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.

Increased atrial contraction contribution to left ventricular filling during early septic shock.

PURPOSE: To assess the atrial systolic function and the contribution of atrial contraction to left ventricular (LV) filling in septic shock patients as compared with healthy volunteers. METHODS: Twenty-seven septic patients evaluated during first 48 h of ICU admission and compared with 27 healthy volunteers. Left atrial (LA) contraction contribution to LV filling was calculated as the active emptying atrial volume/LV end-diastolic volume. Atrial systolic function was evaluated with the atrial kinetic force [LAKE = 0.5 × blood density × LVVactive × (peak A velocity)2] and atrial ejection force [LASF = 0.5 × blood density × mitral annulus area × (peak A velocity)2]. RESULTS: LV ejection fraction was lower in septic patients than in control group: 51 ±â€¯14%vs 60 ±â€¯6% (p < 0.01). Contribution of LA contraction to LV preload was greater in septic patients than in normal subjects (26.7 ±â€¯11.3% vs 15.9 ±â€¯5.9%, p < 0.001), even if adjusted for age (0.49 ±â€¯0.19 vs 0.35 ±â€¯0.13, p = 0.004). LAKE and LASF were also significantly larger in septic patients than in normal subjects (21.8 ±â€¯9.1 vs 7.3 ±â€¯3 kdynes·cm, p < 0.001; 16.1 ±â€¯11.7 vs 9.8 ±â€¯4.3 kdynes, p = 0.048, respectively), and remained unchanged during the next 48 h. CONCLUSION: In septic shock patients, LA systolic function increased and greatly contributed to support LV filling. These results highlight the role of preserving atrial contraction on the hemodynamic resuscitation in early septic shock.

Noradrenaline modifies arterial reflection phenomena and left ventricular efficiency in septic shock patients: A prospective observational study.

PURPOSE: To determine whether noradrenaline alters the arterial pressure reflection phenomena in septic shock patients and the effects on left ventricular (LV) efficiency. MATERIAL AND METHODS: Thirty-seven septic shock patients with a planned change in noradrenaline dose. Timing and magnitude (Reflection Magnitude and Augmentation Index) of arterial reflections were evaluated. Total, steady, and oscillatory LV power (also expressed as fraction of the total power), subendocardial viability ratio (SEVR), energy efficiency and transmission ratios were used as a marker of LV efficiency. RESULTS: An incremental change in noradrenaline increased Reflection Magnitude [0.28(0.09) to 0.31(0.1], Augmentation Index [-6.4(23.6) to 4.8(20.7)%], and LV total power [0.79(IQR:0.47-1) to 0.98(IQR:0.57-1.27)W], all p < 0.001; whereas decreased arrival time of reflected waves [from 95(87 to 121) to 83(79 to 101)ms; p < 0.001]. Variables of LV performance showed a decreased efficiency: oscillatory fraction and energy efficiency ratio increased [20.9(5.7) to 22.8(4.9)%, and 8.2(1.7) to 10.1(2) mW.min.litre-1; p < 0.001, respectively]; and energy transmission ratio and SEVR decreased [73.8(9.9) to 72(9.8)% and 146(IQR:113-188) to 143(IQR:109-172)%, p = 0.003 and p = 0.041, respectively]. CONCLUSIONS: Noradrenaline increased reflection phenomena, increasing LV workload and worsening LV performance in septic shock patients. These conditions could explain the detrimental effects during long-term use of noradrenaline.

Effects of fluid administration on arterial load in septic shock patients.

PURPOSE: To determine the effects of fluid administration on arterial load in critically ill patients with septic shock. METHODS: 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). RESULTS: 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. CONCLUSION: 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.

Non-invasive assessment of fluid responsiveness by changes in partial end-tidal CO2 pressure during a passive leg-raising maneuver.

