Haemodynamic effects of labetalol in isoflurane-anaesthetized dogs that received dexmedetomidine: A randomized clinical trial.

OBJECTIVE: To test whether labetalol improved cardiovascular function in anaesthetized dogs injected with dexmedetomidine. STUDY DESIGN: Prospective, randomized, blinded, clinical trial. ANIMALS: A group of 20 healthy client-owned dogs undergoing ovariohysterectomy. METHODS: Each dog received dexmedetomidine (5 µg kg-1) and methadone (0.2 mg kg-1) intramuscularly. General anaesthesia was induced with propofol and maintained with isoflurane in oxygen. All dogs were mechanically ventilated, and epidural anaesthesia with lidocaine was performed. Standard anaesthetic monitoring, invasive blood pressure, oesophageal Doppler and near-infrared tissue perfusion/oxygenation were applied. Peak velocity (PV), mean acceleration and stroke distance (SD) from the oesophageal Doppler were recorded. Arterial elastance (Ea) was calculated. Tissue oxygenation (rStO2) was also recorded. Prior to surgery, animals received either 0.1 mg kg-1 of labetalol intravenously (IV) over 60 seconds or the equivalent volume of saline. Data were recorded for 20 minutes. Age, weight and propofol dose were compared with a Wilcoxon rank-sum test. The effects of time, treatment and their interaction with haemodynamic and perfusion variables were analysed with mixed-effect models and Tukey's post hoc tests. RESULTS: Significant effects of the interaction between treatment and time were observed whereby heart rate (HR) was higher in dogs given labetalol (p = 0.01), whereas arterial blood pressure and Ea were lower (p < 0.01). Similarly, PV, SD and rStO2 were higher in the labetalol group, and significant effects were detected for the interaction between treatment and time (p < 0.01). CONCLUSIONS AND CLINICAL RELEVANCE: Labetalol at a dose of 0.1 mg kg-1 IV in dogs under general anaesthesia and administered a pre-anaesthetic medication of dexmedetomidine produced mild vasodilation (reduction of Ea), resulting in an increase in HR and left ventricular outflow. Although labetalol could be an effective option to achieve haemodynamic optimization after dexmedetomidine-induced vasoconstriction, future studies are needed to assess long-term effects.

Real-world outcomes of the hypotension prediction index in the management of intraoperative hypotension during non-cardiac surgery: a retrospective clinical study.

The Hypotension Prediction Index (HPI) is a validated algorithm developed by applying machine learning for predicting intraoperative arterial hypotension (IOH). We evaluated whether the HPI, combined with a personalized treatment protocol, helps to reduce IOH (depth and duration) and perioperative events in real practice. This was a single-center retrospective study including 104 consecutive adults undergoing urgent or elective non-cardiac surgery with moderate-to-high risk of bleeding, requiring invasive blood pressure and continuous cardiac output monitoring. Depending on the sensor, two comparable groups were identified: patients managed following the institutional protocol of personalized goal-directed fluid therapy (GDFT, n = 52), or this GDFT supported by the HPI (HPI, n = 52). The time-weighted average of hypotension for a mean arterial pressure < 65 mmHg (TWAMAP<65), postoperative complications and length of hospital stay (LOS) were automatically downloaded from medical records and revised by clinicians blinded to the management received by patients. Differences in preoperative variables (i.e. physical status -ASA class-, acute kidney Injury-AKI- risk) and outcomes were analyzed using non-parametric tests with Hodges-Lehmann estimator for the median of differences. ASA class and AKI risk were similar (p = 0.749 and p = 0.837, respectively). Blood loss was also comparable (p = 0.279). HPI patients had a lower TWAMAP<65 [0.09 mmHg (0-0.48 mmHg)] vs [0.23 mmHg (0.01 to 0.97 mmHg)], p = 0.037. Postoperative complications were less prevalent in the HPI patients (0.46 ± 0.98 vs. 0.88 ± 1.20), p = 0.035. Finally, LOS was significantly shorter among HPI patients with a median difference of 2 days (p = 0.019). The HPI combined with a GDFT protocol may help to minimize the severity of IOH during non-cardiac surgery.

