Response of upper limb blood flow to handgrip exercise after Blalock-Taussig operation (for tetralogy of fallot) or subclavian flap operation (for aortic isthmic coarctation)

Abstract

To evaluate the effects of long-term reductions in perfusion pressure on blood flow responses to increased functional demand, 5 patients (aged 12 to 26 years) without normal aortic to subclavian artery blood flow to 1 arm as a result of surgery to treat congenital heart disease were studied. Five age- and sex-matched healthy (control) subjects were also studied. In the patients, forearm blood flow was not different in the surgical and normal arms at rest (3.6 ± 0.6 vs 4.0 ± 0.7 ml/min/100 ml, respectively, mean ± standard error, difference not significant) despite lower systolic blood pressure in the surgical arm (87 ± 2 vs 115 ± 2 mm Hg, p < 0.05). The increases in heart rate, systolic blood pressure, forearm electromyographic activity (index of muscle fatigue) and postexercise forearm blood flow (index of muscle oxygen deficit) were not different in response to 2.5 minutes of submaximal rhythmic handgrip exercise (50% of maximal force) performed with the surgical versus the normal arms. Peak forearm blood flow elicited by combined ischemia and maximal isometric handgrip exercise was not significantly different in surgical and normal arms in the group as a whole (39 ± 4 vs 43 ± 3 ml/min/100 ml, difference not significant), although some bilateral deficit (20 to 38%) was observed in 2 patients. No bilateral differences were observed in the control subjects under any condition. The finding of normal physiologic adjustments to submaximal rhythmic handgrip exercise with the surgical arm suggests that oxygen delivery during exercise was adequate. Further, the similarity of peak blood flow values demonstrates that the affected limb maintains a remarkable capacity for augmenting blood flow despite a lower perfusion pressure. The compensatory adaptations that permitted normal blood flow at rest and in response to moderate and severe vasodilatory stimuli, despite the reductions in perfusion pressure, may be considered a long-term form of blood flow autoregulation that allows marked hyperemia during conditions of increased functional demand.