Circulatory shock is the inadequacy to supply mitochondria with enough oxygen to sustain aerobic energy metabolism. A novel noninvasive bedside measurement was recently introduced to monitor the mitochondrial oxygen tension in the skin (mitoPo₂). As the most downstream marker of oxygen balance in the skin, mitoPo₂ may provide additional information to improve shock management. However, a physiological basis for the interpretation of mitoPo₂ values has not been established yet. In this paper, we developed a mathematical model of skin mitoPo₂ using a network of parallel microvessels, based on Krogh's cylinder model. The model contains skin blood flow velocity, heterogeneity of blood flow, hematocrit, arteriolar oxygen saturation, and mitochondrial oxygen consumption as major variables. The major results of the model show that normal physiological mitoPo₂ is in the range of 40-60 mmHg. The relationship of mitoPo₂ with skin blood flow velocity follows a logarithmic growth curve, reaching a plateau at high skin blood flow velocity, suggesting that oxygen balance remains stable while peripheral perfusion declines. The model shows that a critical range exists where mitoPo₂ rapidly deteriorates if skin perfusion further decreases. The model intuitively shows how tissue hypoxia could occur in the setting of septic shock, due to the profound impact of microcirculatory disturbance on mitoPo₂, even at sustained cardiac output. MitoPo₂ is the result of a complex interaction between all factors of oxygen delivery and microcirculation. This mathematical framework can be used to interpret mitoPo₂ values in shock, with the potential to enhance personalized clinical trial design.NEW & NOTEWORTHY This is the first paper to simulate mitochondrial oxygen tension in skin in circulatory shock. The relationships of mitoPo₂ with parameters of (microcirculatory) oxygen delivery aid in the understanding of noninvasive bedside measurement of mitoPo₂ values and show that mitochondrial oxygen tension is two orders of magnitude higher than classically assumed. The model can be used to enhance clinical trial design investigating mitoPo₂ as a resuscitation target in circulatory shock.

Reinier F. Crane

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