Pharmacodynamic analysis of a fluid challenge with 4 ml kg-1 over 10 or 20 min: a multicenter cross-over randomized clinical trial.

PURPOSE: A number of studies performed in the operating room evaluated the hemodynamic effects of the fluid challenge (FC), solely considering the effect before and after the infusion. Few studies have investigated the pharmacodynamic effect of the FC on hemodynamic flow and pressure variables. We designed this trial aiming at describing the pharmacodynamic profile of two different FC infusion times, of a fixed dose of 4 ml kg-1. METHODS: Forty-nine elective neurosurgical patients received two consecutive FCs of 4 ml kg-1 of crystalloids in 10 (FC10) or 20 (FC20) minutes, in a random order. Fluid responsiveness was defined as stroke volume index increase ≥ 10%. We assessed the net area under the curve (AUC), the maximal percentage difference from baseline (dmax), time when the dmax was observed (tmax), change from baseline at 1-min (d1) and 5-min (d5) after FC end. RESULTS: After FC10 and FC20, 25 (51%) and 14 (29%) of 49 patients were classified as fluid responders (p = 0.001). With the exception of the AUCs of SAP and MAP, the AUCs of all the considered hemodynamic variables were comparable. The dmax and the tmax were overall comparable. In both groups, the hemodynamic effects on flow variables were dissipated within 5 min after FC end. CONCLUSIONS: The infusion time of FC administration affects fluid responsiveness, being higher for FC10 as compared to FC20. The effect on flow variables of either FCs fades 5 min after the end of infusion.

Reliability of effective arterial elastance using peripheral arterial pressure as surrogate for left ventricular end-systolic pressure.

To compare the effective arterial elastance (Ea) obtained from the arterial pressure with Ea calculated from left-ventricular (LV) pressure-volume analysis. Experimental study. LV pressure-volume data was obtained with a conductance catheter and arterial pressures were measured via a fluid-filled catheter placed in the proximal aorta, femoral and radial arteries. Ea was calculated as LV end-systolic pressure (ESP)/stroke volume (SV). Experimental protocol consisted sequentially changing afterload (phenylephrine/nitroprusside), preload (bleeding/fluid), and contractility (esmolol/dobutamine). 90% of systolic pressure (Eaao_SYS, Eafem_SYS, Earad_SYS), mean arterial pressure (Eaao_MAP, Eafem_MAP, Earad_MAP), and dicrotic notch pressure (Eaao_DIC, Eafem_DIC, Earad_DIC) were used as surrogates for LV ESP. SV was calculated from the LV pressure-volume data. When Ea was compared with estimations based on 90% SAP, the relationship was r2 = 0.95, 0.94 and 0.92; and the bias and limits of agreement (LOA): - 0.01 ± 0.12, - 0.09 ± 0.12, - 0.05 ± 0.15 mmHg ml-1, for Eaao_SYS, Eafem_SYS and Earad_SYS, respectively. For estimates using dicrotic notch, the relationship was r2 = 0.94, 0.95 and 0.94 for Eaao_DIC, Eafem_DIC and Earad_DIC, respectively; with a bias and LOA: 0.05 ± 0.11, 0.06 ± 0.12, 0.10 ± 0.12 mmHg ml-1, respectively. When Ea was compared with estimates using MAP, the relationship was r2 = 0.95, 0.96 and 0.95 for Eaao_MAP, Eafem_MAP and Earad_MAP, respectively; with a bias and LOA: 0.05 ± 0.11, 0.06 ± 0.11, 0.06 ± 0.11 mmHg ml-1, respectively. LV ESP can be estimated from the arterial pressure. Provided that the SV measurement is reliable, the ratio MAP/SV provides a robust Ea surrogate over a wide range of hemodynamic conditions and is interchangeably in any peripheral artery, so it should be recommended as an arterial estimate of Ea in further research.

