title: Association of hemodilution and blood pressure in uncontrolled bleeding.
abstract: BACKGROUND
  Hemodynamic status and coagulation capacity affect blood loss after injury. The most advantageous fluid and blood pressure to optimize resuscitation and minimize perturbation of coagulation are unclear. We investigated interactions of isovolumic hemodilution on hemodynamics, coagulation, and blood loss after injury.
  
  
  METHODS
  Twenty-five male rats were randomized into three groups (Whole Blood Uncontrolled Blood Pressure [WBU], n = 7; Lactated Ringers Uncontrolled Blood Pressure [LRU], n = 10; Whole Blood Controlled Blood Pressure [WBC], n = 8) with isovolumic hemodilution of 50% blood volume, with and without control of pre-injury blood pressure. All rats underwent uniform grade IV liver injury 30 min after serial exchanges. Post-injury blood loss and coagulation function were measured.
  
  
  RESULTS
  Dilution occurred, determined by hematocrit, with LRU having a greater reduction. Pre-injury mean arterial pressure (MAP) decreased compared with baseline (98 ± 7 mmHg) with LRU (62 ± 14 mmHg) and WBC (61 ± 10 mmHg), resulting in WBU (101 ± 13 mmHg) being significantly higher and not changed from baseline. Post-injury, MAP decreased from pre-injury, with LRU significantly lower than the other two groups. No differences were observed in prothrombin time/international normalized ratio or thromboelastography. Bleed volume was significantly different between groups: WBU < WBC < LRU and associated with the pre-injury MAP. Controlling baseline MAP, dilution with Lactated Ringers (LR) resulted in greater blood loss than whole blood (3.0 ± 0.4 versus 1.9 ± 0.3 mL).
  
  
  CONCLUSIONS
  In this rat model of liver injury, blood loss was associated with baseline MAP and type of fluid used for dilution. Hemodilution with LR did not produce coagulopathy based on laboratory values. When controlling baseline MAP, dilution with LR increased bleeding, confirming a functional coagulopathic state.
authors.affiliation: Department of Surgery and Center for Translational Injury Research, University of Texas Health Science Center, Houston, Texas.
authors.forename: Nicholas S
authors.initials: NS
authors.lastname: Pawelczyk
authors.forename: Maria del Pilar
authors.initials: Mdel P
authors.lastname: Huby
authors.forename: John R
authors.initials: JR
authors.lastname: Salsbury
authors.forename: Lisa A
authors.initials: LA
authors.lastname: Baer
authors.forename: Yao-Wei W
authors.initials: YW
authors.lastname: Wang
authors.forename: Nena
authors.initials: N
authors.lastname: Matijevic
authors.forename: John B
authors.initials: JB
authors.lastname: Holcomb
authors.forename: Charles E
authors.initials: CE
authors.lastname: Wade
mesh_terms: D000818:Animals; D001777:Blood Coagulation / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D001809:Blood Viscosity / Q000502:physiology*; D001810:Blood Volume / Q000502:physiology*; D006439:Hemodynamics / Q000502:physiology*; D006470:Hemorrhage / Q000503:physiopathology*; D008099:Liver / Q000098:blood supply / Q000293:injuries / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D011517:Prothrombin Time; D051381:Rats; D017207:Rats, Sprague-Dawley; D013916:Thrombelastography
keywords: Coagulation; Injury; Thromboelastography; Trauma