Abstract
The changes in the two consistent components of epidural pressure (EDP) pulse waves, designated as P1 and P2 waves, and mean velocity of common carotid blood flow (CBFV) were studied in 21 patients with acute intracranial hypertension, to determine the origin of an amplitude change in these components. The dynamics of the intracranial compartment were altered by head elevation, jugular vein compression, hyperventilation, or mannitol administration. The amplitudes of the P2 wave, synchronous with the tidal wave of the blood pressure pulse wave, increased progressively with the rise of EDP. But those of the P1 wave, synchronous with the percussion wave of the blood pressure pulse wave, remained nearly invariable at EDPs more than 20-30 mmHg. This is compatible with the changes of the CBFV during the diastole. Jugular vein compression induced a rapid rise of EDP and a proportionate increase in the magnitudes of both waves. Hyperventilation and mannitol administration caused a disproportionate reduction in the amplitudes of P2 wave with a fall of EDP. But mannitol administration at high EDP (more than 40 mmHg) caused a mild fall of EDP and some increase in the amplitudes of the P2 wave.
These results indicate that the variations in the amplitudes of the P1 wave reflect the changes in vascular resistance of the large intracranial conductive arteries, while those of the P2 wave result from the changes in the volume of the cerebral bulk. The increase of the amplitudes of the P2 wave induced by mannitol at high EDP suggests a defective autoregulation of the cerebral vessels.
