The clinical problems in cardiovascular control following spinal cord injury: an overview

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Abstract

On a daily basis, individuals with cervical and upper thoracic spinal cord injury face the challenge of managing their unstable blood pressure, which frequently results in persistent hypotension and/or episodes of uncontrolled hypertension. This chapter will focus on the clinical issues related to abnormal cardiovascular control in individuals with spinal cord injury, which include neurogenic shock, autonomic dysreflexia and orthostatic hypotension. Blood pressure control depends upon tonic activation of sympathetic preganglionic neurons by descending input from the supraspinal structures (Calaresu and Yardley, 1988). Following spinal cord injury, these pathways are disrupted, and thus spinal circuits are solely responsible for the generation of sympathetic activity (Osborn et al., 1989; Maiorov et al., 1997). This results in a variety of cardiovascular abnormalities that have been well documented in human studies, as well as in animal models (Osborn et al., 1990; Mathias and Frankel, 1992a, b; Krassioukov and Weaver, 1995; Maiorov et al., 1997, 1998; Teasell et al., 2000). However, the recognition and management of these cardiovascular dysfunctions following spinal cord injury represent challenging clinical issues. Moreover, cardiovascular disorders in the acute and chronic stages of spinal cord injury are among the most common causes of death in individuals with spinal cord injury (DeVivo et al., 1999).

Section snippets

Pathophysiology of cardiovascular dysfunction after spinal cord injury

The first description of one of the most common autonomic disturbances in individuals with spinal cord injury, known as autonomic dysreflexia, appeared in 1860 (Hilton, 1860). However, it was not until 1947 that Guttman and Whitteridge described the possible mechanisms responsible for the development of this condition (Guttman and Whitteridge, 1947). Both clinical observations and experimental animal data have contributed significantly to our present understanding of the pathophysiology of

The acute post-injury period and neurogenic shock

Acute spinal cord injury in humans, especially at the cervical level, results in severe hypotension and persistent bradycardia that are common components of the phenomenon known as neurogenic shock (Atkinson and Atkinson, 1996). This event is more profound and long lasting in humans after spinal cord injury than in experimental animals. Moreover, clinical observations strongly suggest that the extent to which prolonged and severe hypotension requiring vasopressive therapy occurs is associated

Autonomic dysreflexia

Individuals with a cervical or high thoracic spinal cord injury face life-long abnormalities of blood pressure control (Mathias and Frankel, 1992a; Teasell et al., 2000). In general, the resting arterial blood pressure in these individuals is lower than in able-bodied subjects, often with disabling episodes of orthostatic hypotension. However, life-threatening episodes of autonomic dysreflexia, characterized by extreme hypertension accompanied by a pounding headache, slow heart rate and upper

Orthostatic hypotension

Low arterial blood pressure is a problem in both acute and chronic high-level spinal cord injured patients. Indeed, Mathias and colleagues noted that there was an inverse linear relationship between the level of spinal cord injury and resting blood pressure (Mathias and Frankel, 1992a; Mathias, 1995). This lower resting blood pressure is thought to be secondary to a reduction in sympathetic nervous activity below the level of the spinal cord injury.

In addition to the low resting blood pressure,

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