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==Pathophysiology==
==Pathophysiology==
It is thought that presyncope is the result of the interaction between the circulatory system and the autonomic nervous system. The autonomic nervous system is vital for the maintenance of internal homeostasis including regulation of blood pressure, heart rate, fluid and electrolyte balance, and body temperature. Syncope or presyncope occurs as a result of brain hypoxia, which is usually secondary to a reduction of cerebral perfusion pressure. However, not every reduction in blood pressure leads to brain hypoxia. This is because the cerebral circulation is autoregulated so that brain perfusion is maintained in the face of significant changes in mean blood pressure. This homeostatic mechanism allows regional cerebral blood flow to remain constant over a range of cerebral perfusion pressure (CPP) of 50 to 150 mm Hg or mean arterial pressure (MAP) of 60 to 160 mm Hg. So, as MAP or CPP increases, resistance in small cerebral arteries increases via vasoconstriction and vice versa.<sup>5</sup> Blood pressure below the lower level result in syncope secondary to brain hypoxia.
It is thought that presyncope is the result of the interaction between the circulatory system and the autonomic nervous system. The autonomic nervous system is vital for the maintenance of internal homeostasis including regulation of blood pressure, heart rate, fluid and electrolyte balance, and body temperature. Syncope or presyncope occurs as a result of brain hypoxia, which is usually secondary to a reduction of cerebral perfusion pressure. However, not every reduction in blood pressure leads to brain hypoxia. This is because the cerebral circulation is autoregulated so that brain perfusion is maintained in the face of significant changes in mean blood pressure. This homeostatic mechanism allows regional cerebral blood flow to remain constant over a range of cerebral perfusion pressure (CPP) of 50 to 150 mm Hg or mean arterial pressure (MAP) of 60 to 160 mm Hg. So, as MAP or CPP increases, resistance in small cerebral arteries increases via vasoconstriction and vice versa.<ref name="pmid27521192">{{cite journal| author=Armstead WM| title=Cerebral Blood Flow Autoregulation and Dysautoregulation. | journal=Anesthesiol Clin | year= 2016 | volume= 34 | issue= 3 | pages= 465-77 | pmid=27521192 | doi=10.1016/j.anclin.2016.04.002 | pmc=4988341 | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=27521192  }} </ref><sup>5</sup> Blood pressure below the lower level result in syncope secondary to brain hypoxia.


When standing, initially the force of gravity pools 500 to 800 mL of blood in the distensible veins below heart level.<ref name="pmid28286221">{{cite journal| author=Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD | display-authors=etal| title=2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. | journal=J Am Coll Cardiol | year= 2017 | volume= 70 | issue= 5 | pages= e39-e110 | pmid=28286221 | doi=10.1016/j.jacc.2017.03.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28286221  }} </ref> This increases capillary pressure and plasma is lost to interstitial fluid. It is estimated that plasma volume decreases by 15% within 20 minutes of standing. Pooling of blood in the veins decreases venous return to the heart with subsequent reduction of cardiac output, which in turn, triggers compensatory mechanisms to prevent the reduction of arterial pressure. Compensatory mechanisms include: sympathetic outflow upregulation by the central autonomic network (CAN); and the venoarterial reflex, leg pumping of skeletal muscles, the cerebral autoregulatory mechanism, and to a lesser extent, the renin angiotensin aldosterone system (RAAS).
When standing, initially the force of gravity pools 500 to 800 mL of blood in the distensible veins below heart level.<ref name="pmid28286221">{{cite journal| author=Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD | display-authors=etal| title=2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. | journal=J Am Coll Cardiol | year= 2017 | volume= 70 | issue= 5 | pages= e39-e110 | pmid=28286221 | doi=10.1016/j.jacc.2017.03.003 | pmc= | url=https://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=28286221  }} </ref> This increases capillary pressure and plasma is lost to interstitial fluid. It is estimated that plasma volume decreases by 15% within 20 minutes of standing. Pooling of blood in the veins decreases venous return to the heart with subsequent reduction of cardiac output, which in turn, triggers compensatory mechanisms to prevent the reduction of arterial pressure. Compensatory mechanisms include: sympathetic outflow upregulation by the central autonomic network (CAN); and the venoarterial reflex, leg pumping of skeletal muscles, the cerebral autoregulatory mechanism, and to a lesser extent, the renin angiotensin aldosterone system (RAAS).

