Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes. The nucleus tractus solitarii 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:

1. On one end of the spectrum is the cardioinhibitory response, characterized by a drop in heart rate (negative chronotropic effect) and in contractility (negative inotropic effect) leading to a decrease in cardiac output that is significant enough to result in a loss of consciousness. It is thought that this response results primarily from enhancement in parasympathetic tone.

2. On the other end of the spectrum is the vasodepressor response, caused by a drop in blood pressure (to as low as 80/20) without much change in heart rate. This phenomenon occurs due to dilation of the blood vessels, probably as a result of withdrawal of sympathetic nervous system tone.

3. 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.

Vasovagal syncope may be an evolution response, specifically the fight-or-flight response.

Pressing upon a certain spot in the neck. This may happen when wearing a tight collar, shaving, or turning the head.

POTS has a favorable prognosis when managed appropriately. Symptoms improve within five years of diagnosis for many patients, and 60% return to their original level of functioning. About 90% of people with POTS respond to a combination of pharmacological and physical treatments. Those who develop POTS in their early to mid teens during a period of rapid growth will most likely see complete symptom resolution in two to five years. Outcomes are more guarded for adults newly diagnosed with POTS. Some people do not recover, and a few even worsen with time. The hyperadrenergic type of POTS typically requires continuous therapy. If POTS is caused by another condition, outcomes depend on the prognosis of the underlying disorder.

The prevalence of POTS is unknown. One study estimated a minimal rate of 170 POTS cases per 100,000 individuals, but the true prevalence is likely higher due to underdiagnosis. Another study estimated that there were between 500,000 and 3,000,000 cases in the United States. POTS is more common in women, with a female-to-male ratio of 5:1. Most people with POTS are aged between 20 and 40, with an average onset of 30. Diagnoses of POTS beyond age 40 are rare, perhaps because symptoms improve with age.

Low blood pressure can be caused by low blood volume, hormonal changes, widening of blood vessels, medicine side effects, anemia, heart problems or endocrine problems.

Reduced blood volume, hypovolemia, is the most common cause of hypotension. This can result from hemorrhage; insufficient fluid intake, as in starvation; or excessive fluid losses from diarrhea or vomiting. Hypovolemia is often induced by excessive use of diuretics. Low blood pressure may also be attributed to heat stroke. The body may have enough fluid but does not retain electrolytes. Absence of perspiration, light headedness and dark coloured urine are also indicators.

Other medications can produce hypotension by different mechanisms. Chronic use of alpha blockers or beta blockers can lead to hypotension. Beta blockers can cause hypotension both by slowing the heart rate and by decreasing the pumping ability of the heart muscle.

Decreased cardiac output despite normal blood volume, due to severe congestive heart failure, large myocardial infarction, heart valve problems, or extremely low heart rate (bradycardia), often produces hypotension and can rapidly progress to cardiogenic shock. Arrhythmias often result in hypotension by this mechanism.

Some heart conditions can lead to low blood pressure, including extremely low heart rate (bradycardia), heart valve problems, heart attack and heart failure. These conditions may cause low blood pressure because they prevent the body from being able to circulate enough blood.

Excessive vasodilation, or insufficient constriction of the resistance blood vessels (mostly arterioles), causes hypotension. This can be due to decreased sympathetic nervous system output or to increased parasympathetic activity occurring as a consequence of injury to the brain or spinal cord or of dysautonomia, an intrinsic abnormality in autonomic system functioning. Excessive vasodilation can also result from sepsis, acidosis, or medications, such as nitrate preparations, calcium channel blockers, or AT1 receptor antagonists (Angiotensin II acts on AT1 receptors). Many anesthetic agents and techniques, including spinal anesthesia and most inhalational agents, produce significant vasodilation.

Meditation, yoga, or other mental-physiological disciplines may reduce hypotensive effects.

Lower blood pressure is a side effect of certain herbal medicines, which can also interact with hypotensive medications. An example is the theobromine in "Theobroma cacao", which lowers blood pressure through its actions as both a vasodilator and a diuretic, and has been used to treat high blood pressure.

Hypotension is low blood pressure, especially in the arteries of the systemic circulation. Blood pressure is the force of blood pushing against the walls of the arteries as the heart pumps out blood. A systolic blood pressure of less than 90 millimeters of mercury (mm Hg) or diastolic of less than 60 mm Hg is generally considered to be hypotension. However, in practice, blood pressure is considered too low only if noticeable symptoms are present.

Hypotension is the opposite of hypertension, which is high blood pressure. It is best understood as a physiological state, rather than a disease. Severely low blood pressure can deprive the brain and other vital organs of oxygen and nutrients, leading to a life-threatening condition called shock.

For some people who exercise and are in top physical condition, low blood pressure is a sign of good health and fitness.

