Abstract
To test, theoretically, the hypothesis that: (1) cyclic extravascular compressional modulation of the terminal venous bed occurs with positive pressure inhalation; and (2) the degree of modulation is diminished with increasing vascular dilation induced by increasing the level of the partial pressure of arterial blood carbon dioxide (PCO2), two modifications of Ursino's model of cerebrospinal fluid dynamics21,22 were made: (1) terminal venous bed resistance was synchronously modulated with the ventilation cycle; and (2) both the depth of modulation and cerebrovascular resistance were progressively reduced with increasing levels of PCO2. Recordings of intracranial pressure (ICP) and arterial blood pressure of piglets were obtained and correlated at different levels of hypercapnia. Simulated and experimental correlation values progressively increased monotonically as the level of PCO2 increased. Group (n=4) mean values of correlation (±standard deviation) were 0.54 (±0.17), 0.61 (±0.08), 0.79 (±0.06), 0.86 (±0.04), 0.87 (±0.05) for respective mean PCO2 levels (±standard deviation) of 32.9 (±1.75), 41.4 (±2.5), 55.9 (±4.0), 72.5 (±6.45), and 87.4 (±7.25) mmHg. These results support the stated premise that dilation of the cerebrovasculature reduces the influence of positive pressure ventilation on the ICP recording by increasing the venous pressure and thus diminishing the likelihood of vascular compression. © 2003 Biomedical Engineering Society.
PAC2003: 8719Uv, 8710+e
Article PDF
Similar content being viewed by others
Avoid common mistakes on your manuscript.
References
Asgeirsson, B., P. O. Grande, and C. H. Nordstrom. A new therapy of post-trauma brain edema based on haemodynamic principles for brain volume regulation. Intensive Care Med. 20:260–267, 1994.
Becker, R. F., J. W. Wilson, and J. A. Gehweiler. The Anatomical Basis of Medical Practice. Baltimore MD: Waverly, 1971, p. 906
Chesnut, R. M. Treating raised intracranial pressure in head injury. In: Neurotrauma, edited by R. K. Narayan, J. E. Wilberger, and J. T. Polvishock. New York: McGraw-Hill, 1996, pp. 445–469.
Chopp, M., H. D. Portnoy, and C. Branch. Hydraulic model of cerebrovascular bed: An aid to understanding the volume-pressure test. Neurosurgery13:5–11, 1983.
Chopp, M., and H. D. Portnoy. System analysis of intracranial pressure. J. Neurosurg. 53:516–527, 1980.
Czosnyka, M., N. G. Harris, J. D. Pickard, and S. Piechnik. CO2 cerebrovascular reactivity as a function of perfusion pressure—A modeling study. Acta Neurochir. 121:159–165, 1993.
Daley, M. L., and C. W. Leffler. Correlation coefficient between ICP and arterial pressure: a gauge of cerebral vascular dilation. Acta Neurochir. Suppl. (Wien)71:285–288, 1998.
Daley, M. L., H. Pasupathy, M. Griffith, J. T. Robertson, and C. W. Leffler. Detection of loss of cerebral vascular tone by correlation of arterial and intracranial pressure signals. IEEE Trans. Biomed. Eng. 42:420–424, 1995.
Daley, M. L., M. Griffith, and J. T. Robertson. Loss of variation of baseline of intracranial pressure with loss of regulation of cerebral blood flow. Proceedings of the Annual International Conference of the IEEE Engineering in Medicine and Biology Society 2:671–674, 1993.
Daley, M. L., M. Pourcyrous, A. Willis, and C. W. Leffler. Variation of proposed correlation indices of cerebrovascular reactivity with change of arteriolar diameter. Acta Neurochir. Suppl. (Wien)81:151–153, 2002.
Daley, M. L., S. Han, and C. W. Leffler. Cyclic variation of cerebral pial arteriolar diameter synchronized with positive-pressure inhalation. Acta Neurochir. Suppl. (Wien)81:143–145, 2002.
Daley, M. L., S. Patterson, A. Marmarou, C. W. Leffler, and G. Stidham. Method of estimating cerebral dilation from clinical recordings of intracranial and arterial pressure. Tenth International Symposium on Intracranial Pressure and Neuromonitoring in Brain Injury Acta Neurochir. Suppl. (Wien)71:207, 1998.
Hammer, J., E. Alberti, S. Hoyer, and K. Wiedemann. Influence of systemic and cerebral vascular factors on the cerebrospinal fluid pulse waves. J. Neurosurg. 46:336–345, 1977.
Karus, J. F., and D. L. McArthur. Epidemiologic aspects of brain injury. Neurol. Clin. 14:435–450, 1996.
Nichols, J. S., J. A. Beel, and L. G. Munro. Detection of impaired cerebral autoregulation using spectral analysis of intracranial pressure waves. J. Neurotrauma13:439–456, 1996.
Piechnik, S. K., M. Czosynka, H. K. Richards, P. C. Whitfield, and J. D. Pickard. Cerebral venous blood outflow: A theoretical model based on laboratory simulation. Neurosurgery49:1214–1223, 2001.
Piper, I. R., J. D. Miller, N. M. Dearden, J. R. Leggate, and I. Robertson. Systems analysis of cerebrovascular pressure transmission: An observational study in head injured patients. J. Neurosurg. 73:871–880, 1993.
Portnoy, H. D., M. Chopp, C. Branch, and M. D. Shannon. Cerebrospinal fluid pulse waveform as an indicator of cerebral autoregulation. J. Neurosurg. 56:666–678, 1982.
Portnoy, H. D., and M. Chopp. Cerebrospinal fluid pulse waveform analysis during hypercapnia and hypoxia. Neurosurgery9:14–27, 1981.
Rosner, M. J., S. D. Rosner, and A. H. Johnson. Cerebral perfusion pressure: Management protocol and clinical results. J. Neurosurg. 83:949–962, 1995.
Ursino, M., and C. Lodi. A simple mathematical model of the interaction between intracranial pressure and cerebral hemodynamics. J. Appl. Physiol. 82:1256–1269, 1997.
Ursino, M. A mathematical study of human intracranial hydrodynamics: Part 1—The cerebrospinal fluid pulse pressure. Ann. Biomed. Eng. 16:379–401, 1988.
Ursino, M. A mathematical study of human intracranial hydrodynamics: Part 2—Simulation of clinical tests. Ann. Biomed. Eng. 16:403–416, 1988.
Yada, K., Y. Nakagawa, and M. Tsuru. Circulatory disturbance of the venous system during experimental intracranial hypertension. J. Neurosurg. 39:723–729, 1973.
Author information
Authors and Affiliations
Rights and permissions
About this article
Cite this article
Pasley, R.L., Leffler, C.W. & Daley, M.L. Modeling Modulation of Intracranial Pressure by Variation of Cerebral Venous Resistance Induced by Ventilation. Annals of Biomedical Engineering 31, 1238–1245 (2003). https://doi.org/10.1114/1.1616935
Issue Date:
DOI: https://doi.org/10.1114/1.1616935