Stroke volume increase to exercise in chronic obstructive pulmonary disease is limited by increased pulmonary artery pressure

• Published in: Heart (British Cardiac Society) Vol. 95; no. 2; p. 137
• Main Authors: Holverda, S, Rietema, H, Westerhof, N, Marcus, J T, Gan, C T-J, Postmus, P E, Vonk-Noordegraaf, A
• Format: Journal Article
• Language: English
• Published: England 01-02-2009
• Subjects: Aged; Cardiac Catheterization; Case-Control Studies; Diastole - physiology; Exercise Test; Exercise Tolerance - physiology; Female; Humans; Hypertension, Pulmonary - diagnosis; Hypertension, Pulmonary - physiopathology; Magnetic Resonance Angiography; Male; Middle Aged; Pulmonary Artery - physiopathology; Pulmonary Disease, Chronic Obstructive - diagnosis; Pulmonary Disease, Chronic Obstructive - physiopathology; Stroke Volume - physiology; Systole - physiology; Vascular Resistance - physiology; Ventricular Function, Right - physiology
• ISSN: 1468-201X
• DOI: 10.1136/hrt.2007.138172

This study was designed to investigate the mechanisms by which the right ventricle is able to increase stroke volume (SV) during exercise in chronic obstructive pulmonary disease (COPD). A second aim was to determine whether resting pulmonary artery pressure (Ppa) is predictive of exercise SV.
16 COPD patients (GOLD stages II-IV) underwent right heart catheterisation at rest and during exercise. In this group and eight age-matched controls resting and exercise right ventricular SV, end-diastolic volume (RVEDV) and end-systolic volume (RVESV) were assessed by magnetic resonance imaging (MRI). The exercise protocol during both measurements consisted of 3 minutes of cycling in supine position at 40% of maximal workload.
In all patients mean Ppa increased significantly in response to exercise (21 (8) vs 33 (11) mm Hg, p<0.01), whereas pulmonary vascular resistance did not change. In the patient group, RVEDV (129 (42) vs 135 (42) ml, p<0.05) and SV (63 (13) vs 69 (14) ml, p<0.05) increased significantly from rest to exercise, but RVESV and RV ejection fraction remained unaltered. In contrast, in healthy controls SV is augmented (81 (22) vs 101 (28) ml, p<0.05) by both increased RVEDV (123 (33) vs 134 134) ml, p<0.05) and reduced RVESV (37 (9) vs 27 (10) ml, p<0.05). Resting mean Ppa was related to SV during exercise (r = -0.59, p<0.02).
As a consequence of unaltered pulmonary vascular resistance to exercise in COPD patients, Ppa increases and SV response to exercise is limited and results from an increased preload only. Ppa at rest predicts exercise SV.