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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, …
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