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Vendhan Ramanujam M.B.B.S [2] Antara Chatterjee, M.D[3]

Synonyms and keywords: Faintness; generalized weakness; lightheadedness; near blackout; near fainting; near syncope

Overview

Presyncope is the sensation of feeling faint, lightheadedness[1] and muscular weakness without actually losing consciousness. The presyncope stage may occur for only a few seconds as a prodrome before losing consciousness. Presyncope is most often due to cardiovascular etiology.

Classification

Presyncope may be classified into following subtypes based on the inciting mechanism leading to the final event of transient global hypoperfusion. Presyncope suggests global cerebral hypoperfusion or a toxic/metabolic derangement. Hypoperfusion usually results from a drop in blood pressure (BP).

Cardiac Non-Cardiac
Dysrythmia Neurally-mediated (reflex)
Structural disease Orthostatic hypotension mediated
Neurological
Psychogenic


Pathophysiology

It is thought that presyncope is the result of the interaction between the circulatory system and the autonomic nervous system. The autonomic nervous system is vital for the maintenance of internal homeostasis including regulation of blood pressure, heart rate, fluid and electrolyte balance, and body temperature. Syncope or presyncope occurs as a result of brain hypoxia, which is usually secondary to a reduction of cerebral perfusion pressure. However, not every reduction in blood pressure leads to brain hypoxia. This is because the cerebral circulation is autoregulated so that brain perfusion is maintained in the face of significant changes in mean blood pressure. This homeostatic mechanism allows regional cerebral blood flow to remain constant over a range of cerebral perfusion pressure (CPP) of 50 to 150 mm Hg or mean arterial pressure (MAP) of 60 to 160 mm Hg. So, as MAP or CPP increases, resistance in small cerebral arteries increases via vasoconstriction and vice versa.[2]5 Blood pressure below the lower level result in syncope secondary to brain hypoxia.

When standing, initially the force of gravity pools 500 to 800 mL of blood in the distensible veins below heart level.[3] This increases capillary pressure and plasma is lost to interstitial fluid. It is estimated that plasma volume decreases by 15% within 20 minutes of standing. Pooling of blood in the veins decreases venous return to the heart with subsequent reduction of cardiac output, which in turn, triggers compensatory mechanisms to prevent the reduction of arterial pressure. Compensatory mechanisms include: sympathetic outflow upregulation by the central autonomic network (CAN); and the venoarterial reflex, leg pumping of skeletal muscles, the cerebral autoregulatory mechanism, and to a lesser extent, the renin angiotensin aldosterone system (RAAS).

The autonomic supply to the cardiovascular system is coordinated at the CAN located in the brain stem. The sympathetic nervous system acts as the main effector in the hemodynamic response to postural stressors. Upon standing, there is an initial reduction of cardiac filling and thus, of stroke volume. Pressure receptors in the heart, carotids, and aortic arch sense the perturbation and send impulses to the CAN. This initiates sympathetic vasomotor outflow and norepinephrine is released to vascular beds in the skeletal muscles and cutaneous vasculature; causing vasoconstriction, venoconstriction, as well as increased heart rate and contractility. Venoconstriction causes a correction of orthostasis by increasing cardiac filling for a given amount of gravitational pooling of blood. At the same time, leg pumping of skeletal muscles enhances venous return to the heart and the venoarterial reflex augments arterial vasoconstriction in response to venous distention.

In the nephron, orthostasis causes a decrease in renal blood flow, which leads to a decrease in glomerular sodium filtration and excretion. Norepinephrine release by the sympathetic response results in reabsorption of filtered sodium and increase in extracellular fluid (ECF) volume. At the same time, the RAAS is activated and promotes sodium and water conservation, but the magnitude of this response is less when compared to that caused by norepinephrine in the immediate setting. This was observed in cases of spinal cord injury and quadriplegia, where OH occurs despite marked stimulation of the RAAS but in the absence of sympathetic postganglionic outflow.

