Our prior studies indicated that postural fainting relates to splanchnic hypervolemia and thoracic hypovolemia during orthostasis. We hypothesize that thoracic hypovolemia causes excessive sympathetic activation, increased respiratory tidal volume and fainting involving the pulmonary stretch reflex. We studied 18 patients 13 to 21 years old, 11 who fainted within 10 minutes of upright tilt (fainters), and 7 healthy control subjects. We measured continuous blood pressure and heart rate, respiration by inductance plethysmography, end tidal CO₂ (ETCO₂) by capnography, regional blood flows and blood volumes using impedance plethysmography, and calculated arterial resistance supine and during 70° upright tilt. Splanchnic resistance (mmHg/L/Min) decreased until faint in fainters (44 ±8 to 21±2), but increased in control subjects (47±5 to 53±4). Percent change in splanchnic blood volume increased (7.5±1.0 vs. 3.0±11.5, p<0.05) after onset of tilt. Upright tilt initially significantly increased thoracic, pelvic and leg resistance in fainters which subsequently decreased until faint. In fainters but not control subjects, normalized tidal volume (1±0.1 to 2.6±0.2, p<0.05) and normalized minute ventilation increased throughout tilt (1±0.2 to 2.1±0.5, p<0.05) while respiratory rate (breaths/min) decreased (19±1 to 15±1, p<0.05). Maximum tidal volume occurred just before fainting. The increase in minute ventilation was inversely proportionate to the decrease in ETCO₂. Our data suggests that excessive splanchnic pooling and thoracic hypovolemia results in increased peripheral resistance and hyperpnea in simple postural faint. Hyperpnea and pulmonary stretch may contribute to the sympathoinhibition that occurs at the time of faint.