Cardiac Reserve and Pulmonary Gas Exchange Kinetics in Patients With Stroke

Abstract

Cardiovascular and pulmonary factors contributing to impaired peak oxygen uptake (VO2) in patients with stroke (SP) are not well known. We assessed cardiovascular function, pulmonary gas exchange, and ventilation in SP and healthy age, gender, and activity-matched control subjects. Ten hemiparetic SP and 10 control subjects were enrolled. Subjects completed cycle ergometry testing to assess peak and reserve VO2, carbon dioxide production, ventilation (tidal volume; breathing frequency; minute ventilation), and cardiac output. VO2, carbon dioxide production, and minute ventilation were measured throughout peak exercise recovery (off-kinetics) and at exercise onset (on-kinetics) along with heart rate during low-level exercise. Peak VO2 was 43% lower (P<0.001) in SP secondary to reduced peak and reserve cardiac output and minute ventilation. The impaired cardiac output reserve (P<0.001) was due to a 34% lower heart rate reserve (P=0.001). The impaired minute ventilation reserve (P=0.013) was due to a 41% lower tidal volume reserve (P=0.009). Stroke volume and breathing frequency reserve were preserved. VO2 off-kinetics were 29% slower in SP (P<0.001) and related to peak VO2 (R=-0.72, P<0.001) and peak cardiac output (R=-0.75, P<0.001) for the study group. Additionally, carbon dioxide production (P=0.016) and minute ventilation (P=0.023) off-kinetics were prolonged in SP. VO2 on-kinetics were 29% slower (P=0.031) during low-level exercise in SP. The impaired peak VO2 in SP is secondary to a decline in peak and reserve cardiac output and ventilation. Prolonged VO2 kinetics in SP are associated in part with deconditioning and may be mediated by reduced O2 availability and/or the rate of muscle O2 use.