Performance comparison of ventricular and arterial dP/dtmax for assessing left ventricular systolic function during different experimental loading and contractile conditions.

BACKGROUND: Maximal left ventricular (LV) pressure rise (LV dP/dtmax), a classical marker of LV systolic function, requires LV catheterization, thus surrogate arterial pressure waveform measures have been proposed. We compared LV and arterial (femoral and radial) dP/dtmax to the slope of the LV end-systolic pressure-volume relationship (Ees), a load-independent measure of LV contractility, to determine the interactions between dP/dtmax and Ees as loading and LV contractility varied. METHODS: We measured LV pressure-volume data using a conductance catheter and femoral and radial arterial pressures using a fluid-filled catheter in 10 anesthetized pigs. Ees was calculated as the slope of the end-systolic pressure-volume relationship during a transient inferior vena cava occlusion. Afterload was assessed by the effective arterial elastance. The experimental protocol consisted of sequentially changing afterload (phenylephrine/nitroprusside), preload (bleeding/fluid bolus), and contractility (esmolol/dobutamine). A linear-mixed analysis was used to assess the contribution of cardiac (Ees, end-diastolic volume, effective arterial elastance, heart rate, preload-dependency) and arterial factors (total vascular resistance and arterial compliance) to LV and arterial dP/dtmax. RESULTS: Both LV and arterial dP/dtmax allowed the tracking of Ees changes, especially during afterload and contractility changes, although arterial dP/dtmax was lower compared to LV dP/dtmax (bias 732 ± 539 mmHg⋅s- 1 for femoral dP/dtmax, and 625 ± 501 mmHg⋅s- 1 for radial dP/dtmax). Changes in cardiac contractility (Ees) were the main determinant of LV and arterial dP/dtmax changes. CONCLUSION: Although arterial dP/dtmax is a complex function of central and peripheral arterial factors, radial and particularly femoral dP/dtmax allowed reasonably good tracking of LV contractility changes as loading and inotropic conditions varied.

Predictors to Intravenous Fluid Responsiveness.

Management with intravenous fluids can improve cardiac output in some surgical patients. Management with static preload indicators, such as central venous pressure and pulmonary artery occlusion pressure, has not demonstrated a suitable relationship with changes in the cardiac output induced by intravenous fluid therapy. Dynamic indicators, such as the variability of arterial pulse pressure or stroke volume variation, have demonstrated a suitable relationship. Since improvement in cardiac output does not guarantee an adequate perfusion pressure, in patients with hypotension, it is also necessary to know whether arterial pressure will also increase with intravenous fluid therapy. In this regard, the functional assessment of arterial load by dynamic arterial elastance could help to determine which patients will improve not only their cardiac output but also their mean arterial pressure.

Impact of arterial load on the agreement between pulse pressure analysis and esophageal Doppler.

INTRODUCTION: The reliability of pulse pressure analysis to estimate cardiac output is known to be affected by arterial load changes. However, the contribution of each aspect of arterial load could be substantially different. In this study, we evaluated the agreement of eight non-commercial algorithms of pulse pressure analysis for estimating cardiac output (PPCO) with esophageal Doppler cardiac output (EDCO) during acute changes of arterial load. In addition, we aimed to determine the optimal arterial load parameter that could detect a clinically significant difference between PPCO and the EDCO. METHODS: We included mechanically ventilated patients monitored with a prototype esophageal Doppler (CardioQ-Combi™, Deltex Medical, Chichester, UK) and an indwelling arterial catheter who received a fluid challenge or in whom the vasoactive medication was introduced or modified. Initial calibration of PPCO was made with the baseline value of EDCO. We evaluated several aspects of arterial load: total systemic vascular resistance (TSVR=mean arterial pressure [MAP]/EDCO*80), net arterial compliance (C=EDCO-derived stroke volume/pulse pressure), and effective arterial elastance (Ea=0.9*systolic blood pressure/EDCO-derived stroke volume). We compared CO values with Bland-Altman analysis, four-quadrant plot and a modified polar plot (with least significant change analysis). RESULTS: A total of 16,964-paired measurements in 53 patients were performed (median 271; interquartile range: 180-415). Agreement of all PPCO algorithms with EDCO was significantly affected by changes in arterial load, although the impact was more pronounced during changes in vasopressor therapy. When looking at different parameters of arterial load, the predictive abilities of Ea and C were superior to TSVR and MAP changes to detect a PPCO-EDCO discrepancy≥10% in all PPCO algorithms. An absolute Ea change>8.9±1.7% was associated with a PPCO-EDCO discrepancy≥10% in most algorithms. CONCLUSIONS: Changes in arterial load profoundly affected the agreement of PPCO and EDCO, although the contribution of each aspect of arterial load to the PPCO-EDCO discrepancies was significantly different. Changes in Ea and C mainly determined PPCO-EDCO discrepancy.

