IntroductionHemodynamic 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 (Eadyn), 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.MethodsWe 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%.ResultsBefore fluid infusion, Eadyn was significantly different between MAP responders (MAP increase ≥15% after VE) and MAP nonresponders. VE-induced increases in MAP were strongly correlated with baseline Eadyn (r2 = 0.83; P < 0.0001). The only predictor of MAP increase was Eadyn (area under the curve, 0.986 ± 0.02; 95% confidence interval (CI), 0.84-1). A baseline Eadyn 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%).ConclusionsFunctional assessment of arterial tone by Eadyn, measured as the PVV to SVV ratio, predicted arterial pressure response after volume loading in hypotensive, preload-dependent patients under controlled mechanical ventilation.

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BackgroundMaximal 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.MethodsWe 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.ResultsBoth 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.ConclusionAlthough 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.Electronic supplementary materialThe online version of this article (10.1186/s13054-018-2260-1) contains supplementary material, which is available to authorized users.

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. First, the ability of the model to correctly simulate pulse waveforms in single arterial segments is verified using literature benchmark test cases. Such cases are 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. 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.variations are determined by the physical and mechanical properties of blood and vessels walls, which are the essence of a complex fluid-structure interaction (FSI) mechanism, as well as by the anatomy of the entire cardiac network [33,48]. Viscoelastic properties of vessels play an essential role in the cardiovascular behavior [39,33,20]. In fact, viscoelasticity is one of the features that must be realistically included in the mathematical model when accurate numerical results are sought [20,1,26]. Vessel walls manifest viscoelastic properties that are summed up in three main attributes: creep, stress relaxation and hysteresis [6,39,22]. Among the existing linear viscoelastic models, the Standard Linear Solid (SLS) model provides a better representation of the arterial wall mechanics than the generally adopted Kelvin-Voigt model [1,26,46,32,23], being the latter unable to describe an exponential decay of stress over time [49,10,45]. On the other hand, when modeling the vessel mechanics by means of an elastic behaviour, the information related to hysteresis (i.e. the energy dissipated by viscoelastic effects) vanishes and pressure peaks are overestimated [1,6,20].The augmented FSI (a-FSI) system for blood flow modeling, presented in [7,8], is herein extended to real case studies in single arteries, to assess the capability of the model to serve as a valuable tool for practical medical applications, cardiovascular diagnosis and the study of circulatory pathologies. The extension of the model underlines the importanc...

IntroductionFunctional assessment of arterial load by dynamic arterial elastance (Eadyn), defined as the ratio between pulse pressure variation (PPV) and stroke volume variation (SVV), has recently been shown to predict the arterial pressure response to volume expansion (VE) in hypotensive, preload-dependent patients. However, because both SVV and PPV were obtained from pulse pressure analysis, a mathematical coupling factor could not be excluded. We therefore designed this study to confirm whether Eadyn, obtained from two independent signals, allows the prediction of arterial pressure response to VE in fluid-responsive patients.MethodsWe analyzed the response of arterial pressure to an intravenous infusion of 500 ml of normal saline in 53 mechanically ventilated patients with acute circulatory failure and preserved preload dependence. Eadyn was calculated as the simultaneous ratio between PPV (obtained from an arterial line) and SVV (obtained by esophageal Doppler imaging). A total of 80 fluid challenges were performed (median, 1.5 per patient; interquartile range, 1 to 2). Patients were classified according to the increase in mean arterial pressure (MAP) after fluid administration in pressure responders (≥10%) and non-responders.ResultsThirty-three fluid challenges (41.2%) significantly increased MAP. At baseline, Eadyn was higher in pressure responders (1.04 ± 0.28 versus 0.60 ± 0.14; P <0.0001). Preinfusion Eadyn was related to changes in MAP after fluid administration (R2 = 0.60; P <0.0001). At baseline, Eadyn predicted the arterial pressure increase to volume expansion (area under the receiver operating characteristic curve, 0.94; 95% confidence interval (CI): 0.86 to 0.98; P <0.0001). A preinfusion Eadyn value ≥0.73 (gray zone: 0.72 to 0.88) discriminated pressure responder patients with a sensitivity of 90.9% (95% CI: 75.6 to 98.1%) and a specificity of 91.5% (95% CI: 79.6 to 97.6%).ConclusionsFunctional assessment of arterial load by Eadyn, obtained from two independent signals, enabled the prediction of arterial pressure response to fluid administration in mechanically ventilated, preload-dependent patients with acute circulatory failure.Electronic supplementary materialThe online version of this article (doi:10.1186/s13054-014-0626-6) contains supplementary material, which is available to authorized users.