pulse, and respiratory pauses that may last for 60 seconds. subclavian steal syndrome arises from retrograde (reversed) flow of blood in the vertebral artery or the internal thoracic artery, due to a proximal stenosis (narrowing) and/or occlusion of the subclavian artery. symptoms such as syncope, lightheadedness, and paresthesias occur while exercising the arm on the affected side (most commonly the left). aortic dissection (a tear in the aorta) and cardiomyopathy can also result in syncope. various medications, such as beta blockers, may cause bradycardia induced syncope. a pulmonary embolism can cause obstructed blood vessels and is the cause of syncope in less than 1% of people who present to the emergency department. blood pressure orthostatic (postural) hypotensive syncope is caused primarily by an excessive drop in blood pressure when standing up from a previous position of lying or sitting down. when the head is elevated above the feet the pull of gravity causes blood pressure in the head to drop. this is sensed by stretch receptors in the walls of vessels in the carotid sinus and aortic arch. these receptors then trigger a sympathetic nervous response to compensate and redistribute blood back into the brain. the sympathetic response causes peripheral vasoconstriction and increased heart rate. these together act to raise blood pressure back to baseline. apparently healthy individuals may experience minor symptoms ("lightheadedness", "greying-out") as they stand up if blood pressure is slow to respond to the stress of upright posture. if the blood pressure is not adequately maintained during standing, faints may develop. however, the resulting "transient orthostatic hypotension" does not necessarily signal any serious underlying disease. it is as common or perhaps even more common than vasovagal syncope. this may be due to medications, dehydration, significant bleeding or infection. the most susceptible individuals are elderly frail individuals, or persons who are dehydrated from hot environments or inadequate fluid intake. for example, medical students would be at risk for orthostatic hypotensive syncope while observing long surgeries in the operating room. there is also evidence that exercise training can help reduce orthostatic intolerance. more serious orthostatic hypotension is often the result of certain commonly prescribed medications such as diuretics, β-adrenergic blockers, other anti-hypertensives (including vasodilators), and nitroglycerin. in a small percentage of cases, the cause of orthostatic hypotensive faints is structural damage to the autonomic nervous system due to systemic diseases (e.g., amyloidosis or diabetes) or in neurological diseases (e.g., parkinson's disease). hyperadrenergic orthostatic hypotension refers to an orthostatic drop in blood pressure despite high levels of sympathetic adrenergic response. this occurs when a person with normal physiology is unable to compensate for >20% loss in intravascular volume. this may be due to blood loss, dehydration or third-spacing. on standing the person will experience reflex tachycardia (at least 20% increased over supine) and a drop in blood pressure. hypoadrenergic orthostatic hypotension occurs when the person is unable to sustain a normal sympathetic response to blood pressure changes during movement despite adequate intravascular volume. there is little to no compensatory increase in heart rate or blood pressure when standing for up to 10 minutes. this is often due to an underlying disorder or medication use and is accompanied by other hypoadrenergic signs. central nervous system ischemia the central ischemic response is triggered by an inadequate supply of oxygenated blood in the brain. common examples include strokes and transient ischemic attacks. while these conditions often impair consciousness they rarely meet the medical definition of syncope. vertebrobasilar transient ischemic attacks may produce true syncope as a symptom. the respiratory system may compensate for dropping oxygen levels through hyperventilation, though a sudden ischemic episode may also proceed faster than the respiratory system can respond. these processes cause the typical symptoms of fainting: pale skin, rapid breathing, nausea, and weakness of the limbs, particularly of the legs. if the ischemia is intense or prolonged, limb weakness progresses to collapse. the weakness of the legs causes most people to sit or lie down if there is time to do so. this may avert a complete collapse, but whether the patient sits down or falls down, the result of an ischaemic episode is a posture in which less blood pressure is required to achieve adequate blood flow. an individual with very little skin pigmentation may appear to have all color drained from his or her face at the onset of an episode. this effect combined with the following collapse can make a strong and dramatic impression on bystanders. vertebro-basilar arterial disease arterial disease in the upper spinal cord, or lower brain that causes syncope if there is a reduction in blood supply. this may occur with extending the neck or with use of medications to lower blood pressure. other causes there are other conditions which may cause or resemble syncope. seizures and syncope can be difficult to differentiate. both often present as sudden loss of consciousness and convulsive movements may be present or absent in either. movements in syncope are typically brief and more irregular than seizures. akinetic seizures can present with sudden loss of postural tone without associated tonic-clonic movements. absence of a long post-ictal state is indicative of syncope rather than an akinetic seizure. subarachnoid hemorrhage may result in syncope. often this is in combination with sudden, severe headache. it may occur as a result of a ruptured aneurysm or head trauma. heat syncope occurs when heat exposure causes decreased blood volume and peripheral vasodilatation. position changes, especially during vigorous exercise in the heat, may lead to decreased blood flow to the brain. closely related to other causes of syncope related to hypotension (low blood pressure) such as orthostatic syncope. lactose intolerance can cause "a release of histamine, resulting in an extreme dilatation of the bloodvessels, resulting in a drop of blood pressure so that not enough blood reaches the brains, leading to dizziness, fainting, syncope, itching, hives, tingling or swelling of the lips, tongue, or throat; chest tightness, shortness of breath, or difficulty breathing, wheezing." (more in the article on lactose intolerance). some psychological conditions (anxiety disorder, somatic symptom disorder, conversion disorder) may cause symptoms resembling syncope. a number of psychological