The autonomic  nervous system provides moment to moment control of blood pressure and heart through baroreceptors.



The autonomic nervous system innervates all body organs, including the cardiovascular system.



Arteries, or arterioles, veins and pericytes  in capillaries receive autonomic innervation of muscles which modulates vascular smooth-muscle tone and vessel diameter.



Negative-feedback neural loops regulate groups of sympathetic neurons sending nerve impulses to the vasculature, the heart, and kidney and there are parasympathetic neurons sending nerve impulses to the sinus node of the heart.



Baroreflexes enable the circulatory system to adapt to conditions and maintain blood pressure, heart rate, and blood volume in a narrow physiologic range.



There are a baroreceptors in the walls of major arteries and veins in the heart which provides distinct reflexes, as they continuously signal to the nucleus of the solitary tract, located in the brainstem, through the vagus and glossopharyngeal nerves and are activated by stretch . blood pressure, blood volume, or both rise.



Increase parasympathetic activity to the sinoatrial node slows the heart rate.



A change to the standing position, allows vasoconstriction and  tachycardias to adjust for the fall in blood pressure that would otherwise occur in these changes were not made through baroreceptors changes.



Both arterial and cardiopulmonary baroreceptors inhibit efferent sympathetic neurons, leading to vasodilation, but only arterial baroreceptors influence the heart rate.



Arterial baroreceptors target the splanchnic circulation and cardio pulmonary baroreceptors inhibit sympathetic renal outflow, reducing renin release and proximal tubular sodium reabsorption.



Baroreceptors activation suppresses vasopressin release and sodium appetite, increasing urinary output.



Vagal efferent neurons are inhibited during inspiration, giving rise to respiratory sinus arrhythmia: When 


baroreflex pathways are damaged these rhythms are lost or blunted.



The nucleus of the solitary tract receives and integrates information from peripheral and central chemoreceptors, renal mechanoreceptors and chemo receptors through renal afferent nerves, muscle ergoreceptors and respiratory neurons as well as cortical and hypothalamus neurons.



Increased input from chemoreceptors increases sympathetic outflow in CHF, pulmonary hypertension, and COPD.



When baroreflex neurons are affected by disease blood pressure is unstable and there is acute symptoms of hypo or hyperperfusion.



When the efferent baroreflex neurons are impaired autonomic failure occurs affecting bladder, gastrointestinal and sexual function. 



When baroreflex failure occurs commonly among afferent neurons which affect cranial nerves IX and X but caused no additional autonomic defects.



Diseases that affect baroreflex sympathetic efferent neurons impair the release of norepinephrine at the neurovascular junction.



With insufficient vasoconstriction on standing or exertion orthostatic hypotension and symptoms of organ hypo perfusion, including lightheadedness or dizziness, visual blurring, and syncope occur.



Baroreflex impairment is associated with a sustained fall in blood pressure of at least 20/10 mmHg within three minutes after assumption of the upright position, but in some cases the fall in blood pressure is delayed, occurring after prolong standing.



Supine hypertension develops in 50% of patients with baroreflex  failure as a result of activation of residual sympathetic fibers and denervation supersensitivity.



The loss of normal nocturnal blood pressure profile impairs extracellular fluid volume regulation increasing excretion of sodium and water with loss of extracellular fluid overnight, with worsening orthostatic hypotension in the morning.



Baroreflex efferent neuron damage is most commonly seen in diabetes. 



Second most common cause of baroreflex neuron damage is synucleinopathies including: pure autonomic failure, Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy.



Synucleinopathies are related to intracellular accumulation of misfolded Alpha-synuclein in nerve tissue.



In light-chain and transthyretin amyloidosis, overproduced, misfolded extracellular amyloid deposits are present in sympathetic neurons.



Rarely genetic mutations can impair norepinephrine synthesis and release that can affect autonomic fibers of the baroreflex.



Baroreflex dysfunction can be the initial presentation of synucleinopathies and they provide an early diagnosis before typical motor or cognitive deficits.



For patients with isolated efferent baroreflex failure risk of future diagnosis of Parkinson’s disease, Lewy body dementia, multiple system atrophy is 10% per year.



Orthostatic hypotension due to neurologic causes need to be distinguish from non–neurogenic causes such as dehydration, hemorrhage, anemia, and medications.



