What is the mechanism by which intraocular pressure (IOP) is normally maintained?
IOP contributes to the refracting properties of the eye.
Significant intraocular hypotension or hypertension may lead to blurred vision or refractive discrepancies. The normal range of IOP is 10–22 mmHg. IOP is much higher than tissue pressure, which is 2–3 mmHg, and intracranial pressure, which is 7–8 mmHg. Pressures greater than 25 mmHg are considered abnormal. There are diurnal variations of modest proportion, 2–3 mmHg. IOP is high-est in the morning secondary to the dilatation of pupils during sleep, carbon dioxide (CO2) retention, the recum-bent position, immobility of the eye, and pressure of the eyelid. Each systole can increase the pressure by another 1–2 mmHg, while inspiration can lower IOP by 5 mmHg.
IOP is normally maintained by several factors. One fac-tor is external pressure exerted by periorbital structures, such as the extraocular muscles, venous congestion of the orbital veins, closure of the eyelid, or contraction of the orbicularis ocularis muscle. A second factor is scleral rigidity. The sclera is normally distensible, but as IOP rises it becomes rigid, thereby exacerbating intraocular hyper-tension. A third factor is the volume of intraocular fluid, such as blood, aqueous humor, and the semisolid struc-tures, which include the lens, the vitreous, and intraocular tumors.
Alterations in fluid contents are crucial to IOP. Intraocular blood is mainly present in the choroid plexus, and the state of dilatation or contracture of these vessels will determine the blood volume in the eye. Although IOP is maintained at a relatively uniform level regardless of the degree of hypertension, an acute rise in arterial blood pres-sure may increase IOP. Over time, if arterial hypertension is chronic, IOP will normalize after adaptation of the choroidal vessels.
Impaired venous drainage increases IOP. Coughing or straining will raise IOP by elevating venous pressure (Table 43.1). A mild cough can raise IOP by 34–40 mmHg. Similarly, retching, coughing, or vomiting during induction of anesthesia may cause a rise in IOP which persists for many minutes. This may be particularly true in patients with a history of smoking.
Another important intraocular constituent is aque-ous humor, two-thirds of which is formed in the poste-rior chamber, and one-third of which is produced in the anterior chamber. It is secreted from epithelial cells of the ciliary process. After formation in the posterior seg-ment, aqueous humor circulates through the pupil into the anterior chamber, which is subsequently drained at the angle of the eye and at the spaces of Fontana. The spaces of Fontana are channels in the trabecular mesh. Impaired drainage through this trabecular mesh results in glaucoma. Aqueous humor continues to pass into Schlemm’s canal and the ophthalmic, cavernous, and jugu-lar veins.
Aqueous humor is similar in composition to plasma, without its proteins. Aqueous humor secretion is an energy-requiring process mediated through a sodium pump mechanism. Its production requires both cytochrome oxidase and carbonic anhydrase. Changes in solute con-centration of plasma can affect the formation of aqueous humor and, consequently, the IOP. Thus, mannitol or glycerol is used for lowering IOP. Acetazolamide may also lower IOP. Each of the aforementioned agents has meta-bolic consequences.
Pupillary dilatation narrows the trabecular mesh and spaces of Fontana, predisposing the patient to glau-coma. Agents causing pupillary constriction (miosis) improve aqueous drainage, whereas agents producing pupillary dilatation (mydriasis) impair aqueous drainage.