Mechanisms of tilt‐induced vasovagal syncope in healthy volunteers and postural tachycardia syndrome patients without past history of syncope

Upright tilt table testing has been used to test for vasovagal syncope (VVS) but can result in “false positives” in which tilt‐induced fainting (tilt+) occurs in the absence of real‐world fainting. Tilt+ occurs in healthy volunteers and in patients with postural tachycardia syndrome (POTS) and show enhanced susceptibility to orthostatic hypotension. We hypothesized that the mechanisms for hypotensive susceptibility differs between tilt+ healthy volunteers (Control‐Faint (N = 12)), tilt+ POTS patients (POTS‐Faint (N = 12)) and a non‐fainter control group of (Control‐noFaint) (N = 10). Subjects were studied supine and during 70° upright tilt while blood pressure (BP), cardiac output (CO), and systemic vascular resistance (SVR), were measured continuously. Impedance plethysmography estimated regional blood volumes, flows, and vascular resistance. Heart rate was increased while central blood volume was decreased in both Faint groups. CO increased in Control‐Faint because of reduced splanchnic vascular resistance; splanchnic pooling was similar to Control‐noFaint. Splanchnic blood flow in POTS‐Faint decreased and resistance increased similar to Control‐noFaint but splanchnic blood volume was markedly increased. Decreased SVR and splanchnic arterial vasoconstriction is the mechanism for faint in Control‐Faint. Decreased CO caused by enhanced splanchnic pooling is the mechanism for faint in POTS‐Faint. We propose that intrahepatic resistance is increased in POTS‐Faint resulting in pooling and that both intrahepatic resistance and splanchnic arterial vasoconstriction are reduced in Control‐Faint resulting in increased splanchnic blood flow and reduced splanchnic resistance.