Sympathetic Nervous System
Autonomic Nervous System
Cardiovascular Physiological Phenomena
Lower Body Negative Pressure
Parasympathetic Nervous System
Autonomic Nervous System Diseases
Central Venous Pressure
Vagus Nerve Diseases
Sympathetic Fibers, Postganglionic
Pure Autonomic Failure
Rats, Inbred SHR
Signal Processing, Computer-Assisted
Effects of amlodipine on sympathetic nerve traffic and baroreflex control of circulation in heart failure. (1/1596)Short-acting calcium antagonists exert a sympathoexcitation that in heart failure further enhances an already elevated sympathetic activity. Whether this is also the case for long-acting formulations is not yet established, despite the prognostic importance of sympathetic activation in heart failure. It is also undetermined whether in this condition long-acting calcium antagonists favorably affect a mechanism potentially responsible for the sympathetic activation, ie, the baroreflex impairment. In 28 heart failure patients (NYHA functional class II) under conventional treatment we measured plasma norepinephrine and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during arterial baroreceptor stimulation and deactivation induced by stepwise intravenous infusions of phenylephrine and nitroprusside, respectively. Measurements were performed at baseline and after 8 weeks of daily oral amlodipine administration (10 mg/d, 14 patients) or before and after an 8-week period without calcium antagonist administration (14 patients). Amlodipine caused a small and insignificant blood pressure reduction. Heart rate, left ventricular ejection fraction, and plasma renin and aldosterone concentrations were not affected. This was the case also for plasma norepinephrine (from 2.43+/-0.41 to 2.50+/-0.34 nmol/L, mean+/-SEM), muscle sympathetic nerve activity (from 54.4+/-5.9 to 51.0+/-4.3 bursts/min), and arterial baroreflex responses. No change in the above-mentioned variables was seen in the control group. Thus, in mild heart failure amlodipine treatment does not adversely affect sympathetic activity and baroreflex control of the heart and sympathetic tone. This implies that in this condition long-acting calcium antagonists can be administered without untoward neurohumoral effects anytime conventional treatment needs to be complemented by drugs causing additional vasodilatation. (+info)
A method for determining baroreflex-mediated sympathetic and parasympathetic control of the heart in pregnant and non-pregnant sheep. (2/1596)1. The cardiac baroreflex was measured in four non-pregnant and six pregnant ewes before and during beta-adrenoreceptor blockade with propranolol and before and during vagal blockade with atropine. Arterial pressure was raised by phenylephrine and lowered by sodium nitroprusside. The relationships between mean arterial pressure (MAP) and heart rate (HR), between MAP and heart rate variability (HRV) measured as the coefficient of variation (c.v.) of the mean pulse interval (PI), and between MAP and HRV measured by power spectral analysis were determined. 2. The MAP-HR relationship showed that in pregnant ewes the gain of the cardiac baroreflex was reduced when compared with non-pregnant ewes. Threshold and saturation pressures were higher, maximum achievable HR was lower and there was a decrease in the operating range. 3. V-shaped relationships were obtained between MAP and HRV (measured as the c.v. of PI) and between MAP and power spectral density in the frequency range 0.04-0. 08 Hz. Using selective autonomic blockade the negative, or downward, slope of the V shape was shown to be a measure of baroreceptor-induced, sympathetically mediated effects on HRV. The upward, or positive, slope of the V shape was a measure of baroreceptor-induced, vagally mediated effects. Similar results were also obtained from the cardiac power spectrum, but it was less sensitive. The MAP at which the two slopes intersected was the same as the resting MAP. 4. In pregnant ewes, the slope of the downward limb of the V-shaped relationship between HRV (when measured as the c.v. of PI) and MAP was less than in non-pregnant ewes. 5. The relationship between MAP and the coefficient of variation of the mean pulse interval can therefore be used to measure the degree to which baroreceptor-induced sympathetic and parasympathetic activity affects the heart. 6. The resting MAP is the pressure at which the net effect of these sympathetic and parasympathetic influences on the heart is at a minimum. Studies of both the MAP-HR and MAP-HRV relationships in pregnant and non-pregnant sheep show that in pregnant sheep, there is attenuation of baroreceptor-mediated sympathetic effects on the heart. (+info)