Postural stress in the atrium is sensed by mechanoreceptors as a decreased in atrial stretch. This causes increase of arginine vasopressin (AVP) and decrease in A-type atrial natriuretic peptide (ANP) secretion. This results in “anti-natriuresis” that leads to an increase of ECF volume and cardiac filling.


The pathophysiology of syncope is summarized as a reduction in systemic blood pressure that causes a decrease in the global cerebral blood flow, which results in loss of consciousness. A sudden cessation of cerebral blood flow for 6 to 8 seconds has been shown to cause loss of consciousness.2


Causes

Presyncope may be caused by [cause1], [cause2], or [cause3].

OR

Common causes of [disease] include [cause1], [cause2], and [cause3].

OR

The most common cause of [disease name] is [cause 1]. Less common causes of [disease name] include [cause 2], [cause 3], and [cause 4].

OR

The cause of [disease name] has not been identified. To review risk factors for the development of [disease name], click here.

Differentiating ((Page name)) from other Diseases

[Disease name] must be differentiated from other diseases that cause [clinical feature 1], [clinical feature 2], and [clinical feature 3], such as [differential dx1], [differential dx2], and [differential dx3].

OR

[Disease name] must be differentiated from [[differential dx1], [differential dx2], and [differential dx3].

Epidemiology and Demographics

The incidence/prevalence of [disease name] is approximately [number range] per 100,000 individuals worldwide.

OR

In [year], the incidence/prevalence of [disease name] was estimated to be [number range] cases per 100,000 individuals worldwide.

OR

In [year], the incidence of [disease name] is approximately [number range] per 100,000 individuals with a case-fatality rate of [number range]%.


Patients of all age groups may develop [disease name].

OR

The incidence of [disease name] increases with age; the median age at diagnosis is [#] years.

OR

[Disease name] commonly affects individuals younger than/older than [number of years] years of age.

OR

[Chronic disease name] is usually first diagnosed among [age group].

OR

[Acute disease name] commonly affects [age group].


There is no racial predilection to [disease name].

OR

[Disease name] usually affects individuals of the [race 1] race. [Race 2] individuals are less likely to develop [disease name].


[Disease name] affects men and women equally.

OR

[Gender 1] are more commonly affected by [disease name] than [gender 2]. The [gender 1] to [gender 2] ratio is approximately [number > 1] to 1.


The majority of [disease name] cases are reported in [geographical region].

OR

[Disease name] is a common/rare disease that tends to affect [patient population 1] and [patient population 2].

Risk Factors

There are no established risk factors for [disease name].

OR

The most potent risk factor in the development of [disease name] is [risk factor 1]. Other risk factors include [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] include [risk factor 1], [risk factor 2], [risk factor 3], and [risk factor 4].

OR

Common risk factors in the development of [disease name] may be occupational, environmental, genetic, and viral.

Screening

There is insufficient evidence to recommend routine screening for [disease/malignancy].

OR

According to the [guideline name], screening for [disease name] is not recommended.

OR

According to the [guideline name], screening for [disease name] by [test 1] is recommended every [duration] among patients with [condition 1], [condition 2], and [condition 3].

Natural History, Complications, and Prognosis

If left untreated, [#]% of patients with [disease name] may progress to develop [manifestation 1], [manifestation 2], and [manifestation 3].

OR

Common complications of [disease name] include [complication 1], [complication 2], and [complication 3].

OR

Prognosis is generally excellent/good/poor, and the 1/5/10-year mortality/survival rate of patients with [disease name] is approximately [#]%.

Diagnosis

Diagnostic Study of Choice

The diagnosis of [disease name] is made when at least [number] of the following [number] diagnostic criteria are met: [criterion 1], [criterion 2], [criterion 3], and [criterion 4].

OR

The diagnosis of [disease name] is based on the [criteria name] criteria, which include [criterion 1], [criterion 2], and [criterion 3].

OR

The diagnosis of [disease name] is based on the [definition name] definition, which includes [criterion 1], [criterion 2], and [criterion 3].