For many people, excessively low blood pressure can cause dizziness and fainting or indicate serious heart, endocrine or neurological disorders.

Treatment of hypotension may include the use of intravenous fluids or vasopressors. When using vasopressors, trying to achieve a mean arterial pressure (MAP) of greater than 70 mmHg does not appear to result in better outcomes than trying to achieve a MAP of greater than 65 mm Hg in adults.

Postpartum chills is a physiological response that occurs within two hours of childbirth. It appears as uncontrollable shivering that is not under voluntary control. It is seen in many women after delivery and can be unpleasant. It lasts for a short time. It is thought to be a result of a nervous system response. It may also be related to fluid shifts and the actual strenuous work of labor. It is considered a normal response and there is no accompanying fever. If a fever does develop further assessments may reveal the presence of an infection. Treatment consists of an explanation from clinicians that the shivering is a normal response and that it only lasts for a short time. Warm blankets are given to the women and fluid replacement is encouraged. It has been described as a fairly common and normal occurrence.

After discharge to home with the baby, chills that accompany uncontrolled bleeding, shortness of breath, cold clammy skin, dizziness, heart pain, and racing heart can be a sign of shock that needs immediate medical attention. Mastitis can also cause shivering.

Exercise hypertension is an excessive rise in blood pressure during exercise. Many of those with exercise hypertension have spikes in systolic pressure to 250 mmHg or greater.

A rise in systolic blood pressure to over 200 mmHg when exercising at 100 W is pathological and a rise in pressure over 220 mmHg needs to be controlled by the appropriate drugs.

Similarly, in healthy individuals the response of the diastolic pressure to 'dynamic' exercise (e.g. walking, running or jogging) of moderate intensity is to remain constant or to fall slightly (due to the improved blood flow), but in some individuals a rise of 10 mmHg or greater is found.

Recent work at Johns Hopkins involving a group of athletes aged 55 to 75 with mild hypertension has found a correlation of those with exercise hypertension to a reduced ability of the major blood vessels to change in size in response to increased blood flow (probably due to impaired function of the endothelial cells in the vessel walls). This is to be differentiated from stiffness of the blood-vessel walls, which was not found to be correlated with the effect.

Septic shock is a serious medical condition that occurs when sepsis, which is organ injury or damage in response to infection, leads to dangerously low blood pressure and abnormalities in cellular metabolism.

The primary infection is most commonly caused by bacteria, but also may be by fungi, viruses or parasites. It may be located in any part of the body, but most commonly in the lungs, brain, urinary tract, skin or abdominal organs. It can cause multiple organ dysfunction syndrome (formerly known as multiple organ failure) and death.

Frequently, people with septic shock are cared for in intensive care units. It most commonly affects children, immunocompromised individuals, and the elderly, as their immune systems cannot deal with infection so effectively as those of healthy adults. The mortality rate from septic shock is approximately 25–50%.

Septic shock is a subclass of distributive shock, a condition in which abnormal distribution of blood flow in the smallest blood vessels results in inadequate blood supply to the body tissues, resulting in ischemia and organ dysfunction. Septic shock refers specifically to distributive shock due to sepsis as a result of infection.

Septic shock may be defined as sepsis-induced low blood pressure that persists despite treatment with intravenous fluids. Low blood pressure reduces tissue perfusion pressure, causing the tissue hypoxia that is characteristic of shock. Cytokines released in a large scale inflammatory response result in massive vasodilation, increased capillary permeability, decreased systemic vascular resistance, and low blood pressure. Finally, in an attempt to offset decreased blood pressure, ventricular dilatation and myocardial dysfunction occur.

Septic shock may be regarded as a stage of SIRS (Systemic Inflammatory Response Syndrome), in which sepsis, severe sepsis and multiple organ dysfunction syndrome (MODS) represent different stages of a pathophysiological process. If an organism cannot cope with an infection, it may lead to a systemic response - sepsis, which may further progress to severe sepsis, septic shock, organ failure, and eventually, result in death.

Resistive fear of needles occurs when the underlying fear involves not simply needles or injections but also being controlled or restrained. It typically stems from repressive upbringing or poor handling of prior needle procedures i.e. with forced physical or emotional restraint.

This form of needle phobia affects around 20% of those afflicted. Symptoms include combativeness, high heart rate coupled with extremely high blood pressure, violent resistance, avoidance and flight. The suggested treatment is psychotherapy, teaching the patient self-injection techniques or finding a trusted health care provider.

Hyperalgesic fear of needles is another form that does not have as much to do with fear of the actual needle. Patients with this form have an inherited hypersensitivity to pain, or hyperalgesia. To them, the pain of an injection is unbearably great and many cannot understand how anyone can tolerate such procedures.

