Abstract
62 year old male was referred for evaluation of exertional breathlessness, predominantly when commuting to work by bicycle. There was no associated chest pain, palpitations, syncope or family history of cardiovascular disease. He had untreated hypertension, a remote history of hairy cell leukemia treated with cladribine in remission and polycythemia rubra vera treated with venesection and pegylated-interferon therapy. Trans-thoracic echocardiogram demonstrated normal biventricular size and systolic function with normal valvular function. There was insufficient tricuspid regurgitation to estimate pulmonary pressure. A stress echocardiogram was negative for ischemia at submaximal exercise capacity due to the protocol used. Previous spirometry testing demonstrated preserved lung volumes, forced expiratory volumes and vital capacity. DLCO (lung diffusion capacity for carbon monoxide) was at the lower limit of normal. A ventilation-perfusion scan excluded pulmonary emboli. Cardiopulmonary exercise testing demonstrated good exercise capacity (peak VO2 40.8 ml/kg/min). An abrupt desaturation was seen at the respiratory compensation point, (Figure 1 - left) with an oxygen saturation nadir of 75% (measured in two peripheral locations), which resolved rapidly in early recovery. This coincided with a profound hypertensive response peaking at systolic blood pressure 252mmHg (Figure 1 - right). The test was ceased due to dyspnea and generalized fatigue. This case demonstrates that while maximal oxygen consumption is a prognostic marker, an above average exercise capacity does not exclude underlying pathology. Pulmonary capillary stress failure resulting in transient pulmonary edema and early pulmonary hypertension cannot be excluded. However, with normal exercise capacity, justification of invasive diagnosis is difficult and there are currently no guidelines regarding an optimal surveillance plan.
Published Version
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