Vasopressin V2 receptor enhances gain of baroreflex in conscious spontaneously hypertensive rats. (3/1596)The aim of the present study was to determine the receptor subtype involved in arginine vasopressin (AVP)-induced modulation of baroreflex function in spontaneously hypertensive rats (SHR) and Wistar-Kyoto (WKY) rats using novel nonpeptide AVP V1- and V2-receptor antagonists. Baroreceptor heart rate (HR) reflex was investigated in both SHR and WKY rats which were intravenously administered the selective V1- and V2-receptor antagonists OPC-21268 and OPC-31260, respectively. Baroreflex function was assessed by obtaining alternate pressor and depressor responses to phenylephrine and sodium nitroprusside, respectively, to construct baroreflex curves. In both SHR and WKY rats baroreflex activity was tested before and after intravenous administration of vehicle (20% DMSO), OPC-21268 (10 mg/kg), and OPC-31260 (1 and 10 mg/kg). Vehicle did not significantly alter basal mean arterial pressure (MAP) and HR values or baroreflex function in SHR or WKY rats. The V1-receptor antagonist had no significant effect on resting MAP or HR values or on baroreflex parameters in both groups of rats, although this dose was shown to significantly inhibit the pressor response to AVP (5 ng iv; ANOVA, P < 0.05). In SHR but not WKY rats the V2-receptor antagonist significantly attenuated the gain (or slope) of the baroreflex curve (to 73 +/- 3 and 79 +/- 7% of control for 1 and 10 mg/kg, respectively), although AVP-induced pressor responses were also attenuated with the higher dose of the V2-receptor antagonist. These findings suggest that AVP tonically enhances baroreflex function through a V2 receptor in the SHR. (+info)
Cardiac baroreflex during the postoperative period in patients with hypertension: effect of clonidine. (4/1596)BACKGROUND: Patients with essential hypertension show altered baroreflex control of heart rate, and during the perioperative period they demonstrate increased circulatory instability. Clonidine has been shown to reduce perioperative circulatory instability. This study documents changes in measures of heart rate control after surgery in patients with essential hypertension and determines the effects of clonidine on postoperative heart rate control in these patients. METHODS: Using a randomized double-blind placebo-controlled design, 20 patients with essential hypertension (systolic pressure >160 mm Hg or diastolic pressure >95 mm Hg for > or =1 yr) were assigned to receive clonidine (or placebo), 6 microg/kg orally 120 min before anesthesia and 3 microg/kg intravenously over 60 min before the end of surgery. The spontaneous baroreflex ("sequence") technique and analysis of heart rate variability were used to quantify control of heart rate at baseline, before induction of anesthesia, and 1 and 3 h postoperatively. RESULTS: Baroreflex slope and heart rate variability were reduced postoperatively in patients given placebo but not those given clonidine. Clonidine resulted in greater postoperative baroreflex slope and power at all frequency ranges compared with placebo (4.9+/-2.9 vs. 2.2+/-2.1 ms/mm Hg for baroreflex slope, 354+/-685 vs. 30+/-37 ms2/Hz for high frequency variability). Clonidine also resulted in lower concentrations of catecholamine, decreased mean heart rate and blood pressure, and decreased perioperative tachycardia and hypertension. CONCLUSIONS: Patients with hypertension exhibit reduced heart rate control during the recovery period after elective surgery. Clonidine prevents this reduction in heart rate control. This may represent a basis for the improved circulatory stability seen with perioperative administration of clonidine. (+info)
Hypoxia inhibits baroreflex vagal bradycardia via a central action in anaesthetized rats. (5/1596)It is known that arterial baroreflexes are suppressed in stressful conditions. The present study was designed to determine whether and how hypoxia affects arterial baroreflexes, especially the heart rate component, baroreflex vagal bradycardia. In chloralose-urethane-anaesthetized rats, baroreflex vagal bradycardia was evoked by electrical stimulation of the aortic depressor nerve, and the effect of 15 s inhalation of hypoxic gas (4% O2) was studied. Inhalation of hypoxic gas was found to inhibit baroreflex vagal bradycardia. The inhibition persisted after bilateral transection of the carotid sinus nerve. Cervical vagus nerves were cut bilaterally and their peripheral cut ends were stimulated to provoke vagal bradycardia of peripheral origin so as to determine whether hypoxia could inhibit vagal bradycardia by acting on a peripheral site. In contrast to baroreflex vagal bradycardia, the vagus-induced bradycardia was not affected by hypoxic gas inhalation. It is concluded that baroreflex vagal bradycardia is inhibited by hypoxia and the inhibition is largely mediated by its direct central action. (+info)
