REHABILITATION OF MODERATE TO SEVERE TBI:
CARDIOVASCULAR DISORDERS IN TBI
Hypertension
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Signs: Common, immediate, probably transient, and characterized by
excessive catecholamine (which may predispose to cardiomyopathy), increased
cardiac output, and tachycardia. However, may persist beyond the acute phase
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Risk factors:
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Severe injury
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Focal insult to selective areas, such as the hypothalamus, periventricular
nucleus, and orbitofrontal cortex
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Causes
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Laboratory evaluation should be done to rule out neuroendocrine causes, renal
or adrenal hemorrhage, and pheochromocytoma
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Medications, such as steroids, should be evaluated for risk of hypertension
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Episodic hypertension, accompanied by headaches and facial flushing, may
indicate a spinal cord lesion
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Other possible causes include pain from decubitus ulcers, poor positioning
or splinting, and tracheostomy or gastrostomy sites
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Treatment
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Usually with beta blockers that control blood pressure and have reduced cognitive
side effects, such as atenolol, metoprolol, or nadolol
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Calcium channel blockers and angiotensin-converting enzyme inhibitors in
patients with motor impairment since they also help replete calcium, magnesium,
and phosphate. Beta blockers may also be necessary to control reflex tachycardia. Exposure to beta blockers for either cardiac or non-cardiac reasons was associated with a significant reduction in mortality in patients with severe TBI, even in older, more severely injured, and with lower predicted survival. (Cotton, et al 2007).
Hypotension
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Causes:
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Frequently due to prolonged immobilization, decreased plasma volume, or side
effects of medications, such as antihypertensive agents, and especially
diuretics, alpha blockers, and vasodilators
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Can be secondary to hemorrhage or neuroendocrine imbalance in the early recovery
period
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Persistent hypotension can be due to autonomic or cardiac dysfunction
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Profound hypotension may be associated with hypopituitarism
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Complications - Transient systolic hypotension (systolic blood pressure
< 100 mm Hg) is associated with increased acute mortality and decreased
functional status, and may have the greatest impact in patients with less
severe primary injury (Winchell, et al
1996)
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Treatment is with compression garments, gradual upright positioning
using a tilt table, and drugs such as ephedrine, if necessary
EKG Abnormalities
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Common during early recovery
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Due to myocardial ischemia or necrosis or to massive catecholamine release
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Dysrhythmias are relatively uncommon
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Based on information in Medical Rehabilitation
of Traumatic Brain Injury, L.J. Horn and N.D. Zasler, eds. St. Louis, MO,
Mosby, 1996, except for information where other papers are cited.
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