Fig. 1. Cardiac-induced pulsatile aqueous outflow mechanisms.

Cardiac source of (a) pulsatile aqueous outflow and (b) resultant pulsatile flow into the aqueous veins. During systole, the left ventricle contracts, which initiates a pulse wave that causes the choroidal volume to expand, thus increasing intraocular pressure (IOP). Increased IOP causes the trabecular meshwork (TM) to move into the lumen of Schlemm’s canal (SC), narrowing it. TM movement that narrows the SC lumen increases pressure in SC. Reduced space and increased pressure in SC favor the pulsatile flow of aqueous from SC into aqueous and episcleral veins (ESV). Movement creates an aqueous pulse wave and increases aqueous vein pressure (AVP) during systole. During diastole, choroidal volume decreases, and IOP falls. The TM recoils, releasing the potential energy stored during systole. TM recoil reduces pressure in SC, favoring aqueous flow from the AC into SC through SC inlet valves, (b) Various manifestations of oscillatory pulsatile flow into the episcleral veins are synchronous with the ocular pulse. Pressure in the aqueous veins falls as SC pressure decreases during diastole. Episcleral venous pressure (EVP) is then transiently higher than aqueous vein pressure (AVP) resulting in oscillatory blood entry into aqueous veins. The next systolic wave causes the AVP to be higher than EVP. From: Johnstone M, Aqueous Veins, The Glaucoma Book. New York: Springer, 2010:65–78. Video - Pulsatile Aqueous Vein Flow 1-s2.0-S1350946220300896-mmc1.mp4).