Baroreflex Failure

Abstract

Abstract-The baroreflex receives less attention nowadays because most students of hypertension are convinced that faulty volume regulation by the kidneys is responsible for long-term blood pressure increases. However, unusual patients with bilateral destruction of the normal blood pressure-sensing mechanisms can develop profound chronic hypertension. We present 2 patients with baroreflex failure. Both had volatile hypertension with systolic readings up to 300 mm Hg documented over years. Both had muscle sympathetic nerve activity that was increased even while resting. Treating these patients was a stochastic challenge. The therapy is frequently based on medicines that are no longer commonly prescribed. Key Words: baroreflex Ⅲ sympathetic nervous system Ⅲ autonomic nervous system Ⅲ hypotension Ⅲ bradycardia T he arterial baroreflex buffers acute fluctuations in blood pressure that occur during posture, stress, or other maneuvers. When blood pressure rises, vascular distension is transduced into nervous electrical activity, triggering reflex parasympathetic activation and sympathetic inhibition. Heart rate is slowed and vascular resistance is decreased, buffering the increase in blood pressure. Conversely, baroreceptor activity decreases when blood pressure falls, producing a reflex-mediated increase in heart rate and peripheral resistance. Baroreceptor activity is reset during sustained increases in blood pressure so that in patients with essential hypertension, baroreceptor responsiveness is maintained. However, the resetting of the baroreflex plays at least a permissive role in perpetuation of hypertension. Guyton argued that the baroreflex is responsible for the minute-to-minute regulation of blood pressure, but that the long-term blood pressure regulation is related to volume mechanisms adjusted by the kidneys. 1 However, faulty baroreflexes can occasionally influence long-term blood pressure regulation. An example is the condition of baroreflex failure. Such patients are a diagnostic challenge and a therapeutic nightmare. Case 1A 65-year-old woman was referred to our center for evaluation of possible baroreflex failure. Her chief symptom was volatile hypertension. The patient had a family history of arterial hypertension. Antihypertensive therapy was initiated at a young age and blood pressure readings were stable for many years. Twenty-two years before admission, a papillary thyroid cancer was diagnosed. She was successfully treated with thyroidectomy and local radiation followed by radioiodine treatment. Six years before admission, the patient experienced a neck trauma during a skiing accident. A left common carotid artery stenosis secondary to radiation injury was treated with angioplasty and stent implantation 4 years before admission. After the skiing accident, blood pressure became highly volatile. Systolic blood pressure values as high as 230 mm Hg had been recorded even during antihypertensive therapy with amlodipine, ramipril, spironolactone, metoprolol, and moxonidine. The hypertension was exacerba...

Baroreflex impairment and morbidity after major surgery

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Carotid Baroreceptor Stimulation, Sympathetic Activity, Baroreflex Function, and Blood Pressure in Hypertensive Patients

“…Continuous nonphysiological electric stimulation might disturb the function of peripheral or central components of the arterial baroreflex and cause a condition resembling baroreflex failure. 32,33 This clinical state was an exclusion criterion for DEBuT-HT, and carotid sinus stimulation did not cause baroreflex deficits, as judged by different methods. If anything, in a few patients the baroreflex sensitivity increased, which could be because of true improvement in baroreflex function with an increase in the maximal slope of the sigmoidal baroreflex curve or by a shift of the operating point to the steeper portion of the curve.…”

Carotid baroreflex activation therapy for resistant hypertension

“…28,29 However, symptomatic orthostatic hypotension is rare unless patients become hypovolaemic, owing to reflex compensation by cardiac vagal afferents (such as low-pressure cardiac baroreceptors) that remain intact. [28][29][30] Patients with familial dysautonomia (Riley-Day syndrome or hereditary sensory neuropathy type III) Note that aortic baroreceptors, which also influence blood pressure, are not paced. The dashed arrows represent inhibitory neural influences, and solid arrows represent excitatory neural influences on sympathetic outflow to the heart, peripheral vasculature, and kidneys.…”