Prognostic value of nocturnal Cheyne-Stokes respiration in chronic heart failure. (6/1596)BACKGROUND: Nocturnal Cheyne-Stokes respiration (CSR) occurs frequently in patients with chronic heart failure (CHF), and it may be associated with sympathetic activation. The aim of the present study was to evaluate whether CSR could affect prognosis in patients with CHF. METHODS AND RESULTS: Sixty-two CHF patients with left ventricular ejection fraction /=30/h and left atria >/=25 cm2. CONCLUSIONS: The AHI is a powerful independent predictor of poor prognosis in clinically stable patients with CHF. The presence of an AHI >/=30/h adds prognostic information compared with other clinical, echocardiographic, and autonomic data and identifies patients at very high risk for subsequent cardiac death. (+info)
The rostral ventrolateral medulla mediates the sympathoactivation produced by chemical stimulation of the rat nasal mucosa. (7/1596)1. We sought to outline the brainstem circuit responsible for the increase in sympathetic tone caused by chemical stimulation of the nasal passages with ammonia vapour. Experiments were performed in alpha-chloralose-anaesthetized, paralysed and artificially ventilated rats. 2. Stimulation of the nasal mucosa increased splanchnic sympathetic nerve discharge (SND), elevated arterial blood pressure (ABP), raised heart rate slightly and inhibited phrenic nerve discharge. 3. Bilateral injections of the broad-spectrum excitatory amino acid receptor antagonist kynurenate (Kyn) into the rostral part of the ventrolateral medulla (RVLM; rostral C1 area) greatly reduced the effects of nasal mucosa stimulation on SND (-80 %). These injections had no effect on resting ABP, resting SND or the sympathetic baroreflex. 4. Bilateral injections of Kyn into the ventrolateral medulla at the level of the obex (caudal C1 area) or into the nucleus tractus solitarii (NTS) greatly attenuated the baroreflex and significantly increased the baseline levels of both SND and ABP. However they did not reduce the effect of nasal mucosa stimulation on SND. 5. Single-unit recordings were made from 39 putative sympathoexcitatory neurons within the rostral C1 area. Most neurons (24 of 39) were activated by nasal mucosa stimulation (+65.8 % rise in discharge rate). Responding neurons had a wide range of conduction velocities and included slow-conducting neurons identified previously as C1 cells. The remaining putative sympathoexcitatory neurons were either unaffected (n = 8 neurons) or inhibited (n = 7) during nasal stimulation. We also recorded from ten respiratory-related neurons, all of which were silenced by nasal stimulation. 6. In conclusion, the sympathoexcitatory response to nasal stimulation is largely due to activation of bulbospinal presympathetic neurons within the RVLM. We suggest that these neurons receive convergent and directionally opposite polysynaptic inputs from arterial baroreceptors and trigeminal afferents. These inputs are integrated within the rostral C1 area as opposed to the NTS or the caudal C1 area. (+info)
Investigating feed-forward neural regulation of circulation from analysis of spontaneous arterial pressure and heart rate fluctuations. (8/1596)BACKGROUND: Analysis of spontaneous fluctuations in systolic arterial pressure (SAP) and pulse interval (PI) reveals the occurrence of sequences of consecutive beats characterized by SAP and PI changing in the same (+PI/+SAP and -PI/-SAP) or opposite (-PI/+SAP and +PI/-SAP) direction. Although the former reflects baroreflex regulatory mechanisms, the physiological meaning of -PI/+SAP and +PI/-SAP is unclear. We tested the hypothesis that -PI/+SAP and +PI/-SAP "nonbaroreflex" sequences represent a phenomenon modulated by the autonomic nervous system reflecting a feed-forward mechanism of cardiovascular regulation. METHODS AND RESULTS: We studied anesthetized rabbits before and after (1) complete autonomic blockade (guanethidine+propranolol+atropine, n=13; CAB), (2) sympathetic blockade (guanethidine+propranolol, n=15; SB), (3) parasympathetic blockade (atropine, n=16), (4) sinoaortic denervation (n=10; SAD), and (5) controlled respiration (n=10; CR). Nonbaroreflex sequences were defined as >/=3 beats in which SAP and PI of the following beat changed in the opposite direction. CAB reduced the number of nonbaroreflex sequences (19. 1+/-12.3 versus 88.7+/-36.6, P<0.05), as did SB (25.3+/-11.7 versus 84.6+/-23.9, P<0.001) and atropine (11.2+/-6.8 versus 94.1+/-32.4, P<0.05). SB concomitantly increased baroreflex sensitivity (1.18+/-0. 11 versus 0.47+/-0.09 ms/mm Hg, P<0.01). SAD and CR did not significantly affect their occurrence. CONCLUSIONS: These results suggest that nonbaroreflex sequences represent the expression of an integrated, neurally mediated, feed-forward type of short-term cardiovascular regulation able to interact dynamically with the feedback mechanisms of baroreflex origin in the control of heart period. (+info)
* Heart block: A condition where the electrical signals that control the heart's rhythm are blocked or delayed, leading to a slow heart rate.
