Tissue hypoxia during acute hemorrhage

Critical Care201317:423

DOI: 10.1186/cc12519

Published: 28 March 2013

Calzia and colleagues argue [1] that tissue hypoxia in a rat model of hemorrhage that led to an oxygen deficit of 120 ml/kg with hyperlactacidemia [2] may be modest, and may not affect hydrogen sulfide oxidation since '... the arterial oxygen partial pressure was still normal ...' [1]. This contention requires clarification.

A relative hyperventilation is the rule in most experimental models of hemorrhage [2, 3], since the reduction in oxygen uptake/consumption http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq1_HTML.gif is always larger than that in alveolar ventilation http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq2_HTML.gif . Alveolar oxygen partial pressure therefore increases during hemorrhage, as it is the ratio between http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif and http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq4_HTML.gif (and not the absolute level of http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq4_HTML.gif ) that dictates the partial pressure of oxygen in the alveolar gas (PAO2):
http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_Equa_HTML.gif

This tells us very little about the level of tissue hypoxia.

In all of the models used to study an acute hemorrhage, the baseline oxygen delivery rate http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq5_HTML.gif is three to four times higher than http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif , despite a large discrepancy in http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif per kilogram between a 500 g rat, a 20 kg pig or a human being: cardiac output, DO2 and http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif do share a similar allometric function with body weight, so that the blood oxygen content is the same in most species. http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq6_HTML.gif drops dramatically during hemorrhage, reducing DO2. The level of DO2 decreases up to 10 times while http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif drops by four times regardless of the size of animal chosen [3, 4] so that both DO2 and http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif reach one-third of the baseline metabolic rate at the end of a severe hemorrhage! This should certainly lead to one of the most severe forms of tissue hypoxia - with normal arterial blood oxygen partial pressure - unless a decrease in oxygen demand contributes significantly to the reduction in http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif induced by the decline in DO2. Indeed, although the relationship between DO2 and http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif is similar across species, the meaning of a reduction in http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif can greatly differ among animal models according to their ability to decrease the oxygen demand [3, 5] - a phenomenon present during hemorrhage in small mammals [3]. It is eventually this ability to modify oxygen demand during a hemorrhage, in keeping with DO2, which controls the level of tissue hypoxia, and not the absolute levels of PaO2, DO2 or http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif .

Abbreviations

CaO2

concentration (content) of oxygen in the arterial gas

DO2

rate of oxygen delivery http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq7_HTML.gif

PAO2

partial pressure of oxygen in the alveolar gas

PIO2

partial pressure of oxygen in the inspired gas

http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq6_HTML.gif

cardiac output

http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq4_HTML.gif

alveolar ventilation

http://static-content.springer.com/image/art%3A10.1186%2Fcc12519/MediaObjects/13054_2013_1668_IEq3_HTML.gif

oxygen uptake/consumption.

Declarations

Authors’ Affiliations

(1)
Division of Pulmonary and Critical Care Medicine, Penn State University College of Medicine, Penn State Hershey Medical Center

References

  1. Calzia E, Radermacher P, Olson KR: Endogenous H 2 S in hemorrhagic shock: innocent bystander or central player? Crit Care 2012, 16:183.PubMedView Article
  2. Van De Louw A, Haouzi P: Oxygen deficit and H 2 S in hemorrhagic shock in rats. Crit Care 2012, 16:178.View Article
  3. Haouzi P, Van de Louw A: Uncoupling mitochondrial activity maintains body VO 2 during hemorrhage-induced O 2 deficit in the anesthetized rat. Respir Physiol Neurobiol 2013, 186:87–94.PubMedView Article
  4. Vincent JL, De Backer D: Oxygen transport - the oxygen delivery controversy. Intensive Care Med 2004, 30:1990–1996.PubMedView Article
  5. Haouzi P: Murine models in critical care research. Crit Care Med 2011, 39:2290–2293.PubMedView Article

Copyright

© BioMed Central Ltd 2013

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