The oxygen content in venous blood has two chief determinants. Firstly, it is obviously strongly influenced by the arterial oxygen content. All things being equal, the higher (or lower) the arterial oxygen content, the higher (or lower) the venous oxygen content.
More interestingly, it is also influenced by the tissue uptake of oxygen. For instance, the higher the (aerobic) metabolism of the tissues, the more oxygen they will take up, and the lower the venous oxygen content will be. There is also another (even more interesting!) way in which tissues can take up more oxygen: tissues can influence the amount of oxygen that haemoglobin (Hb) gives up. How? Well, when they aren't provided with enough oxygen, they metabolise anaerobically, and produce lactate as a byproduct. This lowers the pH, and, in turn, this causes Hb to more readily give off oxygen to the tissues.
So, we've covered the chief determinants of the venous oxygen content, and thus venous oxygen saturation. How do we measure it? Well, our first guess might be that any vein could do. Unfortunately, this will only give us information about local tissue conditions, so if we want to know how the body as a whole is doing, we need to go more centrally. How much more centrally? All the way to the pulmonary arteries, as it turns out. Even taking blood from, say the subclavian vein or inferior vena cava would neglect blood coming from different areas. It is more useful to measure the venous oxygen saturation once all the venous blood has mixed - hence the 'mixed' part of the name. (It might seem a bit odd to measure the mixed venous oxygen saturation in the pulmonary arteries, but recall that they carry deoxygenated blood.)
The piece of equipment that we use to undertake this measurement is called a pulmonary artery (or Swan-Ganz) catheter.
So, finally, how does this all help us? Well, if the mixed venous oxygen saturation is low (less than about 60%), there are a few possibilities to consider. As we mentioned above, tither it means that the oxygen delivery (from the arterial side of things) is diminished:
- Decreased Hb: anaemia
- Decreased oxygen saturation: hypoxia
- Decreased cardiac output: hypovolaemia, shock
...or else it means that there has been an increase in oxygen consumption:
It is usually quite easy to work out which of the above causes is operative. There is also a (slightly less useful) list of causes for an increased mixed venous oxygen saturation, but I won't go into that today.
The mixed venous oxygen saturation (SvO2) has proved very useful in trauma and critical care settings. It is a much more sensitive indicator of tissue oxygen supply-demand dynamics than other paramaters. Any drop in the SvO2 is potentially dangerous, as it implies, at the very least, a developing inadequacy in oxygen demands relative to tissue needs. At this point, the patient's arterial sats and blood pressure may be normal - but the low SvO2 indicates that, without intervention, the patient will soon be in dire straits.