Question 23

College Answer

It was expected candidates would define key concepts, particularly 'mixed venous'. Many 
candidates knew some of the elements that contributed to mixed venous PCO2 but few 
described all of the main factors. There was little mention of tissue capillary flow as a factor 
affecting mixed venous CO2

Discussion

This question is essentially identical to Question 7 from the first paper of 2011. However, here the comments are cold and  abrupt, whereas in 2011 the college gave a full detailed breakdown of their expectations, even though they only wanted us to "briefly describe" this thing. On both occasions, the candidates were caught unprepared, and it was a blood bath. The pass rate for this SAQ in 2011 was 8%.

• Mixed venous PCO₂ is usually about 46 mmHg, and is determined by the total oxygen content of mixed venous blood and the shape of the CO₂ dissociation curve
• The total CO₂ content of mixed venous blood, which is usually about 520 ml/L, is described by the modified Fick equation:

  VCO₂ = CO × k × (PvCO₂ - PaCO₂)

  where

  • VCO₂  is the rate of CO₂ production, 
  • CO is the cardiac output,
  • PvCO₂ - PaCO₂ is the arteriovenous CO₂ difference, and
  • k is a coefficient used to describe the near-linear relationship between CO₂ content and partial pressure in the blood.

  • The CO₂ content of arterial blood - any increase in arterial CO₂ will be inherited by the mixed venous CO₂. This is controlled by the central ventilation reflexes.
  • CO₂ production in the tissues, which is related to the rate of aerobic metabolism and oxygen consumption (VO₂). A low metabolic rate will cause a decrease in mixed venous CO₂ (eg. hypothermia). 
  • Cardiac output, which determines the rate of tissue CO₂ removal.
    • Poor cardiac output (eg. in cardiogenic shock) will cause an increased mixed venous CO₂ by a "stagnation phenomenon"
      • I.e. an abnormally large amount of CO₂  will be added to capillary blood per unit volume if the transit time is increased (i.e. flow is decreased)
• The CO₂-carrying capacity of blood, which is described by the CO₂ dissociation curve:
  • The curve is left-shifted because deoxygenated haemoglobin has a higher affinity for CO₂ (the Haldane effect).

Rivers, Emanuel P., Douglas S. Ander, and Doris Powell. "Central venous oxygen saturation monitoring in the critically ill patient." Current opinion in critical care 7.3 (2001): 204-211.

Pearse, R. M., and A. Rhodes. "Mixed and central venous oxygen saturation." Yearbook of Intensive Care and Emergency Medicine 2005. Springer, New York, NY, 2005. 592-602.

Kandel, Gabor, and Arnold Aberman. "Mixed venous oxygen saturation: its role in the assessment of the critically ill patient." Archives of internal medicine 143.7 (1983): 1400-1402.

Ho, K. M., R. Harding, and J. Chamberlain. "A comparison of central venous-arterial and mixed venous-arterial carbon dioxide tension gradient in circulatory failure." Anaesthesia and intensive care 35.5 (2007): 695-701.

Lamia, B., X. Monnet, and J. L. Teboul. "Meaning of arterio-venous PCO2 difference in circulatory shock." Minerva anestesiologica 72.6 (2006): 597-604.