* Sinus node dysfunction: A condition where the sinus node, which is responsible for setting the heart's rhythm, is not functioning properly, leading to a slow heart rate.
* Medications: Certain medications, such as beta blockers, can slow down the heart rate.
* Heart failure: In severe cases of heart failure, the heart may become so weak that it cannot pump blood effectively, leading to a slow heart rate.
* Electrolyte imbalance: An imbalance of electrolytes, such as potassium or magnesium, can affect the heart's ability to function properly and cause a slow heart rate.
* Other medical conditions: Certain medical conditions, such as hypothyroidism (an underactive thyroid) or anemia, can cause bradycardia.
Bradycardia can cause symptoms such as:
* Dizziness or lightheadedness
* Shortness of breath
* Chest pain or discomfort
In some cases, bradycardia may not cause any noticeable symptoms at all.
If you suspect you have bradycardia, it is important to consult with a healthcare professional for proper diagnosis and treatment. They may perform tests such as an electrocardiogram (ECG) or stress test to determine the cause of your slow heart rate and develop an appropriate treatment plan. Treatment options for bradycardia may include:
* Medications: Such as atropine or digoxin, to increase the heart rate.
* Pacemakers: A small device that is implanted in the chest to help regulate the heart's rhythm and increase the heart rate.
* Cardiac resynchronization therapy (CRT): A procedure that involves implanting a device that helps both ventricles of the heart beat together, improving the heart's pumping function.
It is important to note that bradycardia can be a symptom of an underlying condition, so it is important to address the underlying cause in order to effectively treat the bradycardia.
Examples of abnormal reflexes include:
1. Overactive reflexes: Reflexes that are too strong or exaggerated, such as an oversensitive knee jerk reflex.
2. Underactive reflexes: Reflexes that are too weak or diminished, such as a decreased tendon reflex in the arm.
3. Delayed reflexes: Reflexes that take longer than expected to occur, such as a delayed deep tendon reflex.
4. Abnormal reflex arc: A reflex arc that is not normal or expected for the situation, such as a spastic reflex arc.
5. Reflexes that are out of proportion to the stimulus: Such as an excessive or exaggerated reflex response to a mild stimulus.
6. Reflexes that occur in the absence of a stimulus: Such as a spontaneous reflex.
7. Reflexes that do not resolve: Such as a persistent reflex.
8. Reflexes that are painful or uncomfortable: Such as an abnormal rectal reflex.
It's important to note that not all abnormal reflexes are necessarily indicative of a serious medical condition, but they should be evaluated by a healthcare professional to determine the underlying cause and appropriate treatment.
There are several possible causes of orthostatic hypotension, including:
1. Deconditioning: This is a common cause of orthostatic hypotension in older adults who have been bedridden or hospitalized for prolonged periods.
2. Medication side effects: Certain medications, such as beta blockers and vasodilators, can cause orthostatic hypotension as a side effect.
3. Heart conditions: Conditions such as heart failure, arrhythmias, and structural heart defects can lead to orthostatic hypotension.
4. Neurological disorders: Certain neurological disorders, such as Parkinson's disease, multiple sclerosis, and stroke, can cause orthostatic hypotension.
5. Vasomotor instability: This is a condition where the blood vessels constrict or dilate rapidly, leading to a drop in blood pressure.
6. Anemia: A low red blood cell count can lead to a decrease in oxygen delivery to the body's tissues, causing orthostatic hypotension.
7. Dehydration: Dehydration can cause a drop in blood volume and lead to orthostatic hypotension.
8. Hypovolemia: This is a condition where there is a low volume of blood in the body, leading to a drop in blood pressure.
9. Sepsis: Sepsis can cause vasodilation and lead to orthostatic hypotension.
10. Other causes: Other causes of orthostatic hypotension include adrenal insufficiency, thyroid disorders, and certain genetic conditions.
Symptoms of orthostatic hypotension may include:
* Dizziness or lightheadedness
* Blurred vision
* Nausea and vomiting
If you experience any of these symptoms, it is important to seek medical attention as soon as possible. Your healthcare provider can perform a physical examination and order diagnostic tests to determine the underlying cause of your orthostatic hypotension. Treatment will depend on the specific cause, but may include medications to raise blood pressure, fluid replacement, and addressing any underlying conditions.
