title: Effect of large volume infusion on left ventricular volumes, performance and contractility parameters in normal volunteers.
abstract: OBJECTIVE
  Characterize the normal human cardiovascular response to large volume infusion of normal saline.
  
  
  METHODS
  Prospective, interventional trial.
  
  
  METHODS
  ICU procedure room.
  
  
  METHODS
  Healthy male volunteers ( n=32). INTERVENTIONS. Volumetric echocardiography during 4-L saline infusion (3 L over 3 h followed by 1 L over 2 h).
  
  
  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.
  
  
  CONCLUSIONS
  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.
authors.affiliation: Division of Cardiovascular Disease and Critical Care Medicine, Rush-Presbyterian-St. Luke's Medical Center, 1653 West Congress Parkway, Chicago, IL 60612-3833, USA. akumar61@yahoo.com
authors.forename: Anand
authors.initials: A
authors.lastname: Kumar
authors.forename: Ramon
authors.initials: R
authors.lastname: Anel
authors.forename: Eugene
authors.initials: E
authors.lastname: Bunnell
authors.forename: Kalim
authors.initials: K
authors.lastname: Habet
authors.forename: Alex
authors.initials: A
authors.lastname: Neumann
authors.forename: David
authors.initials: D
authors.lastname: Wolff
authors.forename: Robert
authors.initials: R
authors.lastname: Rosenson
authors.forename: Mary
authors.initials: M
authors.lastname: Cheang
authors.forename: Joseph E
authors.initials: JE
authors.lastname: Parrillo
mesh_terms: D000328:Adult; D002306:Cardiac Volume / Q000187:drug effects / Q000502:physiology*; D004562:Electrocardiography; D006801:Humans; D007262:Infusions, Intravenous; D008297:Male; D009200:Myocardial Contraction / Q000187:drug effects / Q000502:physiology*; D011446:Prospective Studies; D012965:Sodium Chloride / Q000008:administration & dosage; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology*; D013997:Time Factors; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
chemical_list: D012965:Sodium Chloride