Cushing reflex
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Template:WikiDoc Cardiology News Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
The Cushing reflex, consisting of an increase in sympathetic outflow to the heart as an attempt to increase arterial blood pressure and total peripheral resistance[1] and that is conflicting with the baroreceptor attempt to apply vagal tone and decrease heart rate, is a hypothalmic response to ischaemia, usually due to poor perfusion (delivery of blood) in the brain. It was first described by Harvey Cushing in 1902.
The ischaemia activates the sympathetic nervous system, causing an increase in the heart's output via increased rate and contractility along with peripheral constriction of the blood vessels. This accounts for the rise in blood pressure, ensuring blood delivery to the brain.
The increased blood pressure also stimulates the baroreceptors (pressure sensitive receptors) in the carotids, leading to an activation of the parasympathetic nervous system, which slows down the heart rate, causing the bradycardia.
The Cushing reflex is usually seen in the terminal stages of acute head injury.
See also: Cushing's triad
References
- ↑ Physiology, 2nd Edition, Saunders, 2002, page 150.
Also note: intravenous admistration of norepinephrine (or NE-like drug)may produce this reflex. Epinephrine thus the better choice to raise blood pressure, as it has a greater effect upon the Beta-1 receptors in the cardiac tissue.