There are several types of tachycardia, including:
1. Sinus tachycardia: This is the most common type and is caused by an increase in the rate of the normal sinus node. It is often seen in response to physical activity or stress.
2. Atrial fibrillation: This is a type of arrhythmia where the heart's upper chambers (atria) contract irregularly and rapidly, leading to a rapid heart rate.
3. Ventricular tachycardia: This is a type of arrhythmia where the heart's lower chambers (ventricles) contract rapidly, often with a rate above 100 bpm.
4. Premature ventricular contractions (PVCs): These are early or extra beats that originate in the ventricles, causing a rapid heart rate.
Tachycardia can cause a range of symptoms, including palpitations, shortness of breath, chest pain, and dizziness. In severe cases, it can lead to cardiac arrhythmias, heart failure, and even death.
Diagnosis of tachycardia typically involves a physical examination, electrocardiogram (ECG), and other tests such as stress tests or echocardiography. Treatment options vary depending on the underlying cause, but may include medications to regulate the heart rate, cardioversion to restore a normal heart rhythm, or in severe cases, implantation of a pacemaker or defibrillator.
There are several possible causes of dizziness, including:
1. Inner ear problems: The inner ear is responsible for balance and equilibrium. Any disruption in the inner ear can cause dizziness.
2. Benign paroxysmal positional vertigo (BPPV): This is a condition that causes brief episodes of vertigo triggered by changes in head position.
3. Labyrinthitis: This is an inner ear infection that causes dizziness and hearing loss.
4. Vestibular migraine: This is a type of migraine that causes dizziness and other symptoms such as headaches.
5. Meniere's disease: This is a disorder of the inner ear that causes dizziness, tinnitus (ringing in the ears), and hearing loss.
6. Medication side effects: Certain medications can cause dizziness as a side effect.
7. Low blood pressure: A sudden drop in blood pressure can cause dizziness.
8. Anxiety: Anxiety can cause dizziness and other symptoms such as rapid heartbeat and shortness of breath.
9. Heart problems: Certain heart conditions such as arrhythmias or heart failure can cause dizziness.
10. Dehydration: Dehydration can cause dizziness, especially if it is severe.
If you are experiencing dizziness, it is important to seek medical attention to determine the underlying cause and receive appropriate treatment. Your healthcare provider may perform a physical examination, take a detailed medical history, and order diagnostic tests such as a hearing assessment or imaging studies to help identify the cause of your dizziness. Treatment will depend on the underlying cause, but may include medications, vestibular rehabilitation therapy, or lifestyle changes.
There are two types of hypertension:
1. Primary Hypertension: This type of hypertension has no identifiable cause and is also known as essential hypertension. It accounts for about 90% of all cases of hypertension.
2. Secondary Hypertension: This type of hypertension is caused by an underlying medical condition or medication. It accounts for about 10% of all cases of hypertension.
Some common causes of secondary hypertension include:
* Kidney disease
* Adrenal gland disorders
* Hormonal imbalances
* Certain medications
* Sleep apnea
* Cocaine use
There are also several risk factors for hypertension, including:
* Age (the risk increases with age)
* Family history of hypertension
* Lack of exercise
* High sodium intake
* Low potassium intake
Hypertension is often asymptomatic, and it can cause damage to the blood vessels and organs over time. Some potential complications of hypertension include:
* Heart disease (e.g., heart attacks, heart failure)
* Kidney disease (e.g., chronic kidney disease, end-stage renal disease)
* Vision loss (e.g., retinopathy)
* Peripheral artery disease
Hypertension is typically diagnosed through blood pressure readings taken over a period of time. Treatment for hypertension may include lifestyle changes (e.g., diet, exercise, stress management), medications, or a combination of both. The goal of treatment is to reduce the risk of complications and improve quality of life.
There are many different types of ANS diseases, including:
1. Dysautonomia: a general term that refers to dysfunction of the autonomic nervous system.
2. Postural orthostatic tachycardia syndrome (POTS): a condition characterized by rapid heart rate and other symptoms that occur upon standing.
3. Neurocardiogenic syncope: a form of fainting caused by a sudden drop in blood pressure.
4. Multiple system atrophy (MSA): a progressive neurodegenerative disorder that affects the autonomic nervous system and other parts of the brain.
5. Parkinson's disease: a neurodegenerative disorder that can cause autonomic dysfunction, including constipation, urinary incontinence, and erectile dysfunction.
