Different Central Hemodynamic Response Among Patients with Incomplete Spinal Cord Injury

Abstract

The cardiovascular response to physical activity is largely regulated by the autonomic nervous system. Sympathetic innervation of the heart originates between segments T1-5, while innervation originating between segments T6-L2 affects vascular response. Injury to the spinal cord induces loss of supraspinal sympathetic control over the cardiovascular system, which may culminate in blunted speed and magnitude of central hemodynamic responses during transitions in metabolic demand. PURPOSE: To investigate the cardiac output (Qt) response in relation to oxygen consumption (VO2) in patients with incomplete spinal cord injury (iSCI). METHODS: We tested 11 subjects in 3 groups: Tetraplegic group (TG, n=4, 41 ± 21 years); Paraplegic group (PG, n=4, 47 ± 19 years) and healthy controls (HC; n=3, 27 ± 8 years). Each group performed a constant-workload test on the treadmill at a self-selected walking speed. Qt and VO2 were measured simultaneously by impedance cardiography and pulmonary gas exchange analysis. RESULTS: Despite HC walking at a greater speed (1.5 mph vs. TG at 0.6 mph and PG at 1.0 mph), there was no difference in Qt or VO2 amplitude amongst the groups. Qt kinetics (reported as the time constant, τ) was longer (p<0.05) in TG (45 ± 21s) compared to either PG or HC (17±4s; 6±5s, respectively). Phase 2 VO2 on-kinetics were not different among the groups (TG, 33±30s; PG, 25±20s; HC, 20±6s). The ratio of τQt/τVO2 was poor (>1.0) in only TG, however was correlated (r = 0.96, p =0.002) with the responsiveness of the oxidative metabolic system (ΔVO2/τVO2) across all groups. CONCLUSION: Sympathetic innervation appears to influence the temporal profile of Qt depending on the level of lesion. Tetraplegics demonstrated slower Qt adjustment to increased metabolic demand compared to paraplegics. The slow increase in Qt relative to VO2 observed in tetraplegics suggests poor matching between central hemodynamics and metabolic demand in those with a higher level of injury. SCI elicits a lesion-dependent impairment in Qt kinetic profiles that may contribute to oxygen delivery to utilization mismatch occurring during walking in people who have incomplete cervical injury.