Acute Cardiac Responses to Spinal Cord Injury

Overview

The immediate period after spinal cord injury (SCI) is one of the only opportunities that clinicians and care-givers have to make a real difference to patient outcomes. One of the main aims during this period is to preserve blood flow and oxygen delivery to the spinal cord to prevent any further damage from occurring after the injury. The heart acts as the major pump for blood to be pumped to the spinal cord and the body. It has been shown in small animal models and in humans with long-standing SCI that the ability of the heart to pump blood after injury is compromised, which may in turn reduce the amount of blood and oxygen delivered to the injured cord. It is unclear how quickly these changes occur in the heart following SCI and how best to manage heart function such that blood flow and oxygen delivery can be optimized. In the present study, the investigators will examine how the heart functions immediately after SCI. The findings from this study are expected to provide new information that could help clinicians improve the management of people who have just suffered a SCI.

Background: The hemodynamic management of the cervical/high-thoracic spinal cord injured patient represents a remarkably complex clinical scenario, but represents one of the only potentially neuroprotective therapeutic options currently available to the clinician. Presently, the singular goal of hemodynamic management is to increase mean arterial blood pressure (MAP) to 85mmHg by targeting peripheral tone via vasopressor therapy, with a view to increasing perfusion of the spinal cord, preventing ischemia at the injury site, and optimizing neurological outcome. It is often overlooked that the instantaneous removal of descending sympathetic control at the time of SCI renders not only the vast majority of the systemic vasculature devoid of supraspinal input, but it also impairs descending control of the heart. What is yet to be considered in current hemodynamic management protocols is that immediate cardiac dysfunction secondary to impaired supraspinal control of the heart may very well be a significant contributor to poor spinal cord perfusion. Indeed, data collected over the last four years in rodent SCI models suggests that cardiac sympathetic decentralization is the principal cause of the low cardiac output observed in both rodents and people with chronic SCI. As such, the investigator's initiative is to provide a novel approach to hemodynamic management to a porcine model that harnesses both peripheral tone and cardiac function. The investigators believe this approach is an immediately translatable neuroprotective strategy for acute SCI. Overview: 10 individuals aged 18-60 who have sustained an acute traumatic SCI (above T2 spinal level) less than 72 hours prior will be recruited over a period of 2 years. Recruitment will be isolated to those individuals who already have a central venous catheter and arterial line as part of standard clinical care (which actually occurs in most patients). In addition to standard clinical lines, an esophageal Doppler probe will be placed to measure aortic outflow on which beat-by-beat systolic cardiac function (i.e., stroke volume, cardiac output, ejection fraction) can be estimated. During a 120 min monitoring period, beat-by-beat dependent cardiac indices will be recorded and a modified Starling curve will be constructed by examining relationships between central venous pressure (i.e., an index of venous return) and aortic flow (i.e., an index of cardiac output). After 1hr of monitoring (Part A), a 250ml bolus of intravenous crystalloid will be infused over a 5 min period and measure beat-by-beat central venous pressure and aortic flow (stroke volume) responses (Part B). The primary outcomes are daily resting stroke volume and ejection fraction, change in stroke volume and central venous pressure (CVP) in response to fluid challenge. The secondary outcome is the slope of the Starling curve