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==Treating orthostatic hypotension==
==Triggers for vasovagal syncope==
Vasovagal syncope can occur after exposure of a lot of different triggers. Recognised triggers for vasovagal syncope are prolonged orthostatic stress, blood drawing, medical instrumentation and psychological stressors.


The concept of '''head-up tilt sleeping''' to manage [[orthostatic hypotension|orthostatic hypotension]] is based on the clinical observations by MacLean and Allen almost 70 years ago <cite>5</cite>. These clinical investigators observed that [[orthostatic hypotension]] in patients with pure autonomic failure appeared to improve symptomatically and objectively during daytime and that this improvement had disappeared in the morning after sleeping in bed at night. The observation of diurnal changes in orthostatic tolerance led MacLean and Allen to the suggestion that patients with [[orthostatic hypotension]] should not sleep in a flat bed but should lie in a semi inclined or head-up position <cite>5</cite><cite>6</cite>. Definite symptomatic and objective reversible changes were documented.
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===Psychological stressors===
The beneficial symptomatic and objective effects of postural treatment at night in patients with debilitating [[orthostatic hypotension]] due to autonomic failure were confirmed in several case series <cite>7</cite><cite>8</cite><cite>9</cite>. A consistent finding in these reports is that if a high salt diet or fludrocortisone were added to head-up sleeping the beneficial effects on orthostatic tolerance were enhanced.
Psychological stressors include stirring emotional news or witnessing a distressing accident (Lewis, 1932;Engel et al., 1944), unexpected pain or threat (Lewis, 1932;GREENFIELD, 1951). Unpleasant smells may trigger vasovagal syncope (Engel & Romano, 1947;Ganzeboom et al., 2003). During blood drawing, vaccination (Braun et al., 1997) or instrumentation, pain of the procedure may contribute to vasovagal syncope. Sharp pain is reported to be an important factor during arterial blood sampling (Rushmer, 1944). However, in a patient with blood phobia just thinking or talking about blood drawing may elicit a common faint (van Dijk et al., 2001).  
An excessive fall in cardiac output underlie the impairment in tolerance to standing after a night’s sleep on a flat bed, systemic vascular resistance does not change <cite>10</cite>. Although nocturnal polyuria is a typical feature of patients with autonomic failure the degree of impairment in orthostatic tolerance after a night's sleep cannot be explained only by the nocturnal polyuria. Marked diurnal variation in orthostatic tolerance can also be found in patients with small diurnal differences in body weight. Transcapillary fluid shifts are thought to play an important role in these patients <cite>10</cite><cite>11</cite><cite>12</cite>. Despite this, treatment with the vasopressin analogue desmopressin has been found effective in reducing both nocturnal polyuria and the postural BP fall in the morning <cite>13</cite>. Adding to complexity, confinement to bed did not substantially alter the diurnal BP changes <cite>14</cite>. Thus various factors may play a role in the diurnal BP changes including orthostatic fluid shifts, transcapillary fluid shifts and neurohumoral rhythms causing changes in sodium and water excretion 


==Physiological mechanisms==
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The ''physiological mechanisms'' underlying the beneficial effects of head-up sleeping are a decrease in sodium and water excretion during the night resulting in a better maintained and plasma volume; an increase in body weight of  0.5- 1 kg is reported <cite>6</cite><cite>8</cite><cite>9</cite><cite>10</cite><cite>15</cite> (for review see <cite>16</cite>. The observation that head-up sleeping becomes effec¬tive coinci¬dental with appe¬arance of slight edema of the lower legs <cite>5</cite><cite>6</cite><cite>15</cite>  suggests that head-up induced volume shifts with an increased content of the extracellular fluid volume in the lower extremities play an important mechanistic role. The lower leg edema is thought to result in diminished pooling of venous blood in the legs and thereby in decreasing the excessive fall in stroke volume and cardiac output during a stand-up in the early morning <cite>5</cite><cite>6</cite><cite>15</cite>.    
===Post-exercise vasovagal syncope===
Syncope after exercise is often neurally mediated, i.e. post-exercise vasovagal syncope. This condition is typically diagnosed in young fit, furthermore healthy young patients. Foremost, the diagnostic workup of all patients presenting with exercise-related syncope is aimed at excluding dangerous cardiac conditions and includes echocardiography and exercise testing (Krediet et al., 2004b).
Characteristically, syncope may occur while the individual is standing motionless during the first five to ten minutes after exercise (Bjurstedt et al., 1983). Especially athletes in the (ultra) endurance sports are at risk for post exercise vasovagal syncope e.g. after marathon swimming (Finlay et al., 1995) or marathon running (Tsutsumi & Hara, 1979;Holtzhausen & Noakes, 1995;Holtzhausen & Noakes, 1997).
Vasovagal syncope after routine treadmill testing is rare (estimated 0,2% (Schlesinger, 1973)). However, when treadmill testing is immediately followed by passive head-up tilt testing, this percentage can increase up to 50-70% (Bjurstedt et al., 1983). Vasovagal syncope after exercise is considered to be a benign occurrence (Krediet et al., 2004b).


