Oxygen Extraction Ratio

Reviewed and revised 29 August 2014

OVERVIEW

  • Oxygen extraction ratio (O2ER) is the ratio of oxygen consumption (VO2)  to oxygen delivery (DO2)
    • global oxygen delivery (DO2) is the total amount of oxygen delivered to the tissues per minute, irrespective of the distribution of blood flow
    • oxygen consumption (VO2) is the total amount of oxygen removed from the blood due to tissue oxidative metabolism per minute
  • Under resting conditions with normal distribution of cardiac output, DO2 is more than adequate to meet VO2 and ensure that aerobic metabolism is maintained
  • Oxygen that is not extracted returns to the mixed venous circulation
  • ScvO2 of 70% indicates oxygen delivery is adequate (assuming normal microcirculatory function)

CALCULATION

O2ER = VO2 / DO2 = (SaO2-SvO2) / SaO2

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

anearobic-threshold-vincent-de-backer
From Nebout and Pirrachio, 2012
  • 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

References and links

Journal articles

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

CCC 700 6

Critical Care

Compendium

Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health and Clinical Adjunct Associate Professor at Monash University. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.

After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.

He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE.  He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of litfl.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.

His one great achievement is being the father of two amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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