OUTFLOW
II
The Retinal Circulation, ctd.
We follow the blood stream to the optic disc. There,
within a fraction of a millimeter, there occurs a
precipitous drop in pressure, from the 12 or 15 or 20 or 25
or whatever the intraocular pressure happens to be, to a
very low value, perhaps five or three or twomm Hg. The
value of the venous pressure within the optic nerve is
unknown, but the distance from the optic nerve to the
cavernous sinus is small, and we know that in the sinus the
venous pressure is zero or less. Simple algebraic
calculation illustrates what goes on. If we define
resistance as the quotient of pressure gradient divided by
flow, then given a constant volume of flow per unit time,
the large pressure gradient indicates a proportionately
large resistance to flow. The cause of this increase of
resistance, and its fluctuations are readily seen. With the
ophthalmoscope, one can observe that on the optic disc the
increase in resistance to flow is brought about by the
pressure induced collapse of the retinal veins. As its
cross section becomes smaller, if the volume flow per unit
time is to remain the same, as it must, there will be
acceleration of the rate of flow. The vein collapses, of
course, from a disparity between intravascular and
extravascular, i.e. intraocular pressures. The
intravascular pressure is low because of a lack of down-
stream resistance. There is literally nothing, no
resistance, no friction, no back pressure, to prevent the
blood in the retianl vein from draining freely into the
veins behind the globe. That is why a segment of vein on
the disc collapses, sufficient in length to establish a
segment of high resistance to flow which will, in effect
maintain the intravascular pressures within the eye at above
intraocular pressure. It is this resistance which holds
back, as it were, the contents of the venous bed in the
retina, and prevents its being expressed by the intraocular
pressure.
It is instructive now to observe, how this collapsed
segment of vein which serves as a reducing valve, responds
to changes in the various parameters to which it is subject.
Simply by lightly placing a finger over the lateral rectus
muscle and making pressure on the sclera, one may increase
the intraocular pressure, and observing through the
ophthalmoscope at the same time, simultaneously, onenotes
that the segment of collapsed being becomes longer, up to a
point, and then no additional pressure will cause any
additional collapse of the vessel. In other eyes even the
initial increase of intraocular pressure brings about no
change in the length of the compressed vein. As intraocular
pressure is increased, the resistance of the vein will also
increase, and, depending on the physical characetristic of
the vein wall and on the volume of flow, this increase in
resistance will be brought about either by additional
compression of that segment of vein which is already
collapsed, or by the collapsed of an additional distal
length of vein, that is, by lengthening of the total amount
of collapsed vein. We observe the same phenomenon to occur
spontaneously in those eyes where there is spontaneous
pulsation of veins on the disc. There the fluctuation in
the length of the collapsed segment is caused by pulsations
in the intraocular pressure which are transmitted from
pulsatile expansion of the choroid secondary to the
pulsation of its own blood supply. The arterial pulse
momentarily expands the choroidal vasculature, increasing
the intraocular pressure, and it is this pressure increase
which is reflected in the pulsation of the retinal vein.
Consider also the effects on the length of collapsed
vein of variations of retinal arterial flow. When flow
through the vein increases, there is some small diminution
in the length of the collapsed vein at its distal end.
Conversely, as is often the case, when, as from
arteriosclerotic obstruction of the feeding vessels, there
is a diminution of flow, the length of collapsed vein
increased. This relationship becomes obviouis from purely
algebraic considerations, inasmuch as the pressure gradient
is the product of flow times resistance. If the pressure
gradient is to remain the same, then when the flow per
minute decreases, the resistance must increase. The
resistance will increase either as a result of more complete
or of more extensive collapse. Whether the change in
resistance comes about as the result of more complete or
more extensive collapse will be a function of the elastic
properties of the vein. The less pliable, the more
sclerotic the vein, the longer will be the segment required
to bring about the requisite pressure gradient for any given
amount of flow. Similarly, the lower the minute volume of
flow, the longer will be the segment required to account for
any given pressure gradient. We observe that when the flow
diminishes beyond a critical point, for any given value of
wall stiffness, a localized reduction in pressure can no
longer be achieved. The pressure will then be reduced in
the entire venous bed. The entire venous tree will then
sustain a pressure reduction as manifested by partial
collapse of the vein and the broadening of its profile as
described above.