==Application==
====Muscle pump====
MacLean and Allen accomplished the head-up position by placing the posts of the head of a bed on ordinary kitchen chairs (40-45 cm high) <cite>5</cite><cite>6</cite>. Ten Harkel used a head–up angle of 12 degrees (about 30 cm elevation of the head of the bed) <cite>9</cite>. Sleeping in a sitting position has been applied by Bannister et al. <cite>8</cite> Based on the presumed physiological mechanism discussed above, a steep head-up tilt sleeping position is likely to be the most effective. Gravitational stress is a function of the sine of the angle of tilt and not of the angle itself. Thus a tilt-angle of 5 degrees as used by Fan et al will induce 9% and a tilt-angle of 12 degrees 21% of the full 90 degree orthostatic load. However, a steep tilt-angle is difficult to tolerate by the majority of patients and their partners. We instruct our patients to put the head-end of their bed on 20-30 cm blocks. A hard pillow under the mattress at the level of the thighs has been found useful to prevent sliding down. A footboard is another helpful measure <cite>9</cite>. Head-up tilting also reduces supine hypertension in patients with autonomic failure and also causes an additional gravitationally-induced reduction in cerebral arterial pressure. A 20-25 cm elevation of the head of the bed lowers cerebral arterial pressure by about 15 mmHg <cite>16</cite>.
During exercise, rhythmically contracting skeletal muscles in the lower part of the body reduce the degree of venous pooling by squeezing veins, thereby increasing the venous return of blood to the heart. This phenomenon is known as the ‘muscle pump. The sudden removal of the muscle pump after stopping exercise decreases cardiac preload which, together with a rapid return of vagal tone, may promote vasovagal syncope.


==References==
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<biblio>
===Vasovagal syncope in airliners===
#5 MacLean AR, Allen EV. Orthostatic hypotension and orthostatic tachycardia: treatment with the “head-up” bed. JAMA. 1940;115:2162–2167.
Vasovagal episodes are the most common in-flight medical events, and may affect patients of all ages (Gendreau & DeJohn, 2002). In addition to prolonged motionless sitting, the use of alcohol, anxiety  and mild hypoxia during air travel all may predispose to vasovagal faints (Sutton, 1999). Cabin pressure in commercial aircraft is usually adjusted to the equivalent of an altitude of 1500 to 2500 m above sea level. It appears that hypoxic syncope results from the super-imposed vasodilator effects of hypoxia on the cardiovascular system (Halliwill & Minson, 2005).  
#6 MacLean AR, Allen EV, Magath TB. Orthostatic tachycardia and orthostatic hypotension: defects in the return of venous blood to the heart. Am Heart J 1944;27: 145-163.
 
#7 Corcoran AC, Browning JS, Page IH. Renal hemodynamics in Orthostatic Hypotension: effects of Angiotonin and Head-up Bed. J Am Med Ass 1942:119:793-794.
====Treatment====
#8 pmid=4311254
Patients, who otherwise never experienced a (severe) vasovagal episode may suffer from convulsive syncope during air travel (Wieling et al., 2006). These patients should be advised to have a high salt intake in the days prior to travelling by plane, reducing anti-hypertensive medication –if feasible- and drinking non-alcoholic beverages galore during the trip. Especially during long flights (> 2 hours) they should perform in-chair muscle tensing and relaxing exercise and have a regular walk through the isle. In recurrent cases midodrine prior to flying or supportive stockings can be considered.
#9 pmid=1506810
 
#10 pmid=1961353
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#11 pmid=11724647
===Sleep vasovagal syncope===
#12 pmid=6470562
Sleep vasovagal syncope is defined as loss of consciousness in a non-intoxicated adult occurring during the night (e. g. 10:00 pm to 7:00 am), in which the patient wakes up with pre-syncopal and abdominal symptoms (i.e. an urge to defecate) and losses consciousness in bed or immediately upon standing. There is no tongue biting or post-ictal confusion. There is usually a history of daytime vasovagal syncope and there seems to be a more pronounced fear of blood and medical procedures than in other syncope patients (Jardine et al., 2006b). Physical examination, ECG and EEG are within normal limits. The vasovagal reaction is thought to start while asleep (Krediet et al., 2004a;Jardine et al., 2006a), and continuing after waking up, hence the name. During syncope there may be a profound sinus-bradycardia (Krediet et al., 2004a). Vasovagal sleep syncope occurs at all ages.
#13 pmid=3089519
 
#14 pmid=6872160
====Differential Diagnosis====
#15 pmid=10750642
Sleep vasovagal syncope is diagnosed by excluding beyond reasonable doubt the hereafter mentioned disorders (Jardine et al., 2006a).
#16 pmid=12357277
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Epilepsy is the foremost alternative diagnosis to consider, but can often easily be ruled out on clinical grounds. Complex partial, generalized tonic-clonic and myoclonic epilepsy may occur during sleep and can imitate syncope when causing cause sinus-bradycardia (Tinuper et al., 2001).
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There are a number of related conditions, including “'''abdominal epilepsy'''” and '''Panayiotopoulos syndrome''' (typically with vomiting) (Covanis, 2006), in which the associated clinical features are abdominal pain and confusion.
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Sleep paralysis and hypnogogic hallucinations occur in '''narcolepsy''' but also as isolated phenomena, mostly with other characteristic features in the history (e. g., daytime somnolence, in contrast to syncope there’s no amnesia.) and abnormal polysomnography, which can also be used to diagnose sleep apnoea and night terrors.
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Occasionally cardiac disorders may cause cardiac arrhythmias during sleep. Most of these are unlikely if the 12-lead ECG is normal, and in some patients long-term ambulatory ECG monitoring is required (Brierley et al., 2001).
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Some patients with a diagnosis of defaecation syncope (see below) described abdominal and pre-syncopal symptoms that started simultaneously during sleep (Pathy, 1978;Fisher, 1979); there may be some overlap between this condition and sleep syncope (Jardine et al., 2006a).
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