Oxygen consumption-oxygen delivery relationship in children

doi:10.1016/S0022-3476(05)81690-7

The Journal of Pediatrics

Volume 123, Issue 2, August 1993, Pages 208-214

https://doi.org/10.1016/S0022-3476(05)81690-7 Get rights and content

We examined the relationship between oxygen consumption (̇o₂) and oxygen delivery (Do₂) over a range of metabolic demand in two groups of children. We studied 15 children ofter cardiac surgery (plasma lactate levels <2.2 mmol/L, ̇o₂<6 ml/min per kilogram, oxygen extraction ratio <25%); 8 were given transfusions with erythrocytes, 10 to 15 ml/kg, and 7 received adrenaline infusions (0.05 to 0.3 μg/kg per minute). Blood transfusions significantly increased Do₂ (20.5±6.4 to 26.2±7.1 ml/min per kilogram; p<0.05) but did not alter ̇o₂. Adrenaline increased Do₂ (19.9±5.0 to 25.9±6.1 ml/min per kilogram; p<0.05) and ̇o₂ (4.3±0.8 to 5.5±1.2 ml/min per kilogram; p<0.05), but the oxygen excretion ratio and the mixed venous oxygen, saturation were unchanged. We also measured ̇o₂ and Doppler-derived Do₂ in 25 normal children during exercise. The relationship during exercise is given by the following equation: ̇o₂ index (in milliters per minute per kilogram)=0.88×Do₂ index − 6.95. Adrenaline infusions, but not blood transfusions, increased ̇o₂ and Do₂ together. This effect may be due to increased demand, analogous to exercise, and probably does not represent improved perfusion. We also found significant measurement error in Do₂ and spontaneous variation in ̇o₂. We believe that the concept of supplydependent ̇o₂ is based on a number of methodologic and measurement errors. It should not be used to justify potentially dangerous therapies in sick children.

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Cited by (30)

