The mechanism of orthostatic and haemorrhage fainting.

In order to study the adjustment of central circulation to postural changes and the mechanism of orthostatic fainting, the pressure in the brachial artery, the pulmonary artery, the right ventricle and heart rate (HR) were recorded in sixteen healthy young men, both supine and after tilting to 45 degrees and 90 degrees head up, before (normovolaemic, NV) as well as after (hypovolaemic, HV) withdrawal and reinfusion of (mostly) 950 g blood (about 15% of blood volume, BV). Two subjects fainted in supine HV, two in 90 degrees NV, four disclosed impending symptoms of fainting, and two fainted in 90 degrees HV. 'Fainters' differed from the others by smaller BV in relation to body height, higher HR in 90 degrees NV and lower arterial mean pressure in HV. In the three fainting situations, right ventricular enddiastolic pressure (PRveD) was markedly lowered to or below 0 mmHg. Arterial diastolic pressure (PaD) was not correlated with PRveD, but the pulse pressure decreased with the fall in PRveD. In 90 degrees HV, PaD fell in the six subjects who fainted or disclosed impending symptoms. Irrespective of the situation, the fainting attack involved a sudden decrease of HR and arterial pressure, concomitantly with a first unchanged then increased PRveD and/or pulmonary artery diastolic pressure. A reflex control of the filling volume/pressure of the heart is assumed to precipitate fainting by counteracting the arterial blood pressure regulation.