The ClearSight system measures blood pressure non-invasively and determines cardiac output by analyzing the continuous pressure waveform. We performed a multi-center clinical study in China to test the equivalence of cardiac output measured with the ClearSight system (CSCO) and cardiac output measured with the pulmonary artery catheter bolus thermodilution (TDCO) method.

End-stage heart failure (HF) patients are at high risk for mortality and morbidity. We aimed to study the role of cardiac output (CO) assessed by Doppler as a noninvasive tool, to predict mortality, rehospitalization rate, and left ventricular assist device (LVAD) implantation at 6 months.

Arterial pulse-derived cardiac output monitors are routinely employed to guide hemodynamic management during liver transplant surgery. In this study, we sought to assess the reliability by evaluating the agreement of the cardiac output measured by the FloTrac Vigileo versus pulmonary artery catheter (continuous cardiac output) at specified times during liver transplant.

Capstesia is a software designed for smartphones (AndroidTM/iOSTM) to estimate the cardiac output and other haemodynamic variables from the waveform obtained from an invasive arterial cannula. The technology has been validated by studies in simulated environmental conditions. We compared the cardiac output (CO) and stroke volume variation (SVV) obtained by conventional cardiac output monitor VigileoTM with CO and pulse pressure variation (PPV) extracted from CapstesiaTM, under clinical conditions, intraoperatively.

Various non-invasive methods are available to measure cardiac output (CO) during pregnancy. We compared serial measures of CO using various methods to determine which provided the least variability. Ten patients with spontaneous pregnancy had estimation of CO at baseline prior to becoming pregnant and at the end of the first and third trimesters. Echocardiographic data were used to estimate CO using the Teichholz method, Simpson's biplane method, and the Doppler determined velocity time integral (VTI) method. In addition, a Bioz Dx device was used to estimate CO by impedance cardiography. CO estimated with the VTI method had the lowest beat-to-beat variability. CO estimated with the VTI method was higher than CO estimated with the 2D-Teichholz method and Simpson's method. The percent change in CO during pregnancy was similar for all echo methods (VTI, Teichholz, and Simpson's biplane). Baseline CO determined with impedance cardiography was higher than CO determined with the VTI method. However, change in CO during pregnancy was significantly lower when measured with impedance cardiography. There was marked heterogeneity in the degree of rise in CO during the first trimester (-3 to 55%). The wide variation in the gestational rise in CO was unexpected, and at least in part secondary to variable increase in heart rate. We recommend the use of the Doppler determined VTI method for the estimation of CO in pregnancy.

Induction of general anesthesia frequently induces arterial hypotension, which is often treated with a vasopressor, such as phenylephrine. As a pure α-agonist, phenylephrine is conventionally considered to solely induce arterial vasoconstriction and thus increase cardiac afterload but not cardiac preload. In specific circumstances, however, phenylephrine may also contribute to an increase in venous return and thus cardiac output (CO). The aim of this study is to describe the initial time course of the effects of phenylephrine on various hemodynamic variables and to evaluate the ability of advanced hemodynamic monitoring to quantify these changes through different hemodynamic variables. In 24 patients, after induction of anesthesia, during the period before surgical stimulus, phenylephrine 2 µg kg-1 was administered when the MAP dropped below 80% of the awake state baseline value for > 3 min. The mean arterial blood pressure (MAP), heart rate (HR), end-tidal CO2 (EtCO2), central venous pressure (CVP), stroke volume (SV), CO, pulse pressure variation (PPV), stroke volume variation (SVV) and systemic vascular resistance (SVR) were recorded continuously. The values at the moment before administration of phenylephrine and 5(T5) and 10(T10) min thereafter were compared. After phenylephrine, the mean(SD) MAP, SV, CO, CVP and EtCO2 increased by 34(13) mmHg, 11(9) mL, 1.02(0.74) L min-1, 3(2.6) mmHg and 4.0(1.6) mmHg at T5 respectively, while both dynamic preload variables decreased: PPV dropped from 20% at baseline to 9% at T5 and to 13% at T10 and SVV from 19 to 11 and 14%, respectively. Initially, the increase in MAP was perfectly aligned with the increase in SVR, until 150 s after the initial increase in MAP, when both curves started to dissociate. The dissociation of the evolution of MAP and SVR, together with the changes in PPV, CVP, EtCO2 and CO indicate that in patients with anesthesia-induced hypotension, phenylephrine increases the CO by virtue of an increase in cardiac preload.

