Carotid Sinus Hypersensitivity

Carotid Sinus Hypersensitivity is a topic covered in the 5-Minute Clinical Consult.

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  • The carotid sinus, located at the bifurcation of the internal and external carotid arteries, contains baroreceptors that are responsive to increases or decreases in arterial pressure. It plays a central role in blood pressure (BP) homeostasis.
  • An endogenous increase in BP or external pressure applied to a carotid sinus causes an increase in the baroreceptor firing rate and activates vagal efferents and/or inhibits the sympathetic discharge to the heart and blood vessels, resulting in a slowing of the heart rate and/or drop in BP.
  • In carotid sinus hypersensitivity (CSH), stimulation of one or both carotid sinuses causes an exaggerated baroreceptor response that can result in dizziness or syncope.
  • CSH is defined as asystole for at least 3 seconds and/or a drop in systolic BP of at least 50 mm Hg during carotid sinus massage (CSM).
  • CSH is generally divided into three subtypes, based on response to CSM:
    • Cardioinhibitory (70–75%): asystole for at least 3 seconds
    • Vasodepressor (5–10%): fall in systolic BP of at least 50 mm Hg
    • Mixed (20–25%): combination of the first 2 subtypes
  • Carotid sinus syndrome (CSS) typically (but not consistently) refers to CSH with syncope and may be classified as:
    • Spontaneous CSS: syncope after accidental mechanical manipulation (trigger) of the carotid sinuses (e.g., shaving, tight collars, or tumors)
    • Induced CSS: syncope diagnosed by CSM, although no mechanical trigger is found


  • Disease of elderly; virtually unknown in people aged <50 years
  • More prevalent in males by ratio of 4:1
  • Typical patient is an older man, usually with a history of coronary artery disease (CAD) and hypertension (HTN), with right CSH > left CSH.
  • CSH may be a cause of the symptoms in 30% of elderly patients with unexplained syncope (1).
  • CSH was also present in 35% of community-dwelling older individuals without any symptoms of syncope, falls or drop attacks (2).

Etiology and Pathophysiology

  • The exact mechanism of CSH remains unknown. Changes in any part of the reflex arc or the target organs may give rise to this condition, or it may be a part of a generalized autonomic disorder associated with autonomic dysregulation.
  • Associated with resting sympathetic overactivity and increased baroreflex sensitivity (2)
  • Bradycardia and asystole seen in cardioinhibitory and mixed CSH subtypes appear to be mediated by vagal efferents, whereas vasodilatation and arterial hypotension in the vasodepressor and mixed subtypes are attributed to decrease sympathetic tone.
  • Symptomatic CSH has been shown to be associated with impaired cerebral autoregulation, and in asymptomatic CSH, it was found to be normal (2).
  • Atherosclerosis may diminish carotid sinus compliance, resulting in a reduction in afferent impulse traffic in the baroreflex pathway (3).
  • CSH is often idiopathic but can be caused by:
    • Carotid body tumors
    • Inflammatory and malignant lymph nodes in the neck
    • Extensive scarring from prior neck surgery in the area of the carotid sinus
    • Metastatic cancer

Risk Factors

  • Male gender
  • Advanced age
  • CAD
  • HTN
  • DM

Commonly Associated Conditions

  • Sick sinus syndrome
  • Atrioventricular block
  • CAD
  • HTN
  • Orthostatic hypotension
  • Vasovagal syncope
  • Alzheimer disease
  • Parkinson disease

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