Intensive Care Medicine

, Volume 41, Issue 7, pp 1247–1255 | Cite as

Effects of fluid administration on arterial load in septic shock patients

  • Manuel Ignacio Monge GarcíaEmail author
  • Pedro Guijo González
  • Manuel Gracia Romero
  • Anselmo Gil Cano
  • Chris Oscier
  • Andrew Rhodes
  • Robert Michael Grounds
  • Maurizio Cecconi



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.


Fluid therapy Septic shock Arterial pressure Cardiac output Arterial load Esophageal Doppler 



Area under the receiver-operating characteristic curve


Net arterial compliance


Cardiac output


Diastolic arterial pressure


Effective arterial elastance


Dynamic arterial elastance


Electronic supplementary material


Hydroxyethyl starch


Interquartile range


Least significant change


Mean arterial pressure


Receiver-operating characteristic


Systolic arterial pressure


Stroke volume


Systemic vascular resistance


Arterial time constant


Volume expansion


Conflicts of interests

MIMG is consultant for Edwards Lifesciences and received travel expenses from Deltex. AGC has received Honoraria from Edwards Lifesciences. AR has received Honoraria and is on the advisory board for LiDCO, Honoraria for Covidien, Edwards Lifesciences and Cheetah. MC in the last 5 years has received honoraria and/or travel expenses from Edwards Lifesciences, LiDCO, Cheetah, Bmeye, Masimo and Deltex. PGG, MGR, CO and RMG have no conflict of interest to declare.

Supplementary material

134_2015_3898_MOESM1_ESM.docx (158 kb)
Supplementary material 1 (DOCX 157 kb)


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Copyright information

© Springer-Verlag Berlin Heidelberg and ESICM 2015

Authors and Affiliations

  • Manuel Ignacio Monge García
    • 1
    • 2
    Email author
  • Pedro Guijo González
    • 1
  • Manuel Gracia Romero
    • 1
  • Anselmo Gil Cano
    • 1
  • Chris Oscier
    • 2
  • Andrew Rhodes
    • 2
  • Robert Michael Grounds
    • 2
  • Maurizio Cecconi
    • 2
  1. 1.Unidad de Cuidados IntensivosHospital SAS de JerezJerez de la FronteraSpain
  2. 2.Department of General Intensive CareSt. George’s Healthcare NHS Trust and St George’s University of LondonLondonUK

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