This chapter is only very slightly 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". No questions have ever been asked specifically about the practical uses of the SvO2, and they are highly unlikely to be asked in the future because the practice of measuring this parameter has gone out of fashion.
The one question from the First Part papers which asked about this topic was Question 8 from the first paper of 2019. The specific instructions were to compare and contrast the measurement and interpretation of central and mixed venous oxygen saturations. A suggested answer to that question is offered here in lieu of a summary, as this could potentially have some value to the revising exam candidate, in contrast to everything else that follows.
Measurement and Interepretation
of Mixed Venous and Central Venous Oxygen Saturation
Domain Central venous Mixed venous Site of sampling SVC or right atrium Pulmonary artery Measurement
- Intermittent sampling:
- ABG: derivation of the SvO2 value from the PO2, pH and pCO2, using the oxygen-haemoglobin dissociation curve.
- Co-oximetry: relies on measuring the absoprtion of near-IR light by haemoglobin species, and the use of the Beer-Lambert law to calculate the concentrations of oxyhaemoglobin and deoxyhaemoglobin
- Continuous monitoring:
- Reflectance spectrophotometry: relies on measuing the reflected wavelengths of near-IR light, and calculating the concentrations of oxyhaemoglobin and deoxyhaemoglobin from the log ratio of the signal strength (as each Hb species reflects a different wavelength)
Normal values 75% 70% Relationship between them Usually, higher than mixed venous Usually, lower than central venous
(incorporates blood from the coronary sinus, which has sats of ~ 35%)
- Mixed venous oxygen content
- Oxygen carrying capacity of blood
- Oxyhameoglbin dissociation curve shape
- Components of the modified Fick equation:
(CO = VO2 / CaO2 - CvO2):
- Arterial oxygen content
- VO2 (oxygen consumption)
- Cardiac output
- Low in:
- Cardiogenic shock
- Septic shock
- Malignant hyperthermia
- Elevated in:
- Also septic shock
- Cyanide toxicity
- High output cardiac failure
- Anaesthesia and paralysis
For this, you have several options, some of which are even continuous. In other words, rather than sampling the venous blood intermittently and risking blocking the lumen or introducing contamination, you can suspend a sensor in the bloodstream and continuously monitor the parameter of your choice.
That's relatively easy, provided the parameter of your choice is venous oxygen saturation. Popularised by the EGDT cult in the early 2000s, ScvO2 measurement attracted substantial industry attention, and gave rise to the development of various products which promised to monitor the ScvO2 continuously. These were so heavily marketed that the early versions of Surviving Sepsis Guidelines were widely criticised for being essentially an advertising pamphlet for Edwards Life Sciences (although the pork-barrelling by Eli Lilly was probably more egregious). The taint of industry whoring still remains, unfairly discouraging the use of these instruments. In contrast, the results of large-scale modern trials ( ProCESS, ARISE, ProMISE) discourages their use totally fairly, from the standpoint of overwhelming evidence.
Anyway: in Question 8 from the first paper of 2019, the examiners insisted that
"methods of measurement such as co-oximetry and reflectance spectrophotometry needed to be explained", and not just listed. To explain spectrophotometry and co-oximetry in detail is somewhat ambitious for a 40% answer (or this brief chapter) and so only an outline is offered here, to simplify revision.
Infrared oximetry (reflection spectrophotometry) is the gentle art of bouncing a near-IR light beam off erythrocytes, first described by Landsman et al in 1978. Because deoxygenated haemoglobin and oxyhaemoglobin reflect completely different wavelengths, you can calculate the concentration of each from the analysis of the reflected light. One could go on, but they say a picture is worth a thousand cliches:
For those who are not visual learners,
Co-oximetry is upheld as the gold standard of oximetry, as it measures the concentration of oxyhaemoglobin and deoxyhaemoglobin in as direct a fashion as is reasonably possible. It is described in detail elsewhere, as the average ICU trainee usually contacts this technology in the course of learning about dyshaemoglobin species and ABG machine innards. For a good peer-reviewed source, a reader may also refer to the excellent short paper by Elizabeth Mack (2007). In brief:
Calculation of sO2 from PO2, PCO2 and pH is a possible third way of getting am SvO2 value (or any sort of sO2) and should be mentioned here because it exists, but not dwelled upon because it is an anachronism of an era when blood gas analysers were not uniformly outfitted with haemoglobin spectrophotometry. It was dependent on the measurement of other values, and had the effect of amplifying their measurement error. Moreover, it would be confused by the presence of dyshaemoglobin, and could not be done continuously. Nierman & Schechter (1994) compared this technique (unfavourably) to co-oximetry of venous blood
To the question, "how do you interpret SvO2 data", most reasonable people would respond, "with a grain of salt". However diminished the role of this strategy, for exam purposes the CICM trainee still needs to be aware of these techniques; and there is every possibility that one day they may work with a старове́р consultant who incorporates them into their routine practice. A good article by Keith Walley (2010) summarises some of them. In short, the following applications for SvO2 and ScvO2 monitoring have been historically supported, however briefly, by the then-available evidence:
Established uses which remain essential in practice include:
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. That leaves only two variables in this equation which are subject to change: 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, to the point that many respected experts have called to abandon its use. A particularly excellent takedown may be seen at PulmCrit. In short:
Elsewhere, the relationship of SvO2 and tissue oxygen consumption is discussed. Without reproducing much of the contents of that page, it will suffice to say that SvO2 can be said to reflect the oxygen consumption by the tissues, and therefore their perfusion. This conclusion can be reached by the following mental acrobatics:
However, one might point out that:
An interesting alternative to the use of raw untreated SvO2 has been proposed by Mekontso-Dessap et al (2002). Under their proposal, one calculates the arteriovenous differences in CO2 and O2 content, and uses the ratio of these differences to determine how much oxygen is being used for aerobic metabolism. Consider:
By this theory, if one encounters a lactic acidosis and the VCO2/VO2 ratio is normal, one must conclude that this is a Type B lactic acidosis. Of course, detecting anaerobic metabolism does not necessarily mean knowing the management strategy which is required to make it aerobic. Is the ratio low because flow to the issues is poor, or are the patient's mitochondria just not using the oxygen properly, or is there microvascular shunting occurring which prevents proper oxygen use? Su et al (2018) used this to guide therapy (comparing it to SvO2, of all things), and found that there was no difference in outcome. It remains to be seen whether this turns into a valuable bedside instrument.
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.
Of course, anybody who has been paying attention will realise that the contribution of dissolved oxygen is often far from negligible (for example, where Hb is low and FiO2 is high, it could contribute up to 20% to the total oxygen content of whole blood). To actually calculate shunt, SvO2 is still essential
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 had taken it on board as part of their recommendations, and for a period suggested that everybody needs to aim for a SvO2 of 65-70% (Grade 1C).
The use of SvO2 in sepsis resuscitation was subsequently tested in the ProCESS, ARISE and ProMISE studies. The use of ScvO2 was one of the main differences 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. To be fair, many of these patients were not particularly unwell (critics of ARISE will point out that most of the patients improved after a couple of litres of fluid), but even subgroup analysis of truly ICUish patients did not reveal any effect.
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%