Open Access

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 V ˙ O 2 is always larger than that in alveolar ventilation V ˙ A . Alveolar oxygen partial pressure therefore increases during hemorrhage, as it is the ratio between V ˙ O 2 and V ˙ A (and not the absolute level of V ˙ A ) that dictates the partial pressure of oxygen in the alveolar gas (PAO2):
PA O 2  =  PI O 2 - k V ˙ O 2 / V ˙ A

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 ( D O 2 = Q ˙ C a O 2 ) is three to four times higher than V ˙ O 2 , despite a large discrepancy in V ˙ O 2 per kilogram between a 500 g rat, a 20 kg pig or a human being: cardiac output, DO2 and V ˙ O 2 do share a similar allometric function with body weight, so that the blood oxygen content is the same in most species. Q ˙ drops dramatically during hemorrhage, reducing DO2. The level of DO2 decreases up to 10 times while V ˙ O 2 drops by four times regardless of the size of animal chosen [3, 4] so that both DO2 and V ˙ O 2 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 V ˙ O 2 induced by the decline in DO2. Indeed, although the relationship between DO2 and V ˙ O 2 is similar across species, the meaning of a reduction in V ˙ O 2 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 V ˙ O 2 .



concentration (content) of oxygen in the arterial gas


rate of oxygen delivery ( Q ˙ C a O 2 )


partial pressure of oxygen in the alveolar gas


partial pressure of oxygen in the inspired gas

Q ˙

cardiac output

V ˙ A

alveolar ventilation

V ˙ O 2

oxygen uptake/consumption.


Authors’ Affiliations

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


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