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'''True capillaries''' normally branch off the metarteriole and empty in the [[Venous system|postcapillary venule]]. The root of the true capillaries is surrounded by smooth muscle cells. This is called a precapillary sphincter. It acts as a valve that regulates [[Blood flow|blood flow]] through the capillary bed. If the sphincters are contracted, the blood will pass through the vascular shunt, and no exchange of materials will take place. If the valves are relaxed, blood will flow through the capillaries and exchange with the surrounding cells occurs. | '''True capillaries''' normally branch off the metarteriole and empty in the [[Venous system|postcapillary venule]]. The root of the true capillaries is surrounded by smooth muscle cells. This is called a precapillary sphincter. It acts as a valve that regulates [[Blood flow|blood flow]] through the capillary bed. If the sphincters are contracted, the blood will pass through the vascular shunt, and no exchange of materials will take place. If the valves are relaxed, blood will flow through the capillaries and exchange with the surrounding cells occurs. | ||
=Postural Tachycardia Syndrome (POTS)= | |||
POTS is a hetergeneous group of disorders with similar cinlical manifestations. POTS is characterized by a combination of an abnormally high heart frequency (tachycardia) while standing (postural) and symptoms of palpitations, light-headedness, and other sensations that occur due to cerebral hypoperfusion (see [[Symptoms and signs of presyncope|symptoms and signs of presyncope]]) | |||
</div> | |||
An abnormal heart rate respons is defined as: | |||
* Sustained heart rate increment of > 30 bpm within 10 minutes of standing or head-up tilt | |||
* Patients aged 12-19 years require an increment of > 40 bpm | |||
* '''Or''' a heart rate that exceeds 120 bpm | |||
* The heart rate increment cannot be associated conditions as prolonged bed rest, or medications that diminish vascular or autonomic tone | |||
* Symptoms of cerebral hypoperfusion and autonomic overactivity | |||
==Pathophysiology== | |||
The etiology and pathophysiology of POTS are unknown, but are likely to be heterogeneous. The syndrome is associated with deconditioning, recent viral illness, chronic fatigue syndrome and a limited or restricted autonomic neuropathy. The differential diagnosis includes conditions that cause tachycardia, such as thyrotoxicosis, inappropriate sinus tachycardia and other cardiac rhythm abnormalities, pheochromocytoma, hypoadrenalism, anxiety, dehydration, and medications (e.g., vasodilators, diuretics, and b-agonists). Many patients report that their symptoms started after a febrile illness, pregnancy, surgery, trauma or sepsis. The present thought on the pathophysiology of POTS after such an event is that POTS is an autoimmune disorder. | |||
==Epidemiology== | |||
The prevalence of POTS is not known, but estimates suggest at least 500.000 people are affected by POTS in the United States alone<cite>Grubb</cite>. The syndrome is more common in women. | |||
==Clinical presentation== | |||
The orthostatic symptoms of POTS consists of light-headedness, visual blurring or tunnel vision, palpitations, tremulousness, and weakness (especially in the legs). Other symptoms include fatigue, exercise intolerance, hyperventilation, shortness of breath, anxiety, chest pain, nausea, acral coldness or pain, and concentration difficulaties and headaches. On clinical examination, in addition to the heart rate increment, pulse pressure may be reduced and acral coldness may be present. Continued standing may lead to venous prominence, cyanosis and foot swelling. A hyperadrenergic state is present in some patients who have a resting tachycardia, sweating, and tremulousness. | |||
==References== | |||
<biblio> | |||
#Grubb pmid=18506020 | |||
</biblio> | |||