If the person does not fall into a fully flat, supine position, and the head remains elevated above the trunk, a state similar to a seizure may result from the bloods inability to return quickly to the brain, and the neurons in the body will fire off and generally cause muscles to twitch very slightly but mostly remain very tense.The autonomic nervous systems physiological state (see below) leading to loss of consciousness may persist for several minutes, so

If patients try to sit or stand when they wake up, they may pass out again
The person may be nauseated, pale, and sweaty for several minutes or hours

Causes
Reflex syncope occurs in response to a trigger due to dysfunction of the heart rate and blood pressure regulating mechanism. When heart rate slows or blood pressure drops, the resulting lack of blood to the brain causes fainting. Vasovagal
Typical triggers include:

Prolonged standing
Emotional stress
Pain
The sight of blood
Fear of needles
Time varying magnetic field (i.e. transcranial magnetic stimulation)

Situational
After or during urination (micturition syncope)
Straining, such as to have a bowel movement
Coughing
Swallowing
Lifting a heavy weight

Carotid sinus
Pressing upon a certain spot in the neck. This may happen when wearing a tight collar, shaving, or turning the head. Pathophysiology
Regardless of the trigger, the mechanism of syncope is similar in the various vasovagal syncope syndromes.
Pharmacokinetics
Absorption
Doxepin is well-absorbed from the gastrointestinal tract but between 55 and 87% undergoes first-pass metabolism in the liver, resulting in a mean oral bioavailability of approximately 29%. Following a single very low dose of 6 mg, peak plasma levels of doxepin are 0.854 ng/mL (3.06 nmol/L) at 3 hours without food and 0.951 ng/mL (3.40 nmol/L) at 6 hours with food. Plasma concentrations of doxepin with antidepressant doses are far greater, ranging between 50 and 250 ng/mL (180 to 900 nmol/L). Area-under-curve levels of the drug are increased significantly when it is taken with food. Distribution
Doxepin is widely distributed throughout the body and is approximately 80% plasma protein-bound, specifically to albumin and α1-acid glycoprotein. Metabolism
Doxepin is extensively metabolized by the liver via oxidation and N-demethylation. Its metabolism is highly stereoselective. Based on in vitro research, the major enzymes involved in the metabolism of doxepin are the cytochrome P450 enzymes CYP2D6 and CYP2C19, with CYP1A2, CYP2C9, and CYP3A4 also involved to a lesser extent. The major active metabolite of doxepin, nordoxepin, is formed mainly by CYP2C19 (>50% contribution), while CYP1A2 and CYP2C9 are involved to a lesser extent, and CYP2D6 and CYP3A4 are not involved. Both doxepin and nordoxepin are hydroxylated mainly by CYP2D6, and both doxepin and nordoxepin are also transformed into glucuronide conjugates. The elimination half-life of doxepin is about 15–18 hours, whereas that of nordoxepin is around 28–31 hours.