Research in applied cardiopulmonary physiology and extracorporeal support

Don’t go for the sats – physiological note on Oxygenation in COVID-19


A lot of discussion has been going about oxygenation in COVID-19 and when to intubate patients​1​. The question ultimately becomes, when to intubate. Patients without distress, high work of breathing or risk of self inflicted lung injury probably should not be intubated ​2​. Hypoxia can be tolerated up to a very low point. Of note, low saturations reading are inaccurate and should not be relied upon.

This tracing is from a palliative patient with extremely low saturations. The monitor shows no hypotonia, no tachypnoea and not tachycardia.

Calculating oxygen contents and oxygen reserve

Oxygen content (CaO2: arterial oxygen content, CvO2: Venous oxygen content) and oxygen delivery (DO2, assuming CO: cardiac output) can easily be calculated using standard formula. Assuming a oxygen consumption (VO2) of 200ml/min we can then calculate venous oxygen content and estimate mixed venous saturation.

(1) CaO2 = 1.36 * Hb * SaO2 / 100 + 0.003 * PaO2

(2) DO2 = CO * cO2

(3) cvO2 = (DO2 – VO2) / CO

(4) SvO2 = CvO2 / (1.36 * Hb)

(5) Oxygen Reserve = DO2 – VO2

(1) Calculation of arterial oxygen content (CaO2)
(2) Calculation of oxygen delivery (DO2)
(3) Calculation of venous oxygen content (CvO2)
(4) Estimation of venous oxygen saturation (SvO2)
(5) Estimation of oxygen reserve

These formulas can be used to run a simulation with varying Hb, cardiac output and arterial pO2 / arterial saturation values. This might help in evaluating which parameters are most useful in improving tissue oxygenation. This model does not take into account other effects of “normal” oxygen saturations on microcirculation or oxygen gradients into organs.

Calculating mixed venous saturation and oxygen reserve

SvO2 as a function of arterial saturation and cardiac output
Oxygen reserve (calculated as DO2 – VO2) as a function of arterial sats and cardiac output.


Visually it becomes quite clear, that cardiac output is the driving force behind oxygenation and thus venous saturation. From this point of view, clinicians are well advised not to focus on arterial saturation alone. However, in clinical practice guidelines usually recommend clear targets for arterial saturation, while hemodynamic parameters are less obviously defined.

From this I would draw the following conclusions:

  • Our physiological systems have huge reserves. This implies, that if a patient desaturates during mobilization (increased VO2), their physiology has to be severely impaired.
  • If in a clinical setting one has to decide between cardiac output and arterial oxygenation, I would prefer to have a normal to high cardiac output with low PEEP values. This could be a scenario in high PEEP settings or beta blocker administration. Impaired cardiac output is much more dangerous.
  • From a oxygenation point of view, increasing hemoglobin concentrations does help. However, transfusions may have their own morbidity and mortality ​3​.

Bottom Line

There is no point in having great arterial saturation, when there is no cardiac output to deliver oxygen to the tissue.


  1. 1.
    Gattinoni L, Chiumello D, Caironi P, et al. COVID-19 pneumonia: different respiratory treatments for different phenotypes? Intensive Care Med. April 2020. doi:10.1007/s00134-020-06033-2
  2. 2.
    Tobin M. Basing Respiratory Management of Coronavirus on Physiological Principles. Am J Respir Crit Care Med. April 2020. doi:10.1164/rccm.202004-1076ED
  3. 3.
    Zheng Y, Lu C, Wei S, Li Y, Long L, Yin P. Association of red blood cell transfusion and in-hospital mortality in patients admitted to the intensive care unit: a systematic review and meta-analysis. Crit Care. November 2014. doi:10.1186/s13054-014-0515-z

Photo by Cristian Newman on Unsplash

Cite this article (2. October 2022) Don’t go for the sats – physiological note on Oxygenation in COVID-19. Retrieved from
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