Relationship between intraventricular mechanical dyssynchrony and left ventricular systolic and diastolic performance: An in vivo experimental study.

Left ventricular mechanical dyssynchrony (LVMD) refers to the nonuniformity in mechanical contraction and relaxation timing in different ventricular segments. We aimed to determine the relationship between LVMD and LV performance, as assessed by ventriculo-arterial coupling (VAC), LV mechanical efficiency (LVeff ), left ventricular ejection fraction (LVEF), and diastolic function during sequential experimental changes in loading and contractile conditions. Thirteen Yorkshire pigs submitted to three consecutive stages with two opposite interventions each: changes in afterload (phenylephrine/nitroprusside), preload (bleeding/reinfusion and fluid bolus), and contractility (esmolol/dobutamine). LV pressure-volume data were obtained with a conductance catheter. Segmental mechanical dyssynchrony was assessed by global, systolic, and diastolic dyssynchrony (DYS) and internal flow fraction (IFF). Late systolic LVMD was related to an impaired VAC, LVeff , and LVEF, whereas diastolic LVMD was associated with delayed LV relaxation (logistic tau), decreased LV peak filling rate, and increased atrial contribution to LV filling. The hemodynamic factors related to LVMD were contractility, afterload, and heart rate. However, the relationship between these factors differed throughout the cardiac cycle. LVMD plays a significant role in LV systolic and diastolic performance and is associated with hemodynamic factors and intraventricular conduction.

Longitudinal Validation of Right Ventricular Pressure Monitoring for the Assessment of Right Ventricular Systolic Dysfunction in a Large Animal Ischemic Model.

Right ventricular (RV) dysfunction is a major cause of morbidity and mortality in intensive care and cardiac surgery. Early detection of RV dysfunction may be facilitated by continuous monitoring of RV waveform obtained from a pulmonary artery catheter. The objective is to evaluate the extent to which RV pressure monitoring can detect changes in RV systolic performance assess by RV end-systolic elastance (Ees) following the development of an acute RV ischemic in a porcine model. HYPOTHESIS: RV pressure monitoring can detect changes in RV systolic performance assess by RV Ees following the development of an acute RV ischemic model. METHODS AND MODELS: Acute ischemic RV dysfunction was induced by progressive embolization of microsphere in the right coronary artery to mimic RV dysfunction clinically experienced during cardiopulmonary bypass separation caused by air microemboli. RV hemodynamic performance was assessed using RV pressure waveform-derived parameters and RV Ees obtained using a conductance catheter during inferior vena cava occlusions. RESULTS: Acute ischemia resulted in a significant reduction in RV Ees from 0.26 mm Hg/mL (interquartile range, 0.16-0.32 mm Hg/mL) to 0.14 mm Hg/mL (0.11-0.19 mm Hg/mL; p < 0.010), cardiac output from 6.3 L/min (5.7-7 L/min) to 4.5 (3.9-5.2 L/min; p = 0.007), mean systemic arterial pressure from 72 mm Hg (66-74 mm Hg) to 51 mm Hg (46-56 mm Hg; p < 0.001), and mixed venous oxygen saturation from 65% (57-72%) to 41% (35-45%; p < 0.001). Linear mixed-effect model analysis was used to assess the relationship between Ees and RV pressure-derived parameters. The reduction in RV Ees best correlated with a reduction in RV maximum first derivative of pressure during isovolumetric contraction (dP/dtmax) and single-beat RV Ees. Adjusting RV dP/dtmax for heart rate resulted in an improved surrogate of RV Ees. INTERPRETATION AND CONCLUSIONS: Stepwise decreases in RV Ees during acute ischemic RV dysfunction were accurately tracked by RV dP/dtmax derived from the RV pressure waveform.

