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.

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.

Low cardiac output syndrome (LCOS) is an important complication of cardiac surgery. It is associated with increased morbidity and mortality. The incidence of LCOS after surgery is high in patients with congenital heart disease (CHD). Therefore, determining the risk factors of LCOS has clinical significance for the management of CHD. This study aimed to analyze the risk factors of LCOS.

It's necessary to analyze the related risk factors and complications of low cardiac output syndrome (LCOS) after operation in children with congenital heart disease (CHD), to elucidate the management strategy of LCOS.

To describe the relationship between cerebral oxygenation, cardiac output, arterial blood pressure (BP), and cerebral blood flow velocity in extremely low gestational age neonates (ELGANs) during transition.

Despite 5-7 months of physical inactivity during hibernation, brown bears (Ursus arctos) are able to cope with physiological conditions that would be detrimental to humans. During hibernation, the tissue metabolic demands fall to 25% of the active state. Our objective was to assess cardiac function associated with metabolic depression in the hibernating vs. active states in free-ranging Scandinavian brown bears.

Low-cardiac output syndrome (LCOS) after cardiac surgery secondary to systemic hypoperfusion is associated with a higher incidence of renal and neurological damage. A range of effective therapies are available for LCOS. The beneficial systemic effects of levosimendan persist even after cardiac output is restored, which suggests an independent cardioprotective effect.

Previous studies have shown beneficial effects of levosimendan in high-risk patients undergoing cardiac surgery. Two large randomized controlled trials (RCTs), however, showed no advantages of levosimendan.

Low cardiac output syndrome (LCOS) is a severe complication after valve surgery, with no uniform standard for early identification. We developed interpretative machine learning (ML) models for predicting LCOS risk preoperatively and 0.5 h postoperatively for intervention in advance.

Cardiac surgery employing cardiopulmonary bypass exposes infants to a high risk of morbidity and mortality. The objective of this study was to assess the utility of clinical and laboratory variables to predict the development of low cardiac output syndrome, a frequent complication following cardiac surgery in infants. We performed a prospective observational study in the pediatric cardiovascular ICU in an academic children's hospital. Thirty-one patients with congenital heart disease were included. Serum levels of nucleosomes and a panel of 20 cytokines were measured at six time points in the perioperative period. Cardiopulmonary bypass patients were characterized by increased levels of interleukin-10, -6, and -1α upon admission to the ICU compared to non-bypass cardiac patients. Patients developing low cardiac output syndrome endured longer aortic cross-clamp time and required greater inotropic support at 12 h postoperatively compared to bypass patients not developing the condition. Higher preoperative interleukin-10 levels and 24 h postoperative interleukin-8 levels were associated with low cardiac output syndrome. Receiver operating characteristic curve analysis demonstrated a moderate capability of aortic cross-clamp duration to predict low cardiac output syndrome but not IL-8. In conclusion, low cardiac output syndrome was best predicted in our patient population by the surgical metric of aortic cross-clamp duration.

Veno-arterial extracorporeal life support (VA-ECLS) results in cardiopulmonary shunting with reduced native cardiac output (NCO). Low NCO occurrence is common and associated with risk of thromboembolic and pulmonary complications. Practical tools for monitoring NCO during VA-ECLS would therefore be valuable. Pulse pressure (PP) and end-tidal carbon dioxide (EtCO2) are known to be related to cardiac output. We have designed a study to test whether PP and EtCO2 were efficient for the monitoring of NCO during VA-ECLS.

Cardiovascular adaptations to exercise, particularly at the individual level, remain poorly understood. Previous group level research suggests the relationship between cardiac output and oxygen consumption ([Formula: see text]-[Formula: see text]) is unaffected by training as submaximal [Formula: see text] is unchanged. We recently identified substantial inter-individual variation in the exercise [Formula: see text]-[Formula: see text] relationship that was correlated to stroke volume (SV) as opposed to arterial oxygen content. Therefore we explored the effects of sprint interval training (SIT) on modulating [Formula: see text]-[Formula: see text] given an individual's specific [Formula: see text]-[Formula: see text] relationship. 22 (21±2 yrs) healthy, recreationally active males participated in a 4-week SIT (8, 20 second sprints; 4x/week, 170% of the work rate at [Formula: see text] peak) study with progressive exercise tests (PET) until exhaustion. Cardiac output ([Formula: see text] L/min; inert gas rebreathe, Finometer Modelflow™), oxygen consumption ([Formula: see text] L/min; breath-by-breath pulmonary gas exchange), quadriceps oxygenation (near infrared spectroscopy) and exercise tolerance (6-20; Borg Scale RPE) were measured throughout PET both before and after training. Data are mean Δ from bsl±SD. Higher [Formula: see text] ([Formula: see text]) and lower [Formula: see text] ([Formula: see text]) responders were identified post hoc (n = 8/group). SIT increased the [Formula: see text]-[Formula: see text] post-training in [Formula: see text] (3.8±0.2 vs. 4.7±0.2; P = 0.02) while [Formula: see text] was unaffected (5.8±0.1 vs. 5.3±0.6; P = 0.5). [Formula: see text] was elevated beyond 80 watts in [Formula: see text] due to a greater increase in SV (all P<0.04). Peak [Formula: see text] (ml/kg/min) was increased in [Formula: see text] (39.7±6.7 vs. 44.5±7.3; P = 0.015) and [Formula: see text] (47.2±4.4 vs. 52.4±6.0; P = 0.009) following SIT, with [Formula: see text] having a greater peak [Formula: see text] both pre (P = 0.02) and post (P = 0.03) training. Quadriceps muscle oxygenation and RPE were not different between groups (all P>0.1). In contrast to [Formula: see text], [Formula: see text] responders are capable of improving submaximal [Formula: see text]-[Formula: see text] in response to SIT via increased SV. However, the increased submaximal exercise [Formula: see text] does not benefit exercising muscle oxygenation.

