image‐based patient‐specific in silico modeling

In recent years, transcatheter aortic valve replacement (TAVR) has become the leading method for treating aortic stenosis. While the procedure has improved dramatically in the past decade, there are still uncertainties about the impact of TAVR on coronary blood flow. Recent research has indicated that negative coronary events after TAVR may be partially driven by impaired coronary blood flow dynamics. Furthermore, the current technologies to rapidly obtain non-invasive coronary blood flow data are relatively limited. Herein, we present a lumped parameter computational model to simulate coronary blood flow in the main arteries as well as a series of cardiovascular hemodynamic metrics. The model was designed to only use a few inputs parameters from echocardiography, computed tomography and a sphygmomanometer. The novel computational model was then validated and applied to 19 patients undergoing TAVR to examine the impact of the procedure on coronary blood flow in the left anterior descending (LAD) artery, left circumflex (LCX) artery and right coronary artery (RCA) and various global hemodynamics metrics. Based on our findings, the changes in coronary blood flow after TAVR varied and were subject specific (37% had increased flow in all three coronary arteries, 32% had decreased flow in all coronary arteries, and 31% had both increased and decreased flow in different coronary arteries). Additionally, valvular pressure gradient, left ventricle (LV) workload and maximum LV pressure decreased by 61.5%, 4.5% and 13.0% respectively, while mean arterial pressure and cardiac output increased by 6.9% and 9.9% after TAVR. By applying this proof-of-concept computational model, a series of hemodynamic metrics were generated non-invasively which can help to better understand the individual relationships between TAVR and mean and peak coronary flow rates. In the future, tools such as these may play a vital role by providing clinicians with rapid insight into various cardiac and coronary metrics, rendering the planning for TAVR and other cardiovascular procedures more personalized.

Cardiovascular responses to static handgrip exercise and postexercise ischemia in heart failure with preserved ejection fraction.

Heart failure with preserved ejection fraction (HFpEF) is characterized by reduced ability to sustain physical activity that may be due partly to disease-related changes in autonomic function that contribute to dysregulated cardiovascular control during muscular contraction. Thus, we used a combination of static handgrip exercise (HG) and postexercise ischemia (PEI) to examine the pressor response to exercise and isolate the skeletal muscle metaboreflex, respectively. Mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR) were assessed during 2-min of static HG at 30 and 40% of maximum voluntary contraction (MVC) and subsequent PEI in 16 patients with HFpEF and 17 healthy, similarly aged controls. Changes in MAP were lower in patients with HFpEF compared with controls during both 30%MVC (Δ11 ± 7 vs. Δ15 ± 8 mmHg) and 40%MVC (Δ19 ± 14 vs. Δ30 ± 8 mmHg), and a similar pattern of response was evident during PEI (30%MVC: Δ8 ± 5 vs. Δ12 ± 8 mmHg; 40%MVC: Δ13 ± 10 vs. Δ18 ± 9 mmHg) (group effect: P = 0.078 and P = 0.017 at 30% and 40% MVC, respectively). Changes in HR, CO, and TPR did not differ between groups during HG or PEI (P > 0.05). Taken together, these data suggest a reduced pressor response to static muscle contractions in patients with HFpEF compared with similarly aged controls that may be mediated partly by a blunted muscle metaboreflex. These findings support a disease-related dysregulation in neural cardiovascular control that may reduce an ability to sustain physical activity in HFpEF.NEW & NOTEWORTHY The current investigation has identified a diminution in the exercise-induced rise in arterial blood pressure (BP) that persisted during postexercise ischemia (PEI) in an intensity-dependent manner in patients with heart failure with preserved ejection fraction (HFpEF) compared with older, healthy controls. These findings suggest that the pressor response to exercise is reduced in patients with HFpEF, and this deficit may be mediated, in part, by a blunted muscle metaboreflex, highlighting the consequences of impaired neural cardiovascular control during exercise in this patient group.

Toward smartphone-based blood pressure monitoring

A single-centre, prospective longitudinal study to assess changes in maternal arterial stiffness and cardiac output parameters among low-risk healthy pregnant women.Thirty low-risk, healthy, pregnant women attending their routine antenatal dating ultrasound scan were recruited. Non-invasive assessment of arterial stiffness and cardiac output was undertaken at five gestational windows from 11 to 40 weeks of pregnancy. Data were analysed using a linear mixed model incorporating time and other relevant predictors as fixed effects, and patient as a random effect.Gestational age had a significant effect on all arterial stiffness parameters, including brachial augmentation index (AIx) (p = .001), aortic AIx (p = .002) and aortic pulse wave velocity (p = .002). The aortic AIx (%) reduced during pregnancy: the lowest mean (standard error, SE) was 4.07 (1.01) at 28 weeks before it increased to 7.04 (SE 1.64) at 40 weeks.Similarly, non-invasive assessments of cardiac output (p < .001), stroke volume (p = .014), heart rate (p < .001) and total peripheral resistance (p < .001) demonstrated significant changes with gestational age. Mean cardiac output (l/m) increased during pregnancy reaching a peak at 28 weeks gestation 6.66 (SE 0.28), but dropped thereafter to reach 5.71 (SE 0.25) around term.The current study provides pregnancy normograms for gestational changes in arterial stiffness and cardiac output parameters among low-risk, healthy pregnant women. Further work will be required to assess the risk of placental mediated diseases and pregnancy outcome among pregnant women with parameters outside the normal range.