Intraoperative hypotension when using hypotension prediction index software during major noncardiac surgery: a European multicentre prospective observational registry (EU HYPROTECT).

Background: Intraoperative hypotension is associated with organ injury. Current intraoperative arterial pressure management is mainly reactive. Predictive haemodynamic monitoring may help clinicians reduce intraoperative hypotension. The Acumen™ Hypotension Prediction Index software (HPI-software) (Edwards Lifesciences, Irvine, CA, USA) was developed to predict hypotension. We built up the European multicentre, prospective, observational EU HYPROTECT Registry to describe the incidence, duration, and severity of intraoperative hypotension when using HPI-software monitoring in patients having noncardiac surgery. Methods: We enrolled 749 patients having elective major noncardiac surgery in 12 medical centres in five European countries. Patients were monitored using the HPI-software. We quantified hypotension using the time-weighted average MAP <65 mm Hg (primary endpoint), the proportion of patients with at least one ≥1 min episode of a MAP <65 mm Hg, the number of ≥1 min episodes of a MAP <65 mm Hg, and duration patients spent below a MAP of 65 mm Hg. Results: We included 702 patients in the final analysis. The median time-weighted average MAP <65 mm Hg was 0.03 (0.00-0.20) mm Hg. In addition, 285 patients (41%) had no ≥1 min episode of a MAP <65 mm Hg; 417 patients (59%) had at least one. The median number of ≥1 min episodes of a MAP <65 mm Hg was 1 (0-3). Patients spent a median of 2 (0-9) min below a MAP of 65 mm Hg. Conclusions: The median time-weighted average MAP <65 mm Hg was very low in patients in this registry. This suggests that using HPI-software monitoring may help reduce the duration and severity of intraoperative hypotension in patients having noncardiac surgery.

Changes of operative performance of pulse pressure variation as a predictor of fluid responsiveness in endotoxin shock.

Several limitations regarding pulse pressure variation (PPV) use have been reported. Our aim was to describe changes in the PPV operative performance as a predictor of fluid responsiveness during the development of a swine endotoxin shock model and to assess hemodynamic variables associated with PPV changes. A swine porcine endotoxin shock model was established (Escherichia Coli 055:B5 endotoxin) in 7 pigs, and 3 pigs were included in the control group. The endotoxin was infused until the mean arterial pressure (MAP) dropped below 50 mmHg (TH0); then, the model animal was reanimated with fluids and vasopressors. We performed fluid challenges every hour for 6 h. ROC curve analysis and a linear mixed model were performed. The area under the curve of PPV decreased from 0.95 (0.81-1.00) to 0.60 (0.17-1.00) at TH0. Its cutoff increased from 10.5 to 22.00% at TH0. PPV showed an inverse relationship with stroke volume, mean systemic filling pressure, MAP, and systemic vascular resistance (SVR) (p < 0.001, AIC = 111.85). The PPV operative performance as a predictor of fluid responsiveness decreased with the progression of shock. This could lead to an inverse association between PPV and the following variables: MAP and SVR.

Hypotension Prediction Index Software to Prevent Intraoperative Hypotension during Major Non-Cardiac Surgery: Protocol for a European Multicenter Prospective Observational Registry (EU-HYPROTECT).