The ketone body 3-hydroxybutyrate (3-OHB) increases cardiac output and myocardial perfusion without affecting blood pressure in humans, but the cardiovascular sites of action remain obscure. Here, we test the hypothesis in rats that 3-OHB acts directly on the heart to increase cardiac contractility and directly on blood vessels to lower systemic vascular resistance. We investigate effects of 3-OHB on (a) in vivo hemodynamics using echocardiography and invasive blood pressure measurements, (b) isolated perfused hearts in Langendorff systems, and (c) isolated arteries and veins in isometric myographs. We compare Na-3-OHB to equimolar NaCl added to physiological buffers or injection solutions. At plasma concentrations of 2-4 mM in vivo, 3-OHB increases cardiac output (by 28.3±7.8%), stroke volume (by 22.4±6.0%), left ventricular ejection fraction (by 13.3±4.6%), and arterial dP/dtmax (by 31.9±11.2%) and lowers systemic vascular resistance (by 30.6±11.2%) without substantially affecting heart rate or blood pressure. Applied to isolated perfused hearts at 3-10 mM, 3-OHB increases left ventricular developed pressure by up to 26.3±7.4 mmHg and coronary perfusion by up to 20.2±9.5%. Beginning at 1-3 mM, 3-OHB relaxes isolated coronary (EC50=12.4 mM), cerebral, femoral, mesenteric, and renal arteries as well as brachial, femoral, and mesenteric veins by up to 60% of pre-contraction within the pathophysiological concentration range. Of the two enantiomers that constitute racemic 3-OHB, D-3-OHB dominates endogenously; but tested separately, the enantiomers induce similar vasorelaxation. We conclude that increased cardiac contractility and generalized systemic vasorelaxation can explain the elevated cardiac output during 3-OHB administration. These actions strengthen the therapeutic rationale for 3-OHB in heart failure management.

To determine the increment in cardiac output and in O2 consumption (Vo2) from quiet breathing to maximal sustained ventilation, Vo2 and cardiac output were measured using an acetylene rebreathing technique in five subjects. Cardiac output and Vo2 were measured multiple times in each subject at rest and during sustained maximal ventilation. During maximal ventilation subjects breathed 5% CO2 to prevent hypocapnia. The increase in cardiac output from rest to maximal breathing was taken as an estimate of respiratory muscle blood flow and was used to calculate the arteriovenous O2 content difference across the respiratory muscles from the Fick equation. Cardiac output increased by 4.3 +/- 1.0 l/min (mean +/- SD), from 5.6 +/- 0.7 l/min at rest to 9.9 +/- 1.1 l/min, during maximal ventilations ranging from 127 to 193 l/min. Vo2 increased from 312 +/- 29 to 723 +/- 69 ml/min during maximal ventilation. O2 extraction across the respiratory muscles during maximal breathing was 9.6 +/- 1.0 vol% (range 8.5 to 10.7 vol%). These values suggest an upper limit of respiratory muscle blood flow of 3-5 l/min during unloaded maximal sustained ventilation.

Prophylactic milrinone is commonly used to prevent Low Cardiac Output Syndrome (LCOS) after pediatric cardiac surgery. This study compares the use of levosimendan with milrinone when used as the primary inotrope following pediatric cardiac surgery.

Subclinical reductions in cardiac output correspond to lower cerebral blood flow (CBF), placing the brain at risk for functional changes.

There is little published data investigating non-invasive cardiac output monitoring in the emergency department (ED). We assess here the accuracy of five non-invasive methods in detecting fluid responsiveness in the ED: (1) common carotid artery blood flow, (2) suprasternal aortic Doppler, (3) bioreactance, (4) plethysmography with digital vascular unloading method, and (5) inferior vena cava collapsibility index. Left ventricular outflow tract echocardiography derived velocity time integral is the reference standard. This follows an assessment of feasibility and repeatability of these methods in the same cohort of ED patients.

Caveolae are strikingly abundant in endothelial cells, yet the physiological functions of caveolae in endothelium and other tissues remain incompletely understood. Previous studies suggest a mechanoprotective role, but whether this is relevant under the mechanical forces experienced by endothelial cells in vivo is unclear. In this study we have sought to determine whether endothelial caveolae disassemble under increased hemodynamic forces, and whether caveolae help prevent acute rupture of the plasma membrane under these conditions. Experiments in cultured cells established biochemical assays for disassembly of caveolar protein complexes, and assays for acute loss of plasma membrane integrity. In vivo, we demonstrate that caveolae in endothelial cells of the lung and cardiac muscle disassemble in response to acute increases in cardiac output. Electron microscopy and two-photon imaging reveal that the plasma membrane of microvascular endothelial cells in caveolin 1(-/-) mice is much more susceptible to acute rupture when cardiac output is increased. These data imply that mechanoprotection through disassembly of caveolae is important for endothelial function in vivo.

Bioreactance is the continuous analysis of transthoracic voltage variation in response to an applied high frequency transthoracic current and was recently introduced for non-invasive cardiac output measurement (NICOM). We evaluated NICOM compared to thermodilution (TD) in adult horses. Six healthy horses were used for this prospective, blinded, experimental study. Cardiac output (CO) measurements were performed simultaneously using TD and the bioreactance method. Different cardiac output scenarios were established using xylazine (0.5 mg/kg IV) and dobutamine (1.5-3 mcg/kg/min). Statistical analysis was performed by calculating the concordance rate, performing a regression analysis, Pearson correlation, and Bland Altman. The TD-based CO and NICOM values were highly correlated for low, normal and high CO values with an overall correlation coefficient. A 4-quadrant plot showed an 89% rate of concordance. The linear regression calculated a relationship between NICOM and TDCO of Y = 0.4874 · X + 0.5936. For the corrected Bland Altman agreement, the mean bias and lower/upper limits of agreement were -0.26 and -3.88 to 3.41 L/min, respectively. Compared to TD, bioreactance- based NICOM showed good accuracy at induced low, normal, and high CO states in normal horses. Future studies performed under more clinical conditions will show if this monitor can help to assess hemodynamic status and guide therapy in horses in ICU settings and under general anesthesia.