These observations in physicology, in addition to
their explanatory value for a-v nicking and the increase v/a
ration commonly seen in obstructive retinal vascular disease
of all kinds, will also shed some light on the possible
etiology of glaucomatous disc damage. Observation with the
ophthalmosocpe, readily confirmed with fluorescein
angiography, reveals that the temporal and nasal poles of
the disc, those areas in other words that subserve the
macula and the temporal field which are as is well known
most resistant to glaucomatous damage, have a venours
drainage through small horizonatlly cousing veins which
enter the central retinal vein near the center of the disc
in the proximity of the lamina cribrosa. The central vein
in this area is almost always collapsed and the pressure
within it is substantially lower than the intraocular
pressure. Equally important is the circumstance that when
the intraocular pressure is increased the venous pressure in
this central segment of vein is unaffected. It is different
with the venous drainage from the upper and lower poles of
the optic disc. This drainage feeds into the superior and
inferior retinal veins at or near the disc margin, where the
retinal veins are not collapsed, distal to the collapsed
segments. Therefore this venous drainage must contend with
the intraocular pressure. Therefore venous drainage from
the upper and lower poles of the disc which show the
greatest sensitivity to glaucomatous damage, occurs into a
segment of vein at or slightly above the intraocular
pressure. At least as important, when the intraocular
pressure rises, unless, as is usually not the case, the area
of collapse extends to this region, the pressure against
which the capillary drainage from the upper and lower poles
of the disc must contend, increases with the intraocular
pressure.
Consider then what might happen to the venous
circulation on the disc as the intraocular pressure is
increased. The venous drainage from the temporal and nasal
portions of the disc is affected not at all, inasmuch as it
feeds into a segment of retinal vein which is collapsed, and
therefore under lower pressure, and an increase in the
intraocular pressure will not be transmitted to it. The
venous drainage on the other hand from the upper and lower
poles of the disc feeds into branches of the retinal vein
which are not usually collapsed either at nromal or at
elevated intraocular pressures. This fact means that the
venous pressure in these segments is equal to or slightly
higher than the prevailing intraocular pressure and, more
importantly, that as intraocular pressure rises, the
pressure in this segment of vein rises with it. At the
upper and lower poles of the disc, as distinct from the
temporal and nasal poles, the veins act like funnels which
serve to conduct increases in intraocular pressure into the
disc substance in just those regions where atrophy and
excavation from elevated intraocular pressure are most
likely to occur.
The Choroidal Circulation
Let us make a model of drainage from the choroidal
circulation.
In Issue No. 11 of the Glaucoma Letter we discussed the
venous drainage from the retinal circulation. Inferences
that can readily me made from retinoscopic observation alone
made it possible for us to give explanations for the
phenomena of A-V nicking, of increased V/A ratio in
arteriosclerotic and hypertensive vascular disease. Such
observations also suggested a possible mechanism for the
selective distribution of glaucomatous optic nerve damage,
and by extension suggested that it might be impairment of
the venous circulation that was responsible for the optic
atrophy and excavation in glaucoma rather than impairment of
arterial circulation as has hitherto been assumed. In
addition, and perhaps not least in importance, reflections
on the mechanisms of venous drainage from the retinal
circulation forced on us as they were by the simple process
of observation, by the need to explain and the desire to
understand what is so readily observable, provide us with
tools to think about venous drainage in general and give us
courage to consider other mechanisms of venous drainage in
the eye that are more or less inaccessible to inspection.
The outlines of the choroidal circulation are well
understood. The choroid is supplied by posterior ciliary
arteries perforating the sclera in a circular patter around
the optic nerve and by the two long posterior ciliary
arteries that course beneath the retina at the temporal and
nasal meridians respectively. There are also recurrent
arterial branches that perforate the sclera at the sites of
the insertions of the recti muscles. All these arteries
feed a rich and convoluted capillary bed, whose distinctive
character is reflected in a distinctive name: the
choriocapillaris. The choriocapillaris then drains into the
vortex veins. Our knowledge of this circulation derives
largely from anatomic and physiologic studies, since the
choroid itself is largely obscured from view on
ophthalmoscopy by the intervening pigment epithelium. A few
salient observations, however, are possible. The long
posterior ciliary artery can usually be seen as it courses
forward beneath the retina. The vortex veins are visible,
and feeding them, a spoke-like network of broad veins. From
its location, we can reliably infer that the entire intra-
ocular choroidal circulation is subject to the intraocular
pressure. We know, also, that on the outside of the globe,
the pressure in the ophthalmic vein into which the vortex
circulation drains is relatively much lower than the
intravascular pressure of the choriocapillaris. As in the
case of the retinal circulation, we infer the existence of a
pressure gradient. What can we say about its extent and
location?
