Stephen E. Epstein1, M Stampfer1, G. DAVID BEISER1
1From the Cardiology Branch, National Heart Institute, Bethesda, Maryland 20014.
Tóm tắt
Withdrawal of sympathetic tone to the veins resulting in peripheral pooling of blood has been suggested as an important factor contributing to the decrease in cardiac output and hence arterial pressure that occurs during vasovagal syncope. However, no measurements of venous tone during syncope have been reported. In the course of other studies on the circulatory effects of negative pressure below the iliac crests, and 80° head-up tilt, vasovagal reactions occurred in 10 subjects. Heart rate, central venous pressure, arterial pressure, forearm blood flow, forearm vascular resistance, and forearm or hand venous tone were measured. The typical vasovagal reaction could be divided into two phases. A gradual fall in arterial pressure signified the onset of phase I, during which forearm vascular resistance did not change significantly. The duration of phase I was highly variable. The onset of phase II was denoted by an abrupt fall in arterial pressure and heart rate and a decrease of 62% in forearm vascular resistance, from 36 to 14 mm Hg/ml/100 g/min. However, venoconstriction rather than venodilatation occurred in the forearm or hand veins. Since central venous pressure did not change prior to or during the onset of the reaction, it is unlikely that venodilatation occurred in other vascular beds. It is concluded that two of the major mechanisms responsible for the hypotension of vasovagal syncope initiated by orthostasis or lower body negative pressure are bradycardia and dilatation of the resistance vessels. In contrast, it appears that the venous bed, by constricting, tends to maintain filling pressure and thereby cardiac output, and thus works in an opposite direction.
