The acute impact of spinal cord injury on cardiac function, and novel approaches to hemodynamic management.
One of the only neuroprotective strategies available to clinicians for acute spinal cord injury (SCI) patients is appropriate hemodynamic management. Presently, vasopressor therapy is used to augment blood pressure to a similar level in all patients, with the aim of improving blood flow to the spinal cord and minimizing damage to the surrounding tissue. However, this approach does not always produce positive outcomes, and can actually worsen neurological outcomes in some SCI patients. Although the use of vasopressors efficaciously targets the impairments to peripheral vasomotor tone, it does not account for potential impairments in cardiac function that also result from loss of central sympathetic outflow following SCI. To date, little to no data exist surrounding the acute impact of SCI on cardiac function or the application of cardiac interventions for hemodynamic management in these patients. Targeting the optimization of cardiac output does not have some of the negative side-effects related to increasing blood pressure (i.e. hemorrhage at the injury site) and thus may provide a more robust method of augmenting spinal cord blood flow (SCBF) and effectively managing hemodynamics immediately following SCI.
Our research aims to characterize the alterations to cardiac function immediately following traumatic SCI, and determine whether restoring cardiac output can optimize SCBF and improve neurological outcomes. This work will significantly improve our understanding of how cardiac function is altered post-SCI and how to best manipulate cardiac function to maintain SCBF. The findings from these studies will be immediately translatable to inform clinical practices and optimize neurological outcomes for SCI patients.