OR

There are no established criteria for the diagnosis of [disease name].

History and Symptoms

The majority of patients with presyncope report:

  • lightheadedness, general weakness
  • dizziness
  • confusion
  • tunnel vision, blurry vision
  • slurred speech
  • trouble hearing
  • sweating
  • nausea or vomiting
  • headache
  • heart palpitations

These symptoms can last from just a few seconds to several minutes before they pass.


Physical Examination

Patients with [disease name] usually appear [general appearance]. Physical examination of patients with [disease name] is usually remarkable for [finding 1], [finding 2], and [finding 3].

OR

Common physical examination findings of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

The presence of [finding(s)] on physical examination is diagnostic of [disease name].

OR

The presence of [finding(s)] on physical examination is highly suggestive of [disease name].

Laboratory Findings

An elevated/reduced concentration of serum/blood/urinary/CSF/other [lab test] is diagnostic of [disease name].

OR

Laboratory findings consistent with the diagnosis of [disease name] include [abnormal test 1], [abnormal test 2], and [abnormal test 3].

OR

[Test] is usually normal among patients with [disease name].

OR

Some patients with [disease name] may have elevated/reduced concentration of [test], which is usually suggestive of [progression/complication].

OR

There are no diagnostic laboratory findings associated with [disease name].

Electrocardiogram

There are no ECG findings associated with [disease name].

OR

An ECG may be helpful in the diagnosis of [disease name]. Findings on an ECG suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

X-ray

There are no x-ray findings associated with [disease name].

OR

An x-ray may be helpful in the diagnosis of [disease name]. Findings on an x-ray suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

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There are no x-ray findings associated with [disease name]. However, an x-ray may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Echocardiography or Ultrasound

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OR

Echocardiography/ultrasound may be helpful in the diagnosis of [disease name]. Findings on an echocardiography/ultrasound suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no echocardiography/ultrasound findings associated with [disease name]. However, an echocardiography/ultrasound may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

CT scan

There are no CT scan findings associated with [disease name].

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[Location] CT scan may be helpful in the diagnosis of [disease name]. Findings on CT scan suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

There are no CT scan findings associated with [disease name]. However, a CT scan may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

MRI

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[Location] MRI may be helpful in the diagnosis of [disease name]. Findings on MRI suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

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There are no MRI findings associated with [disease name]. However, a MRI may be helpful in the diagnosis of complications of [disease name], which include [complication 1], [complication 2], and [complication 3].

Other Imaging Findings

There are no other imaging findings associated with [disease name].

OR

[Imaging modality] may be helpful in the diagnosis of [disease name]. Findings on an [imaging modality] suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

Other Diagnostic Studies

There are no other diagnostic studies associated with [disease name].

OR

[Diagnostic study] may be helpful in the diagnosis of [disease name]. Findings suggestive of/diagnostic of [disease name] include [finding 1], [finding 2], and [finding 3].

OR

Other diagnostic studies for [disease name] include [diagnostic study 1], which demonstrates [finding 1], [finding 2], and [finding 3], and [diagnostic study 2], which demonstrates [finding 1], [finding 2], and [finding 3].

Treatment

Medical Therapy

There is no treatment for [disease name]; the mainstay of therapy is supportive care.

OR

Supportive therapy for [disease name] includes [therapy 1], [therapy 2], and [therapy 3].

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The majority of cases of [disease name] are self-limited and require only supportive care.

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[Disease name] is a medical emergency and requires prompt treatment.

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The mainstay of treatment for [disease name] is [therapy].

OR The optimal therapy for [malignancy name] depends on the stage at diagnosis.

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[Therapy] is recommended among all patients who develop [disease name].

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Pharmacologic medical therapy is recommended among patients with [disease subclass 1], [disease subclass 2], and [disease subclass 3].

OR

Pharmacologic medical therapies for [disease name] include (either) [therapy 1], [therapy 2], and/or [therapy 3].

OR

Empiric therapy for [disease name] depends on [disease factor 1] and [disease factor 2].

