A theoretical investigation of the increase in venous oxygen saturation levels in glaucoma patients

Abstract

 

Purpose

 

Several clinical studies (e.g. Olafsdottir and Vanderwalle et al. 2014) have observed increased retinal venous oxygen (O₂) saturation in glaucoma patients as compared with healthy persons (Fig. 1A). Here, a theoretical model is used to propose three possible explanations for these observed increases in saturation.

 

Methods

 

A previously developed theoretical model of the retina (Arciero et al. 2013) is used to predict changes in blood flow and O₂ saturation in retinal arterioles, capillaries, and venules. Tissue O₂ consumption is calculated using a Krogh cylinder model. Given clinical measurements of intraocular pressure (IOP), mean arterial pressure (MAP), and arterial O₂ saturation from healthy persons and advanced (visual field MD≥10dB) primary open angle glaucoma (POAG, IOP>21mmHg) and normal tension glaucoma (NTG, IOP≤21mmHg) patients, the model is used to predict the O₂ demand (M₀) or capillary density (N) that would yield the clinically-measured venous O₂ saturation in each population.

 

Results

 

The model predicts that a decrease in M₀, an impairment of autoregulation (IA), or an increase in N can individually lead to increased venous saturation for certain ocular perfusion pressures (OPP=2/3 MAP - IOP), as depicted in Fig. 1B. The model also predicts that a decrease in M₀ or increase in N yields increased venous saturation in POAG patients, while no change in M₀ or N is predicted in NTG patients when compared with healthy persons.

 

Conclusions

 

Decreased M₀, impaired regulation, and increased N can independently lead to increased venous saturation, although to different degrees depending on an individual’s OPP level. The study also suggests that the mechanisms leading to increased venous saturation in advanced cases of glaucoma differ between POAG and NTG patients. We hypothesize that the increased saturation levels are explained by decreased M₀ in POAG and IA in NTG patients.  

 

Fig. 1 A) Venous saturation data collected from healthy, advanced POAG, and advanced NTG patients. B) Model predicted effects of decreased M₀ (black), impaired autoregulation (IA, red), and increased capillary density (green) on venous saturation, compared with the model prediction for healthy patients (blue). C) Model predicted levels of M₀ (gray, left scale) and N (blue, right scale) that yield the venous saturation clinical data collected from the three populations.