Background: Intraoperative hypotension is common in patients having non-cardiac surgery and associated with postoperative acute myocardial injury, acute kidney injury, and mortality. Avoiding intraoperative hypotension is a complex task for anesthesiologists. Using artificial intelligence to predict hypotension from clinical and hemodynamic data is an innovative and intriguing approach. The AcumenTM Hypotension Prediction Index (HPI) software (Edwards Lifesciences; Irvine, CA, USA) was developed using artificial intelligence­specifically machine learning­and predicts hypotension from blood pressure waveform features. We aimed to describe the incidence, duration, severity, and causes of intraoperative hypotension when using HPI monitoring in patients having elective major non-cardiac surgery. Methods: We built up a European, multicenter, prospective, observational registry including at least 700 evaluable patients from five European countries. The registry includes consenting adults (≥18 years) who were scheduled for elective major non-cardiac surgery under general anesthesia that was expected to last at least 120 min and in whom arterial catheter placement and HPI monitoring was planned. The major objectives are to quantify and characterize intraoperative hypotension (defined as a mean arterial pressure [MAP] < 65 mmHg) when using HPI monitoring. This includes the time-weighted average (TWA) MAP < 65 mmHg, area under a MAP of 65 mmHg, the number of episodes of a MAP < 65 mmHg, the proportion of patients with at least one episode (1 min or more) of a MAP < 65 mmHg, and the absolute maximum decrease below a MAP of 65 mmHg. In addition, we will assess causes of intraoperative hypotension and investigate associations between intraoperative hypotension and postoperative outcomes. Discussion: There are only sparse data on the effect of using HPI monitoring on intraoperative hypotension in patients having elective major non-cardiac surgery. Therefore, we built up a European, multicenter, prospective, observational registry to describe the incidence, duration, severity, and causes of intraoperative hypotension when using HPI monitoring in patients having elective major non-cardiac surgery.

Dynamic arterial elastance to predict arterial pressure response to volume loading in preload-dependent patients.

INTRODUCTION: Hemodynamic resuscitation should be aimed at achieving not only adequate cardiac output but also sufficient mean arterial pressure (MAP) to guarantee adequate tissue perfusion pressure. Since the arterial pressure response to volume expansion (VE) depends on arterial tone, knowing whether a patient is preload-dependent provides only a partial solution to the problem. The objective of this study was to assess the ability of a functional evaluation of arterial tone by dynamic arterial elastance (Ea(dyn)), defined as the pulse pressure variation (PPV) to stroke volume variation (SVV) ratio, to predict the hemodynamic response in MAP to fluid administration in hypotensive, preload-dependent patients with acute circulatory failure. METHODS: We performed a prospective clinical study in an adult medical/surgical intensive care unit in a tertiary care teaching hospital, including 25 patients with controlled mechanical ventilation who were monitored with the Vigileo(®) monitor, for whom the decision to give fluids was made because of the presence of acute circulatory failure, including arterial hypotension (MAP ≤65 mmHg or systolic arterial pressure <90 mmHg) and preserved preload responsiveness condition, defined as a SVV value ≥10%. RESULTS: Before fluid infusion, Ea(dyn) was significantly different between MAP responders (MAP increase ≥15% after VE) and MAP nonresponders. VE-induced increases in MAP were strongly correlated with baseline Ea(dyn) (r(2) = 0.83; P < 0.0001). The only predictor of MAP increase was Ea(dyn) (area under the curve, 0.986 ± 0.02; 95% confidence interval (CI), 0.84-1). A baseline Ea(dyn) value >0.89 predicted a MAP increase after fluid administration with a sensitivity of 93.75% (95% CI, 69.8%-99.8%) and a specificity of 100% (95% CI, 66.4%-100%). CONCLUSIONS: Functional assessment of arterial tone by Ea(dyn), measured as the PVV to SVV ratio, predicted arterial pressure response after volume loading in hypotensive, preload-dependent patients under controlled mechanical ventilation.

