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