Abstract

The baroreflex is an important component of the physiological short-term control of the blood pressure. Baroreceptors are mainly located in the wall of the aortic arch and of the internal carotid artery (ICA). The carotid sinus nerve (CSN) contains afferent fibres travelling from the carotid sinus’ baroreceptors located in the adventitia of the ICA. It joins the glossopharyngeal (IX) nerve and ends in the nucleus tractus solitarius in the brain stem. The efferent loop is conducted by the vagus (X) nerve to the heart leading to a physiologic bradycardia and inhibited atrioventricular conduction, in response to systemic hypertension. Also, a blocked sympathetic nerve system causes venodilatation, decreasing ventricular preload, and vasodilatation, both leading to decreased blood pressure. Carotid sinus syndrome (CSS) is caused by a pathologic overshoot of this baroreflex and is characterised by exaggerated bradycardia and hypotension in response to carotid sinus stimulation, in situations such as shaving, wearing tight collar or head turning. The triggering events might vary considerably overtime in any individual patient, but the syndrome can be reproduced by carotid sinus massage. CSS prevalence could be as high as 45% in elderly patients. If left untreated, CSS mortality rates could exceed 25% within 5 years.

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