Analysis of mixed venous blood provides valuable information in evaluating the oxygen supply-demand axis. Mixed venous oxygen saturation (SvO₂) is the O₂ saturation of blood in the pulmonary artery after the venous effluent from various organs has mixed thoroughly in the right ventricle (normal SvO₂ = 70% to 80%, normal mixed venous oxygen pressure [PvO₂] =35 to 45 mm Hg). Normally, blood from the inferior vena cava is more fully saturated (5% to 7%) than blood from the superior vena cava due to highly saturated blood from the renal vein entering the inferior vena cava, but the reverse is true in shock states because of redistribution of flow away from the splanchnic, renal, and mesenteric beds.

The SvO₂ can be measured intermittently by slowly withdrawing a sample of blood from the distal port of the unwedged pulmonary artery catheter or continuously with a fiberoptic pulmonary artery catheter that measures O₂ saturation by reflectance oximetry. Intermittent sampling of SvO₂ is accomplished by discarding the initial 3 mL of blood and then withdrawing a sample very slowly in order to avoid contamination with capillary blood, which may artifactually increase the oxygen content.

The value of mixed venous blood analysis is best understood in the framework of tissue O₂ delivery-supply dynamics. Oxygen delivery is the product of cardiac output and arterial O₂ content, the latter being determined by the hemoglobin and arterial O₂ saturation (SaO₂). Each organ receives a variable percentage of the total amount, a flow that may be luxuriant, just adequate, or insufficient to satisfy the aerobic metabolism demand. The O₂ tension (PvO₂) and saturation of the venous effluent reflect the balance between supply and demand. Normally, peripheral oxygen consumption is independent of the oxygen delivery. Therefore, as cardiac output and oxygen delivery decline, peripheral extraction increases to keep consumption constant. This results in decreased mixed venous oxygen saturation. Under normal conditions, the SaO₂-SvO₂ difference is 20% to 25%, yielding an SvO₂ of 65% to 75% when arterial blood is well oxygenated. Increased SvO₂ is seen in a variety of conditions. In sepsis, SvO₂ is often normal, but in some cases there is extreme peripheral vasodilatation, and cardiac
output increases disproportionately to metabolic demands, resulting in increased SvO₂. Cirrhosis is one of the more common causes of marked increase in SvO₂, with values usually >85%. A number of vasodilating agents and left-to-right shunts (either intracardiac or peripheral) also result in increased SvO₂. Wedging of the catheter and mitral regurgitation (which tend to bring the catheter tip into contact with arterialized blood) are additional factors that raise the SvO₂. Finally, agents that interfere with mitochondrial cytochrome activity (e.g., cyanide) may produce an elevated SvO₂ value owing to inability of the tissues to utilize oxygen.