This form of fear of needles affects around 10% of needle phobes. The symptoms include extreme explained anxiety, and elevated blood pressure and heart rate at the immediate point of needle penetration or seconds before. The recommended forms of treatment include some form of anesthesia, either topical or general.

BII phobia is one of the more common psychiatric disorders, affecting about 3 to 4% of the general population, and in about 80% of the BII phobia cases, the patient experiences syncope or presyncope. After a random survey was completed in Aligarh, India, with 1648 male and 1613 female, it was found that a significantly higher percentage of females compared to males had BII phobia; 23.36% of females were diagnosed with BII phobia while only 11.19% of males were diagnosed. Females also fainted more often than males, at 64.09% compared to a male rate of 39.4%.

Furthermore, only 5.3% of BII phobia patients reported to have visited the hospital once or twice for consultation about BII phobia, however, without engaging in any kind of treatment.

Another study, involving participants from all 50 states and the District of Columbia, ages 65 years and older, found that a total of 386 participants disclosed having BII Phobia throughout their whole lifetime, 90% of those cases consisted of patients dealing with BII Phobia as well as other lifetime fears.

Acute stress reaction (also called acute stress disorder, psychological shock, mental shock, or simply shock) is a psychological condition arising in response to a terrifying or traumatic event, or witnessing a traumatic event that induces a strong emotional response within the individual. It should not be confused with the unrelated circulatory condition of shock/hypoperfusion. Acute stress reaction (ASR) may develop into delayed stress reaction (better known as PTSD) if stress is not correctly managed. ASR is characterized by re-living and avoiding reminders of an aversive event, as well as generalized hypervigilance after initial exposure to a traumatic event. ASD is differentiated from PTSD as a disorder that precedes it, and if symptoms last for more than one month, it will develop into PTSD. It can thus be thought of as the acute phase of PTSD.

Antidepressant treatment tachyphylaxis (ADT tachyphylaxis), also known as Prozac poop-out, is a medical condition in which progressive or acute tolerance effects are seen following chronic administration of a drug. ADT tachyphylaxis specifically refers to a sudden decrease in response to selective serotonin reuptake inhibitors (SSRIs), which are the most commonly prescribed antidepressants. Although less commonly prescribed as antidepressants (having lost popularity following the introduction of SSRIs), monoamine oxidase inhibitors, or MAOIs, have also incurred a "poop-out" effect among depressed patients.

Patients affected by ADT tachyphylaxis experience a noticeably sudden progressive decrease in response to SSRIs. The reported rates of this condition vary from 9% to 33% of SSRI users, and the majority of those affected are less responsive to subsequent treatments. In most observational studies, these individuals suffer a recurrence or relapse of depression without changing the previously effective dose.

ADT tachyphylaxis incorporates drug sensitivity as a potential causal factor for the decreased response. However, tolerance provides a more accurate explanation. While the exact cause of ADT tachyphylaxis in individual cases is unknown, drug tolerance is a more comprehensive model, as it includes mechanisms of pharmacodynamic tolerance, metabolic tolerance, and others.

The cause of BII phobia is not well known. Some studies show that specific genes make one more vulnerable to the phobia. Other studies suggest that just like any other phobia, BII phobia could be caused by a traumatic experience (Chapman). It has been proved that social stress amplifies BII symptoms, however, it is not a main cause.

Allodynia (Ancient Greek "" "állos" "other" and "" "odúnē" "pain") refers to central pain sensitization (increased response of neurons) following normally non-painful, often repetitive, stimulation. Allodynia can lead to the triggering of a pain response from stimuli which do not normally provoke pain. Temperature or physical stimuli can provoke allodynia, which may feel like a burning sensation, and it often occurs after injury to a site. Allodynia is different from hyperalgesia, an extreme, exaggerated reaction to a stimulus which is normally painful.

Lethargy is a state of tiredness, weariness, fatigue, or lack of energy. It can be accompanied by depression, decreased motivation, or apathy. Lethargy can be a normal response to inadequate sleep, overexertion, overworking, stress, lack of exercise, improper nutrition, boredom, or a symptom of a disorder. It may also be a side-effect of medication or caused by an interaction between medications or medication(s) and alcohol. When part of a normal response, lethargy often resolves with rest, adequate sleep, decreased stress, physical exercise and good nutrition.

When someone starts to feel the sensation of being scared or nervous they start to experience anxiety. According to a Harvard Mental Health Letter, "Anxiety usually has physical symptoms that may include a racing heart, a dry mouth, a shaky voice, blushing, trembling, sweating, lightheadedness, and nausea". It triggers the body to activate its sympathetic nervous system. This process takes place when the body releases adrenaline into the blood stream causing a chain of reactions to occur. This bodily response is known as the "fight or flight" syndrome, a naturally occurring process in the body done to protect itself from harm. "The neck muscles contract, bringing the head down and shoulders up, while the back muscles draw the spine into a curve. This, in turn, pushes the pelvis forward and pulls the genitals up, slumping the body into a classic fetal position".

