It is recognized that exercise produces abnormally large increases in pulmonary artery pressure in patients with pulmonary vascular disease as a consequence of a variety of disorders, but the relationship between pressure and cardiopulmonary exercise performance is poorly understood. This lack of understanding is due (in part) to difficulty making measurements of pulmonary haemodynamics using conventional fluid filled catheters. This article seeks to improve understanding by comparing variables measured during formal exercise testing with simultaneous measurements of pulmonary artery pressure using a micro-manometer tipped catheter.Ten patients with suspected pulmonary hypertension were studied using a micromanometer tipped pulmonary artery catheter, during cardiopulmonary exercise testing.Ventilatory equivalents for oxygen and carbon dioxide correlated with the pulmonary artery pressure measured on exercise, but oxygen pulse and oxygen uptake did not. Ventilatory equivalents, noninvasively measured during exercise, may merit further study as potential surrogates of pulmonary artery pressure and hence be useful in identifying individuals at risk of developing pulmonary hypertension. Eur Respir J 2000; 16: 282±287.
Background-The specific contribution of secondary pulmonary hypertension to the morbidity and mortality of patients with underlying lung disease can be diYcult to assess from single measurements of pulmonary artery pressure. We have studied patients with secondary pulmonary hypertension using an ambulatory system for measuring continuous pulmonary artery pressure (PAP). We chose to study patients with connective tissue disease because they represent a group at high risk of pulmonary vascular disease, but with little disturbance of lung function. Methods-Six patients (five with progressive systemic sclerosis and one with systemic lupus erythematosis) were studied. They underwent preliminary cardiopulmonary investigations followed by Doppler echocardiography, right heart catheterisation, and ambulatory pulmonary artery pressure monitoring to measure changes in pressure over a 24 hour period including during a formal exercise test. Results-All patients had pulmonary hypertension as measured by Doppler echocardiography with estimated pulmonary artery systolic pressures of 40-100 mm Hg. Pulmonary function testing revealed virtually normal spirometric values (mean FEV 1 86.9% predicted) but marked reduction in CO gas transfer factor (KCO 57.8% predicted). Exercise responses were impaired with mean VO 2 max 50.6% predicted. Ambulatory PAP monitoring indicated significant changes in pressures with variation in posture and activity throughout 24 hours. Resting PAP did not predict the change in PAP seen on exercise. Conclusion-Conventional methods of assessment of the pulmonary circulation based on single measurements in the supine position may underestimate the stresses faced by the right side of the circulation. This ambulatory system allows monitoring of pulmonary haemodynamics continuously over 24 hours during normal activities of daily living. These measurements may increase our understanding of the contribution made by secondary pulmonary hypertension to the morbidity and mortality of the underlying lung disease. (Thorax 1998;53:857-862)
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