COVID-19-related echocardiographic patterns of cardiovascular dysfunction in critically ill patients: A systematic review of the current literature.

PURPOSE: Coronavirus disease 2019 (COVID-19) infection may trigger a multi-systemic disease involving different organs. There has been growing interest regarding the harmful effects of COVID-19 on the cardiovascular system. This systematic review aims to systematically analyze papers reporting echocardiographic findings in hospitalized COVID-19 subjects. MATERIALS AND METHODS: We included prospective and retrospective studies reporting echocardiography data in >10 hospitalized adult subjects with COVID-19; from 1st February 2020 to 15th January 2021. RESULTS: The primary electronic search identified 1120 articles. Twenty-nine studies were finally included, enrolling 3944 subjects. Overall the studies included a median of 68.0% (45.5-100.0) of patients admitted to ICU. Ten studies (34.4%) were retrospective, and 20 (68.9%) single-centred. Overall enrolling 1367 subjects, three studies reported normal echocardiographic findings in 49 ± 18% of cases. Seven studies (24.1%) analyzed the association between echocardiographic findings and mortality, mostly related to right ventricular (RV) dysfunction. CONCLUSIONS: Data regarding the use of echocardiography on hospitalized, predominantly ICU, COVID-19 patients were retrieved from studies with heterogeneous designs, variable sample sizes, and severity scores. Normal echocardiographic findings were reported in about 50% of subjects, with LVEF usually not affected. Overall, RV dysfunction seems more likely associated with increased mortality. TRIAL REGISTRATION: CRD42020218439.

Understanding ventriculo-arterial coupling.

In the late 19th century, Otto Frank published the first description of a ventricular pressure-volume diagram, thus laid the foundation for modern cardiovascular physiology. Since then, the analysis of the pressure-volume loops became a reference tool for the study of the ventricular pump properties. However, understanding cardiovascular performance requires both the evaluation of ventricular properties and the modulating effects of the arterial system, since the heart and the arterial tree are anatomically and functionally related structures. The study of the coupling between the cardiac function and the properties of the arterial system, or ventriculo-arterial (VA) coupling, provides then a comprehensive characterization of the performance of the cardiovascular system in both health and disease. The assessment of cardiovascular function is an essential element of the hemodynamic evaluation of critically ill patients. Both left and right ventricular dysfunction and arterial system disturbances are frequent in these patients. Since VA coupling ultimately defines de performance and efficiency of the cardiovascular system, the analysis of the interaction between the heart and the arterial system could offer a broader perspective of the hemodynamic disorders associated with common conditions, such as septic shock, heart failure, or right ventricular dysfunction. Moreover, this analysis could also provide valuable information about their pathophysiological mechanisms and may help to determine the best therapeutic strategy to correct them. In this review, we will describe the basic principles of the VA coupling assessment, its limitations, and the most common methods for its estimation at the bedside. Then, we will summarize the current knowledge of the application of VA coupling in critically ill patients and suggest some recommendations for further research.

Dynamic Arterial Elastance as a Ventriculo-Arterial Coupling Index: An Experimental Animal Study.

Dynamic arterial elastance (Eadyn), the ratio between arterial pulse pressure and stroke volume changes during respiration, has been postulated as an index of the coupling between the left ventricle (LV) and the arterial system. We aimed to confirm this hypothesis using the gold-standard for defining LV contractility, afterload, and evaluating ventricular-arterial (VA) coupling and LV efficiency during different loading and contractile experimental conditions. Twelve Yorkshire healthy female pigs submitted to three consecutive stages with two opposite interventions each: changes in afterload (phenylephrine/nitroprusside), preload (bleeding/fluid bolus), and contractility (esmolol/dobutamine). LV pressure-volume data was obtained with a conductance catheter, and arterial pressures were measured via a fluid-filled catheter in the proximal aorta and the radial artery. End-systolic elastance (Ees), a load-independent index of myocardial contractility, was calculated during an inferior vena cava occlusion. Effective arterial elastance (Ea, an index of LV afterload) was calculated as LV end-systolic pressure/stroke volume. VA coupling was defined as the ratio Ea/Ees. LV efficiency (LVeff) was defined as the ratio between stroke work and the LV pressure-volume area. Eadyn was calculated as the ratio between the aortic pulse pressure variation (PPV) and conductance-derived stroke volume variation (SVV). A linear mixed model was used for evaluating the relationship between Ees, Ea, VA coupling, LVeff with Eadyn. Eadyn was inversely related to VA coupling and directly to LVeff. The higher the Eadyn, the higher the LVeff and the lower the VA coupling. Thus, Eadyn, an easily measured parameter at the bedside, may be of clinical relevance for hemodynamic assessment of the unstable patient.

