• Manuel Ignacio Monge García, Pedro Guijo González, Manuel Gracia Romero, Anselmo Gil Cano, Chris Oscier, Andrew Rhodes, Robert Michael Grounds, and Maurizio Cecconi.
• Unidad de Cuidados Intensivos, Hospital SAS de Jerez, Jerez de la Frontera, Spain, ignaciomonge@gmail.com.
• Intensive Care Med. 2015 Jul 1;41(7):1247-55.

PurposeTo determine the effects of fluid administration on arterial load in critically ill patients with septic shock.MethodsAnalysis 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).ResultsEighty-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.ConclusionFluid 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.

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