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.

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.

ECMO is the most frequently used mechanical support for patients suffering from low cardiac output syndrome. Combining IABP with ECMO is believed to increase coronary artery blood flow, decrease high afterload, and restore systemic pulsatile flow conditions. This study evaluates that combined effect on coronary artery flow during various load conditions using an in vitro circuit. In doing so, different clinical scenarios were simulated, such as normal cardiac output and moderate-to-severe heart failure. In the heart failure scenarios, we used peripheral ECMO support to compensate for the lowered cardiac output value and reach a default normal value. The increase in coronary blood flow using the combined IABP-ECMO setup was more noticeable in low heart rate conditions. At baseline, intermediate and severe LV failure levels, adding IABP increased coronary mean flow by 16%, 7.5%, and 3.4% (HR 60 bpm) and by 6%, 4.5%, and 2.5% (HR 100 bpm) respectively. Based on our in vitro study results, combining ECMO and IABP in a heart failure setup further improves coronary blood flow. This effect was more pronounced at a lower heart rate and decreased with heart failure, which might positively impact recovery from cardiac failure.

Introduction: Low cardiac output syndrome is one of the postoperative complications that are associated with significant morbidity and mortality after surgical closure of atrial septal defect (ASD) with small-sized left ventricle (LV). This study investigated whether preoperative left ventricular end-diastolic volume index (LVEDVi) could accurately predict low cardiac output syndrome (LCOS) after surgical closure of ASD with small-sized LV. Method: This retrospective cohort study involved adult ASD patients with small-sized LV from January 2018 to December 2019 in National Cardiovascular Center Harapan Kita. Preoperative MRI data to assess the left and right ventricle volume were collected. A bivariate analysis using independent Student's t-test was done. Diagnostic test using receiver operating characteristic (ROC) curve was also done to obtain the area under the curve (AUC) value. The best cutoff point was determined by Youden's index. Result: Fifty-seven subjects were involved in this study [age (mean ± SD) 32.56 ± 13.15 years; weight (mean ± SD) 48.82 ± 12.15 kg]. Subjects who had post-operative LCOS (n = 30) have significantly lower LVEDVi (45.0 ± 7.42 ml/m2 vs. 64.15 ± 13.37 ml/m2; p < 0.001), LVEDV (64.6 ± 16.0 ml vs. 85.9 ± 20.7 ml; p < 0.001), LVSV (38.97 ± 11.5 ml vs. 53.13 ± 7.5 ml; p < 0.001), and LVSVi (27.28 ± 8.55 ml/m2 vs. 37.42 ± 5.35 ml/m2; p < 0.001) compared to subjects who did not have post-operative LCOS (n = 27). ROC analysis showed that the best AUC was found on LVEDVi (AUC 95.3%; 95% confidence interval: 90.6-100%). The best cutoff value for LVEDVi to predict the occurrence of LCOS after surgical closure of ASD was 53.3 ml/m2 with a sensitivity of 86.7% and a specificity of 85.2%. Conclusion: This study showed that preoperative LVEDVi could predict LCOS after surgical closure of ASD with small-sized LV with a well-defined cutoff. The best cutoff value of LVEDVi to predict the occurrence of LCOS after surgical ASD closure was 53.5 ml/m2.

Enhanced carotid body (CB) chemoreflex function is strongly related to cardiorespiratory disorders and disease progression in heart failure (HF). The mechanisms underlying CB sensitization during HF are not fully understood, however previous work indicates blood flow per se can affect CB function. Then, we hypothesized that the CB-mediated chemoreflex drive will be enhanced only in low output HF but not in high output HF. Myocardial infarcted rats and aorto-caval fistulated rats were used as a low output HF model (MI-CHF) and as a high output HF model (AV-CHF), respectively. Blood flow supply to the CB region was decreased only in MI-CHF rats compared to Sham and AV-CHF rats. MI-CHF rats exhibited a significantly enhanced hypoxic ventilatory response compared to AV-CHF rats. However, apnea/hypopnea incidence was similarly increased in both MI-CHF and AV-CHF rats compared to control. Kruppel-like factor 2 expression, a flow sensitive transcription factor, was reduced in the CBs of MI-CHF rats but not in AV-CHF rats. Our results indicate that in the setting of HF, potentiation of the CB chemoreflex is strongly associated with a reduction in cardiac output and may not be related to other pathophysiological consequences of HF.

