Oxygen extraction index (O₂ER)

Oxygen extraction index is interrelated to the cell membrane permeability, where cholesterol and phospholipids are of great importance. By hypothesis for the nature of bonds, involved in the interaction of phospholipids polar sites and cholesterol, cholesterol hydroxyl and ethereal oxygen become hydrogen bonded. At a phase transition temperature, phospholipids pass from a solid gel to a liquidcrystal state. Molecular nature of phase transition is attributed to the changes of average speed of oxygen supply, depending in the temperature. In special literature, when assessing cholesterol role in the membrane structure and function it is considered that cholesterol facilitates decrease in mobility of fatty acid chains at high temperatures and increase in mobility at low temperatures.

O₂ER is VO2 / DO2; the normal ratio is 0.2-0.3, which corresponds to an ScVO2 (Central venous saturation) of 70-80%.

A high O₂ER (i.e. a low ScVO2) is a feature of "flow insufficiency" states, i.e. anything which causes a decreased cardiac output (or an increased tissue oxygen demand, for that matter)

A low O₂ER (i.e. a high ScVO2) demonstrates either a diminished tissue oxygen demand, or inefficient oxygen utilisation by the tissues, or some sort of pathologically increased cardiac output (well in excess of the organism's physiological requirements).

Calculation of the oxygen extraction ratio

The simple O₂ER equation can be expressed as follows:

O₂ER  = VO2 / DO2

VO2 = CO ×(CaO2 - CvO2)  ...this is the global oxygen consumption

DO2 = CO ×CaO2 ...this is the global oxygen delivery.

In order to calculate this, one requires the cardiac output (from the PA catheter) and the oxygen content of the blood. The oxygen-carrying capacity of blood is discussed in another chapter, and remains fairly stable in ICU patients (given that the hemoglobin and arterial saturation is carefully monitored and controlled). So, really, the only variable which actually varies is the mixed venous saturation. Thus the O₂ER equation can be simplified as follows:

O₂ER  = (SaO2-SvO2) / SaO2

Or even more simply,

O₂ER  = 100% - SvO2 (in percent)

(assuming that the arterial saturation is close to 100%).

(SvO2- mixed venous saturation)

Normal values

In a normal 75 kg adult undertaking routine activities:

·       VO2 is approximately 250 ml/min (cf. VO2max in a non-athlete 75kg person is about 3L/min)

·       DO2 is approx 1 L/min

·       O₂ER is 25% (increases to ~70% during maximal exercise in an athlete)

·       SvO2 70%

O2ER varies for different organs:

·       cardiac O₂ER = >60%

·       hepatic O₂ER = 45-55%

·       renal O₂ER = <15%

RELATIONSHIP BETWEEN VO2 and DO2

Initially, as metabolic demand (VO2) increases, or DO2 diminishes, O₂ER rises to maintain aerobic metabolism and consumption remains independent of delivery.

However, at a point called critical DO2 (cDO2)—the maximum O₂ER is reached. This is believed to be ~70%.

Beyond cDO2 any further increase in VO2, or decline in DO2, must lead to tissue hypoxia and anaerobic metabolism (lactate production is a surrogate for this)

In reality each tissue/organ has its own cDO2 — the higher the O₂ER for a given tissue, the greater the dependence on DO2 (supply dependence).

Interpretation of abnormal O₂ER

High O₂ER suggests inadequate oxygen delivery (OH CRAP; shock)

oxygen (hypoxic hypoxia: low FiO2 gas or high altitude; lung disease)

hemoglobin (anemia)

contractility

rate/ rhythm

afterload

preload

shock/ hypoperfusion due to other causes

or increased oxygen consumption (VO2)

fever and inflammatory states, e.g. sepsis, burns, trauma, surgery

increased metabolic rate, e.g. hyperthyroidism, adrenergic drugs, hyperthermia, burns

increased muscular activity, e.g. exercise, shivering, seizures, agitation/anxiety/pain, weaning from ventilation/ increased respiratory effort

Low O₂ER suggests increased oxygen delivery

hyperoxia, e.g high FiO2 gas, hyperbaric oxygen or ECMO

or decreased oxygen consumption

decreased metabolic rate, e.g. hypothyroidism, sedatives/ hypnotics, hypothermia

decreased muscular activity e.g. sedation/analgesics, muscle paralysis, ventilatory support

antipyretics

Starvation/hyponutrition

Sepsis due to shunting and histotoxic hypoxia

Histotoxic hypoxia, e.g. cyanide poisoning

https://derangedphysiology.com/main/required-reading/equipment-and-procedures/Chapter%202.4.3/oxygen-extraction-ratio#:~:text=O2ER%20is%20VO,oxygen%20demand%2C%20for%20that%20matter

https://derangedphysiology.com/main/required-reading/equipment-and-procedures/Chapter%20242/central-and-mixed-venous-saturation-monitoring

https://litfl.com/oxygen-extraction-ratio/

https://www.mayoclinic.org/tests-procedures/ecmo/about/pac-20484615#:~:text=In%20extracorporeal%20membrane%20oxygenation%20(ECMO,to%20tissues%20in%20the%20body.

https://www.ncbi.nlm.nih.gov/books/NBK560867/#:~:text=The%20fraction%20of%20inspired%20oxygen%2C%20FiO2%2C%20is%20an%20estimation%20of,treatment%20of%20patients%20with%20hypoxemia.

1. McLellan SA, Walsh TS. Oxygen delivery and haemoglobin. Contin Educ Anaesth Crit Care Pain (2004) 4 (4): 123-126. [Free Full Text]
2. Nebout S, Pirracchio R. Should We Monitor ScVO2 in Critically Ill Patients? Cardiol Res Pract. 2012;2012:370697. PMC3177360.