Syncope (Fainting)

Failure to distinguish between causes (underlying disease) and mechanisms (event allowing it to happen) of syncope has lead to confusions of terminology and simplistic conclusions in the past. Many different entities were often discussed- neurocardiogenic syncope, vasovagal syncope, vasodepressor syncope, neurally-mediated syncope, and orthostatic syncope-even though the clinical features were similar or overlapping.

In 1932 Thomas Lewis introduced the term "vasovagal" syncope to stress that both the heart and blood vessels were involved in fainting. The exact mechanisms of vasovagal syncope remained unclear, however. People were often observed to pass out without a preceding change in heart rate. Later it was noted that syncope could be readily elicited in patients with transplanted hearts that lacked cardiac innervation. Vascular regulation was thought to be controlled by two branches of the autonomic nervous system, the so-called sympathetic and parasympathetic systems, which act outside of conscious control. It was accepted that syncope was predominantly due to a sudden imbalance between sympathetic and parasympathetic influences, however, in recent years it has become obvious that mechanisms determining the tone of blood vessels are much more complex.

Very potent substances released by all vessels such as the vasoconstrictor endothelin and the vasodilator NO (nitric oxide) were discovered in recent years. Importantly, some of these substances have been shown to be released by new "autonomic" nerves that are neither sympathetic nor parasympathetic (nonadrenergic-noncholinergic nerves). These and other newly discovered substances and nerves strongly influence the regulation of the sympathetic and parasympathetic systems and could play a pivotal role in the mechanisms provoking sudden drops in blood pressure and loss of consciousness.