To describe early, continuous, non-invasive measures of cardiac output (CO) and evolution over time in infants with hypoxic-ischaemic encephalopathy (HIE).

Cardiac power output (CPO), derived from the product of cardiac output and mean aortic pressure, is an important yet underexploited parameter for hemodynamic monitoring of critically ill patients in the intensive-care unit (ICU). The conductance catheter-derived pressure-volume loop area reflects left ventricular stroke work (LV SW). Dividing LV SW by time, a measure of LV SW min- 1 is obtained sharing the same unit as CPO (W). We aimed to validate CPO as a marker of LV SW min- 1 under various inotropic states.

Monitoring cardiac output (CO) is important to optimize hemodynamic function in critically ill patients. The prevalence of aortic valve insufficiency (AI) is rising in the aging population. However, reliability of CO monitoring techniques in AI is unknown. The aim of this study was to investigate the impact of AI on accuracy, precision, and trending ability of transcardiopulmonary thermodilution-derived COTCPTD in comparison with pulmonary artery catheter thermodilution COPAC.

Hepatic fibrosis progresses with right heart failure, and becomes cardiac cirrhosis in a severe case. Although its causal factor still remains unclear. Here we evaluated the progression of hepatic fibrosis using a pulmonary artery banding (PAB)-induced right heart failure model and investigated whether cardiac output (CO) is responsible for the progression of hepatic fibrosis.

During vertebrate evolution there has been a shift in the way in which the heart varies cardiac output (the product of heart rate and stroke volume). While mammals, birds, and amphibians increase cardiac output through large increases in heart rate and only modest increases (approximately 30%) in stroke volume, fish and some reptiles use modest increases in heart rate and very large increases in stroke volume (up to 300%). The cellular mechanisms underlying these fundamentally different approaches to cardiac output modulation are unknown. We hypothesized that the divergence between volume modulation and frequency modulation lies in the response of different vertebrate myocardium to stretch. We tested this by progressively stretching individual cardiac myocytes from the fish heart while measuring sarcomere length (SL), developed tension, and intracellular Ca2+ ([Ca2+]i) transients. We show that in fish cardiac myocytes, active tension increases at SLs greater than those previously demonstrated for intact mammalian myocytes, representing a twofold increase in the functional ascending limb of the length-tension relationship. The mechanism of action is a length-dependent increase in myofilament Ca2+ sensitivity, rather than changes in the [Ca2+]i transient or actin filament length in the fish cell. The capacity for greater sarcomere extension in fish myocardium may be linked to the low resting tension that is developed during stretch. These adaptations allow the fish heart to volume modulate and thus underpin the fundamental difference between the way fish and higher vertebrates vary cardiac output.

Critical care ultrasonography (CCUS) is increasingly applied also in the intensive care unit (ICU) and performed by non-experts, including even medical students. There is limited data on the training efforts necessary for novices to attain images of sufficient quality. There is no data on medical students performing CCUS for the measurement of cardiac output (CO), a hemodynamic variable of importance for daily critical care.

Background Sepsis is the overwhelming host response to infection leading to shock and multiple organ dysfunction. Cardiovascular complications greatly increase sepsis-associated mortality. Although murine models are routinely used for preclinical studies, the benefit of using genetically engineered mice in sepsis is countered by discrepancies between human and mouse sepsis pathophysiology. Therefore, recent guidelines have called for standardization of preclinical methods to document organ dysfunction. We investigated the course of cardiac dysfunction and myocardial load in different mouse models of sepsis to identify the optimal measurements for early systolic and diastolic dysfunction. Methods and Results We performed speckle-tracking echocardiography and assessed blood pressure, plasma inflammatory cytokines, lactate, B-type natriuretic peptide, and survival in mouse models of endotoxemia or polymicrobial infection (cecal ligation and puncture, [ CLP ]) of moderate and high severity. We observed that myocardial strain and cardiac output were consistently impaired early in both sepsis models. Suppression of cardiac output was associated with systolic dysfunction in endotoxemia or combined systolic dysfunction and reduced preload in the CLP model. We found that cardiac output at 2 hours post- CLP is a negative prognostic indicator with high sensitivity and specificity that predicts mortality at 48 hours. Using a known antibiotic (ertapenem) treatment, we confirmed that this approach can document recovery. Conclusions We propose a non-invasive approach for assessment of cardiac function in sepsis and myocardial strain and strain rate as preferable measures for monitoring cardiovascular function in sepsis mouse models. We further show that the magnitude of cardiac output suppression 2 hours post- CLP can be used to predict mortality.