This chapter is vaguely relevant to Section G4(vi) of the 2017 CICM Primary Syllabus, which asks the exam candidate to "describe the factors that affect venous oxygen saturation".
A mixed venous blood gas is a sample aspirated from the most distal port of the PA catheter, offering a mixture of inferior vena cava blood, superior vena cava blood, and the coronary sinuses. Thus, the result is an average of venous blood.
But what if I don't have a PA catheter, you might ask?
Difference between mixed venous blood samples and central venous blood samples
Weirdly, there seems to be some disagreement as to which is higher.
Our glorious scripture specifies that under normal physiological conditions central venous saturation (ScvO2) is 2-3% lower than mixed venous oxygen saturation (SvO2); if one's cross-table viva examiner happens to be Thomas John Morgan or Balasubramanian Venkatesh, one would be wise to quote Chapter 14 and regurgitate this information.
In contrast, a 2004 study published in Chest would have us believe that the ScvO2 is 5% higher than the SvO2, and implies that the difference may be a measure of myocardial oxygen consumption (given that the source of the discrepancy is probably blood washing out of the coronary sinus). Yet another review article reports that this difference changes with the CVC sampling tip position (at 15cm from the tricuspid valve, the ScvO2 was 8% higher, but in the right atrium it was only 1% higher).
A pictorial demonstration of this discrepancy:
So, in short, one can simply conclude that ScvO2 is not SvO2, and that the closer one approaches the heart the more the two measurements will agree. ScvO2 is usually slightly lower than SvO2, but this relationship may reverse in states of shock.
Estimation of cardiac output from mixed venous saturation using Ficks equation
Now, with some suspended disbelief, we can convince ourselves that some of the above parameters will not change much in the course of our daily work. For instance, the SaO2 would rarely be outside the 90-100 range - as it is not routine for an ICU patient to be kept at an SaO2 60% for long.
Similarly, we can take a bit of a guess at what the VO2I should be - for most people, its 3.5ml/kg/min, or 125ml/min.
In short, the only two variables in this equation which are subject to change are cardiac index and SvO2.
Now, if we rearrange the equation even more, by substituting the assumptions we have made, we have an even simpler form of the formula:
So... lets plug in some numbers: if our patient has a Hb of about 70, SaO2 of 96% and an SvO2 of 70%, the cardiac index is 1.42 x (1 / 0.26), or about 5.5 L/min/m2. If the SvO2 drops to 50%, the CI generated by this equation is 3L/min/m2. And so forth.
Mind you, this is not what one could call a precise and meaningful measurement. Many assumptions are made on the way to deriving this formula, and the value it generates is rather divorced from reality. However, as a "quick and dirty" means of assessing cardiac output, it is a useful bedside tool.
Estimation of efficiency of tissue oxygen delivery using ScvO2
So, some average of oxygen utilisation by both the lazy chondroblast and the hard-working myocytes must exist, and it is related to the mixed venous saturation. Thus, ScvO2 gives us an impression of average end-capillary blood: the "leftovers" of the oxygen, whatever the cells didn't use. This can be used to determine the effectiveness of tissue oxygen delivery.
Obviously, a very low ScvO2 suggests that there is an increased need for oxygen in the tissues (such is the case with hyperthermia, shivering, or exercise) or a decreased delivery of oxygen to the tissues (as in any sort of shock, anaemia, decreased cardiac output, or hypoxia).
Conversely, a very high ScvO2 suggests that the tissues are either not hungry (i.e. their demand is decreased, as in something like hypothermia or when under the effects of a muscle relaxant) or that they are unable to extract the oxygen for whatever reason (such as in the case of cyanide poisoning, or anything else that interferes with mitochondrial function).
By experiment, it has been established that under normal conditions, in the absence of critical illness, the critical oxygen extraction ratio (ERO2) is about 70%, corresponding to an SvO2 of around 30%. Of course, normal well-perfused people are not going around getting their pulmonary arterial blood sampled. No ICU patient falls into this category. Ronco et al have established empirically that for the critically ill population, the critical ERO2 is around 60%, corresponding to a SvO2 of around 40%.
Use of SvO2 to estimate shunt fraction
If you ignore the negligible contribution from dissolved oxygen, the shunt fraction equation can be rearranged into this:
Thus, if you have an arterial saturation of 99% and a venous saturation of 70%, your shunt fraction is 3%;
if the arterial saturation is 90% and venous saturation is 60%, the shunt fraction is 25%.
And so on.
Use of SvO2 in guiding resuscitation of septic shock
Rivers famously used an SvO2 of 70% as one of the goals of early goal-directed therapy. Though the trial has its critics, the Surviving Sepsis people have taken it on board as part of their recommendations, and they suggest you aim for a SvO2 of 65-70% (Grade 1C)
The use of SvO2 in sepsis resuscitation was tested in the ProCESS, ARISE and ProMISE studies. The use of ScvO2 was one of differenced between groups. These studies did not demonstrate any survival benefit from protocolised care, in which the use of ScvO2 was one of the major components.
Use of SvO2 in assessing readiness for extubation
A study published in 2010 has reported on changes in SvO2 in response to a spontaneous breathing trial. These investigators do things slightly differently to the general norm of Australian ICU; the patients were subjected to a 2-hour trial of being intubated but not ventilated - on a T-tube blow-over. This was essentially a test of their respiratory muscle power. If you can suck on a straw for two hours without building up a sweat, then you can probably breathe without a straw.
The SvO2 was used as a measure of whole-body oxygen demand (given a stable level of oxygen delivery). If you are physiologically crippled, with poor gas exchange and poor cardiac output, the increased metabolic demands of breathing though a hellishly narrow tube will increase your SvO2. The abovelinked study showed that if during such a 2-hour trial your SvO2 decreases by more than 4.5mmHg, you are at greater risk of re-intubation over the coming 48 hours.
This study has its flaws. Apart from doing T-piece spontaneous breathing trials (which many don't bother with any more, even though they are probably equivalent in effectiveness to PSV) the small studied groups were heterogenous, and the institutional reintubation rate was very high, even accounting for the fact that the study selected only "difficult to wean" patients (i.e. those who had already failed the T-piece torture). Their reintubation rate was 42%, whereas in large Australian ICUs the rate of re-intubation of electively extubated patients seems to be 1.8%