About Arterial Blood Gase

pH 7.44 (7.34-7.45)
paCO2 32 (32-36)
PaO2 67 (75-100)
HCO3 21 (20-26)
BE -2 (-3 - +3)
SaO2 92%

This patient has idiopathic pulmonary fibrosis (chronic presentation).

My hypothesised mechanism (can someone please give me the thumbs up or tell me where i’ve gone wrong if so?):

Due to the disease process, the patient has developed insensitivity to the CO2 drive - because she has had chronically high CO2. As a result, she has switched to the hypoxic drive.

Because she has decreased surface area and increased thickness of membrane, it is more difficult for gas to be exchanged. This has lead to low PO2. Due to the hypoxic drive, she is now hyperventilating to increase her PO2. However, this hyperventilation is not adequate to raise her PO2 to normal, hence the low PO2 and SaO2.

Because CO2 diffuses more easily across the membrane than O2, the increased hyperventilation causes this patient to blow off an excess amount of CO2.

The loss of CO2 causes respiratory alkalosis in this patient.

This respiratory alkalosis is compensated by the kidneys ie metabolic compensation. The resorption of bicarb is decreased so that more of it is lost in the urine. In this way, the pH is normal (though in the high range of normal).