The symptoms of<unk>  can be caused by several distinct pathophysiological mechanisms. These mechanisms are poorly understood, and can overlap, with many people showing features of multiple<unk>  types. Many people with<unk>  exhibit low blood volume (hypovolemia), which can decrease the rate of blood flow to the heart. To compensate for this, the heart increases its cardiac output by beating faster, leading to the symptoms of presyncope and reflex<unk> . In the 30% to 60% of cases classified as hyperadrenergic<unk> , norepinephrine levels are elevated on standing, often due to hypovolemia or partial autonomic neuropathy. A smaller minority of people with<unk>  have (typically very high) standing norepinephrine levels that are elevated even in the absence of hypovolemia and autonomic neuropathy; this is classified as central hyperadrenergic<unk> . The high norepinephrine levels contribute to symptoms of<unk> . Another subtype, neuropathic<unk> , is associated with denervation of sympathetic nerves in the lower limbs. In this subtype, it is thought that impaired constriction of the blood vessels causes blood to pool in the veins of the lower limbs. Heart rate increases to compensate for this blood pooling. In up to 50% of cases, there was an onset of symptoms following a viral illness. It may also be linked to vaccination, physical trauma, concussion, pregnancy, or surgery. It is believed that these events could act as a trigger for an autoimmune response that result in<unk> .<unk>  is more common in females than males. It has also been shown to be linked in patients with acute stressors such as pregnancy, recent surgery, or recent trauma.<unk>  also has been linked to patients with a history of autoimmune diseases, irritable bowel<unk> , anemia, hyperthyroidism, fibromyalgia, diabetes, amyloidosis, sarcoidosis, systemic lupus erythematosus, and cancer. Genetics likely plays a role, with one study finding that one in eight<unk>  patients reported a history of<unk>  intolerance in their family. Associated Co-morbidities : Migraine headaches (11-40%) : Ehlers–Danlos<unk>  (20-25%) : Fibromyalgia (11-20%) : Irritable bowel<unk>  (7-30%) : Chronic fatigue<unk>  (7-21%) : Mast cell activation disorder (6-9%) Autoimmunity There is an increasing number of studies indicating that<unk>  is an autoimmune disease. A high number of patients has elevated levels of autoantibodies against the adrenergic alpha 1 receptor and against the muscarinic acetylcholine M4 receptor. Especially elevations of adrenergic α1 receptor is associated with symptoms severity in patients with<unk> . Secondary If<unk>  is caused by another condition, it may be classified as secondary<unk> . Chronic diabetes mellitus is one common cause.<unk>  can also be secondary to gastrointestinal disorders that are associated with low fluid intake due to nausea or fluid loss through diarrhea, leading to hypovolemia. Systemic lupus erythematosus and other autoimmune diseases have also been linked to<unk> . There is a subset of patients who present with both<unk>  and mast cell activation<unk>  (MCAS), and it is not yet clear whether MCAS is a secondary cause of<unk>  or simply comorbid, however, treating MCAS for these patients can significantly improve<unk>  symptoms.<unk>  can also co-occur in all types of Ehlers–Danlos<unk>  (EDS), a hereditary connective tissue disorder marked by loose hypermobile joints prone to subluxations and dislocations, skin that exhibits moderate or greater laxity, easy bruising, and many other symptoms. A trifecta of<unk> , EDS, and Mast Cell Activation<unk>  (MCAS) is becoming increasingly more common, with a genetic marker common among all three conditions.<unk>  is also often accompanied by vasovagal syncope, with a 25% overlap being reported. There are some overlaps between<unk>  and chronic fatigue<unk> , with evidence of<unk>  in 10–20% of CFS cases. Fatigue and reduced exercise tolerance are prominent symptoms of both conditions, and dysautonomia may underlie both conditions.<unk>  can sometimes be a paraneoplastic<unk>  associated with cancer. There are case reports of people developing<unk>  and other forms of dysautonomia post-COVID. There is no good large-scale empirical evidence yet to prove a connection, so for now the evidence is preliminary .
Postural orthostatic tachycardia syndrome
Da Costa's syndrome  Da Costa's syndrome  1
Heat syncope
Laughter-induced syncope
Vasoplegic syndrome
Reflex syncope
Permissive hypotension
Postanesthetic shivering