title: Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: can irreversibility be anticipated?
abstract: BACKGROUND
  The causes of cardiovascular collapse (CC) during hemorrhagic shock (HS) are unknown. We hypothesized that vascular tone loss characterizes CC, and that arterial pulse pressure/stroke volume index ratio or vascular tone index (VTI) would identify CC.
  
  
  METHODS
  Fourteen Yorkshire-Durock pigs were bled to 30 mmHg mean arterial pressure and held there by repetitive bleeding until rendered unable to compensate (CC) or for 90 min (NoCC). They were then resuscitated in equal parts to shed volume and observed for 2 h. CC was defined as a MAP < 30 mmHg for 10 min or <20 mmHg for 10 s. Study variables were recorded at baseline (B0), 30, 60, 90 min after bleeding and at resuscitation (R0), 30, and 60 min afterward.
  
  
  RESULTS
  Swine were bled to 32% ± 9% of total blood volume. Epinephrine (Epi) and VTI were low and did not change in NoCC after bleeding compared with CC swine, in which both increased (0.97 ± 0.22 to 2.57 ± 1.42 mcg/dL, and 173 ± 181 to 939 ± 474 mmHg/mL, respectively), despite no differences in bled volume. Lactate increase rate (LIR) increased with hemorrhage and was higher at R0 for CC, but did not vary in NoCC. VTI identified CC from NoCC and survivors from non-survivors before CC. A large increase in LIR was coincident with VTI decrement before CC occurred.
  
  
  CONCLUSIONS
  Vasodilatation immediately prior to CC in severe HS occurs at the same time as an increase in LIR, suggesting loss of tone as the mechanism causing CC, and energy failure as its probable cause.
authors.affiliation: Department of Critical Care Medicine, University of Pittsburgh, 3550 Terrace Street, Scaife Hall, PIttsburgh, PA 15261, USA. gomezh@upmc.edu
authors.forename: Hernando
authors.initials: H
authors.lastname: Gómez
authors.forename: Jaume
authors.initials: J
authors.lastname: Mesquida
authors.forename: Linda
authors.initials: L
authors.lastname: Hermus
authors.forename: Patricio
authors.initials: P
authors.lastname: Polanco
authors.forename: Hyung Kook
authors.initials: HK
authors.lastname: Kim
authors.forename: Sven
authors.initials: S
authors.lastname: Zenker
authors.forename: Andrés
authors.initials: A
authors.lastname: Torres
authors.forename: Rajaie
authors.initials: R
authors.lastname: Namas
authors.forename: Yoram
authors.initials: Y
authors.lastname: Vodovotz
authors.forename: Gilles
authors.initials: G
authors.lastname: Clermont
authors.forename: Juan Carlos
authors.initials: JC
authors.lastname: Puyana
authors.forename: Michael R
authors.initials: MR
authors.lastname: Pinsky
mesh_terms: D000818:Animals; D001341:Autonomic Nervous System / Q000502:physiology; D001794:Blood Pressure / Q000502:physiology*; D002395:Catecholamines / Q000097:blood; D016207:Cytokines / Q000097:blood; D004195:Disease Models, Animal; D004734:Energy Metabolism / Q000502:physiology; D007022:Hypotension / Q000401:mortality / Q000503:physiopathology*; D019344:Lactic Acid / Q000097:blood; D009566:Nitrates / Q000097:blood; D009573:Nitrites / Q000097:blood; D010100:Oxygen / Q000097:blood; D012151:Resuscitation; D012720:Severity of Illness Index; D012771:Shock, Hemorrhagic / Q000401:mortality / Q000503:physiopathology*; D013318:Stroke Volume / Q000502:physiology*; D034421:Sus scrofa; D014655:Vascular Resistance / Q000502:physiology; D014664:Vasodilation / Q000502:physiology*
chemical_list: D002395:Catecholamines; D016207:Cytokines; D009566:Nitrates; D009573:Nitrites; D019344:Lactic Acid; D010100:Oxygen