Final answer:
Anatomical shunts cause PO₂ differences between alveolar gas and arterial blood by allowing blood to bypass oxygenation areas, resulting in lower arterial PO₂. Hydrostatic forces and ventilation-perfusion mismatches, further aggravated by physiological positions like standing, enhance these shunts, impairing gas exchange and counteractive mechanisms that normally regulate blood flow to well-ventilated alveoli.
Step-by-step explanation:
Anatomical shunts in the bronchial circulation cause an oxygen pressure (PO₂) difference between alveolar gas and arterial blood because they lead to a mismatch of ventilation and perfusion within the lungs. The partial pressure of oxygen in alveolar air is typically about 104 mm Hg, while in oxygenated blood in the pulmonary veins it is about 100 mm Hg. In cases of anatomical shunts, blood bypasses areas where oxygenation occurs, leading to arterial blood having lower PO₂ levels than expected. Additionally, in conditions like gravity affecting the upright lung, the perfusion is not uniform due to hydrostatic forces, causing anatomical shunts where the blood flow does not match the air reaching certain lung areas, thus reducing the rate of gas exchange.
The body uses mechanisms to counteract these shunts, such as constricting pulmonary arterioles to redirect blood flow to better-ventilated alveoli. Internal physiological controls adjust blood flow in response to CO₂, O₂, and pH levels, ensuring adequate gas exchange in functional areas. However, an anatomical shunt in the bronchial circulation directly bypasses the alveoli, hampering this compensatory mechanism, resulting in a significant PO₂ difference between alveolar gas and arterial blood.