The clinical features of cardiac and carotid sinus syncope are in some ways the same as those described above except that the onset may be absolutely abrupt, without any warning symptoms, and is independent of the patient being in an upright posture. The clinical particulars of these and other forms of syncope are described further on.
This term refers to all forms of syncope that result directly from the vascular effects of neural signals coming from the central nervous system. In essence, all the types of syncope in this category are “vasovagal,” meaning a combination of vasodepressor and vagal effects in varying proportions; the only differences are in the stimuli that elicit the reflex response.
A number of stimuli, mostly from the viscera but some of psychologic or emotional origin, are capable of eliciting this response, which consists of a reduction or loss of sympathetic vascular tone coupled with a heightened vagal activity. The nucleus of the tractus solitarius (NTS) in the medulla integrates these afferent stimuli and normal baroreceptor signals with the efferent sympathetic mechanisms that maintain vascular tone (see further on and Chap. 25).
Several lines of study suggest that there are disturbances of both sympathetic control of vascular tone and also of the responsiveness of baroreceptors in neurogenic syncope, but the precise mechanisms are unclear. By the use of microneurography, Wallin and Sundlof have demonstrated an increase in sympathetic outflow in peripheral nerves just prior to syncope, as would be expected; however, this activity then ceases at the onset of fainting. Unmyelinated (postganglionic sympathetic) fibers cease firing during vasovagal fainting at a point when the blood pressure falls below 80/40 mm Hg and the pulse, below 60. This would signify that there is an initial attempt to compensate for the falling blood pressure, following which there is a centrally mediated withdrawal of sympathetic activity. Which one of these mechanisms (perhaps both) is responsible for syncope is not clear. More recently, Bechir and colleagues showed that muscle sympathetic activity as assessed using microneurography is increased in the resting state in patients with orthostatic hypotension and, importantly, does not increase further with venous pooling (induced by lower-body negative pressure). Moreover, in the same patients, the response of the cardiac baroreceptors to pooling was significantly diminished. These data are only partially in agreement with those of Wallin and Sundlof, and they are not in accord with an initial increase in sympathetic activity prior to syncope.
There is agreement that peripheral vascular resistance is greatly reduced just prior to and at the onset of fainting. This drop in resistance has been attributed to an initial adrenergic discharge that, at high levels, causes a vasodilatation (rather than constriction) in intramuscular blood vessels. High levels of epinephrine and the vasodilating effects of nitric oxide acting on vascular endothelium, as well as greatly augmented levels of circulating acetylcholine during syncope, also have been invoked as additional or intermediary factors, but all remain speculative. In the current view, the drop in blood pressure is the result of a transient but excessive activity of sympathetic nerves that paradoxically leads to vascular dilatation in muscle and viscera from an imbalance between β-adrenergic and α-adrenergic activity peripherally.
It has been further suggested, on the basis of reasonable physiologic evidence, that the early sympathotonic attempt to maintain blood pressure leads to overly vigorous contractions of the cardiac chambers and that this, in turn, acts as the afferent stimulus for withdrawal of sympathetic tone in common fainting (see “Neurocardiogenic Syncope,” later).