AUTONOMIC CONTROL OF VASOVAGAL SYNCOPE

In the pathophysiological study of vasovagal syncope, the nature of th e interaction between baroreceptor sensitivity (BS), sympathetic withd rawal, and parasympathetic activity has yet to be ascertained. Altered BS may predispose toward abnormal sympathetic and parasympathetic res ponses to orthostasis, causing hypotension that may progress to syncop e if there is sympathetic withdrawal. To examine this hypothesis, we m onitored blood pressure (BP), heart rate (HR), BS, forearm blood flow and muscle nerve sympathetic activity (MNSA) continuously in 18 vasova gal patients during 60 degrees head-up tilt, syncope, and recovery. Re sults were compared with those of 17 patients who were able to tolerat e tilt for 45 min. During early tilt, BP was maintained in both groups by an increase in HR and MNSA from baseline (P < 0.01), but BS decrea sed more in the syncopal group (P < 0.05). At the start, of presyncope (mean 2.7 +/- 0.2 min before syncope and 15.2 +/- 12 min after tilt), when BP fell, HR and sympathetic activity remained increased from bas eline (P < 0.01). Thereafter BP and HR correlated directly with sympat hetic activity and regressed in Linear fashion until syncope (P < 0.00 1), whereas BS increased to baseline. At syncope, BP, HR, and sympathe tic activity fell below baseline (P ( 0.01, P < 0.05, and P < 0.01, re spectively), but BS did not increase. During recovery, sympathetic act ivity increased to baseline and BS increased (P < 0.05), whereas HR an d BP remained low (P < 0.01 and P ( 0.05, respectively). The mechanism for the initiation of hypotension during presyncope remains unknown, but BS may contribute. Vasodilatation and bradycardia during presyncop e appear to be more closely related to withdrawal of sympathetic activ ity than to increased parasympathetic cardiac activity.