Background. Surgical correction of mitral regurgitation (MR) can lead to postoperative low cardiac output state. We aimed to assess the acute hemodynamic changes after percutaneous MitraClip therapy (a unique model without influence of factors linked to surgical procedure) in patients with functional MR without the influence of general anaesthesia. Methods. We studied invasive hemodynamic parameters in 23 patients before procedure (conscious, nonsedated patients), during procedure (intubated patients), and the first day after MitraClip implantation (conscious, extubated patients). Results. Mitral valve clipping significantly increased cardiac index (CI) (from 2.0 ± 0.5 to 3.3 ± 0.6 L/min/m2; p < 0.01). Conversely, there was significant reduction in the mean pulmonary capillary wedge pressure (PCWP) (from 18.6 ± 5.7 to 10.5 ± 3.8 mmHg; p < 0.01), mean pulmonary artery pressure (from 29.8 ± 10.9 to 25.2 ± 10.3 mmHg; p = 0.03), and pulmonary vascular resistance index (from 531 ± 359 to 365 ± 193 dyn·s·cm-5/m2; p = 0.03). Conclusions. The functional MR therapy with percutaneous MitraClip device results in significant increase in CI (+66%) and concomitant decrease in PCWP (-42%). None of our patients developed low cardiac output state. Our results support the idea that significant part of low cardiac output state after cardiac surgery is due to surgery related factors rather than due to increase in afterload after MR elimination.

Cardiac output monitoring is used in critically ill and high-risk surgical patients. Intermittent pulmonary artery thermodilution and transpulmonary thermodilution, considered the gold standard, are invasive and linked to complications. Therefore, many non-invasive cardiac output devices have been developed and studied. One of those is electrical cardiometry. The results of validation studies are conflicting, which emphasize the need for definitive validation of accuracy and precision. We performed a database search of PubMed, Embase, Web of Science and the Cochrane Library of Clinical Trials to identify studies comparing cardiac output measurement by electrical cardiometry and a reference method. Pooled bias, limits of agreement (LoA) and mean percentage error (MPE) were calculated using a random-effects model. A pooled MPE of less than 30% was considered clinically acceptable. A total of 13 studies in adults (620 patients) and 11 studies in pediatrics (603 patients) were included. For adults, pooled bias was 0.03 L min-1 [95% CI - 0.23; 0.29], LoA - 2.78 to 2.84 L min-1 and MPE 48.0%. For pediatrics, pooled bias was - 0.02 L min-1 [95% CI - 0.09; 0.05], LoA - 1.22 to 1.18 L min-1 and MPE 42.0%. Inter-study heterogeneity was high for both adults (I2 = 93%, p < 0.0001) and pediatrics (I2 = 86%, p < 0.0001). Despite the low bias for both adults and pediatrics, the MPE was not clinically acceptable. Electrical cardiometry cannot replace thermodilution and transthoracic echocardiography for the measurement of absolute cardiac output values. Future research should explore it's clinical use and indications.

We examined the relationship between changes in cardiac output and middle cerebral artery mean blood velocity (MCA V(mean)) in seven healthy volunteer men at rest and during 50% maximal oxygen uptake steady-state submaximal cycling exercise. Reductions in were accomplished using lower body negative pressure (LBNP), while increases in were accomplished using infusions of 25% human serum albumin. Heart rate (HR), arterial blood pressure and MCA V(mean) were continuously recorded. At each stage of LBNP and albumin infusion was measured using an acetylene rebreathing technique. Arterial blood samples were analysed for partial pressure of carbon dioxide tension (P(a,CO2). During exercise HR and were increased above rest (P < 0.001), while neither MCA V(mean) nor P(a,CO2) was altered (P > 0.05). The MCA V(mean) and were linearly related at rest (P < 0.001) and during exercise (P = 0.035). The slope of the regression relationship between MCA V(mean) and at rest was greater (P = 0.035) than during exercise. In addition, the phase and gain between MCA V(mean) and mean arterial pressure in the low frequency range were not altered from rest to exercise indicating that the cerebral autoregulation was maintained. These data suggest that the associated with the changes in central blood volume influence the MCA V(mean) at rest and during exercise and its regulation is independent of cerebral autoregulation. It appears that the exercise induced sympathoexcitation and the change in the distribution of between the cerebral and the systemic circulation modifies the relationship between MCA V(mean) and .