title: Effects of fluid administration on arterial load in septic shock patients.
abstract: OBJECTIVE
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Unidad de Cuidados Intensivos, Hospital SAS de Jerez, Jerez de la Frontera, Spain, ignaciomonge@gmail.com.
authors.forename: Manuel Ignacio
authors.initials: MI
authors.lastname: Monge García
authors.forename: Pedro
authors.initials: P
authors.lastname: Guijo González
authors.forename: Manuel
authors.initials: M
authors.lastname: Gracia Romero
authors.forename: Anselmo
authors.initials: A
authors.lastname: Gil Cano
authors.forename: Chris
authors.initials: C
authors.lastname: Oscier
authors.forename: Andrew
authors.initials: A
authors.lastname: Rhodes
authors.forename: Robert Michael
authors.initials: RM
authors.lastname: Grounds
authors.forename: Maurizio
authors.initials: M
authors.lastname: Cecconi
mesh_terms: D000368:Aged; D062186:Arterial Pressure / Q000502:physiology*; D001794:Blood Pressure / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D015150:Echocardiography, Doppler / Q000295:instrumentation; D005260:Female; D005440:Fluid Therapy / Q000379:methods*; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic / Q000295:instrumentation; D012189:Retrospective Studies; D012772:Shock, Septic / Q000503:physiopathology / Q000628:therapy*; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance