An experimental study of cerebrovascular resistance, pressure transmission, and craniospinal compliance.
To successfully match the treatment to the cause for raised intracranial pressure (ICP) after a severe head injury, it is important to know the underlying mechanism at a given moment for the raised pressure. In particular, it is important to distinguish between active cerebral vasodilation, indicating functional autoregulation, and a passive vascular dilation as the cause for raised ICP. An experimental study was performed in feline models of diffusely raised ICP (n = 6), of active arterial vasodilation caused by arterial hypercarbia (n = 6), and of passive arterial dilation caused by pharmacologically induced arterial hypertension (n = 6) to determine if wave form analysis of ICP can distinguish active from passive arteriolar vasodilation. Pulsatile pressure transmission from the blood pressure pulse to the ICP pulse (cerebrovascular pressure transmission [CVPT]), cerebrovascular resistance, and craniospinal compliance were measured simultaneously at each level of raised ICP, arterial hypercarbia, and arterial hypertension. Arterial hypercarbia, caused by both 5 and 10% inspired CO2 increased low-frequency CVPT, which was followed by an increasingly negative phase shift between the blood pressure and ICP wave form (P < 0.05). Diffusely raised ICP caused by intraventricular infusion of mock cerebrospinal fluid caused increased low-frequency CVPT (P < 0.01) but resulted in no overall change in phase shift, although the sign of the phase shift remained negative. After arterial hypertension, caused by the infusion of angiotensin II, where there was loss of myogenic tone, an increased low-frequency CVPT was accompanied by a positive phase shift (P < 0.01). These data demonstrate it may be possible to distinguish active arteriolar vasodilation from a passive loss of autoregulatory vascular tone through simultaneous measurement of the low-frequency CVPT and phase shift. Analysis of the ICP wave form provides information relevant to the management of raised ICP.
Piper
I R
IR
Department of Clinical Neurosciences, University of Edinburgh, Scotland.
Chan
K H
KH
Whittle
I R
IR
Miller
J D
JD
D000818:Animals; D001921:Brain / Q000098:blood supply* / Q000503:physiopathology; D001925:Brain Damage, Chronic / Q000503:physiopathology; D002245:Carbon Dioxide / Q000097:blood; D002415:Cats; D015170:Cerebrospinal Fluid Pressure / Q000502:physiology; D003187:Compliance; D006706:Homeostasis / Q000502:physiology*; D006973:Hypertension / Q000503:physiopathology; D007427:Intracranial Pressure / Q000502:physiology*; D011559:Pseudotumor Cerebri / Q000503:physiopathology*; D013116:Spinal Cord / Q000503:physiopathology*; D014655:Vascular Resistance / Q000502:physiology*
D002245:Carbon Dioxide