Vein Pulsation

The phenomenon of vein pulsation

The venous retinal pulsation is occurring due to the blood pressure difference in the central retinal vein. The pressure difference occurs due to the condition of the systole and diastole pressure.

The following are experimental studies carried out so far on physician experiment set-ups and existing theoretical models considered, wave surface with the Pulsations phenomena of collapsible vessels in the body deal. Few of these models are based on the anatomical and physiological conditions of the CRV, which is why most only the effect must be interpreted.

Theoretical models

Model according to DN Levine

The theoretical model by Levine relates the phenomenon of pulsating Vein on the observed pulsations of the CRV.

4.9) and represent the portion of the vein at the optic disc as it exits the eye (I), the intra-neural portion (II), the region through the nerve sheath where it crosses the subarachnoid space (III) and the extra-neural portion where the central retinal vein traverses outside the nerve to join the ophthalmic vein (IV), respectively. In the portion of the vein towards the rear of the eye (compartment I), the elastic wall is externally surrounded by vitreous humour at the IOP, while in the portion of the vein passing through the nerve sheath (compartment III), the elastic wall is externally surrounded by CSF at the ICP. Coupling between the IOP and ICP dictates the onset of the RVP. Other more sophisticated models for the elastic response of the vein are available, including for example its bending stiffness, but this study focuses on the simplest possible model. In compartment II the retinal vein is assumed to pass down the center of the optic nerve and so is unsheathed by nerve and connective tissue; therefore the vein wall can be assumed rigid. The vein wall in compartment IV is also assumed

This threshold intraocular pressure depends on the phase shift, varying over a range of approximately 1.5mmHg for mean ICP of 0mmHg. There are two encouraging features emerging from this model: first, the threshold for the onset of large amplitude oscillations appears to be an approximately linear relationship between the IOP and the CSF pressure over a significant range, consistent with measurements in canines; second, predictions show only a modest dependency on the phase shift between the IOP and the ICP oscillations – for the model parameters chosen the maximal difference in the predicted onset IOP was 1.5mmHg across the range of phase shift. The model employs an idealized representation of the elastic vessel wall (neglecting bending stiffness), assumes simple sinusoidal waveforms for the ICP and IOP and neglects pulsatility in the inlet flow into the vein. The model also assumes that the diameter of the vein is constant along its length and ignores bifurcations. When the mean IOP is 18.5mmhg then the ICP is 0mmhg, IOP is increased to 18.5mmHg, the vessel wall in compartment