May 2007
Volume 48, Issue 13
ARVO Annual Meeting Abstract  |   May 2007
Electrical Analog Model of Ocular Pulse Amplitude as a Function of Systemic Pulse Pressure and Ocular Rigidity
Author Affiliations & Notes
  • H. J. Karol
    The Ohio State University, Columbus, Ohio
    Biomedical Engineering,
  • C. J. Roberts
    The Ohio State University, Columbus, Ohio
    Biomedical Engineering,
  • R. H. Small
    The Ohio State University, Columbus, Ohio
  • Footnotes
    Commercial Relationships H.J. Karol, None; C.J. Roberts, None; R.H. Small, None.
  • Footnotes
    Support None.
Investigative Ophthalmology & Visual Science May 2007, Vol.48, 4946. doi:
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      H. J. Karol, C. J. Roberts, R. H. Small; Electrical Analog Model of Ocular Pulse Amplitude as a Function of Systemic Pulse Pressure and Ocular Rigidity. Invest. Ophthalmol. Vis. Sci. 2007;48(13):4946.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose:: To model the ocular pulse waveform and determine its relationship to systemic blood pressure and ocular rigidity.

Methods:: The interdependent pulsatile ocular blood flow and equilibrium aqueous circulation can be represented by an electrical analog system where pressure and flow translate to voltage and current, respectively. Resistance, vessel compliance and inertia are analogous to resistance, capacitance and inductance, respectively. A model of the interdependent circuits was created using TopSPICE [Penzar Development, Canoga Park, CA] with intraocular pressure (IOP) and ocular pulse amplitude (OPA) as output variables. Ocular blood flow was modeled as a series of two windkessels, each consisting of 3 elements. The posterior ciliary arteries of the eye were lumped as the first windkessel and the capillaries as the second. The input was provided by a look-up table controlled voltage source programmed to produce a carotid pulse waveform. The aqueous circulation was modeled with a current source to represent the steady inflow, a battery to represent the episcleral venous pressure, with capacitance and resistance to represent ocular rigidity and outflow resistance, respectively. The interdependence of ocular blood flow and aqueous circulation was represented by a capacitor between the two circuits. The model was driven using a representation of the carotid waveform with baseline systolic and diastolic pressures of 110/80mmHg, providing a pulse pressure (PP) of 30mmHg. These pressures, along with ocular rigidity, were varied to determine the effect on OPA and IOP.

Results:: Using the baseline driving pressures, the model generated a waveform of the ocular pulse with a mean IOP of 14.49mmHg and an OPA of 2.058mmHg. This waveform closely resembled the physiological waveform of the ocular pulse. As PP was varied by 10mmHg, OPA and mean IOP varied by 0.69mmHg and 0.175mmHg, respectively with an increase in PP resulting in an increase of OPA and mean IOP. Changes in OPA and mean IOP were a function of PP only. Decreasing the ocular rigidity (increasing capacitance by a factor of 100), resulted in a 0.25mmHg and 0.065mmHg decrease in OPA and mean IOP respectively.

Conclusions:: In the literature, OPA is considered as an isolated parameter related to ocular blood flow, which is an incomplete description. This model successfully represents the ocular pulse waveform and demonstrates how OPA, and to a lesser extent IOP, are dependent on both ocular rigidity and systemic pulse pressure. The next step is to drive the model with physiological data.

Keywords: computational modeling • intraocular pressure 

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