Carotid sinus hypersensitivity

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

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Overview

The carotid sinus contains a baroreceptor that senses arterial blood pressure and allows the body to regulate blood pressure and perfusion. Excessive sensitivity of this receptor may lead to reduced heart rate and/or blood pressure that can lead to syncope, called Carotid Sinus Hypersensitivity (CSH).

Weiss and Baker first described the syndrome in 15 patients in 1933.

Epidemiology and Demographics

CSH appears to be more common in men and in elderly patients. Other studies have suggested that CSH is more common in patients with Coronary artery disease (CAD), Hypertension (HTN) and in those with abnormal EKGs. Studies have also shown that CSH is more common in patients taking digitalis, alpha-methyldopa, clonidine and beta-blockers, presumably due to increased vagal activity. Some studies have suggested that CSH is more common in patients with carotid artery atherosclerosis.

Huang, et al, found CSH in 28% of patients with unexplained syncope, and other studies have found it in up to 45% of such patients. Huang Other studies have found CSH in up to 20% of the elderly population, though only a fraction of these individuals actually suffer from signs and symptoms of CSH.

Pathophysiology & Etiology

The carotid sinus baroreceptor is located in the internal carotid artery sinus just above the bifurcation of the common carotid artery. It senses arterial blood pressure and in response sends afferent signals to the sensory nucleus of the vagus, via the sinus nerve of Hering, a branch of the glossopharyngeal nerve. Increased afferent signals lead to increased vagal tone and reduced sympathetic tone.

Two general types of CSH have been described, though patients may have mixed features:

Vagal or cardioinhibitory type - Increased signal leads to a slowed heart rate.

• The slowed rate is usually due to sinus arrest or SA exit block. Some degree of AV block may occur as well in some patients.
  

Vasodepressor type - Blood pressure falls without slowing of the heart rate. Loss of sympathetic tone may be particularly important in this subtype.

The mechanism of the hypersensitivity has not been fully elucidated. Carotid sinus denervation does not always result in cure, so there may be several contributing features. Many people believe that the defect lies in the CNS.

• One theory is increased alpha-2 adrenergic receptor mediated activity in the afferent or brainstem pathway of the carotid sinus reflex.
• Other theories include high resting vagal tone, hyperresponsiveness to acetylcholine, inadequate cholinesterase, etc. in affected patients.

The syndrome has been observed in patients with tumors or lymph node enlargement in the region of the carotid sinus. If severe atheromatous narrowing of the carotid arteries is present, compression of the carotid artery can lead to syncope due to inadequate CNS perfusion and not necessarily due to carotid sinus hypersensitivity.

Diagnosis

Persons with CSH may have reproducible signs and symptoms with carotid sinus pressure, and this may be used diagnostically. If patients have audible bruits on exam or known significant carotid atherosclerosis, carotid sinus massage (CSM) is generally not recommended.

The usual criteria for diagnosis are >3 seconds of ventricular asystole and/or a fall of SBP of >50 mmHg during carotid sinus massage.

• The massage is defined as firm steady pressure to the carotid sinus for ~5 seconds with the neck in the hyperextended position while supine.
• The carotid sinus can be found along the carotid artery medial to the sternocleidomastoid (SCM) at the level of the thyroid cartilage.
• Heart rate, blood pressure, EKG and clinical response are monitored for change.
• The procedure is then repeated on the other side. The procedure may be repeated standing to evaluate carotid sinus vasodepressor hypersensitivity.

Patients may have either a heart rate fall, the cardioinhibitory response, or fall in blood pressure, the vasodepressor response. Weiss and Baker also reported that some patients suffered from syncope without any fall in heart rate or blood pressure, they called the primary cerebral type.

The test is not all-together sensitive or specific. If normal patients are tested, some will have a fall in blood pressure and heart rate despite no history of syncope. Other patients with history of syncope will have a fall in HR or BP but no reproducible symptoms at the time of the test.

Differential Diagnosis

The differential diagnosis of syncope includes true syncope and other non-syncopal causes. Below is listed one of many classification schemes.