Computational hemodynamics in arteries with the one-dimensional augmented fluid-structure interaction system: viscoelastic parameters estimation and comparison with in-vivo data.

Mathematical models are widely recognized as a valuable tool for cardiovascular diagnosis and the study of circulatory diseases, especially to obtain data that require otherwise invasive measurements. To correctly simulate body hemodynamics, the viscoelastic properties of vessels walls are a key aspect to be taken into account as they play an essential role in cardiovascular behavior. The present work aims to apply the augmented fluid-structure interaction system of blood flow to real case studies to assess the validity of the model as a valuable resource to improve cardiovascular diagnostics and the treatment of pathologies. Main contributions of the paper include the evaluation of viscoelastic tube laws, estimation of viscoelastic parameters and comparison of models with literature results and in-vivo experiments. The ability of the model to correctly simulate pulse waveforms in single arterial segments is verified using literature benchmark test cases, designed taking into account a simple elastic behavior of the wall in the upper thoracic aorta and in the common carotid artery. Furthermore, in-vivo pressure waveforms, extracted from tonometric measurements performed on four human common carotid arteries and two common femoral arteries, are compared to numerical solutions. It is highlighted that the viscoelastic damping effect of arterial walls is required to avoid an overestimation of pressure peaks. Finally, an effective procedure to estimate the viscoelastic parameters of the model is herein proposed, which returns hysteresis curves of the common carotid arteries dissipating energy fractions in line with values calculated from literature hysteresis loops in the same vessel.

Dynamic Arterial Elastance During Experimental Endotoxic Septic Shock: A Potential Marker of Cardiovascular Efficiency.

Dynamic arterial elastance (Eadyn), the ratio between pulse pressure variation (PPV) and stroke volume variation (SVV), has been suggested as a dynamic parameter relating pressure and flow. We aimed to determine the effects of endotoxic septic shock and hemodynamic resuscitation on Eadyn in an experimental study in 18 New Zealand rabbits. Animals received placebo (SHAM, n = 6) or intravenous lipopolysaccharide (E. Coli 055:B5, 1 mg⋅kg - 1) with or without (EDX-R, n = 6; EDX, n = 6) hemodynamic resuscitation (fluid bolus of 20 ml⋅kg - 1 and norepinephrine for restoring mean arterial pressure). Continuous arterial pressure and aortic blood flow measurements were obtained simultaneously. Cardiovascular efficiency was evaluated by the oscillatory power fraction [%Osc: oscillatory work/left ventricular (LV) total work] and the energy efficiency ratio (EER = LV total work/cardiac output). Eadyn increased in septic animals (from 0.73 to 1.70; p = 0.012) and dropped after hemodynamic resuscitation. Eadyn was related with the %Osc and EER [estimates: -0.101 (-0.137 to -0.064) and -9.494 (-11.964 to -7.024); p < 0.001, respectively]. So, the higher the Eadyn, the better the cardiovascular efficiency (lower %Osc and EER). Sepsis resulted in a reduced %Osc and EER, reflecting a better cardiovascular efficiency that was tracked by Eadyn. Eadyn could be a potential index of cardiovascular efficiency during septic shock.