Decrease in cardiac output and muscle sympathetic activity during vasovagal syncope

Abstract

The importance of cardiac output (CO) to blood pressure level during vasovagal syncope is unknown. We measured thermodilution CO, mean blood pressure (MBP), and leg muscle mean sympathetic nerve activity (MSNA) each minute during 60 degrees head-up tilt in 26 patients with recurrent syncope. Eight patients tolerated tilt (TT) for 45 min (mean age 60 +/- 5 yr) and 15 patients developed syncope during tilt (TS) (mean age 58 +/- 4 yr, mean tilt time 15.4 +/- 2 min). In TT patients, CO decreased during the first minute of tilt (from 3.2 +/- 0.2 to 2.5 +/- 0.3 l x min(-1) x m(-2), P = 0.001) and thereafter remained stable between 2.5 +/- 0.3 (P = 0.001) and 2.4 +/- 0.2 l x min(-1) x m(-2) (P = 0.004) at 5 and 45 min, respectively. In TS patients, CO decreased during the first minute (from 3.3 +/- 0.2 to 2.7 +/- 0.1 l x min(-1) x m(-2), P = 0.02) and was stable until 7 min before syncope, falling to 2.0 +/- 0.2 at syncope (P = 0.001). Regression slopes for CO versus time during tilt were -0.01 min(-1) in TT versus -0.1 l x min(-1) x m(-2) x min(-1) in TS (P = 0.001). However, MBP was more closely correlated to total peripheral resistance (R = 0.56, P = 0.001) and MSNA (R = 0.58, P = 0.001) than CO (R = 0.32, P = 0.001). In vasovagal reactions, a progressive decline in CO may contribute to hypotension some minutes before syncope occurs.

Hemodynamics of orthostatic intolerance: implications for gender differences

“…For both men and women, MAP remained relatively stable during progressive LBNP until hemodynamic collapse and prominent hypotension occurred suddenly. There was not a threshold BP that was reached earlier in women, but rather a neurally mediated event, presumably sympathetic withdrawal (20,25,49), that occurred when the heart was markedly unloaded.…”

“…Thus, although not dispositive, the weight of evidence suggests that the absence of any differences between genders in norepinephrine or total peripheral resistance, which is the ultimate downstream determinant of the effect of increasing sympathetic nerve activity, argues against a physiologically meaningful impairment in vasomotor control in women. Numerous investigations have shown that the ultimate precipitant of hypotension and syncope is sympathetic withdrawal and vasodilation (10,24,25,45). Although the exact stimulus that causes this final common pathway is unknown, it has been argued that stimulation of ventricular mechanoreceptors in the setting of a small, hypercontractile heart may be one potential mechanism (26,33,37).…”

“…Ultimately, the individual determinant of fainting is likely to be the vasoconstrictor reserve, or the ability to respond to central hypovolemia with vasoconstriction. For example, Jardine et al (25) reported recently that during the progressive hypotension before syncope, MAP was more closely correlated to total peripheral resistance and muscle sympathetic nerve activity than SV and CO; however, in orthostatic hypotension, progressive declines in SV and CO are the primary stimuli that ultimately lead to neurally mediated syncope.…”

Diagnostic utility of the head-up tilt test in syncope and the related complications

“…[16,17] The temporal sequence of changes in blood pressure and heart rate during tilt induced syncope parallel those seen with spontaneous syncope. [18] Single-stage isoproterenol tilt table test has been found to be more effective in inducing a positive vasovagal response in an adult population than the standard (drug free) passive tilt table test, and it significantly reduced the procedural time. [19] These observations are in agreement with our study.…”

The pathophysiologic mechanisms associated with hypotensive susceptibility

“…Indeed, more than 2 decades ago, VVS was reported in heart transplant recipients and more recently several investigators made the observation that decreases in cardiac output contributed to the hypotension independent of reflex-mediated changes [14,20,39]. Fu et al showed that up to one third of subjects with tilt induced pre-syncope had a severe drop in cardiac output with no change in total peripheral resistance.…”