VQ Mismatch

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 P_O2 in any lung unit is determined by the ratio of ventilation to blood flow

• 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

• 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 P_O2, 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