Intensive Care Medicine

, Volume 30, Issue 7, pp 1361–1369 | Cite as

Effect of large volume infusion on left ventricular volumes, performance and contractility parameters in normal volunteers

  • Anand Kumar
  • Ramon Anel
  • Eugene Bunnell
  • Kalim Habet
  • Alex Neumann
  • David Wolff
  • Robert Rosenson
  • Mary Cheang
  • Joseph E. Parrillo



Characterize the normal human cardiovascular response to large volume infusion of normal saline.


Prospective, interventional trial.


ICU procedure room.


Healthy male volunteers (n=32).


Volumetric echocardiography during 4-L saline infusion (3 L over 3 h followed by 1 L over 2 h).

Measurements and results

Following 3-L saline infusion, stroke volume and cardiac output increased approximately 10% without a significant change in heart rate or blood pressure. A decrease in end-systolic volume contributed to the increase in stroke volume to an extent similar to that provided by the increase in end-diastolic volume. All contractility indices except end-systolic wall stress/end-systolic volume index were increased at 3 h post-initiation of saline infusion. Stroke volume but not cardiac output remained elevated at 5 h with persistence of ventricular volume responses; only ejection fraction was significantly elevated among the contractility indices. Afterload measures including total peripheral resistance and end-systolic wall stress were significantly decreased after 3-L infusion but were unchanged compared to baseline following infusion of an additional 1 L over 2 h. Modeled blood viscosity studies demonstrate that changes in apparent contractility after 3-L saline infusion can be explained solely by viscosity reduction associated with hypervolemic hemodilution.


The initial increase in stroke volume associated with high volume saline infusion in normal volunteers is associated with increases of most load-dependent and ostensibly load-independent parameters of left ventricular contractility. This phenomenon is unlikely to represent a true increase in contractility and appears to be caused by reduced afterload as a consequence of decreased blood viscosity. This decrease in blood viscosity may complicate analysis of some previous in vivo studies examining the effect of volume loading on cardiac function using low-viscosity solutions.


Volunteers Saline Resuscitation Heart Cardiac output Contractility 

Supplementary material

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Supplementary Material (PDF 73 KB)


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Copyright information

© Springer-Verlag 2004

Authors and Affiliations

  • Anand Kumar
    • 1
    • 5
  • Ramon Anel
    • 1
  • Eugene Bunnell
    • 1
  • Kalim Habet
    • 1
  • Alex Neumann
    • 1
  • David Wolff
    • 2
  • Robert Rosenson
    • 2
  • Mary Cheang
    • 3
  • Joseph E. Parrillo
    • 4
  1. 1.Division of Cardiovascular Disease and Critical Care MedicineRush-Presbyterian-St. Luke’s Medical CenterChicagoUSA
  2. 2.Section of Preventative Cardiology, Northwestern University Medical CenterNorthwestern University Medical SchoolChicagoUSA
  3. 3.Biostatistical Consulting Unit, Department of Community Health Sciences, Faculty of MedicineUniversity of ManitobaWinnipegCanada
  4. 4.Division of Cardiovascular Disease and Critical Care Medicine, Cooper Hospital/University Medical CenterRobert Wood Johnson Medical SchoolCamdenUSA
  5. 5.Section of Critical Care Medicine, GE-706Health Sciences CentreWinnipegCanada

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