Oxygen Delivery and Consumption Relationships in Sepsis — The Role of Inotropic and Vasoactive Drugs

Abstract

Oxygen delivery (DO₂) and oxygen consumption ($\mathop \text{V}\limits^\text{.}$O₂) relationships are a confusing subject with contradictory research findings. Whole body DO₂, also termed oxygen availability, is calculated: DO₂ = Hb x SaO₂ x CO x 0.134, where Hb = hemoglobin concentration, g/dl; SaO₂ = arterial oxygen saturation, %; CO = cardiac output, 1/min. $\mathop \text{V}\limits^\text{.}$O₂ can either be calculated indirectly, Hb x (SaO₂ — SvO₂) X CO X 0.134, where SvO₂ = venous oxygen saturation, or be directly measured as the difference between inspired and expired gases. In normal individuals $\mathop \text{V}\limits^\text{.}$O₂ is closely regulated to provide for the bodies needs and remains relatively constant over a wide range of DO₂. If DO₂ falls however, a critical point is reached after which $\mathop \text{V}\limits^\text{.}$O₂ also falls. A different situation might occur in critically ill patients, particularly septic patients, where $\mathop \text{V}\limits^\text{.}$O₂ appears to be related to DO₂ over a wide range of DO₂, a phenomenon termed “supply dependence” [1].