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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.

Psychological stressors

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).

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).

Muscle pump

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.

Vasovagal syncope in airliners

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).

Treatment

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.

Sleep vasovagal syncope

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.

Differential Diagnosis

Sleep vasovagal syncope is diagnosed by excluding beyond reasonable doubt the hereafter mentioned disorders (Jardine et al., 2006a).
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).
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.
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.
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).
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).