Vasovagal syncope is the most common type of syncope (fainting). There are a number of different syncope syndromes which all fall under the umbrella of vasovagal syncope. The common element among these conditions is the central mechanism leading to loss of consciousness. The differences among them are in the factors which trigger this mechanism.
abdominal straining or 'bearing down' (as in defecation)
random onsets due to nerve malfunctions
Pressing upon certain places on the throat, sinuses, and eyes.
People with vasovagal syncope typically have recurrent episodes, usually when exposed to a specific trigger. The initial episode often occurs when the person is a teenager, then recurs in clusters throughout his or her life. Prior to losing consciousness, the individual frequently experiences a prodrome of symptoms such as lightheadedness, nausea, sweating, ringing in the ears, and visual disturbances. These last for at least a few seconds before consciousness is lost, which typically happens when the person is sitting up or standing. When they pass out, they fall down; and when in this position, effective blood flow to the brain is immediately restored, allowing the person to wake up.
The autonomic nervous system's physiologic state (see below) leading to loss of consciousness may persist for several minutes, so:
if the person tries to sit or stand when they wake up, they may pass out again; and
the person may be nauseated, pale, and sweaty for several minutes after they wake up.
Pathophysiology and mechanism
Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. In it, the nucleus tractus solitarius of the brainstem is activated directly or indirectly by the triggering stimulus, resulting in simultaneous enhancement of parasympathetic nervous system (vagal) tone and withdrawal of sympathetic nervous system tone.
This results in a spectrum of hemodynamic responses:
On one end of the spectrum is the cardioinhibitory response, characterized by a drop in heart rate. The drop in heart rate leads to a drop in blood pressure that is significant enough to result in a loss of consciousness. It is thought that this response results primarily from enhancement in parasympathetic tone.
On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure without much change in heart rate. This phenomenon occurs due to vasodilation, probably as a result of withdrawal of sympathetic nervous system tone.
The majority of people with vasovagal syncope have a mixed response somewhere between these two ends of the spectrum.
One account for these physiological responses is the Bezold-Jarisch Reflex. This reflex involves a variety of cardiovascular and neurological processes, which can be summarized as follows: Prolonged upright posture results in some degree of pooling of blood in the lower extremities that can lead to diminished intracardiac volume. This phenomenon is accentuated if the individual is dehydrated. The resultant arterial hypotension is sensed in the carotid body baroreceptors, and afferent fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility. However, pressure receptors in the wall and trabeculae of the underfilled left ventricle may then sense stimuli, indicating high-pressure C-fiber afferent nerves from these receptors. They may respond by sending signals that trigger paradoxical bradycardia and decreased contractility, resulting in additional and relatively sudden arterial hypotension. 
In addition to the mechanism described above, a number of other medical conditions may cause syncope. Making the correct diagnosis for loss of consciousness is one of the most difficult challenges that a physician can face. The core of the diagnosis of vasovagal syncope rests upon a clear description by the patient of a typical pattern of triggers, symptoms, and time course.
Also is pertinent to differentiate lightheadedness, vertigo and hypoglycemia as other causes
In patients with recurrent syncope, diagnostic accuracy can often be improved with one of the following diagnostic tests:
Vasovagal syncope is rarely life-threatening in itself, but may be associated with injury from falling. It may also be associated with certain psychiactric disorders.
Treatment for vasovagal syncope focuses on avoidance of triggers, restoring blood flow to the brain during an impending episode, and measures which interrupt or prevent the pathophysiologic mechanism described above.
The cornerstone of treatment is avoidance of triggers known to cause syncope in that person. Before known triggering events, the patient may increase consumption of salt and fluids to increase blood volume. Sports and energy drinks may be particularly helpful.
Discontinuation of medications known to lower blood pressure may be helpful, but stopping antihypertensive drugs can also be dangerous. This process should be managed by an expert.
Patients should be educated on how to respond to further episodes of syncope, especially if they experience prodromal warning signs: They should lie down and raise their legs; or at least lower their head to increase blood flow to the brain. If the individual has lost consciousness, he or she should be laid down with his or her head turned to the side. Tight clothing should be loosened. If the inciting factor is known, it should be removed if possible (for instance, the cause of pain).
Wearing graded compression stockings may be helpful.
There are certain orthostatic training exercises which have been proven to improve symptoms in people with recurrent vasovagal syncope.
Certain medications may be helpful, but are rarely effective by themselves:
Beta blockers (β-adrenergic antagonists) are the most common medication given. However, in several recent controlled randomized trials they were not effective.
Other medications which may be effective include fludrocortisone, midodrine, SSRIs such as paroxetine or sertraline, disopyramide, and, in healthcare settings where a syncope is anticipated, atropine.
For people with the cardioinhibitory form of vasovagal syncope, implantation of a permanent pacemaker may be beneficial or even curative.
^ Sheldon R, Connolly S, Rose S, Klingenheben T, Krahn A, Morillo C, Talajic M, Ku T, Fouad-Tarazi F, Ritchie D, Koshman ML; Circulation. Prevention of Syncope Trial (POST): a randomized, placebo-controlled study of metoprolol in the prevention of vasovagal syncope. 2006 Mar 7;113(9):1164-70.
^ Madrid AH, Ortega J, Rebollo JG, Manzano JG, Segovia JG, Sánchez A, Peña G, Moro C. Lack of efficacy of atenolol for the prevention of neurally mediated syncope in a highly symptomatic population: a prospective, double-blind, randomized and placebo-controlled study. J Am Coll Cardiol. 2001 Feb;37(2):554-9.
Daroff, Robert B. & Carlson, Mark D. (2001). Faintness, Syncope, Dizziness, and Vertigo. In Eugene Braunwald, Anthony S. Fauci, Dennis L. Kasper, Stephen L. Hauser, Dan L. Longo, & J. Larry Jameson (Eds.), Harrison's Principles of Internal Medicine (15th Edition), pp. 111–115. New York: McGraw-Hill these can stand to be attributed with other sources as well.