6. Dopamine deficiency: a condition characterized by low levels of the neurotransmitter dopamine, which can affect the ANS and other body systems.
7. Autonomic nervous system disorders associated with autoimmune diseases, such as Guillain-Barré syndrome and lupus.
8. Trauma: physical or emotional trauma can sometimes cause dysfunction of the autonomic nervous system.
9. Infections: certain infections, such as Lyme disease, can affect the autonomic nervous system.
10. Genetic mutations: some genetic mutations can affect the functioning of the autonomic nervous system.
Treatment for ANS diseases depends on the specific condition and its underlying cause. In some cases, medication may be prescribed to regulate heart rate, blood pressure, or other bodily functions. Lifestyle changes, such as regular exercise and stress management techniques, can also be helpful in managing symptoms. In severe cases, surgery may be necessary to correct anatomical abnormalities or repair damaged nerves.
1. Vagus nerve paralysis: A condition in which the vagus nerve is damaged or degenerated, leading to weakness or paralysis of the muscles involved in swallowing and breathing.
2. Vagus nerve neuritis: Inflammation of the vagus nerve, which can cause symptoms such as hoarseness, dysphagia, and pain in the throat.
3. Vagus nerve tumors: Abnormal growths on the vagus nerve that can cause a variety of symptoms, including difficulty swallowing, voice changes, and seizures.
4. Vagus nerve trauma: Damage to the vagus nerve due to injury or surgery, which can result in long-term consequences such as dysphagia and vocal cord paralysis.
5. Vagus nerve syndromes: A group of disorders that affect the vagus nerve and its connections with other organs, such as the heart and lungs. These syndromes can cause a range of symptoms, including seizures, difficulty breathing, and abnormal heart rhythms.
These are some examples of Vagus Nerve Diseases that can affect the quality of life of an individual. It is important to be aware of these conditions and seek medical attention if symptoms persist or worsen over time.
In other words, pure autonomic failure refers to a situation where an individual experiences a decline in their autonomic nervous system's ability to regulate involuntary functions, such as heart rate, blood pressure, digestion, and body temperature, without any identifiable underlying cause. This can result in a range of symptoms, including fatigue, dizziness, lightheadedness, and difficulty maintaining balance.
Pure autonomic failure is rare and often presents challenges for diagnosis and treatment. It may be associated with other medical conditions, such as autoimmune disorders or neurodegenerative diseases, but in some cases, the cause remains unknown. Treatment options are limited and may include medication, lifestyle modifications, and management of symptoms.
The exact cause of vasovagal syncope is not fully understood, but it is thought to be related to an imbalance in the autonomic nervous system (which controls involuntary functions such as heart rate and blood pressure). It can be triggered by a variety of factors, including:
* Strong emotions such as fear or anxiety
* Pain or discomfort
* Intense physical activity
* Dehydration or low blood sugar
* Certain medications
During a vasovagal syncope episode, the person may experience symptoms such as:
* Dizziness or lightheadedness
* Blurred vision
* Nausea or vomiting
* Feeling of impending doom or loss of control
* Eventually, fainting or falling to the ground
Diagnosis of vasovagal syncope is typically made based on a combination of symptoms and physical examination findings. Tests such as an electrocardiogram (ECG) or blood tests may be ordered to rule out other conditions that may be causing the symptoms. Treatment for vasovagal syncope usually involves addressing any underlying triggers, such as managing stress or avoiding certain stimuli that may cause the episodes. In some cases, medications such as beta blockers or antidepressants may be prescribed to help regulate the heart rate and blood pressure.
There are several causes of hypotension, including:
1. Dehydration: Loss of fluids and electrolytes can cause a drop in blood pressure.
2. Blood loss: Losing too much blood can lead to hypotension.
3. Medications: Certain medications, such as diuretics and beta-blockers, can lower blood pressure.
4. Heart conditions: Heart failure, cardiac tamponade, and arrhythmias can all cause hypotension.
5. Endocrine disorders: Hypothyroidism (underactive thyroid) and adrenal insufficiency can cause low blood pressure.
6. Vasodilation: A condition where the blood vessels are dilated, leading to low blood pressure.
7. Sepsis: Severe infection can cause hypotension.
Symptoms of hypotension can include:
1. Dizziness and lightheadedness
2. Fainting or passing out
3. Weakness and fatigue
4. Confusion and disorientation
5. Pale, cool, or clammy skin
6. Fast or weak pulse
7. Shortness of breath
8. Nausea and vomiting
If you suspect that you or someone else is experiencing hypotension, it is important to seek medical attention immediately. Treatment will depend on the underlying cause of the condition, but may include fluids, electrolytes, and medication to raise blood pressure. In severe cases, hospitalization may be necessary.
