Mesenteric blood flow and muscle sympathetic nerve activity during vasovagal syncope

Vasovagal syncope is thought to be mediated by a progressive fall in cardiac output secondary to venous pooling of blood in the splanchnic circulation. How and when this occurs before syncope has not been determined.

A total of 20 patients who became hypotensive during head-up tilt (age 40.9 ± 3.4 years; 10 females) were divided into two groups—the glyceryl trinitrate (GTN) group (n = 12) and the vasovagal syncope (VVS) group (n = 8) – on the basis of whether or not nitroglycerine provocation was required. They were compared with a control group (age 38.6 ± 3.3; 8 females; n = 13). Hemodynamics, including superior mesenteric artery blood flow (SMABF) and muscle sympathetic nerve activity (MSNA) were recorded continuously during early tilt, presyncope and recovery. We used pixel-weighting to calculate average velocity from the pulsed Doppler velocity envelope.

During baseline and early tilt, resistance to mesenteric blood flow was lower in the VVS group: 0.30 ± 0.02 to 0.30 ± 0.02 mmHg/ml/min versus controls 0.30 ± 0.03 to 0.38 ± 0.04 mmHg/ml/min (p = 0.05). During presyncope, as blood pressure and stroke volume gradually fell, SMABF was higher in the VVS group, falling from 370 ± 46 to 248 ± 35 ml/min, versus controls, falling from 342 ± 51 to 233 ± 19 (p = 0.03). At this time, MSNA was lower in the VVS group than controls: 39 ± 4 to 34 ± 3 bursts/min versus 45 ± 2 to 48 ± 3 (p = 0.001).

During presyncope, increased splanchnic blood flow may pool more blood in capacitance vessels resulting in decreased venous return and cardiac output. This may be secondary to decreased vasoconstrictor sympathetic activity.