Cardiovascular Complications in Spinal Cord Injury

Posted by e-Medical PPT Thursday, July 21, 2011
Spinal cord injury can result in significant compromise of cardiovascular control due to an impaired autonomic nervous system and skeletal muscle paralysis

Evolution of the control of the cardiovascular system
Immediately after SCI occurs, blood pressure rises due to release of norepinephrine from the adrenal glands and by a pressor response from mechanical disruption of vasoactive neurons and tracts in the spinal cord.
This is followed by a period of spinal shock (decreased cortical spinal and sympathetic activity and unopposed vagal tone).
Over time reflexes and spasticity return due to compensatory changes occur in the vascular beds, skeletal muscle, and rennin-angiotensin aldosterone system.

Short- and long-term consequences
Cardiac arrhythmias
Autonomic dysreflexia
Deep vein thrombosis
Coronary heart disease
Exercise response

Decreased compensatory vasoconstriction
 Venous pooling (skeletal muscle and splanchnic regions),
 venous pooling in the extravascular tissues lower extremities (leg swelling)
 reduced venous blood return resulting in reduced stroke volume, and blood pressure.
Hypotension, and especially orthostasis, usually improves within days to weeks as compensatory changes occur in the vascular beds, skeletal muscle, and rennin-angiotensin aldosterone system.

The ANS modulates cardiac electrophysiology and autonomic dysfunction can lead to ventricular arrhythmias.
Bradycardia is often precipitated by tracheal or rectal stimulation (eg, during suctioning or bowel program) and hypoxia.
Atropine may be needed, and temporary (sometimes permanent) cardiac pacemakers have been used.
This problem usually resolves over the first 2-6 weeks after SCI.

Due to loss of supraspinal control of hyperreflexic Sympathetic Nervous System activity, caused by noxious stimuli below the level of injury in individuals with SCI. This can lead to dangerously high blood pressures that can result in cerebral hemorrhage.

Poikylothermia:  Patients with lesions above T6 are poikilothermic and cannot regulate their body temperature. The lack of vasoconstrictors and ability shift blood flow to warm or cool the body.The inability to sweat below the level of the lesion...

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