Baroreflex activation therapy
Heart rate turbulence
Rostral ventrolateral medulla
Pathophysiology of hypertension
Inappropriate sinus tachycardia
Effects of alcohol on memory
Central venous pressure
Endoscopic thoracic sympathectomy
Impaired cardiac baroreflex sensitivity predicted renal denervation response
Browsing Biological Research by Subject "baroreflex"
Baroreflex Activation Therapy: A Novel Approach for HFrEF Patients
Longterm peripheral baroreflex and chemoreflex function after bilateral eversion carotid endarterectomy
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Functional symmetry of the aortic baroreflex in female spontaneously hypertensive rats. | J Hypertens;41(9): 1456-1465, 2023...
Comparison of aortic and carotid baroreflex stimulus-response characteristics in humans<...
Enhanced pressor responsiveness to central cholinergic activation by physostigmine and impaired baroreflex function in...
Enhanced sympathetic outflow and decreased baroreflex sensitivity are associated with intermittent hypoxia-induced systemic...
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Spontaneous baroreflex sensitivity3
- From the analysis of these parameters the software provides the estimates of spontaneous baroreflex sensitivity (BRS). (unibo.it)
- The mean arterial pressure (MAP) and interpulse interval (PPI) signals were then used to assess the autonomic functions and spontaneous baroreflex sensitivity by auto- and cross-spectral analysis, respectively. (tmu.edu.tw)
- Sugar-sweetened soft drink consumption acutely decreases spontaneous baroreflex sensitivity and heart rate variability. (cdc.gov)
- Functional symmetry of the aortic baroreflex in female spontaneously hypertensive rats. (bvsalud.org)
- We have previously demonstrated a left-sided dominance in the expression of aortic baroreflex function in male spontaneously hypertensive rats (SHRs) and normotensive rats of either sex . (bvsalud.org)
- If lateralization in aortic baroreflex function extends to hypertensive female rats remains undetermined. (bvsalud.org)
- These data show that female SHRs, unlike male SHRs, express similar central integration of left versus right aortic baroreceptor afferent input and thus show no laterization in the aortic baroreflex during hypertension . (bvsalud.org)
- To assess aortic-cardiac responses, neck pressure (NP) and suction (NS) were applied during PE and SN administration, respectively, to counter alterations in CSP thereby isolating the aortic baroreflex. (unthsc.edu)
- In addition, this investigation describes a model of aortic baroreflex function in normal healthy humans, which may prove useful in identifying the origin of baroreflex dysfunction in disease- and training-induced conditions. (unthsc.edu)
- The results of this study indicate that chronic IH-induced hypertension is associated with a facilitation of cardiovascular sympathetic outflow and inhibition of baroreflex sensitivity in conscious rats. (tmu.edu.tw)
- In healthy humans, fructose-sweetened water consumption increases blood pressure variability (BPV) and decreases spontaneous cardiovagal baroreflex sensitivity (cBRS) and heart rate variability (HRV). (cdc.gov)
- increases in baroreflex sensitivity, relaxation, and nitric oxide bioavailability seem to play important roles. (ifm.org)
- Patients are contraindicated if they have been assessed to have bilateral carotid bifurcations located above the level of the mandible, baroreflex failure or autonomic neuropathy, uncontrolled symptomatic cardiac bradyarrhythmias, carotid atherosclerosis that is determined by ultrasound or angiographic evaluation greater than 50%, ulcerative plaques in the carotid artery as determined by ultrasound or angiographic evaluation, known allergy to silicone or titanium. (cvrx.com)
- In order to characterize the stimulus-response relationships of the arterial, aortic, and carotid baroreflexes in mediating cardiac chronotropic function, we measured heart rate (HR) responses elicited by acute changes in mean arterial pressure (MAP) and carotid sinus pressure (CSP) in 11 healthy individuals. (unthsc.edu)
- Graded levels of NP and NS were delivered to the carotid sinus using a customized neck collar device to assess the carotid-cardiac baroreflex, independent of drug infusion. (unthsc.edu)
- Vasoconstriction Response to Mental Stress in Sickle Cell Disease: The Role of the Cardiac and Vascular Baroreflexes Front Physiol. (usc.edu)
- Arterial (aortic+carotid) baroreflex control of HR was quantified using ramped changes in MAP induced by bolus injection of phenylephrine (PE) and sodium nitroprusside (SN). (unthsc.edu)
