Fainting syncope, commonly known as fainting

Neurally mediated syncope
Reflex syncope or neurally mediated syncope occurs when blood vessels expand and heart rate decreases inappropriately leading to poor blood flow to the brain.^[1] This may occur from either a triggering event such as exposure to blood, pain, strong feelings, or a specific activity such as urination, vomiting, or coughing.^[1]
Vasovagal syncope
Main article: Vasovagal syncope
Vasovagal (situational) syncope is one of the most common types which may occur in response to any of a variety of triggers, such as scary, embarrassing or uneasy situations, during blood drawing, or moments of sudden unusually high stress.^[3] There are many different syncope syndromes which all fall under the umbrella of vasovagal syncope related by the same central mechanism.^[3] First, the person is usually predisposed to decreased blood pressure by various environmental factors. A lower than expected blood volume, for instance, from taking a low-salt diet in the absence of any salt-retaining tendency. Or heat causing vaso-dilation and worsening the effect of the relatively insufficient blood volume. The next stage is the adrenergic response. If there is underlying fear or anxiety (e.g., social circumstances), or acute fear (e.g., acute threat, needle phobia), the vaso-motor centre demands an increased pumping action by the heart (flight or fight response). This is set in motion via the adrenergic (sympathetic) outflow from the brain, but the heart is unable to meet requirements because of the low blood volume, or decreased return. A feedback response to the medulla is triggered via the afferent vagus nerve. The high (ineffective) sympathetic activity is thereby modulated by vagal (parasympathetic) outflow leading to excessive slowing of heart rate. The abnormality lies in this excessive vagal response causing loss of blood flow to the brain.^[9] The tilt-table test typically evokes the attack. Avoiding what brings on the syncope and possibly greater salt intake is often all that is needed.^[10]
Associated symptoms may be felt in the minutes leading up to a vasovagal episode and are referred to as the prodrome. These consist of light-headedness, confusion, pallor, nausea, salivation, sweating, tachycardia, blurred vision, and sudden urge to defecate among other symptoms.^[9]
Vasovagal syncope can be considered in two forms:

• 
  Isolated episodes of loss of consciousness, unheralded by any warning symptoms for more than a few moments. These tend to occur in the adolescent age group and may be associated with fasting, exercise, abdominal straining, or circumstances promoting vaso-dilation (e.g., heat, alcohol). The subject is invariably upright. The tilt-table test, if performed, is generally negative.
  
• 
  Recurrent syncope with complex associated symptoms. This is neurally mediated syncope (NMS). It is associated with any of the following: preceding or succeeding sleepiness, preceding visual disturbance ("spots before the eyes"), sweating, lightheadedness.^[3] The subject is usually but not always upright. The tilt-table test, if performed, is generally positive. It is relatively uncommon.
  

Syncope has been linked with psychological triggers.^[3] This includes fainting in response to the sight or thought of blood, needles, pain, and other emotionally stressful situations. One theory in evolutionary psychology is that fainting at the sight of blood might have evolved as a form of playing dead which increased survival from attackers and might have slowed blood loss in a primitive environment.^[11] "Blood-injury phobia", as this is called, is experienced by about 15% of people.^[12] It is often possible to manage these symptoms with specific behavioral techniques.
Another evolutionary psychology view is that some forms of fainting are non-verbal signals that developed in response to increased inter-group aggression during the paleolithic. A non-combatant who has fainted signals that she or he is not a threat. This would explain the association between fainting and stimuli such as bloodletting and injuries seen in blood-injection-injury type phobias such as needle phobia as well as the gender differences.
Much of this pathway was discovered in animal experiments by Bezold (Vienna) in the 1860s. In animals, it may represent a defence mechanism when confronted by danger ("playing possum").