The Diagnosis and Treatment of Baroreflex Failure

The baroreflex, also known as the baroreceptor reflex, is a homeostatic system in the body that serves to keep blood pressure at approximately constant levels. The baroreflex creates a quick negative feedback loop in which increased blood pressure induces a reduction in heart rate. Reduced blood pressure reduces baroreflex activation, causing heart rate to increase and blood pressure to return to normal. Their role is to detect pressure changes by responding to variations in artery wall tension [1].

Anatomy of baroreflex :

The carotid sinuses and aortic arch contain the most sensitive baroreceptors. The aortic arch baroreceptor axons travel inside the vagus nerve (CN X), whereas the carotid sinus baroreceptor axons travel within the glossopharyngeal nerve (CN IX). Baroreceptor activation passes directly into the central nervous system to stimulate glutamatergic neurons in the brainstem's solitary nucleus [2].

 

Baroreflex Therapy To Reduce Sympathetic Nerve Activity:

The ability of baroreflex activation therapy to reduce sympathetic nerve activity suggests a potential application in the treatment of chronic heart failure because, in this condition, there is frequently intense sympathetic activation and patients with such sympathetic activation have a significantly increased risk of fatal arrhythmias and death. 

Causes of Baroreflex :

Abnormalities in the vascular baroreceptors, the glossopharyngeal nerve, its brain stem connections, or afferent nerve disruption can all result in baroreflex failure. Accidental trauma, unilateral or bilateral carotid endarterectomy trauma (3,4) or subsequent surgical therapy for pathology in the relevant anatomic locations, local tumor growth (6), and brain stem stroke are all established causes of baroreflex failure (7).

 

"Clinical Signs of Baroreflex Insufficiency"

Hypertensive Emergency:

As it necessitates prompt treatment, the acute form of baroreflex dysfunction is most frequently seen in hospital settings. Surgery performed on patients frequently results in loss of glossopharyngeal or vagus nerve function. Acute baroreflex failure can also result from unintentional injury. The clinical picture of injury to the afferent limb of the baroreflex is acute, continuous hypertension, tachycardia, and headache (12).

 

Orthostatic Tachycardia:

One of the most frequent findings among patients referred to tertiary hospitals with complaints of orthostatic intolerance is orthostatic tachycardia, which is defined as an increase in heart rate by >30 bpm from the supine to an upright position. The majority of patients with orthostatic tachycardia are diagnosed with neuropathic postural tachycardia syndrome (11).

 

Malignant Vagotonia:

The malignant vagotonia lesions more frequently result in the total or almost total elimination of afferent baroreflex input, causing denervation of the heart and cardiovascular system as well as tachycardia (12).

Malignant vagotonia is associated with Baroreflex insufficiency:  

When the parasympathetic efferent vagal fibers are not simultaneously destroyed along with the baroreflex, malignant vagotonia with severe bradycardia, hypotension, and sinus arrest episodes can develop.

 

Treatment of Baroreflex Failure:

The primary goal of baroreflex failure therapy is to lessen the frequency and amplitude of life-threatening blood pressure and heart rate surges. A secondary goal of therapy is to reduce the frequency of symptomatic hypotensive episodes. Pacemaker implantation may be required in patients with selective baroreflex dysfunction. A bionic baroreflex system has been proposed as an innovative therapy (7).

 

Baroreflex Improvement :

During BP increase and reduction, improvement in baroreflex sensitivity is mediated in part by an increase in aortic depressor nerve sensitivity (8,9).

 

Conclusion:

Many more prevalent illnesses mirror baroreflex dysfunction and are frequently misdiagnosed. Hypertensive crises, volatile hypertension, pheochromocytoma, poorly managed hypertension, orthostatic tachycardia, headache, hyperhidrosis, bradycardia, and syncope should all be evaluated in the differential diagnosis. Medical, surgical, family, and pharmacological histories are all important historical information (10).

 

References:

1. Osby U, Correia N, Brandt L, Ekbom A, Sparen P. Mortality and causes of death in schizophrenia in Stockholm county, Sweden. Schizophr Res (2000) 45:21–8.

2. Yuan, Jason; Brooks, Heddwen L.; Barman, Susan M.; Barrett, Kim E. (2019). Ganong's Review of Medical Physiology. ISBN 978-1-26-012240-4.

3. Biller J, Feinberg WM, Castaldo JE, et al. Guidelines for carotid endarterectomy: a statement for healthcare professionals from a special writing group of the stroke council, American Heart Association. Stroke. 1998; 29: 554–562.

4. Towne JB, Bernhard VM. The relationship of postoperative hypertension to complications following carotid endarterectomy. Surgery. 1980; 88: 575–580.

5. DeToma G, Nicolanti V, Plocco M, et al. Baroreflex failure syndrome after bilateral excision of carotid body tumors: an underestimated problem. J Vasc Surg. 2000; 31: 806–810.

6. Phillips AM, Jardine DL, Parkin PJ, et al. Brain stem stroke causing baroreflex failure and paroxysmal hypertension. Stroke. 2000; 31: 1997–2001.

7. Sato T, Kawada T, Shishido T, et al. Novel therapeutic strategy against central baroreflex failure: a bionic baroreflex system. Circulation. 1999; 100: 299–304.

8. Silva GJJ, Brum PC, Negrão CE, Krieger EM. Acute and chronic effects of exercise on baroreflex in spontaneously hypertensive rats. Hypertension. 1997; 30: 714–719.

9. Brum PC, Silva GJJ, Moreira ED, Ida F, Negrão CE, Krieger EM. Exercise training increases baroreceptor gain sensitivity in normal and hypertensive rats. Hypertension. 2000; 36: 1018–1022.

10. Reis DJ. The brain and hypertension: reflections on 35 years of inquiry into the neurobiology of the circulation. Circulation. 1984; 70 (suppl III): 31–45

 

 By: Rida Iqbal