A patient with idiopathic pulmonary fibrosis (IPF) has reduced DLCO (diffusing capacity for CO) and reduced total lung capacity. In which clinical scenario would DLCO be paradoxically elevated despite normal or reduced lung volumes?

• A Pulmonary arterial hypertension — elevated pulmonary capillary pressure increases DLCO by recruiting alveolar capillaries
• B Acute pulmonary embolism — increased ventilation-perfusion mismatch increases the driving gradient for CO diffusion
• C Obesity — increased thoracic blood volume recruits additional pulmonary capillaries in the apical zones
• D Polycythaemia vera — increased haemoglobin concentration increases the pulmonary capillary blood's CO-binding capacity, raising DLCO above predicted values ✓

Explanation

DLCO (DLco = DM × θ × Vc) depends on alveolar–membrane diffusion capacity (DM) and capillary blood CO-binding capacity (θ × Vc). θ is the CO-binding rate per mL blood, proportional to haemoglobin concentration. In polycythaemia vera, markedly elevated Hb increases the rate at which haemoglobin in pulmonary capillaries binds CO, raising DLCO even with normal lung volumes. DLCO must be corrected for Hb when interpreting results. Pulmonary hypertension reduces capillary transit time and eventually reduces DLCO. Acute PE reduces DLCO by reducing perfused capillary surface area. Obesity slightly reduces TLC but DLCO is usually normal or mildly reduced, not elevated.

Reference: Guyton & Hall, Textbook of Medical Physiology, 14th ed.

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