In trying to resist this position, the body will begin to shake in places such as the legs and hands. Several other things happen besides this. Muscles in the body contract, causing them to be tense and ready to attack. Second, "blood vessels in the extremities constrict". This can leave a person with the feeling of cold fingers, toes, nose, and ears. Constricted blood vessels also gives the body extra blood flow to the vital organs.

In addition, those experiencing stage fright will have an increase in blood pressure, which supplies the body with more nutrients and oxygen in response to the "fight or flight" instincts. This, in return, causes the body to overheat and sweat. Breathing will increase so that the body can obtain the desired amount of oxygen for the muscles and organs. Pupils will dilate giving someone the inability to view any notes they have in close proximity; however, long range vision is improved making the speaker more aware of their audience's facial expressions and nonverbal cues in response to the speaker's performance. Lastly, the digestive system shuts down to prepare for producing energy for an immediate emergency response. This can leave the body with the effects of dry mouth, nausea, or butterflies.

Blood phobia is often caused by direct or vicarious trauma in childhood or adolescence. Though some have suggested a possible genetic link, a study of twins suggests that social learning and traumatic events, rather than genetics, is of greater significance.

The inclusion of “blood-injury phobia” within the category of specific or simple phobias in classificatory systems reflects a perception that fear has a primary role in the disorder. Consistent with this assumption, blood-injury phobia appears to share a common etiology with other phobias. Kendler, Neale, Kessler, Heath, and Eaves (1992) have argued from data comparing monozygotic with dizygotic twins that the genetic factor common to all phobias (agoraphobia, social phobia, and specific phobias), strongly predisposes a person to specific phobias.

The recognition of an inherited vulnerability common to all phobias is consistent with the notion that elevated trait anxiety predisposes one to anxiety disorders. Trait anxiety provides a background of affective arousal that permits a more rapid activation of the fight or flight response. With respect to specific activating events, conditioning is one way that stimuli become able to elicit anxiety (Rachman, 1991).

Accordingly, painful experiences can condition fear to blood-injury stimuli. Investigators typically classify around 60% of self-reported onsets of blood-injury phobia as beginning with conditioning experiences (Ost, 1991; Ost,

1992; Ost & Hugdahl, 1985; Thyer et al., 1985). However, examinations of available case-by-case verbal summaries call into question the conclusion that conditioning episodes are as prevalent as reported (see Mattick, Page, & Lampe, in press). For example, Thyer et al. (1985) identified a conditioning episode when a “patient received an injection at age 13 and fainted” (p. 455), and in another person when ‘at age six she heard her elementary school teacher give a talk on the circulatory system. This frightened the patient to the

point of syncope” (Thyer et al., 1988.)

Although this hypothesis is well known among clinicians and individuals with diabetes, there is little scientific evidence to support it. Clinical studies indicate that a high fasting glucose in the morning is more likely because the insulin given on the previous evening fails to last long enough. Studies from 2007 onwards using continuous glucose monitoring show that a high glucose in the morning is not preceded by a low glucose during the night. Furthermore, many individuals with hypoglycemic episodes during the night don't wake due to a failure of release of epinephrine during nocturnal hypoglycemia. Thus, Somogyi's theory is not assured and may be refuted.

Allodynia is a clinical feature of many painful conditions, such as neuropathies, complex regional pain syndrome, postherpetic neuralgia, fibromyalgia, and migraine. Allodynia may also be caused by some populations of stem cells used to treat nerve damage including spinal cord injury. Static mechanical allodynia is a paradoxical painful hypoaesthesia, one etiology of which is lesions of A-beta fibers.

Tachyphylaxis is characterized by the rate sensitivity: the response of the system depends on the rate with which a stimulus is presented. To be specific, a high-intensity prolonged stimulus or often-repeated stimulus may bring about a diminished response also known as desensitization.

Chronic Somogyi rebound is a contested explanation of phenomena of elevated blood sugars in the morning. Also called the Somogyi effect and posthypoglycemic hyperglycemia, it is a rebounding high blood sugar that is a response to low blood sugar. When managing the blood glucose level with insulin injections, this effect is counter-intuitive to insulin users who experience high blood sugar in the morning as a result of an overabundance of insulin at night.

This theoretical phenomenon was named after Michael Somogyi, a Hungarian-born professor of biochemistry at the Washington University and Jewish Hospital of St. Louis, who prepared the first insulin treatment given to a child with diabetes in the USA in October 1922. Somogyi showed that excessive insulin makes diabetes unstable and first published his findings in 1938.

Compare with the dawn phenomenon, which is a morning rise in blood sugar in response to waning insulin and a growth hormone surge (that further antagonizes insulin).