Carotid sinus hypersensitivity (CSH) is an exaggerated response to carotid sinus baroreceptor stimulation. It results in dizziness or syncope from transient diminished cerebral perfusion.
Although baroreceptor function usually diminishes with age, some people experience hypersensitive carotid baroreflexes. For these individuals, even mild stimulation to the neck results in marked bradycardia and a drop in blood pressure.
CSH predominantly affects older males. It is a potent contributory factor and a potentially treatable cause of unexplained falls and neurocardiogenic syncopal episodes in elderly people.[1, 2] Yet, CSH is often overlooked in the differential diagnosis of presyncope and syncope.[3]
CSH, orthostatic hypotension, and vasovagal syncope are common conditions that are likely to coexist in patients with syncope and falls.[4]
NextPathophysiologyThe carotid sinus reflex plays a central role in blood pressure homeostasis. Changes in stretch and transmural pressure are detected by baroreceptors in the heart, carotid sinus, aortic arch, and other large vessels. Afferent impulses are transmitted by the carotid sinus, glossopharyngeal, and vagus nerves to the nuclei tractus solitarius and the para median nucleus in the brain stem. Efferent limbs are carried through sympathetic and vagus nerves to the heart and blood vessels, controlling heart rate and vasomotor tone.
In CSH, mechanical deformation of the carotid sinus (located at the bifurcation of the common carotid artery) leads to an exaggerated response with bradycardia or vasodilatation, resulting in hypotension, presyncope, or syncope.
The hemodynamic changes following carotid sinus stimulation are independent of body position. These changes have a distinct temporal pattern, with an initial fall in the cardiac output driven by heart rate, followed by a later fall in total peripheral resistance.[5]
CSH may be a part of a generalized autonomic disorder associated with autonomic dysregulation.[6] Data have been reported on neuronal degeneration with accumulation of hyperphosphorylated tau or alpha-synuclein in neurones in medulla, leading to impairment of central regulation of baroreflex responses and predispose elderly patients to CSH.[7]
However, the exact mechanism and site of abnormal sensitivity is unknown. The exaggerated response may be due to changes in any part of the reflex arc or the target organs.
Clinically and historically, 3 types of CSH have been described.
The cardioinhibitory type comprises 70-75% of cases. The predominant manifestation is a decreased heart rate, which results in sinus bradycardia, atrioventricular block, or asystole due to vagal action on sinus and atrioventricular nodes. This response can be abolished with atropine.[8] The vasodepressor type comprises 5-10% of cases. The predominant manifestation is a vasomotor tone decrease without a change in heart rate. The significant resulting drop in blood pressure is due to a change in the balance of parasympathetic and sympathetic effects on peripheral blood vessels. This response is not abolished with atropine. The mixed type comprises 20-25% of cases. A decrease in heart rate and vasomotor tone occurs.A recent proposal by a group of international experts suggests that the classification of CSH into 3 types as above should be revised. It has been suggested that all patients with CSH should be classified as "mixed" between vasodepression and cardioinhibition. This is because isolated cardioinhibitory CSH (asystole without fall in arterial pressure) does not occur.[9]
The terms spontaneous carotid sinus syndrome and induced carotid sinus syndrome have also been introduced to categorize patients who are presumed to have CSH.
The term spontaneous carotid sinus syndrome refers to a clinical situation in which the symptoms can be clearly attributed to a history of accidental mechanical manipulation of the carotid sinuses (eg, taking pulses in the neck, shaving) and CSH is reproduced by carotid sinus massage. Spontaneous carotid sinus syndrome is rare and accounts for about 1% of causes of syncope. The term induced carotid sinus syndrome refers to a clinical situation in which a patient has no clear history of accidental mechanical manipulation of the carotid sinuses and has a negative result from workup for syncope, except for a hypersensitive response to carotid sinus massage, which can be attributed to the patient's symptoms. Induced carotid sinus syndrome is more prevalent than spontaneous carotid sinus syndrome and accounts for the bulk of patients with an abnormal response to carotid sinus massage observed in the clinical setting. PreviousNextEpidemiologyFrequencyUnited StatesCSH is found in 0.5-9.0% of patients with recurrent syncope.
InternationalCSH is observed in up to 14% of elderly nursing home patients and 30% of elderly patients with unexplained syncope and drop attacks.
Mortality/MorbidityCSH is associated with an increased risk of falls, drop attacks, bodily injuries, and fractures in elderly patients.In the general population, the rates of mortality, sudden death, myocardial infarction, or stroke are unaffected by the presence of CSH. SexCSH is more common in males than in females.
AgeCSH is predominantly a disease of elderly people; it is virtually unknown in people younger than 50 years.
PreviousProceed to Clinical Presentation , Carotid Sinus Hypersensitivity
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ReplyDeleteSupervision of carotid sinus hypersensitivity is based on the frequency, severeness, and consequences of each and every patient's symptoms. Most patients could be treated with training, lifestyle changes, requirement, and This routine follow-up. Some individuals who have incapacitating and recurrent symptoms may need the following therapies: Pharmacotherapy has been utilized to treat recurrent, systematic conditions. However, no single agent has shown to provide long-term performance in large-scale, randomized, handled trials.
ReplyDeletePermanent pacemaker implantation is often considered an effective treatment for cardioinhibitory CSH and mixed forms of CSH. Current American School of Cardiology/American Coronary heart Association/Heart Rhythm Society clinical practice guidelines consider permanent pacing therapy to become class I indicator (ie, general agreement exists the therapy is effective and useful) inside patients with recurrent syncope attributable to carotid sinus stimulation inside the absence of almost any drug that depresses this sinus node or atrioventricular conduction. Permanent pacing is known as a class IIa indicator in patients together with recurrent syncope with out clear, provocative events is actually a hypersensitive cardioinhibitory reply. Permanent pacing can be discouraged in patients having a hypersensitive cardioinhibitory respond to carotid sinus stimulation inside the absence of signs and symptoms.
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