Also of interest are abnormalities in the response to hypocarbia of patients who are prone to syncope. Norcliffe-Kaufmann and colleagues recorded a greater-than-normal reduction in cerebral blood flow velocity (gauged by transcranial Doppler) and an excessively reduced vascular resistance in the forearm in response to hypocarbia, and the opposite reactions to hypercarbia. They relate the degree of these changes to variations in orthostatic tolerance among patients and suggest that the two aforementioned changes relate to decreased cerebral blood flow that may engender syncope.
This entity, a component or perhaps a subtype of vasodepressor syncope, has received attention as a cause of otherwise unexplained fainting in healthy and athletic children and young adults. As mentioned earlier, it may be the final precipitant in the common vasodepressor faint, and the term is used synonymously with vasovagal or vasodepressor syncope by some authors.
Oberg and Thoren were the first to observe that the left ventricle itself can be the source of neurally mediated syncope in much the same way as the carotid sinus when stimulated, produces vasodilatation and bradycardia. During acute blood loss in cats, they noted a paradoxical bradycardia that was preceded by increased afferent activity in autonomic fibers arising from the ventricles of the heart, a reaction that was eliminated by sectioning these nerves. This concept of the heart as the afferent source of vasodepressor reflexes had been suggested by Bezold, as well as by Jarisch and Zoterman, and came to be known as the Bezold-Jarisch reflex (see Mark). The inferoposterior wall of the left ventricle is the site of most of the subendocardial mechanoreceptors that are responsible for afferent impulses to the nucleus tractus solitarius.
For this mechanism to become active, very vigorous cardiac contractions must occur in the presence of deficient filling of the cardiac chambers (hence “neurocardiogenic”). In the simple faint, an initial burst of sympathetic activity is thought to precipitate physiologic circumstances of excessive cardiac contraction. Echocardiographic findings of a diminished ventricular chamber size and vigorous contractions just prior to syncope support this notion (the “empty-heart syndrome”). The remaining baroreceptors in the aorta may be responsible for the increased afferent activity.
According to Kaufmann, a proclivity to primary neurocardiogenic syncope can be identified by the finding of delayed fainting when the patient is placed at a 60-degree upright position on a tilt table. After approximately 10 min of upright posture, the blood pressure drops below 100 mm Hg; soon thereafter, the patient complains of dizziness and sweating and subsequently faints. In contrast, patients with primary sympathetic failure will faint soon after upward tilting. Half of patients with unexplained syncope display a delayed tilt-table reaction, but it is also seen in 5 percent of controls (see “Tilt-Table Testing” further on). The value of isoproterenol as a cardiac stimulant and peripheral vasodilator to enhance the effect of upright posture and expose neurocardiogenic syncope during the tilt-table test is controversial. The subject has been reviewed by Abboud.