- We found no significant effect of promethazine on resting mean R-R interval, arterial pressure, R-R interval power spectra, carotid baroreflex function, and venous plasma catecholamine levels. (aspetjournals.org)
Spontaneously hypertensive rats1
- Kawashima, K, Miwa, Y & Fujimoto, K 1988, ' Enhanced pressor responsiveness to central cholinergic activation by physostigmine and impaired baroreflex function in spontaneously hypertensive rats ', Therapeutic Research , vol. 9, no. 2, pp. 144-153. (elsevier.com)
- Because the effects of promethazine on autonomic cardiovascular mechanisms in general and baroreflex function in particular were not known, we were unable to exclude a possible influence of promethazine on our results. (aspetjournals.org)
- Marrocco Trischitta, Massimiliano Maria (2008) Longterm peripheral baroreflex and chemoreflex function after bilateral eversion carotid endarterectomy , [Dissertation thesis], Alma Mater Studiorum Università di Bologna. (unibo.it)
- The aim of this study is to assess the long-term effect of the e-CEA on arterial baroreflex and peripheral chemoreflex function in humans. (unibo.it)
- ACE inhibition did not change the spontaneous baroreflex indices (gain and baroreflex effectiveness index) in ELA-2 KO mice. (nih.gov)
- Stay up-to-date on the latest news, insights and best practices on Barostim Baroreflex Activation Therapy. (cvrx.com)
- Baroreflex mechanisms in major depressions. (bvsalud.org)
- Notably, baroreflex function was better maintained in e-CEA, compared to standard CEA. (unibo.it)
- Massage of the carotid sinus demonstrated the presence of a carotid sinus syndrome (CSS), an abnormal baroreflex response of the carotid sinus that leads to asystole and extreme hypotension. (minervamedica.it)
- This finding indicates each baroreflex functions as both an important anti-hypotensive and anti-hypertensive mechanism. (unthsc.edu)
- Spontaneous baroreflex was assessed by the sequencing method. (nih.gov)
- Adekunle and Akintomide: Exercise treadmill test in type 2 diabetes mellitus patients étaient en sous-groupe de risque duc modéré et il n'y n'avait aucune différence statistiquement significative entre les mâles et les femelles à cet égard. (who.int)
- The prospective, nonrandomized, feasibility DEBuT-HT (Device Based Therapy in Hypertension trial) study showed that, in patients with resistant hypertension (systolic BP [SBP] ≥160 mmHg or diastolic ≥90 mmHg despite ≥3 antihypertensive medications), BAT therapy using the Rheos® Baroreflex Hypertension Therapy™ (CVRx, Inc.) reduced mean BP by 21/12 mmHg after 3 months of therapy with a favorable safety profile. (medscape.com)
- Baroreflex activation therapy (BAT) is a device-based approach that consists of an implanted pulse generator (implanted in the pectoral region), external programming system, and leads placed adjacent to the carotid sinus to deliver electrical pulses to the carotid baroreceptors. (medscape.com)
- Because the baroreceptors are tonically active, the baroreflex can compensate rapidly for both increases and decreases in blood pressure. (bvsalud.org)
- Identifying physiological origins of baroreflex dysfunction in salt-sensitive hypertension in the Dahl SS rat.Physiol. (nih.gov)
- Baroreflex failure is a rare disorder that causes fluctuations in blood pressure with episodes of severe hypertension (high blood pressure) and elevated heart rate in response to stress, exercise, and pain. (nih.gov)
- Symptoms of Baroreflex failure may include headache, sweating, and a heart rate that does not respond to medications. (nih.gov)
- In many cases, the cause of Baroreflex failure is not known. (nih.gov)
- TI - Post-exercise depression of baroreflex slowing of the heart in humans. (nih.gov)
- Baroreflex responses were analyzed in anesthetized STZ-AD rats using femoral catheterization for blood pressure and heart rate, and autonomic activity was assessed using specific blockers and splanchnic sympathetic nerve recordings. (nih.gov)
- Baroreflex function in STZ-AD showed a blunted heart rate (HR) response to low blood pressure challenges, and the maximal sympathetic nerve activity was reduced. (nih.gov)
- This is a phenomenological ODE model of baroreflex open-loop control of heart rate. (nih.gov)
- [ 5 ] Electrical stimulation of the carotid baroreceptors results in activation of the baroreflex system with subsequent increase in the parasympathetic outflow and inhibition of the sympathetic activity. (medscape.com)