An intact spinal cord is required for proper autonomic function and thus, cardiovascular stability. Changes in cardiovascular function are lesion-dependent and unique to each SCI. Generally, higher-level injuries along the spinal cord result in the greatest degree of cardiovascular impairment as as such, cardiovascular complications subsequent to SCI are directly related to the neurological level of injury. After SCI, autonomic control of regions below the level of the lesion are severely disrupted. Higher-level SCIs, particularly cervical or high-thoracic injuries (T6 or above), are associated with significant SNS dysfunction as a consequence of the loss of supraspinal control of the SNS; this is considered as the major cause of hemodynamic imbalance and regulatory changes that occur following SCI. Parasympathetic control of cardiac function si preserved following injury since innervation to the heart is carried out via the vagal nerve and does not transmit through the spinal cord. Therefore, the disruption of autonomic function caused by SCI results in disproportional involvement of the SNS in comparison to the PNS in terms of hemodynamic regulation. Hypoactive sympathetic outflow together with unopposed parasympathetic activity through the intact vagal nerve lead to imbalanced autonomic control and disordered cardiac function, including clinical manifestations such as bradycardia, low resting blood pressure, and even cardiac arrest (Furlan & Fehlings, 2008; Phillips et al. 2012; Teasell et al. 2000; West et al. 2012). In terms of SCIS below the level of T6, there is enough sympathetically innervated peripheral vasculature under supraspinal control to allow for hemodynamic homeostasis with limited clinical indicators of SNS dysfunction (Teasell et al. 2000).
The relationship between injury severity (complete vs. incomplete) and resulting cardiovascular dysregulation is less well understood and no clear association has yet been established (West et al. 2013). Baroreflex funciton and sensitivity is disrupted in SCI, although this is a more consistent finding in high-level injuries (Phillips et al. 2012). Baroreflex dysfunction in SCI is thought to be influenced by increased stiffening of arteries, where stretch-receptors are located that transmit information on systemic BP (Phillips et al. 2014).
The association between physiological dysfunction and cardiovascular complications occurring during acute SCI has been evaluated by four studies.
Phillips et al. (2014) conducted a cross-over randomized controlled trial (RCT) to study the association between baroreflex sensitivity (BRS) and common carotid artery (CCA) stiffness, as well as the influence of midodrine on BRS and arterial stiffness. The majority of SCI participants included in this study were within 6.5-11 weeks of injury, although 1 participant had chronic SCI and was 144 weeks after injury at the time of the study. Arterial stiffness was elevated in SCI patients compared to able-bodied controls when in the upright position (p<0.05). BRS and arterial stiffness were found to be negatively associated in the upright position in SCI patients (p=0.03), indicating that reduced BRS is related to increased arterial stiffness following SCI. Midodrine administration led to increased BP and reduced HR in SCI patients, however, it had no effect on BRS or CCA parameters.
An observational study by Krstačić et al. (2013) aimed to assess autonomic dysfuntion after SCI and the effect of the resulting altered sympathetic activity on the cardiovascular system. Acute cervical SCI patients were included in this study who were monitored beginning on their first day of hospital admission. The patients were evaluated for cardiac autonomic balance using electrocardiogram data to analyze heart rate variability (HRV) in time and frequnecy domains. As a parameter of HRV, the ratio of low to high freqencies represents sympathovagal balance, and was significantly reduced in the SCI patient group compared to the control group (0.41 vs. 1.71, p<0.001); this indicates the presence of altered sympathetic activity having an effect on the cardiovascular system in acute cervical SCI patients.
Furlan et al. (2003) demonstrated an association between the location and severity of pathology in the spinal cord and cardiovascular dysfunction following SCI. In this observational study, cervical SCI patients were retrospectively reviewed to compare those that had developed severe cardiovascular dysfunction (Group 1) with those that had developed no to minor cardiovascular dysfunction (Group 2). A control group of patients (Group 3) who had intact central nervous systems was also included for comparison purposes, and all patient information was collected during a 5-week post-injury period. Axonal preservation in the dorsal aspects of the lateral funiculus (Area I) and in the white matter adjacent to the dorsolateral aspects of the intermediolateral cell column (Area II) was significantly lower in Group 1 than in Group 2 participants (p<0.034 and p=0.013, respectively). There was an observed axonal loss of ~70% in Area I in Group 1 compared to 20% in Group 2 patients, and a 20% loss in Area II in Group 1 compared to 15% in Group 2 patients, suggesting the dorsal aspects of the lateral funiculus as being the more likely site of descending vasomotor pathways contributing to cardiovascular dysfunction after SCI.
Finally, in an observational study by Summers et al. (2013), patients were studied within the early stages of their emergency department resuscitation to determine the pathophysiology underlying neurogenic shock. Hemodynamic variables were collected from patients who were diagnosed with neurogenic shock using impedance cardiography. Etiology was variable; it was observed as a decrease in peripheral vascular resistance in 33% of patients, a loss of vascular capacitance in 22% of patients, or a combination of both, as seen in 33% of patients. Etiology was purely cardiac in the remaining 11% of patients.
Cardiovascular complications arising in the acute phase of SCI are primarily related to decreased sympathetic output and increased vagal activity in the absence of compensatory mechanisms, and the physiological dysfunction that occurs as a result.