Neurologic-associated causes

• Neurocardiogenic syncope – due to direct cardiac inhibition
• Vasovagal syncope
• Micturition syncope
• Carotid sinus hypersensitivity
• Seizure
• Transient ischemic attack (TIA) / Stroke
• Vertigo
• Hypoglycemia
• Narcolepsy
• Psychogenic – panic attack, anxiety disorder, somatization

Cardiac syncope

• Arrhythmia
• Outflow obstruction – valve disease, myxoma, idiopathic hypertrophic sub-aortic stenosis (IHSS), pulmonary embolism
• Insufficient cardiac output – CAD/USA/Myocardial infarction (MI), cardiac tamponade

Peripheral syncope - inability to maintain peripheral vascular tone

• Volume loss – including orthostatic hypotension and blood loss
• Medication effect – common agents include anticholinergics, nitrates, diuretics, other HTN meds.
• Autonomic and peripheral neuropathies – including diabetic neuropathy and other dysautonomias
• Neurodegenerative changes with orthostatic hypotension

History and Symptoms

Many patients will give a history of syncope or near-syncope with movement of the neck, wearing of a tight collar, shaving, etc. This history is not necessary, however, to make the diagnosis. Patients are usually upright, often standing, and develop a sudden episode of syncope, often with an associated fall. Small convulsive movements often occur with the loss of consciousness. The loss of consciousness is usually <30 seconds, and patients awake quickly with no clouding of consciousness.

The syndrome has been described in patients in chronic Afib, in addition to patients in normal sinus rhythm (NSR).

Physical Examination

Eyes

Pressing on the eyes can elicit a vagal response, but this is not part of the syndrome.

Ear Nose and Throat

Careful examination should be done to assess for carotid bruits and to assure that there is no obvious mass compressing the carotid (such as tumors or lymph nodes).

Risk Stratification and Prognosis

Many but not all patients with syncope due to CSH have recurrent symptoms if not treated. In one study, up to 2/3 of patients did not have recurrence, so it is prudent to reserve significant interventions for those patients with recurrent symptoms. Patients with CSH have a higher rate of hip fracture, laceration and recurrent syncope than in age-matched controls. Brignole, et al evaluated 312 patients with CSH, and found similar mortality to controls. Brignole

Treatment

Pharmacotherapy

• Anticholinergics - atropine
• Sympathomimetic meds – ephedrine. May be particularly useful in patients with vasodepressor type.
• Volume agents – fludrocortisone
• Selective serotonin reuptake inhibitors (SSRI) – two recent studies have shown a good response to SSRIs in five patients with the vasodepressor type CSH.

Surgery and Device Based Therapy

• Patients with cardioinhibitory / vagal type CSH often do quite well with pacemaker placement. Because some patients have AV node blockade, ventricular as well as atrial pacing is often indicated.
• Carotid sinus denervation by surgery or radiation.

ACC / AHA Guidelines- Permanent Pacing After the Acute Phase of Myocardial Infarction (DO NOT EDIT)

“

Class I 1. Permanent ventricular pacing is indicated for persistent second-degree AV block in the His-Purkinje system with alternating bundle-branch block or third-degree AV block within or below the His-Purkinje system after ST-segment elevation MI. (Level of Evidence: B) 2. Permanent ventricular pacing is indicated for transient advanced second- or third-degree infranodal AV block and associated bundle-branch block. If the site of block is uncertain, an electrophysiological study may be necessary. (Level of Evidence: B) 3. Permanent ventricular pacing is indicated for persistent and symptomatic second- or third-degree AV block. (Level of Evidence: C) Class IIb 1. Permanent ventricular pacing may be considered for persistent second- or third-degree infranodal AV block at the AV node level, even in the absence of symptoms. (Level of Evidence: B) Class III 1. Permanent ventricular pacing is not indicated for transient AV block in the absence of intraventricular conduction defects. (Level of Evidence: B) 2. Permanent ventricular pacing is not indicated for transient AV block in the presence of isolated left anterior fascicular block. (Level of Evidence: B) 3. Permanent ventricular pacing is not indicated for new bundle-branch block or fascicular block in the absence of AV block. (Level of Evidence: B) 4. Permanent ventricular pacing is not indicated for persistent asymptomatic first-degree AV block in the presence of bundle-branch or fascicular block. (Level of Evidence: B)

”

Acknowledgements

The content on this page was first contributed by Ellison L. Smith, M.D., Editor-In-Chief: C. Michael Gibson, M.S., M.D. [3]

List of contributors:

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