A right-to-left shunt occurs when a portion of the blood bypasses the lung and mixes with oxygenated blood. This results in a variation in the partial pressure of oxygen (PaO2) depending on the size of the shunt. Alveolar ventilation remains normal. The partial pressures of alveolar carbon dioxide (PACO2), alveolar oxygen (PAO2), inspired carbon dioxide (PiCO2), inspired oxygen (PiO2), carbon dioxide in portal venous blood (PpvCO2), oxygen in portal venous blood (PpvO2), carbon dioxide in mixed venous blood (PvCO2), and oxygen in mixed venous blood (PvO2) are all factors to consider.

An important characteristic of an anatomical shunt is that if an affected individual is given 100% oxygen to breathe, the response is severely blunted. The blood that bypasses the gas-exchanging units is not exposed to the enriched oxygen, so it continues to be deoxygenated. As a result, the blood with increased oxygen mixes with the deoxygenated blood, leading to persistent hypoxemia. The degree of hypoxemia depends on the volume of the shunted blood. Normally, the hemoglobin in the blood that perfuses the ventilated alveoli is almost fully saturated, so most of the added oxygen is in the form of dissolved oxygen.

In an anatomical shunt, the partial pressure of carbon dioxide (PaCO2) is not usually increased, despite the elevated CO2 levels in the shunted blood. This is because the central chemoreceptors respond to any rise in CO2 with an increase in ventilation, thus reducing PaCO2 to the normal range. However, in severe cases of hypoxemia, the increased respiratory drive caused by the hypoxemia can further increase ventilation and lower PaCO2 below the normal range.

A physiological shunt, also known as venous admixture, can occur when there is no ventilation to lung units but perfusion continues. In this scenario, all the ventilation is directed to the lung unit with functional gas exchange, while perfusion is evenly distributed between both lung units. The lung unit without ventilation but with perfusion has a V̇ /Q̇ ratio of 0. The blood perfusing this unit is mixed venous blood, as no gas exchange occurs. The effect of a physiological shunt on oxygenation is similar to that of an anatomical shunt. Deoxygenated blood bypasses a gas-exchanging unit and mixes with arterial blood. Atelectasis, which is the obstruction to ventilation in a gas-exchanging unit resulting in loss of volume, is a clinical example of a situation where the lung region has a V̇ /Q̇ ratio of 0. Causes of atelectasis include mucous plugs, airway edema, foreign bodies, and airway tumors.
• Fig. 23.9 Right-to-Left Shunt. Alveolar ventilation is normal, but a portion of the cardiac output bypasses the lung and mixes with oxygenated blood. PaO2 varies according to the size of the shunt. PACO2, partial pressure of alveolar carbon dioxide; PAO2, partial pressure of alveolar oxygen; PiCO2, partial pressure of inspired carbon dioxide; PiO2, partial pressure of inspired oxygen; PpvCO2, partial pressure of carbon dioxide in portal venous blood; PpvO2, partial pressure of oxygen in portal venous blood; PvCO2, partial pressure of carbon dioxide in mixed venous blood; PvO2, partial pressure of oxygen in mixed venous blood.
An important feature of an anatomical shunt is that if an affected individual is given 100% O2 to breathe, the response is blunted severely. The blood that bypasses the gas-exchanging units is never exposed to the enriched O2, and thus it continues to be deoxygenated. The PO2 in the blood that is not being shunted increases and it mixes with the deoxygenated blood. Thus the degree of persistent hypoxemia in response to 100% O2 varies with the volume of the shunted blood. Normally, the hemoglobin in the blood that perfuses the ventilated alveoli is almost fully saturated. Therefore, most of the added O2 is in the form of dissolved O2 (see
The PaCO2 in an anatomical shunt is not usually increased even though the shunted blood has an elevated level of CO2. The reason for this is that the central chemoreceptors (see ) respond to any elevation in CO2 with an increase in ventilation and reduce PaCO2 to the normal range. If the hypoxemia is severe, the increased respiratory drive secondary to the hypoxemia increases the ventilation and can decrease PaCO2 to below the normal range.
A physiological shunt (also known as venous admixture) can develop when ventilation to lung units is absent in the presence of continuing perfusion (
Fig. 23.10 ). In this situation, in the two–lung unit model, all the ventilation goes to the other lung unit, whereas perfusion is equally distributed between both lung units. The lung unit without ventilation but with perfusion has a V̇ /Q̇ ratio of 0. The blood perfusing this unit is mixed venous blood; because • Fig. 23.10 Schema of a Physiological Shunt (Venous Admixture). Notice the marked decrease in PaO2 in comparison to PCO2. The alveolar-arterial difference for oxygen (AaDO2) in this example is 85 mm Hg. PACO2, partial pressure of alveolar carbon dioxide; PAO2, partial pressure of alveolar oxygen; PiCO2, partial pressure of inspired carbon dioxide; PiO2, partial pressure of inspired oxygen; PpvCO2, partial pressure of carbon dioxide in portal venous blood; PpvO2, partial pressure of oxygen in portal venous blood; PvCO2, partial pressure of carbon dioxide in mixed venous blood; PvO2, partial pressure of oxygen in mixed venous blood.
there is no ventilation, no gas is exchanged in the unit, and the blood leaving this unit continues to resemble mixed venous blood. The effect of a physiological shunt on oxygenation is similar to the effect of an anatomical shunt; that is, deoxygenated blood bypasses a gas-exchanging unit and admixes with arterial blood. Clinically, atelectasis (which is obstruction to ventilation of a gas-exchanging unit with subsequent loss of volume) is an example of a situation in which the lung region has a V̇ /Q̇ of 0. Causes of atelectasis include mucous plugs, airway edema, foreign bodies, and tumors in the airway.