Mixed venous oxygen saturation (SvO2) monitoring


  • measurement of oxygenation saturation from mixed venous blood (SvO2) in the pulmonary artery
  • requires Pulmonary Artery Catheter insertion in most clinical settings


  • measures the end result of O2 consumption and delivery


O2 flux = (cardiac output x (Hemoglobin concentration x SpO2 x 1.34) + (PaO2 x 0.003)) – oxygen consumption

  • SvO2 = mixed venous oxygen saturation
  • measured via a sample of blood from a pulmonary artery catheter (PAC)
  • measures the end result of O2 consumption and delivery
  • is used in ICU as a measure of O2 extraction by the body
  • normal SvO2 = 65-70%
  • SvO2 > ScvO2 as it contains blood from both SVC and IVC
  • if SvO2 low then either consumption elevated or demand high
  • 0.5 corresponds to a theoretical critical PvO2 of 26mmHg -> level where tissue dysoxia is highly likely
  • > 0.8 corresponds with high flow states: sepsis, hyperthyroidism, severe liver disease



  • it can be used as a marker of how well O2 is being delivered to the peripheral tissues by extrapolation (if SvO2 low and patient in multiorgan failure then we can add a inotrope to help increase cardiac output ie. in severe sepsis)
  • its surrogate ScvO2 has used as a treatment goal in severe sepsis and has been shown to decrease mortality and morbidity (Rivers study)
  • continuous measurement obtained once inputting data about patient (thus can see trends with changes in therapy – fluid, inotropes, vasodilators, dialysis)
  • good information quickly


  • must be measured from a PAC thus patient exposed to risks associated with pulmonary artery catheterization (arrhythmia, pulmonary infarction, embolism, bleeding, pneumothorax, line sepsis)
  • blood taken from a normal central line to estimate SvO2 (referred to as ScvO2 not true result and not as accurate and may mainly be blood from SVC which has a different O2 saturation than SvO2 -> used as a treatment goal in severe sepsis and has been shown to decrease mortality and morbidity (Rivers))
  • can be high in a number of situations (sepsis, liver failure, wedged PAC, administration of high FiO2)
  • can be low in a number of situation (multiple organ failure, cardiac arrest)
  • requires calibration for changing haematocrit
  • Gattinoni RCT showed no benefit from SvO2 monitoring


  • see complications associated with PAC use


High SvO2

  • increased O2 delivery (increased FiO2, hyperoxia, hyperbaric oxygen)
  • decreased O2 demand (hypothermia, anaesthesia, neuromuscular blockade)
  • high flow states: sepsis, hyperthyroidism, severe liver disease

Low SvO2

  • decreased O2 delivery:

1. decreased Hb (anaemia, haemorrhage, dilution) 2. decreased SaO2 (hypoxaemia) 3. decreased Q (any form of shock, arrhythmia)

  • increased O2 demand (hyperthermia, shivering, pain, seizures)

Causes of High SvO2 despite evidence of End-organ Hypoxia

  • microvascular shunting (e.g. sepsis)
  • histotoxic hypoxia (e.g. cyanide poisoning)
  • abnormalities in distribution of blood flow

References and Links


Journal articles

  • Robin E, Costecalde M, Lebuffe G, Vallet B. Clinical relevance of data from the pulmonary artery catheter. Crit Care. 2006;10 Suppl 3:S3. Review. PubMed PMID: 17164015; PubMed Central PMCID: PMC3226125.

CCC 700 6

Critical Care


Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also a 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 three amazing children.

On Twitter, he is @precordialthump.

| INTENSIVE | RAGE | Resuscitology | SMACC

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