While not an intuitively obvious or typically self-sufficient cause for severe hypoxemia, decreased mixed venous oxygen saturation acts synergistically with each of the previous lesions to worsen hypoxemia. Conversely, interventions which increase mixed venous oxygen saturation can be used to compensate for the other lesions.
The saturation of mixed venous blood influences oxygenation in the presence of pure shunt as well as VlQ mismatch. The saturation of the shunt blood flow is approximately equal to that of the mixed venous blood and, because of the sigmoid shape of the oxyhemoglobin dissociation curve, even a small amount of poorly saturated shunt flow significantly reduces the saturation of systemic blood. As the saturation of mixed venous blood decreases, the stimulus for hypoxic pulmonary vasoconstriction increases according to the formula
It should be noted that as the stimulus for generalized hypoxic pulmonary vasoconstriction increases, pulmonary resistance rises and the flow through anatomical
shunts may also increase, creating a self-reinforcing cycle. Decreases in mixed venous oxygen saturation interrelate with VlQ mismatch in a similar fashion.
Mixed venous oxygen saturation is determined by oxygen delivery and oxygen consumption. Oxygen delivery, in turn, is a function of hemoglobin quantity (Hb), arterial hemoglobin saturation, and cardiac output (CO):
Normal resting oxygen delivery for a 70-kg adult is approximately 1000 ml/min. Oxygen is consumed as blood circulates and normal resting oxygen consumption is about 250 ml/min. The combined blood from the superior vena cava, inferior vena cava, and coronary sinus normally has a saturation between 60 and 75 per cent. Normal resting oxygen delivery is approximately 16 ml/kg/min. 'Critical' oxygen delivery, which is the delivery below which consumption begins to decrease, is about half normal delivery or roughly 8 ml/kg/min. Therefore there is a substantial reserve. The fact that consumption remains constant over the range described implies that mixed venous oxygen decreases linearly over the same range.
Anemia, arterial hypoxemia, low cardiac output, and increased systemic oxygen consumption all contribute to reduced mixed venous oxygen saturation through their effects on oxygen delivery or consumption. However, it should be noted that the contributing factors have different relative 'weights' in terms of their impact on mixed venous oxygenation. A 2-l/min decrease in cardiac output may represent a 40 per cent reduction in oxygen delivery, while a decrease in arterial oxygen saturation from 100 to 90 per cent only decreases oxygen delivery by 10 per cent.
It is obvious that the combination of arterial desaturation and anemia or decreased cardiac output will have substantial effects on systemic oxygen delivery as well as mixed venous oxygen saturation. Under some circumstances, arterial hypoxemia and mixed venous hypoxemia can become self-reinforcing, as is evident from Fig 7.
In these conditions, oxygenation can be ameliorated by therapies aimed at improving mixed venous oxygenation, such as red cell transfusion, inotropic support, or sedation.
Fig. 7 The changes in oxygen concentration as blood passes through the lung. Note that if the mixed venous oxygen concentration is sufficiently low, it will affect all other oxygen concentrations. (Reproduced with permission from Guyton (,1991))
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