Review
The carotid sinus reflexes

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Abstract

Forty years have elapsed since Hering defined the carotid sinus reflex. Present theory indicates that the reflexes act by “buffering” the outflow from the brain of sympathetic and parasympathetic nervous system activity. Through changes in this autonomic nervous system outflow, decreases in systemic arterial pressure would be opposed by (a) decreases in the distensibility and volume of the systemic postarteriolar capacity vessels, (b) increases in cardiac work, and (c) increases in total peripheral resistance. Conversely, increases in arterial pressure would be opposed by effects in the opposite direction.

Until the last decade, baroreceptor experimental neurogenic hypertension was produced by bilateral carotid sinus denervation and partial vagotomy. The hypertension so caused was singularly unlike essential hypertension. It was very labile, and the increase in arterial pressure was associated with tachycardia and an elevation of cardiac output. However, since 1954, it has been clearly demonstrated that permanent, stable hypertension without tachycardia can readily be produced in dogs by bilaterally interfering with the carotid sinus reflexes alone (vagi intact). Furthermore, it has been shown that the carotid sinus reflexes may be of significance in the production of renal hypertension. Also, carotid sinus pacemakers have recently been shown to be capable of reducing blood pressure in hypertensive dogs and man.

It has been held for more than 30 years that spontaneous syncopal attacks are caused by stimulation of the carotid sinus reflexes. Nevertheless, in the great majority of patients with a diagnosis of carotid sinus syndrome, spontaneous syncope is not associated with an immediately apparent stimulation of the carotid sinus, such as direct pressure, a tight collar, shaving, or scratching. It is argued in the present communication that in those cases without apparent stimulation of the carotid sinus the diagnosis of carotid sinus syndrome cannot be made or classified by the tests presently employed. Even the results of surgical denervation cannot prove the existence of the carotid sinus syndrome in most cases.

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      This initiates a reflex arc to the upper brainstem and produces a compensatory bradycardia and a subsequent lowering in blood pressure.11 Some vascular surgeons advocate nerve –sparing dissection and/or local anaesthetic blockade of the carotid sinus nerve at the time of CEA to minimise fluctuations in blood pressure,12 although the purported benefits are based primarily on animal studies13 and several randomised studies have refuted this assertion.14,15 Therefore the role of local anaesthetic infiltration into the carotid sinus during CEA to prevent post-operative haemodynamic instability remains unclear.

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    This study was supported by research grants from the National Heart Institute, United States Public Health Service, HE08756 and HE06546-04(CV), and the Eli Lilly and Company, Indianapolis, Ind.

    Address: Mt. Sinai Hospital, 100th St. and Fifth Ave., New York, N. Y., 10029.

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