The acute impacts 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 hemodynamic management. Presently, vasopressor therapy is most widely used to augment blood pressure to a specific target in all patients, with the aim of improving spinal cord perfusion and minimizing hypoxic damage in the surrounding tissue. However, this approach does not always produce positive outcomes, and may actually worsen neurological outcomes in some SCI patients. While vasopressors are effective in reversing an injury-induced loss of peripheral vasomotor tone, it does not account for potential impairments in cardiac function that occur via a loss of descending sympathetic outflow following SCI. To date, little is known regarding the acute impacts of SCI on the heart, nor the potential advantages of targetting the heart during hemodynamic management in these patients. Hemodynamic therapies that aim to optimize cardiac function may avoid the negative side-effects related to increasing blood pressure (i.e. hemorrhage at the injury site) and thus provide a more robust method of improving spinal cord blood flow and oxygenation acutely following SCI.
Our research aims to characterize the alterations to cardiac function immediately following traumatic high-level (i.e. ≥T6) SCI, and determine whether restoring left ventricular function can optimize spinal cord perfusion, cord oxygenation and neurological outcomes. The findings from this work will improve our understanding the cardiac consequences of SCI, and ultimately help to inform clinical practices and optimize neurological outcomes for SCI patients.