WY: An 18-year-old footballer with no previous significant medical history sustained a tendon injury during a football match. This was repaired successfully under general anaesthetic, but the SaO₂ (% saturation of haemoglobin) was found to be 78.5% on air. Following recovery from the injury, he returned to playing football six times per week while he was investigated further. Chest X-ray and CT scan demonstrated three pulmonary arteriovenous malformations (PAVMs) that were thought to be due to underlying hereditary haemorrhagic telangiectasia (HHT).

CLS: That would be the most likely cause of the clinical picture. PAVMs1 affect approximately 1 in 2600 people,2 have usually completed growth by puberty and frequently result in hypoxaemia.3 The PAVM vessels provide an anatomic right-to-left shunt that allows a fraction of pulmonary arterial blood to bypass the pulmonary capillary bed and hence gas exchange. Greater shunt flow (as a proportion of cardiac output) results in lower PaO₂/SaO₂, but this is frequently asymptomatic. The majority of patients have underlying HHT, especially if they have multiple PAVMs.

WY: How was it possible for him to be so sporty?

CLS: The relevant term for oxygen transport to the tissues is not the SaO₂ or PaO₂ (in kPa or mm Hg), but the arterial oxygen content (CaO₂ (mL of oxygen per unit blood volume)). CaO₂ depends on the concentration of haemoglobin in addition to the commonly measured oxygen parameters. I would predict that the patient had secondary polycythaemia at presentation.

WY: Yes, the haemoglobin was 20.9 g/dL and haematocrit 0.61%.

CLS: So this will have maintained his CaO₂, which we can calculate as SaO₂×haemoglobin×1.34/100. His CaO₂ was 22 mL/dL, which is higher than normal, as seen in 23 athletes with PAVMs, …