A bedside test that helps distinguish neurogenic from non-neurogenic causes of orthostatic hypotension is the ratio of the increased heart rate to the decrease in systolic blood pressure. 



The heart rate response to hypotension is pronounced in patients with non–neurogenic orthostatic hypotension, but is blinded in efferent baroreflex failure.



A ratio below 0.5 indicates baroreflex failure.



In patients with efferent baroreflex failure there is a reduced or missing blood pressure overshoot after the Valsalva maneuver and frequently reduced respiratory sinus arrhythmia.



Sympathetic activity is blunted  in efferent baroreflex failure but is unrestrained and overactive in afferent baroflex failure.



In afferent baroreflex impairment barosensitive  sympathetic neurons are unrestrained and the release of  norepinephrine causes the causes vasoconstriction, tachycardia, and increased blood pressure.



In afferent baroreflex impairment headaches, flushing, and agitation are common and blood pressure is unstable. 



Orthostatic hypotension is part of the syndrome, but is not always present.



An acquired afferent baroreflex failure is a complication of damage to the glossopharyngeal and vagal nerves due to radiotherapy to the neck, radical neck surgery, after carotid endarterectomy, and rare tumors that affect the nucleus of the solitary tract.



Afferent baroreflex failure is associated with the Guillain- syndrome with wild swings in blood pressure.



Familial dysautonomia is it hereditary sensory and or Namic neuropathy due to a mutation that causes a spicing defect check in the E LP1 in children with Jewish ancestors.



ELP1  refers to elongated complex protein1  which is reduced in familial dysautonomia and prevents the growth and survival of afferent neurons including those involved in baroreflexes.



Acquired afferent baroreflex failure indicate that sympathetic efferent activities is no longer coupled to the cardiac cycle: complete failure of the baroreceptor afferents result in orthostatic hypotension with a paradoxical slowing of the heart rate that is not blocked by atropine, indicating that it is not mediated by activation of vagal efferents.



Most of the patients with autonomic  disease have no detectable nerve disease and the episodes and symptoms with acute cardiovascular changes blood pressure regulation is normal.



Vasovagal syncope is triggered by a reflex which causes sympathetic inhibition and parasympathetic stimulation.



Vasovagal syncope results in an acute fall in blood pressure and heart rate with transient loss, or near loss, of consciousness due to global cerebral decreased perfusion.



Vasovagal syncope is very common: the highest prevalence among teenagers, athletes, and the elderly. With a sufficient degree of autistic stress it can be induced in more than 75% of healthy people.



It is not a predictor of adverse cardiovascular outcomes. 



Consciousness is regained rapidly and then no neurologic see quickly although it can result in head trauma and bone fractures.



Postural tachycardia syndrome with marked tachycardia in the standing position, no fall in blood pressure but with sympathetic activation manifested by palpitations, chest pain, shortness of breath, and anxiety.



Postural tachycardia syndrome prevalence is high among young white women.



Postural tachycardia syndrome May be associated with subtle abnormalities in the baroreflexes.



Postural tachycardia syndrome is diagnosed when symptoms occur within 10 minutes after the patient has assumed an upright position with a sustained rising heart rate of 30 bpm.



[[Stress cardiomyopathy]] is caused by abnormal increased sympathetic activity.



Stress cardiomyopathy is usually seen among postmenopausal women, with neurologic was psychiatric disorders and more than 50% of patients, but without clinically significant coronary artery disease.



An acute phase of stress cardiomyopathy catecholamine levels are high suggesting a barrel reflects in balance.



Baroreflex dysfunction management includes avoiding triggers, salt and water loading, physical training when fitness is slow, use of countermaneuvers when premonitory symptoms appear, and the avoidance of falls.



In chronic baroreflex disorders patients can stand very low blood pressures because of an expanded autoregulatory range.



In chronic baroreflex disorders symptoms usually appear when the mean blood pressure is below 75 mg  mm Hg.



Treatment of chronic baroreflex disorders  is aimed at preventing severe hypotension that might result in syncope: sleeping with the head of the bed elevated, reduce overnight diuresis, abdominal binders targeting the splanchnic circulation, rapidly drinking water can raise blood pressure.



Drug treatment of neurogenic orthostatic hypotension combines intravascular volume expansion and avasoconstrictor drug.





































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