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.

The use of pulse pressure variation and stroke volume variation in spontaneously breathing patients to assess dynamic arterial elastance and to predict arterial pressure response to fluid administration.

BACKGROUND: Dynamic arterial elastance (Eadyn), defined as the pulse pressure variation (PPV) to stroke volume variation (SVV) ratio, has been suggested as a predictor of the arterial pressure response to fluid administration. In this study, we assessed the effectiveness of Eadyn to predict the arterial blood pressure response to a fluid challenge (FC) in preload-dependent, spontaneously breathing patients. METHODS: Patients admitted postoperatively and monitored with the Nexfin monitor (BMEYE, Amsterdam, The Netherlands) were enrolled in the study. Patients were included in the analysis if they were spontaneously breathing and had an increase in cardiac output ≥10% during an FC. Patients were classified according to the increase in mean arterial blood pressure (MAP) after FC into MAP-responders (MAP increase ≥10%) and MAP-nonresponders (MAP increase <10%). Eadyn was continuously calculated from the PPV and SVV values obtained from the monitor. RESULTS: Thirty-four FCs from 26 patients were studied. Seventeen FCs (50%) induced a positive MAP response. Preinfusion Eadyn was significantly higher in MAP-responders (1.39 ± 0.41 vs 0.85 ± 0.23; P = 0.0001). Preinfusion Eadyn predicted a positive MAP response to FC with an area under the receiver-operating characteristic curve of 0.92 ± 0.04 of standard error (95% confidence interval, 0.78-0.99; P < 0.0001). A preinfusion Eadyn value ≥1.06 (gray zone: 0.9-1.15) discriminated MAP-responders with a sensitivity and specificity of 88.2% (approximate 95% confidence interval, 64%-99%), respectively. CONCLUSIONS: Noninvasive Eadyn, defined as the PPV to SVV ratio, predicted the arterial blood pressure increase to fluid administration in spontaneously breathing, preload-dependent patients.

Dynamic arterial elastance as a predictor of arterial pressure response to fluid administration: a validation study.

INTRODUCTION: Functional 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. METHODS: We 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. RESULTS: Thirty-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 (R (2) = 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%). CONCLUSIONS: Functional 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.

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.