Middle cerebral artery velocity during head-up tilt induced hypovolaemic shock in humans.

Middle cerebral artery mean velocity (Vmean) and pulsatility index (PI) were followed during head-up tilt induced hypovolaemic shock in nine subjects. Mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP) and thoracic (TI) electrical impedance were also recorded. Vmean, PI, and CVP did not change during head-up tilt to 50 degrees, while MAP increased from 92 (81-106) (median and range) to 100 (97-112) mmHg, HR from 63 (53-74) to 84 (68-89) beats min-1 and TI100kHz from 30 (27-36) to 32 (30-39) Ohm (P < 0.01) (n = 8). During maintained tilt, Vmean decreased from 52 (32-72) to 34 (16-59) cm s-1, whereas HR increased to 87 (52-108) beats min-1 and TI100 kHz to 33 (31-39) Ohm (P < 0.01). Presyncopal symptoms appeared after 33 (3-46) min and were associated with a MAP of 65 (32-84) mmHg (P < 0.01) and a HR of 58 (52-71) beats min-1 (P < 0.05). Vmean decreased to 25 (16-36) cm s-1, and cerebral conductance index (Vmean/MAPbrain) and PI increased (P < 0.01). Arterial collapse was observed (diastolic velocity of zero) in one subject at a brain (diastolic) blood pressure of 21 mmHg and he developed tachycardia (131 beats min-1) during presyncope. PaCO2 did not change. Maintained tilt resulted in central volume depletion reflected by changes in MAP, HR, and thoracic electrical impedance but not in CVP. Transcranial Doppler derived indices of cerebral perfusion demonstrated critically low values despite marked increase in conductance index.