Hypotension is considered to be the cause of syncope during lower body negative pressure (LBNP). However, hypocapnia induced by hyperventilation has been observed in subjects preceding syncope, and may contribute to the onset of syncope by reducing cerebral blood flow during orthostatic stress (Morgan et al. 1997). Enhancing the ‘respiratory pump’ may partially attenuate the reduction in venous return that occurs during LBNP (Lipsitz et al. 1998; Novak et al. 1998), but the associated hyperventilation may actually exacerbate orthostatic intolerance. The aims of this study were to examine the effect of plasma volume expansion on tolerance to LBNP, and to consider the role of hypocapnia in the development of syncope.

Following approval by King’s College London Ethics Committee, five subjects volunteered to participate in the study. Subjects performed two LBNP stress tests. LBNP was applied at 10 mmHg increments every 3 min until cessation at pre-syncope, or due to breathing difficulties. Subjects performed one test after ingesting 12 ml/kg body weight of electrolyte fluid (F trial), and one test following no fluid (NF trial). Measurements included change in plasma volume (cyanmethaemoglobin and microhaematocrit values from venous blood samples incorporated into equation by Dill & Costill, 1974), end-tidal PCO₂ (nasal catheter), blood pressure (Finapres), heart rate (ECG). Data presented as means ± S.E.M., and compared using paired t tests.

Following fluid ingestion, plasma volume increased (P < 0.05) by 3.25 %, and time to cessation of LBNP increased (P < 0.05) by 4.28 min (NF: 18.85 ± 1.28 min; F: 23.13 ± 1.81 min). End-tidal PCO₂ (n = 4) did not change from baseline values during mild LBNP up to -20 mmHg (NF: 42.13 ± 0.86; F: 42.23 ± 1.66 mmHg). However, as suction pressure increased to ^–30 mmHg and above, end-tidal PCO₂ fell. Hypocapnia was greater during the NF trial, with a significantly lower (P < 0.05) end-tidal PCO₂ at suction of -50 mmHg (NF: 36.24 ± 1.67; F: 40.9 ± 1.55 mmHg). Mean end-tidal PCO₂ at time of LBNP cessation were similar between trials (NF: 31.70 ± 3.04; F: 33.27 ± 2.35 mmHg).

In conclusion, the smaller reduction in end-tidal PCO₂ during suction following plasma volume expansion was associated with increased tolerance to LBNP. Therefore, hypocapnia may be an important factor that contributes to orthostatic intolerance. However, plasma volume expansion may play an important role in reducing the hypocapnic contribution implicated in syncope during orthostatic stress by perhaps reducing the degree of hyperventilation that often leads to cerebral vasoconstriction.