OR

Patients with [disease subclass 1] are treated with [therapy 1], whereas patients with [disease subclass 2] are treated with [therapy 2].

Surgery

Surgical intervention is not recommended for the management of [disease name].

OR

Surgery is not the first-line treatment option for patients with [disease name]. Surgery is usually reserved for patients with either [indication 1], [indication 2], and [indication 3]

OR

The mainstay of treatment for [disease name] is medical therapy. Surgery is usually reserved for patients with either [indication 1], [indication 2], and/or [indication 3].

OR

The feasibility of surgery depends on the stage of [malignancy] at diagnosis.

OR

Surgery is the mainstay of treatment for [disease or malignancy].

Primary Prevention

There are no established measures for the primary prevention of [disease name].

OR

There are no available vaccines against [disease name].

OR

Effective measures for the primary prevention of [disease name] include [measure1], [measure2], and [measure3].

OR

[Vaccine name] vaccine is recommended for [patient population] to prevent [disease name]. Other primary prevention strategies include [strategy 1], [strategy 2], and [strategy 3].

Secondary Prevention

There are no established measures for the secondary prevention of [disease name].

OR

Effective measures for the secondary prevention of [disease name] include [strategy 1], [strategy 2], and [strategy 3].



Overview. In many patients, lightheadedness is a symptom of orthostatic hypotension. Orthostatic hypotension occurs when blood pressure drops significantly when the patient stands from a supine or sitting position. If loss of consciousness occurs in this situation, it is termed syncope. Presyncope is frequently reported in patients with forms of Dysautonomia such as the Postural Tachycardia Syndrome. According to McGraw-Hill Concise Dictionary of Modern Medicine © 2002, presyncope is "An episode of near-fainting which may include lightheadedness, dizziness, severe weakness, blurred vision, which may precede a syncopal episode."

Causes

Life-Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular Acute coronary syndrome, acute myocardial infarction, acute myocarditis, Adams-Stokes syndrome, anomalous origins of coronary arteries, aortic aneurysm, aortic dissection, aortic stenosis, arrhythmogenic right ventricular dysplasia, atrial myxoma, atrioventricular block, AV nodal reentrant tachycardia, bifascicular block, bradyarrhythmia, brugada syndrome, cardiac tamponade, catecholaminergic polymorphic ventricular tachycardia, channelopathy, complete atrioventricular block, dehydration, dilated cardiomyopathy, epsilon wave, hemorrhage, hypertrophic cardiomyopathy, hypotension, Jervell and Lange-Nielsen syndrome, long QT syndrome, mitral stenosis, orthostatic hypotension, paroxysmal ventricular tachycardia, persistent atrial flutter, preexcitation syndrome, prolonged corrected QT interval, pulmonic stenosis, retroperitoneal hemorrhage, ruptured abdominal aortic aneurysm, saddle embolus, second degree AV block, short corrected QT interval, short QT syndrome, sick sinus syndrome, significant sinus pause, subclavian steal syndrome, supraventricular tachyarrhythmia, third degree heart block, ventricular arrhythmia, ventricular tachycardia, Wolff-Parkinson-White syndrome
Chemical/Poisoning Carbon monoxide, cocaine, ethanol
Dental No underlying causes
Dermatologic No underlying causes
Drug Side Effect ACE inhibitor, alpha blockers, amitriptyline, antiarrhythmics, antidepressants, antiemetics, antihypertensive medications, antipsychotic agents, barbiturates, beta blockers, bromocriptine, calcium channel blockerchlorpheniramine, cinnarizine, clonidine, desipramine, digoxin, diphenhydramine, diuretics, dothiepin, erectile dysfunction medications, Flurazepam, ganglionic blocker, hydralazine, hydroxyzine, L-dopa, nitrates, nortriptyline, opiates, phenothiazines, rizatriptan, tricyclic antidepressants, vasodilators
Ear Nose Throat No underlying causes
Endocrine No underlying causes
Environmental No underlying causes
Gastroenterologic Gastrointestinal bleeding
Genetic Channelopathy
Hematologic No underlying causes
Iatrogenic No underlying causes
Infectious Disease No underlying causes
Musculoskeletal/Orthopedic No underlying causes
Neurologic Carotid sinus hypersensitivity, dysautonomia, Lewy body dementia, multiple system atrophy, parkinson disease, seizure, spinal cord injury, subarachnoid hemorrhage, transient ischemic attack, vagal stimulation, vertebrobasilar insufficiency
Nutritional/Metabolic No underlying causes
Obstetric/Gynecologic No underlying causes
Oncologic Atrial myxoma, carcinoid syndrome
Ophthalmologic No underlying causes
Overdose/Toxicity No underlying causes
Psychiatric Anorexia nervosa, anxiety, emotional stress, hysterical faint, psychogenic pseudosyncope
Pulmonary Hypoxia
Renal/Electrolyte Uremia
Rheumatology/Immunology/Allergy Anaphylaxis, Takayasu's arteritis
Sexual No underlying causes
Trauma No underlying causes
Urologic No underlying causes
Miscellaneous Breath holding spells, choking game, cough, defecation, deglutition, drop attack, hair combing, heat illness, hyperventilation, hypocapnia, hypoglycemia, implanted cardioverter defibrillator malfunction, laughing, micturition, post-exercise, postprandial hypotension, prolonged bed rest, sneeze, significant blood loss, valsalva maneuver, vomiting, weightlifting

