Orthostatic stress induced by prolonged motionless standing, results in blood ‘pooling’ in dependent regions and may lead to hypotension and syncope. In addition to its hydrostatic effects prolonged orthostasis is often accompanied by hyperventilation, with resulting hypocapnia and it is possible that this may also contribute to the development of syncope. The purpose of this study was to try to evaluate the likely role of hypocapnia in the development of syncope both by its effects on the cerebral circulation and on peripheral vascular resistance.

We studied patients who had been referred for orthostatic stress testing due to suspected attacks of posturally related syncope. Subjects were studied on a combined tilt/lower body suction device to determine orthostatic tolerance as time to presyncope. Patients were categorised as having normal or low orthostatic tolerance by comparison with previous data. We recorded the following: ECG (chest wall leads), finger and brachial arterial blood pressures (Finapres photoplethysmography and oscillometric sphygmomanometer), end-tidal CO₂ (infrared analyser), brachial arterial blood velocity (Doppler) and middle cerebral artery velocity (transcranial Doppler). From changes in brachial and middle cerebral pressures and velocities we calculated changes in vascular resistances. The effects were then determined of changes in end-tidal CO₂ achieved by hypoventilation (aided by added dead-space) and hyperventilation. All data were then compared using Student’s unpaired t tests; values are expressed as means ± S.E.M.

Twenty patients had lower than predicted times to presyncope (16.5 ± 2.0 min) and twelve were normal (32.8 ± 0.8 min). There was no difference in the values of end-tidal CO₂ at the end of the test in the two groups (3.9 ± 0.2 % in early fainters, and 3.7 ± 0.19 % in normals). Changes in end-tidal CO₂ induced opposite changes in vascular resistance in the two regions: a decrease in CO₂ caused cerebral vasoconstriction and forearm vasodilatation. The sensitivities of the two vascular beds to CO₂ were calculated as percentage changes in resistance divided by changes in end-tidal CO₂. In the cerebral circulation, the sensitivities of the two groups of patients were not significantly different (-26.3 ± 2.4 and -22.7 ± 1.8 units, in early fainters and normals, respectively). In the forearm circulation the CO₂ sensitivity was significantly greater in the early fainters (17.8 ± 2.0 and 10.6 ± 2.3 units, P < 0.003).

The results are compatible with the view that hyperventilation and hypocapnia contribute to orthostatic intolerance and that the reason that some patients have a poor tolerance to orthostatic stress may be partly explained by the greater sensitivity of their peripheral circulation, and hence vasodilatation, to a lowering of blood levels of CO₂.

All procedures accord with current local guidelines.