Cerebrovascular pressure transmission: Changes in highest modal frequency induced by vasodilation

Introduction

The ultimate goal of this work is to continuously assess cerebrovascular autoregulation of patients with brain injury to permit improved intensive care management and therapy. To accomplish this goal we have been exploring system identification modeling techniques that could be applied to arterial blood pressure (ABP) and intracranial pressure (ICP) recordings typically available in intensive care settings. Our numerical modeling approach has been to use a Windkessel model to define the mathematical structure of cerebrovascular pressure transmission of ABP to ICP. Given this mathematical structure an analytical description of cerebrovascular pressure transmission is constructed for the segment of time defined by each recording interval. Just as the modal frequencies, critical vibration modes, of a tuning fork reflect its structural properties; the modal frequencies of cerebrovascular pressure transmission reflect the structural and functional properties of the cerebrovascular bed. To quantify changes in cerebrovascular pressure transmission, we chose to evaluate changes in the highest modal frequency (HMF) which represents the highest critical vibration frequency of transmission. Vasodilation and vasoconstriction change the structural and functional properties of the vessels within the arterial-arteriolar bed and result in a change of cerebrovascular pressure transmission. The purpose of this experimental study is to examine changes in HMF and pial arterial diameter (PAD), before, during, and following vasodilatory challenge induced by brief hypercapnia.

Methods

ABP and ICP recordings sampled at 250 Hz, cerebral perfusion pressure (CPP), HMF, PAD obtained by video micrometry, partial pressure of arterial blood gases, and pH, before, during, and following induction of a brief five min hypercapnic challenge were evaluated in six piglets equipped with a cranial window.

Results

Group mean measurements of HMF, CPP, PAD, PCO2, PO2, and pH taken at baseline, during challenge, and post-challenge conditions and statistical comparison are given (see Table 1).

Table 1

Summary of Means (+ S.D.) of HMF, CPP, PAD, PCO₂, PO₂, and pH

	N5	HMF (Hz)	CPP (mmHg)	PAD (um)	PCO2 (mmHg)	PO2 (mmHg)	pH
Baseline	6	21.3(±12.3) 4	65.1(±13.2)	92.3(±10.2) 2	30.0(±2.6) 1	90.2(±22.1)	7.34(±0.11) 1
Challenge	6	58.5(±42.9) 4	54.9(±17.5)	124.3(±19) 2	68.3(±7.7) 1	74.8(±10.1)	7.06(±0.06) 1
Post-Challenge	6	29.9(±15.2)	63.7(±20.7)	95.9(±8.5) 3	33.0(±5.2) 1	88.2(±18.4)	7.3(±.06) 1

1

Significant difference between mean values p<0.005.

2

Significant difference between mean values at p<0.01.

3

Significant difference between mean values at p<0.025.

4

significant difference between mean values at p<0.05.

5

N is the number of piglets with 10 minute pressure recordings sampled at 250 Hz with value of HMF determined on each 8 s segment. Entriesin table represent grand mean values across all piglets.

Conclusions

Significant increases of mean HMF and mean PAD occur during vasodilation induced by brief hypercapnia. Such a result suggests that high values of HMF associated with high values of CPP are indicative of inappropriate vasodilation and loss of pressure regulation.