VQ Mismatch

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Venous Admixture

  • Degree of admixture of mixed venous blood with pulmonary end-capillary blood that would be required to produce the observed difference between arterial and pulmonary end-capillary pCO2
  • Includes both shunt and V/Q mismatch
  • Calculated by the shunt equation - but differs from the actual amount of venous blood that mingles, as:
  • Bronchial venous drainage does not always have the same PO2 as mixed venous blood
  • Venous admixture includes alveoli blood with V/Q mismatch
  • These are in addition to the pulmonary pathology and congenital heart disease examples we normally consider when thinking of shunts
  • Decreasing cardiac output affects PO2 by
  • Decreasing mixed venous oxygen content, which decreases PO2
  • Fraction of the shunt proportionally decreases with decreasing cardiac output, increasing PO2
  • These effects are approximately opposite and equal, therefore cardiac output doesn't affect PO2 much
  • Hypoxia due to shunting cannot be abolished by giving the subject 100% oxygen to breathe
  • Giving a patient 100% O2 to breathe is a very sensitive measure of shunt because when PAO2 is high, a small depression of arterial O2 concentration causes a large fall in pulmonary vein PO2 due to the flat slope of the O2 dissociation curve in this region - meaning a huge gradient will be present between predicted arterial PO2 and actual. This would otherwise be much smaller.


  • Effect of shunting on arterial PCO2 is usually minimal and ignored, as a shunt causing hypoxia causes ventilatory compensation that decreases PCO2 regardless
  • Physiological Shunts:
  • Coronary blood enters LV via the thebesian veins
  • Some bronchial artery blood enters the pulmonary veins
(Blood from these sources is NOT mixed venous blood and thus would have different PO2 from PvO2)
  • Pathological Shunts:
(These may involve mixed venous blood)
  • Congenital heart disease with R->L shunt
  • Perfusion of non-ventilated alveoli (V/Q=0) (atelectasis, bronchial obstruction)
  • Pulmonary arterio-venous shunts (haemangioma)

Ventilation-Perfusion Mismatch

  • Most common cause of hypoxia
  • The PO2 in any lung unit is determined by the ratio of ventilation to blood flow

Screen shot 2012-09-19 at 8.41.20 PM.png

  • Ventilation increases slowly from the top of the lung to the bottom, while blood flow increases more rapidly
  • As a result of this, ventilation-perfusion ratio is abnormally high at the top of the lung and lower at the bottom

Screen shot 2012-09-19 at 8.44.00 PM.png

  • Horizontal "slices" of the lung correspond to positions on O2-CO2 diagram:
  • Decreased PCO2 and high PO2 at the lung apex where VQ ratio is high
  • Increased PCO2 and low PO2 at the lung bases where VQ ratio is low

Overall Effect of VQ Mismatch on Gas Exchange

  • Overall, a lung with variable VQ ratios is not able to transfer as much O2 and CO2 as a uniformly ventilated and perfused lung
  • This is because most blood leaving the lung comes from lower zones whereas ventilation occurs in upper zones
  • Also, alveoli with high VQ ratios add little oxygen to the blood compared with alveoli in low VQ areas, therefore on average mixed capillary blood has more contribution from low VQ units
  • Overall this causes a depression of the arterial PO2 below that of mixed alveolar PO2 - by about 4mmHg in a normal upright lung, but can be much worse in a diseased lung 1234

Distribution of Ventilation-Perfusion Ratios

  • Distribution of V/Q ratios can be measured by infusing inert gases with a range of solubilities and measuring concentrations in arterial blood and expired gas
  • In patients with chronic bronchitis or emphysema, much of the ventilation/blood flow goes to near normal compartments, but considerable blood flow is going to poorly ventilated compartments causing depressed arterial PO2
  • There is also excessive ventilation to lung units with VQ ratios up to 10, which are ineffective in eliminating CO2

VQ Inequality Causing CO2 Retention

  • In theory, V/Q mismatch causes decreased O2 uptake and increased CO2 retention
  • In practice, patients with V/Q mismatch usually have normal arterial CO2
  • Extra ventilation required above normal to compensate for V/Q mismatch is called wasted ventilation
  • Lung units with high V/Q ratios which are inefficient at eliminating CO2 constitute alveolar dead space
  • Hyperventilation is much less effective at increasing arterial PO2, due to the shape of their respective dissociation curves
  • The CO2 dissociation curve is almost straight, meaning that an increase in ventilation will raise the lung's CO2 output of lung units with both high and low V/Q ratios
  • The almost flat O2 dissociation curve means that only units with moderately low ventilation-perfusion ratios will benefit much from increased ventilation.
  • Units with abnormally high V/Q ratios increase O2 of effluent blood very little, while those with low V/Q ratios continue to put out blood with an O2 concentration close to that of mixed venous blood
  • Therefore with hyperventilation, mixed arterial PO2 rises modestly, and some hypoxia always remains