interventions are available. low blood sugar can be a rare cause of syncope. narcolepsy may present with sudden loss of consciousness similar to syncope. diagnostic approach a medical history, physical examination, and electrocardiogram (ecg) are the most effective ways to determine the underlying cause of syncope. guidelines from the american college of emergency physicians and american heart association recommend a syncope workup include a thorough medical history, physical exam with orthostatic vitals, and a 12-lead ecg. the ecg is useful to detect an abnormal heart rhythm, poor blood flow to the heart muscle and other electrical issues, such as long qt syndrome and brugada syndrome. heart related causes also often have little history of a prodrome. low blood pressure and a fast heart rate after the event may indicate blood loss or dehydration, while low blood oxygen levels may be seen following the event in those with pulmonary embolism. routine broad panel laboratory testing detects abnormalities in <2–3% of results and is therefore not recommended. based on this initial workup many physicians will tailor testing and determine whether a person qualifies as 'high-risk', 'intermediate risk' or 'low-risk' based on risk stratification tools. more specific tests such as implantable loop recorders, tilt table testing or carotid sinus massage may be useful in uncertain cases. computed tomography (ct) is generally not required unless specific concerns are present. other causes of similar symptoms that should be considered include seizure, stroke, concussion, low blood oxygen, low blood sugar, drug intoxication and some psychiatric disorders among others. treatment depends on the underlying cause. those who are considered at high risk following investigation may be admitted to hospital for further monitoring of the heart. a hemoglobin count may indicate anemia or blood loss. however, this has been useful in only about 5% of people evaluated for fainting. the tilt table test is performed to elicit orthostatic syncope secondary to autonomic dysfunction (neurogenic). a number of factors make a heart related cause more likely including age over 35, prior atrial fibrillation, and turning blue during the event. electrocardiogram electrocardiogram (ecg) finds that should be looked for include signs of heart ischemia, arrhythmias, atrioventricular blocks, a long qt, a short pr, brugada syndrome, signs of hypertrophic obstructive cardiomyopathy (hocm), and signs of arrhythmogenic right ventricular dysplasia (arvd/c). signs of hcm include large voltages in the precordial leads, repolarization abnormalities, and a wide qrs with a slurred upstroke. signs of arvd/c include t wave inversion and epsilon waves in lead v1 to v3. it is estimated that from 20 to 50% of people have an abnormal ecg. however, while an ecg may identify conditions such as atrial fibrillation, heart block, or a new or old heart attack, it typically does not provide a definite diagnosis for the underlying cause for fainting. sometimes, a holter monitor may be used. this is a portable ecg device that can record the wearer's heart rhythms during daily activities over an extended period of time. since fainting usually does not occur upon command, a holter monitor can provide a better understanding of the heart's activity during fainting episodes. for people with more than two episodes of syncope and no diagnosis on "routine testing", an insertable cardiac monitor might be used. it lasts 28–36 months and is inserted just beneath the skin in the upper chest area. ecg showing hocm long qt syndrome a short pr in wolff–parkinson–white syndrome type 2 brugada ecg pattern imaging echocardiography and ischemia testing may be recommended for cases where initial evaluation and ecg testing is nondiagnostic. for people with uncomplicated syncope (without seizures and a normal neurological exam) computed tomography or mri is not generally needed. likewise, using carotid ultrasonography on the premise of identifying carotid artery disease as a cause of syncope also is not indicated. although sometimes investigated as a cause of syncope, carotid artery problems are unlikely to cause that condition. additionally an electroencephalogram (eeg) is generally not recommended. a bedside ultrasound may be performed to rule out abdominal aortic aneurysm in people with concerning history or presentation. differential diagnosis other diseases which mimic syncope include seizure, low blood sugar, certain types of stroke, and paroxysmal spells. while these may appear as "fainting", they do not fit the strict definition of syncope being a sudden reversible loss of consciousness due to decreased blood flow to the brain. management management of syncope focuses on treating the underlying cause. this can be challenging as the underlying cause is unclear in half of all cases. several risk stratification tools (explained below) have been developed to combat the vague nature of this diagnosis. people with an abnormal ecg reading, history of congestive heart failure, family history of sudden cardiac death, shortness of breath, hct<30, hypotension or evidence of bleeding should be admitted to the hospital for further evaluation and monitoring. low-risk cases of vasovagal or orthostatic syncope in younger people with no significant cardiac history, no family history of sudden unexplained death, and a normal ekg and initial evaluation may be candidates for discharge to follow-up with their primary care provider. recommended acute treatment of vasovagal and orthostatic (hypotension) syncope involves returning blood to the brain by positioning the person on the ground, with legs slightly elevated or sitting leaning forward and the head between the knees for at least 10–15 minutes, preferably in a cool and quiet place. for individuals who have problems with chronic fainting spells, therapy should focus on recognizing the triggers and learning techniques to keep from fainting. at the appearance of warning signs such as lightheadedness, nausea, or cold and clammy skin, counter-pressure maneuvers that involve gripping fingers into a fist, tensing the arms, and crossing the legs or squeezing the thighs together can be used to ward off a fainting spell. after the symptoms have passed, sleep is recommended. lifestyle modifications are important for treating people experiencing repeated syncopal episodes. avoiding triggers and situations where loss of consciousness would be seriously hazardous (operating heavy machinery, commercial pilot, etc.) has been shown to be effective. if fainting spells occur often without a triggering event, syncope may be a sign of an underlying heart disease. in the case where syncope is caused by cardiac disease, the treatment