Yap J C, Moore D M, Cleland J G, Pride N B
Respiratory Division and Clinical Cardiology, Imperial College School of Medicine, Hammersmith Campus, London, United Kingdom.
Am J Respir Crit Care Med. 2000 Oct;162(4 Pt 1):1285-91. doi: 10.1164/ajrccm.162.4.9911097.
The mechanisms of orthopnea and the role of changes in respiratory mechanics in left ventricular failure (LVF) are poorly understood. We have measured total respiratory airflow resistance (Rrs) using forced oscillation in the sitting and supine positions in 10 patients with chronic LVF (NYHA II-III) shortly after recovery from acute LVF and in 10 matched control subjects (CON). Seated, the patients with LVF had small lung volumes but no evidence of airway obstruction (mean FEV(1)/FVC, 81%). Mean Rrs at 6 Hz was only slightly higher in LVF (3.4 cm H(2)O. L(-1). s) than in CON (2.6 cm H(2)O. L(-1). s). After 5 min supine, breathlessness in LVF increased. Despite much smaller mean falls in mid-tidal lung volume (MTLV) in LVF than in CON, the supine rise in Rrs was 80.5% in LVF and 37.6% in CON; mean increases in specific Rrs (SRrs = Rrs.MTLV) were 75.8% in LVF and 16.6% in CON (p 0.001). Five minutes after resuming the sitting position all values had reverted almost to the original sitting values. In 5 LVF patients, nebulized ipratropium, a muscarinic antagonist, only slightly attenuated the supine rise in SRrs. We conclude that patients with chronic LVF, who had little evidence of airways obstruction when seated, showed a large rise in airflow resistance after lying supine for 5 min. This cannot be attributed to reduction in lung volume when supine and no evidence was found of vagally-induced bronchoconstriction. Further experiments are required to establish the cause of the rapid supine rise in airflow resistance in LVF.
