Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: Can irreversibility be anticipated?

Hernando Gómez, Jaume Mesquida, Linda Hermus, Patricio Polanco, Hyung Kook Kim, Sven Zenker, Andrés Torres, Rajaie Namas, Yoram Vodovotz, Gilles Clermont, Juan Carlos Puyana, Michael R. Pinsky

Research output: Contribution to journalArticle

14 Citations (Scopus)

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.

Original languageEnglish (US)
Pages (from-to)358-369
Number of pages12
JournalJournal of Surgical Research
Volume178
Issue number1
DOIs
StatePublished - Nov 2012

Fingerprint

Hemorrhagic Shock
Blood Vessels
Hemorrhage
Lactic Acid
Swine
Arterial Pressure
Blood Volume
Vasodilation
Resuscitation
Stroke Volume
Epinephrine
Blood Pressure

Keywords

  • Animal model
  • Autonomic control
  • Lactate
  • Vasomotor tone

ASJC Scopus subject areas

  • Surgery

Cite this

Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse : Can irreversibility be anticipated? / Gómez, Hernando; Mesquida, Jaume; Hermus, Linda; Polanco, Patricio; Kim, Hyung Kook; Zenker, Sven; Torres, Andrés; Namas, Rajaie; Vodovotz, Yoram; Clermont, Gilles; Puyana, Juan Carlos; Pinsky, Michael R.

In: Journal of Surgical Research, Vol. 178, No. 1, 11.2012, p. 358-369.

Research output: Contribution to journalArticle

Gómez, H, Mesquida, J, Hermus, L, Polanco, P, Kim, HK, Zenker, S, Torres, A, Namas, R, Vodovotz, Y, Clermont, G, Puyana, JC & Pinsky, MR 2012, 'Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: Can irreversibility be anticipated?', Journal of Surgical Research, vol. 178, no. 1, pp. 358-369. https://doi.org/10.1016/j.jss.2011.12.015
Gómez, Hernando ; Mesquida, Jaume ; Hermus, Linda ; Polanco, Patricio ; Kim, Hyung Kook ; Zenker, Sven ; Torres, Andrés ; Namas, Rajaie ; Vodovotz, Yoram ; Clermont, Gilles ; Puyana, Juan Carlos ; Pinsky, Michael R. / Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse : Can irreversibility be anticipated?. In: Journal of Surgical Research. 2012 ; Vol. 178, No. 1. pp. 358-369.
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T1 - Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse

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AU - Gómez, Hernando

AU - Mesquida, Jaume

AU - Hermus, Linda

AU - Polanco, Patricio

AU - Kim, Hyung Kook

AU - Zenker, Sven

AU - Torres, Andrés

AU - Namas, Rajaie

AU - Vodovotz, Yoram

AU - Clermont, Gilles

AU - Puyana, Juan Carlos

AU - Pinsky, Michael R.

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N2 - 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.

AB - 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.

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