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

Gómez, H and Mesquida, J and Hermus, L and Polanco, P and Kim, HK and Zenker, S and Torres, A and Namas, R and Vodovotz, Y and Clermont, G and Puyana, JC and Pinsky, MR (2012) Physiologic responses to severe hemorrhagic shock and the genesis of cardiovascular collapse: Can irreversibility be anticipated? Journal of Surgical Research, 178 (1). 358 - 369. ISSN 0022-4804

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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. © 2012 Elsevier Inc. All rights reserved.


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Item Type: Article
Status: Published
CreatorsEmailPitt UsernameORCID
Gómez, H
Mesquida, J
Hermus, L
Polanco, P
Kim, HKhyk11@pitt.eduHYK11
Zenker, S
Torres, A
Namas, R
Vodovotz, Y
Clermont, Gcler@pitt.eduCLER0000-0002-0163-1379
Puyana, JC
Pinsky, MRpinsky@pitt.eduPINSKY0000-0001-6166-700X
Centers: Other Centers, Institutes, Offices, or Units > McGowan Institute for Regenerative Medicine
Date: 1 November 2012
Date Type: Publication
Journal or Publication Title: Journal of Surgical Research
Volume: 178
Number: 1
Page Range: 358 - 369
DOI or Unique Handle: 10.1016/j.jss.2011.12.015
Schools and Programs: School of Medicine > Critical Care Medicine
Refereed: Yes
ISSN: 0022-4804
PubMed Central ID: PMC3424406
PubMed ID: 22475354
Date Deposited: 29 Oct 2012 15:41
Last Modified: 14 Mar 2021 11:56


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