BACKGROUND: 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. METHODS: Thirty-seven mechanically ventilated patients with acute circulatory failure were monitored with the CardioQ-ODM esophageal Doppler. A 2-minutes PLR maneuver was performed. Fluid responsiveness was defined according to CO increase (responders ≥ 15%) after volume expansion. RESULTS: PLR-induced increases in CO and PETCO2 were strongly correlated (R2 = 0.79; P < 0.0001). The areas under the receiver-operating characteristics (ROC) curve for a PLR-induced increase in CO and PETCO2 (0.97 ± 0.03 SE; CI 95%: 0.85 to 0.99 and 0.94 ± 0.04 SE; CI 95%: 0.82 to 0.99; respectively) were not significantly different. An increase ≥ 5% in PETCO2 or ≥ 12% in CO during PLR predicted fluid responsiveness with a sensitivity of 90.5% (95% CI: 69.9 to 98.8%) and 95.2% (95% CI: 76.2 to 99.9%), respectively, and a specificity of 93.7% (95% CI: 69.8 to 99.8%). CONCLUSION: Induced changes in PETCO2 during a PLR maneuver could be used to track changes in CO for prediction of fluid responsiveness in mechanically ventilated patients with acute circulatory failure, under fixed minute ventilation and assuming a constant tissue CO2 production.

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.

Brachial artery peak velocity variation to predict fluid responsiveness in mechanically ventilated patients.

INTRODUCTION: Although several parameters have been proposed to predict the hemodynamic response to fluid expansion in critically ill patients, most of them are invasive or require the use of special monitoring devices. The aim of this study is to determine whether noninvasive evaluation of respiratory variation of brachial artery peak velocity flow measured using Doppler ultrasound could predict fluid responsiveness in mechanically ventilated patients. METHODS: We conducted a prospective clinical research in a 17-bed multidisciplinary ICU and included 38 mechanically ventilated patients for whom fluid administration was planned due to the presence of acute circulatory failure. Volume expansion (VE) was performed with 500 mL of a synthetic colloid. Patients were classified as responders if stroke volume index (SVi) increased >or= 15% after VE. The respiratory variation in Vpeakbrach (DeltaVpeakbrach) was calculated as the difference between maximum and minimum values of Vpeakbrach over a single respiratory cycle, divided by the mean of the two values and expressed as a percentage. Radial arterial pressure variation (DeltaPPrad) and stroke volume variation measured using the FloTrac/Vigileo system (DeltaSVVigileo), were also calculated. RESULTS: VE increased SVi by >or= 15% in 19 patients (responders). At baseline, DeltaVpeakbrach, DeltaPPrad and DeltaSVVigileo were significantly higher in responder than nonresponder patients [14 vs 8%; 18 vs. 5%; 13 vs 8%; P < 0.0001, respectively). A DeltaVpeakbrach value >10% predicted fluid responsiveness with a sensitivity of 74% and a specificity of 95%. A DeltaPPrad value >10% and a DeltaSVVigileo >11% predicted volume responsiveness with a sensitivity of 95% and 79%, and a specificity of 95% and 89%, respectively. CONCLUSIONS: Respiratory variations in brachial artery peak velocity could be a feasible tool for the noninvasive assessment of fluid responsiveness in patients with mechanical ventilatory support and acute circulatory failure. TRIAL REGISTRATION: ClinicalTrials.gov ID: NCT00890071.

Arterial pressure changes during the Valsalva maneuver to predict fluid responsiveness in spontaneously breathing patients.

OBJECTIVE: To evaluate whether arterial pressure response during a Valsalva maneuver could predict fluid responsiveness in spontaneously breathing patients. DESIGN AND SETTING: Prospective clinical study in a 17-bed multidisciplinary intensive care unit. PATIENTS: Thirty patients without mechanical ventilation and equipped with a radial arterial catheter for whom the decision to give fluids was taken due to suspected hypovolemia. INTERVENTION: A 10-s Valsalva maneuver was performed before and after volume expansion (VE). Patients were classified as responders if stroke volume index (SVi) increased >/=15% after VE. MEASUREMENTS AND RESULTS: Pulse pressure changes during the Valsalva maneuver (VPP) were calculated as the difference between maximal pulse pressure during phase 1 and minimal pulse pressure during phase 2 of the Valsalva maneuver divided by the mean of the two values and expressed as a percentage. Valsalva changes in systolic pressure (VSP) were calculated in similar way. SVi changes induced by VE was correlated with baseline values of VPP and VSP (r (2) = 0.71 and r (2) = 0.60; P < 0.0001, respectively), and with VE-induced changes in VPP and VSP (r (2) = 0.56 and r (2) = 0.44; P < 0.0001 and P < 0.001, respectively). A VPP value of 52% and VSP of 30% predicted fluid responsiveness with a sensitivity of 91% and 73% and a specificity of 95 and 90%, respectively. CONCLUSIONS: Arterial response during the Valsalva maneuver is a feasible tool for predicting fluid responsiveness in patients without mechanical ventilatory support.