Causes in Alphabetical Order

Clinical test

The tilt table test is an evaluative clinical test to help identify presyncope or syncope.[8] A tilt angle of 60 and 70 degrees is optimal and maintains a high degree of specificity.[8] A positive sign with the tilt table test must be taken in context of patient history, with consideration of pertinent clinical findings before coming to a conclusion.

References

  1. Reeves, Alexander G. "Chapter 14: Evaluation of the Dizzy Patient". Disorders of the nervous system: a primer. Dartmouth Medical School. Retrieved 2012-01-06. Unknown parameter |coauthors= ignored (help)
  2. Armstead WM (2016). "Cerebral Blood Flow Autoregulation and Dysautoregulation". Anesthesiol Clin. 34 (3): 465–77. doi:10.1016/j.anclin.2016.04.002. PMC 4988341. PMID 27521192.
  3. Shen WK, Sheldon RS, Benditt DG, Cohen MI, Forman DE, Goldberger ZD; et al. (2017). "2017 ACC/AHA/HRS Guideline for the Evaluation and Management of Patients With Syncope: A Report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society". J Am Coll Cardiol. 70 (5): e39–e110. doi:10.1016/j.jacc.2017.03.003. PMID 28286221.
  4. Khoo, C.; Chakrabarti, S.; Arbour, L.; Krahn, AD. (2013). "Recognizing life-threatening causes of syncope". Cardiol Clin. 31 (1): 51–66. doi:10.1016/j.ccl.2012.10.005. PMID 23217687. Unknown parameter |month= ignored (help)
  5. Kapoor, WN. (2000). "Syncope". N Engl J Med. 343 (25): 1856–62. doi:10.1056/NEJM200012213432507. PMID 11117979. Unknown parameter |month= ignored (help)
  6. Nishida, K.; Hirota, SK.; Tokeshi, J. (2008). "Laugh syncope as a rare sub-type of the situational syncopes: a case report". J Med Case Rep. 2: 197. doi:10.1186/1752-1947-2-197. PMID 18538031.
  7. Benbadis, SR.; Chichkova, R. (2006). "Psychogenic pseudosyncope: an underestimated and provable diagnosis". Epilepsy Behav. 9 (1): 106–10. doi:10.1016/j.yebeh.2006.02.011. PMID 16697264. Unknown parameter |month= ignored (help)
  8. 8.0 8.1 Natale, A., Akhtar, M., Jazayeri, M., Dhala, A., Blanck, Z., Deshpande, S., et al. (1995). Provocation of Hypotension During Head-Up Tilt Testing in Subjects With No History of Syncope or Presyncop. American Heart Association, (92), 54-58. doi: 10.1161/01.CIR.92.1.54; url: http://circ.ahajournals.org/content/92/1/54.full

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