The mechanism of orthostatic and haemorrhagic fainting

Abstract

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° and 90° 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° NV, four disclosed impending symptoms of fainting, and two fainted in 90° HV. ‘Fainters’ differed from the others by smaller BV in relation to body height, higher HR in 90° NV and lower arterial mean pressure in HV. In the three fainting situations, right ventricular end-diastolic pressure (PRV_CD) was markedly lowered to or below 0 mmHg. Arterial diastolic pressure (Pa_D) was not correlated with P_RVcD, but the pulse pressure decreased with the fall in P_RVcD. In 90° HV, Pa_D 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 at first unchanged then increased P_RVcD 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

Key Words:

• experimental haemorrhage
• orthostasis
• central circulation
• blood volume