Haemoglobin transfusion threshold in very preterm newborns: A theoretical framework derived from prevailing oxygen physiology
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Citation Excerpt :
Active manipulation of the [Hb] is the least studied variable of the oxygen delivery equation in the very preterm newborn. Packed red cell transfusion in adult [32] and paediatric [33] intensive care populations has been shown to improve oxygen delivery without increasing oxygen consumption. Further, emerging evidence supports significant beneficial alterations to cardiac output and systemic oxygen extraction in response to packed red blood cell transfusion in preterm infants [34].
The overwhelming majority of very preterm newborns receive at least one transfusion during their in hospital stay. However, despite two recent randomised trials, the appropriate haemoglobin transfusion threshold in these high risk infants remains unclear. Typically, clinicians consider gestation, chronologic age and illness severity in order to determine the need for transfusion. There is, however, no simple way to balance these heterogeneous variables in order to arrive at a transfusion threshold without considering the prevailing oxygen physiology. This is particularly important during the transition to extra-uterine life, a time when the risk of brain injury is highest. We hypothesise that dysregulated cerebral oxygen handling, characterised by restricted oxygen consumption from suboptimal oxygen delivery increases the risk of hypoxic ischaemic brain injury in very preterm newborns and is the single common patho-physiologic process underlying early acquired brain injury in the preterm newborn. Our proposed framework, based on the physiology of oxygen handling, considers the prevailing oxygen kinetics in the very preterm newborn as a means of deriving the appropriate Hb transfusion threshold thereby balancing oxygen delivery and consumption and avoiding hypoxic ischaemic early brain injury. Manipulation of the oxygen delivery equation, with consideration of the likely chronologic changes to cardiac output in particular, permit derivation of a transfusion threshold in the first week of life and represents a novel therapeutic intervention aimed solely at prevention of early acquired brain injury and its associated long term neuro-developmental burden.
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Le transport artériel en O₂ (TaO₂ =Q × CaO₂, avec Q : débit cardiaque, et CaO₂, concentration artérielle en O₂) adapté aux besoins (VO₂) de l’organisme en cas d’anémie aiguë est celui qui permet d’obtenir TaO₂ >TaO₂crit (TaO₂crit : TaO₂ critique, valeur pour laquelle toute diminution de TaO₂ s’accompagne d’une baisse de VO₂). La nécessité d’un apport en globules rouges pour un sujet donné repose donc sur la détermination d’un CaO₂crit, et donc d’un taux d’hémoglobine ([Hb]) critique ([Hb]crit) puisque CaO₂ ≈ 1,39 × [Hb] × SaO₂ (avec SaO₂ : saturation artérielle en O₂). La possibilité de réponse de l’organisme par une augmentation de Q est tout aussi déterminante que [Hb] dans la décision de transfusion puisque CaO₂crit est inversement proportionnel à Qcrit (Qcrit : valeur critique de Q). La saturation veineuse en O₂ du sang veineux mêlé (SvO₂) est une grandeur qui intègre les différents paramètres de l’oxygénation tissulaire puisque SvO₂ =SaO₂ –VO₂/(Q × [Hb] × 1,39). Pour TaO₂crit, SvO₂ est de l’ordre de 40 % et l’extraction périphérique de l’O₂, ERO₂, est de l’ordre de 60 % pour SaO₂ ≈ 100 %. Une grandeur telle que la SvO₂ centrale, ou ScvO₂ — bien corrélée à la SvO₂ mesurée par cathéter de Swan-Ganz — peut être aisément recueillie sur voie veineuse centrale (équipée ou non de fibres optiques) et peut faciliter la décision et le suivi transfusionnels chez le patient présentant une baisse rapide de [Hb].
The correct oxygen (O₂) transport (TaO₂ =Q $̇$ CaO₂, with Q: cardiac output, and CaO₂, arterial O₂ concentration) that matches body O₂ requirements (VO₂) during acute anemia is that one which allows TaO₂ > TaO₂crit (TaO₂crit: critical TaO₂, value at which any further decrease in TaO₂ is associated with a decrease in VO₂). Transfusion decision in an individual relies on critical CaO₂ (CaO₂crit), and critical hemoglobin concentration ([Hb]crit) since CaO₂ ≈ 1.39 $̇$ [Hb] $̇$ SaO₂ (with SaO₂: arterial O₂ saturation). The way the body can increase Q is as much determining as [Hb] in transfusion decision since CaO₂crit is inversely related to Qcrit (Qcrit: critical value for Q). Mixed O₂ venous saturation (SvO₂) is a value, which incorporates key tissue oxygenation determinants. Indeed, SvO₂ = SaO₂ – VO_2/(Q $̇$ [Hb] $̇$ 1.39). At TaO₂crit, SvO₂ is close to 40% and O₂ extraction capabilities, ERO₂, are close to 60% when SaO₂ ≈ 100%. It is, therefore, tempting to consider central venous-derived SvO₂, ScvO₂, as an easy-to-obtain surrogate marker of Swan-derived SvO₂ measurement, which can help in transfusion decision and monitoring when [Hb] is decreasing acutely.

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Original articleOxygen consumption-oxygen delivery relationship in children

Clin Chest Med

Chest

Chest

Chest

J Am Coll Cardiol

Chest

Clin Perinatol

Sequential cardiopulmonary variables of infants and children in septic shock

Crit Care Med

Distribution of cardiopulmonary variables in pediatric survivors and nonsurvivors of septic shock

Crit Care Med

Local control of tissue oxygen delivery and its contribution to the regulation of cardiac output

Am J Physiol

Hemodynamic and oxygen transport effects of dobutamine in critically ill general surgical patients

Crit Care Med

Persistence of supply dependency of oxygen uptake at high levels of delivery in adult respiratory distress syndrome

Crit Care Med

Oxygen consumption is independent of changes in oxygen delivery in severe adult respiratory distress syndrome

Am Rev Respir Dis

Original article
Oxygen consumption-oxygen delivery relationship in children