Perfusion Pressure of the Eye

Update Item Information
Identifier Perfusion_pressure_of_the_Eye
Title Perfusion Pressure of the Eye
Creator Andrew G. Lee, MD; Jeremy Auerbach
Affiliation (AGL) Chairman, Department of Ophthalmology, The Methodist Hospital, Houston, Texas; Professor of Ophthalmology, Weill Cornell Medicine, New York City, New York; (JA) Class of 2023, Baylor College of Medicine, Houston, Texas
Subject Neuro-Ophthalmology; Perfusion Pressure; Neuropathy
Description Dr. Lee lectures medical students on perfusion pressure of the eye.
Transcript We're going to talk about a very simple concept today, which is the perfusion pressure of the eye equals the mean arterial pressure and, as you know, we spend more time in diastole so its two-thirds diastole and one third systole, minus the intraocular pressure. In neuro-ophthalmology, we are dealing with conditions that result in ischemia that are either from a drop in mean arterial pressure or an acute rise in intraocular pressure or both. The conditions that come to us are non-arteritic anterior ischemic optic neuropathy. As you know, this is differentiated from giant cell arteritis. This is a non-arteritic ischemia of the optic nerve and many people believe that NAION is caused by a nocturnal drop in MAP. The nocturnal reduction in blood pressure is a natural process. When you're standing up, you have to autoregulate and increase your blood pressure. But when you're going to sleep, you don't have to do that, so the blood pressure can go down. Nocturnal hypotension is one of the presumptive causes, even though its unproven, of garden variety non-arteritic anterior ischemic optic neuropathy. However, there are other conditions that can drop your blood pressure that you need to know about that could produce what looks like NAION. One of the most common is hemodialysis. During the dialysis exchange process of hemodialysis, we have a number of things that are going wrong on the autoregulatory side in terms of sympathetic control, fluid exchange, and they are vasculopaths in general also. Intradialytic hypotension is one of the causes of NAION. When we have a patient whose stem says ‘this is a 60-year-old white male, end stage renal disease, who is hemodialysis-dependent and presents with acute unilateral loss of vision and a swollen nerve,' even though garden variety NAION is on that list, we have to recognize that the drop in MAP from intradialytic hypotension during hemodialysis is a treatable risk factor to reduce the risk of the fellow eye. Countermeasures could be done against this hemodialysis. In addition, surgery of any kind. On the IOP side, that's intraocular surgeries that raise the intraocular pressure, including just general cataract extraction, but in particular surgeries where they're injecting things into the eye. Glaucoma surgeries, retina surgeries, injections of silicon oil, any type of retinal surgery, can cause a rise in the intraocular pressure independent of the mean arterial pressure that can drop the perfusion pressure. Both intraocular surgeries and non-ocular surgeries. Non-ocular surgeries, however, usually work on the MAP side. The most common non-ocular surgeries that cause NAION or posterior ischemic optic neuropathy-the disc is not swollen, both are ischemic optic neuropathies after non-ocular surgery-spine surgery and cardiac surgery. In spine surgery, we have the additional risk factor of the face-down position and the head down, face-down position might impair the venous return and raise the intraocular pressure. There is going to be blood loss at the time of surgery and they often have to be transfused. And the use of a Wilson device, which is used to push the spine up so they can get better access. The face-down, the Wilson device, the blood loss, and the hypotension in spine surgery can predispose to a drop in MAP plus a decreased venous return and a potential elevated IOP, which can lead to non-garden variety NAION after spine surgery. Cardiac surgery is a lot easier to understand because they're working on the heart, but any surgery can result in post-operative cardiac arrest or atrial fibrillation, and these are mechanisms by which the perfusion pressure might drop from non-ocular types of surgery. In addition, we have other things that we have to worry about with MAP, which is iatrogenic. If we give too much blood pressure medication, that can make the nocturnal hypotension worse, especially if the patient is being treated for white coat hypertension-they're actually not hypertensive but their blood pressure goes up every time their doctor measures them. Inappropriate iatrogenic treatment of white coat hypertension could also drop the MAP. Finally, there are conditions that transiently raise the intraocular pressure and that can cause amarousis fugax. When we have transient vision loss episodes, one of the mechanisms is hypotension-orthostatic hypotension, failure of autoregulatory mechanisms, cardiac arrhythmias, pre-syncopal episodes, all are MAP side. But if you have rapid rise in the intraocular pressure, like intermittent angle closure glaucoma, or intermittent uveitis or Posner-Schlossman Syndrome, you can get transient blackouts in your vision from the IOP side rather than the MAP side. If you just know that the perfusion pressure equals MAP minus the IOP then you can try and figure out which side of the equation we're dealing with. Are we arterial pressure side dropping, or IOP rising? Either, neither, or both? That is the super important concept that I hope you've learned today.
Date 2020-05-27
Language eng
Format video/mp4
Type Image/MovingImage
Collection Neuro-Ophthalmology Virtual Education Library: Andrew G. Lee Collection: https://novel.utah.edu/Lee/
Publisher North American Neuro-Ophthalmology Society
Holding Institution Spencer S. Eccles Health Sciences Library, University of Utah
Rights Management Copyright 2019. For further information regarding the rights to this collection, please visit: https://NOVEL.utah.edu/about/copyright
ARK ark:/87278/s6hx6sp7
Setname ehsl_novel_lee
ID 1561519
Reference URL https://collections.lib.utah.edu/ark:/87278/s6hx6sp7