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 (r² = 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.

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.

To determine the effects of fluid administration on arterial load in critically ill patients with septic shock. Analysis of septic shock patients monitored with an oesophageal Doppler and equipped with an indwelling arterial catheter in whom a fluid challenge was performed because of the presence of systemic hypoperfusion. Measures of arterial load [systemic vascular resistance, SVR = mean arterial pressure (MAP)/cardiac output (CO); net arterial compliance, C = stroke volume (SV)/arterial pulse pressure; and effective arterial elastance, Ea = 90 % of systolic arterial pressure/SV] were studied both before and after volume expansion (VE). Eighty-one patients were analysed, 54 (67 %) increased their CO by at least 10 % after VE (preload responders). In the whole population, 29 patients (36 %) increased MAP by at least 10 % from preinfusion level (pressure responders). In the preload responder group, only 24 patients (44 %) were pressure responders. Fluid administration was associated with a significant decrease in Ea [from 1.68 (1.11–2.11) to 1.57 (1.08–1.99) mmHg/mL; P = 0.0001] and SVR [from 1035 (645–1483) to 928 (654–1452) dyn s cm⁻⁵; P < 0.01]. Specifically, in preload responders in whom arterial pressure did not change, VE caused a reduction in Ea from 1.74 (1.22–2.24) to 1.55 (1.24–1.86) mmHg/mL (P < 0.0001), affecting both resistive [SVR: from 1082 (697–1475) to 914 (624–1475) dyn s cm⁻⁵; P < 0.0001] and pulsatile [C: from 1.11 (0.84–1.49) to 1.18 (0.99–1.44) mL/mmHg; P < 0.05] components. There was no relationship between preinfusion arterial load parameters and VE-induced increase in arterial pressure. Fluid administration significantly reduced arterial load in critically patients with septic shock and acute circulatory failure, even when increasing cardiac output. This explains why some septic patients increase their cardiac output after fluid administration without improving blood pressure.

The passive leg-raising (PLR) maneuver provides a dynamic assessment of fluid responsiveness inducing a reversible increase in cardiac preload. Since its effects are sudden and transitory, a continuous cardiac output (CO) monitoring is required to appropriately assess the hemodynamic response of PLR. On the other hand, changes in partial end-tidal CO2 pressure (PETCO2) have been demonstrated to be tightly correlated with changes in CO during constant ventilation and stable tissue CO2 production (VCO2). In this study we tested the hypothesis that, assuming a constant VCO2 and under fixed ventilation, PETCO2 can track changes in CO induced by PLR and can be used to predict fluid responsiveness.

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. 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. 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. 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.