It appears that the outflow from the choroidal
circulation via the four vortex veins differs in significant
respects from the outflow mechanisms of the retinal veins.
The vortex veins take, as is well known, an oblique course
through the sclera, and it has long been observed through
the sclera, and it has been assumed that with increasing
intraocular pressure there is progressive compression of the
vortex veins, producing an increased resistance to flow and
thereby preventing the pressure-induced collapse of the
choriocapillaris. It was assumed that it was the pressure
of the sclera on these obliquely coursing veins that created
the necessary resistance to prevent the emptying of the
choroidal vascular bed. That this hypothesis is probably
incorrect is suggested by the results of a recent study.
John Battaglioli experimentally determined the compressive
modulus of sample of sclera from enucleated human eyes, and
found that a vessel running circumferentially within the
sclera would not become collapsed, and its resistance would
remain relatively unaffected until the intraocular pressure
had increased to the vicinity of 50 mm. Hg. For vessels
that coursed not tangentially, but relatively more
obliquely, this pressure would become correspondingly
higher, presumably asymptotically approaching infinity,
inasmuch as a vessel running radially through the sclera
would as the intraocular pressure increased, not only not be
compressed, but it would actually dilate with increasing
intraocular pressure. It appears therefore that under
physiologic conditions, the scleral tuunnel is not likely to
be locus of resistance to vortex vein outflow. The
implications of Battaglioli's thesis suggested that it might
be worthwhile to take another look at the choroidal
circulation, to the extent that this can be studies
ophthalmoscopically, obscured as it is by the pigment
epithelial barrier. When one looks at the fundus with the
ophthalmoscope, or with the slit lamp and the contact lens,
one sees the vortex: broad bands of choroidal vein like the
curved spokes of a wheel converging onto the exit foramen.
On first thought one accepts the profile of these vessels as
indicative of a large volume, compatible with the well
established vascularity of the choroid. Yet the observation
that broad venous profiles in the retinal veins represent
not engorged but partially collapsed vessels, raises the
question whether or not the breadth of these structures that
feed the outflow veins of the choroid might not reflect
partial collapse rather than engorgement. This suspicion
appears to be confirmed in the occasional situation when,
because of atrophy of the retinal pigment epithelium one has
an opportunity to study choroidal veins stereoscopically
with the slit lamp. One sees than that at least some, and
perhaps most of the choroidal veins whose shadows one sees
are not cylindrical at all. They are flat ribbons. I have
never seen one that dis not appear to be in a state of
partial collapse.
If this observation is borne out by further studies, it
may turn out that unlike the healthy retinal venous vascular
bed whose volume remains practically unaffected by changes
in the intraocular pressure, the volume of the choroidal
venous vasculature may not be similarly stable. For if a
choroidal vein is collapsed, it means, in effect that its
contents have been partially expressed by the intraocular
pressure, and that its volume may be expected to vary
inversely with the intraocular pressure.
The resulting fluctuation of choroidal volume with
intraocular pressure would unavoidably be reflected in
fluctuating meridional stresses of the choroid itself and
specifically of Bruch's membrane. When the intraocular
pressure decreases, the volume of blood in the choroidal
veins increases, the inner layers of the choroid are
displaced centrally, and the stress induced in them by the
intraocular pressure diminishes. On the other hand, if the
intraocular pressure increases, then the choroid tends to
collapse, and Bruch's membrane is displaced toward the
periphery of the globe and it becomes correspondingly
stretched. This tension in the choroid is transmitted to
the ciliary body to which the choroid is anchored, and
through it to the scleral spur. With an increase in
intraocular pressure then, the choroid tends to collapse,
its inner layers are pushed outward by the intraocular
pressure, there is increased meridional stress which makes
posterior traction on the scleral spur thereby tending to
open the canal of Schlemm and restore the intraocular
pressure to amore normal level. Although the existence of
such a mechanism is likely, there is insufficient data to
permit any conclusion as to its importance, if any, in the
control of intraocular pressure.
The anatomic relationships at the point where the
artery crosses the vein prevent the tangentially oriented
collapse of the vein. Such collapse, if it occurred,
would require a sharp deflection of the artery, as
in B. Instead, radially oriented collapse may occur.
Alternatively, stiffness of the artery combined with
stiffness of the enveloping fibrous tissue may so impede the
collapse of the vein at the crossing as to create a dead
space of relatively stagnant blood. Such stagnation
explains the branch vein occlusions that begin at A-V
crossings. A vein crossing over rather than under the
artery will not exhibit A-V nicking because in that location
collapse of the vein can and does occur without deflection
of the artery.
* * * * *
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