hi this is Andrew Wolf, so in this video
hi this is Andrew Wolf so in this video you will learn about stable angina and
how it's caused by an imbalance between oxygen supply and demand to the
myocardium of the heart muscle and how this is caused by a stable plaque or in
atheroma that is causing the coronary arteries to be partially
constructed and causing reversible ischaemia that occurs with exercise
but was resolves at rest so what do I mean by a mismatch between oxygen demand
and supply so demand actually increases oxygen demand increases in the
myocardium when the heart rate increases so when there's an increasing in heart
rate when there is increased contractility so the muscles are working
faster and they're working harder okay and supply actually is you know
primarily when we talk about supply of oxygen to the myocardium were mostly
talking about perfusion and to a lesser degree to systemic oxygen saturation and
inadequate so these are our variables as well but the primary variable is is
perfusion now typically the body can increase perfusion quite
significantly so at rest are perfusion is a baseline of a
baseline multiple of one and this can increase during exercise to up to six
times normal perfusion to to the myocardium so what happens with in
stable angina is that the ability to increase our perfusion to the myocardium
gets significantly reduced because of atheroma so we're going to talk about
that next so how does that happen
ok so here we have a cross-section of the normal coronary artery and as you
can see it's wide open there's nothing obstructing the balloon
and now with patients that have coronary artery disease they start to develop a
athoeromas, or fatty plaques in the coronary arteries and these can occur in
various places and they're more troublesome in some places than others
and what these plaques look like if you look at the cross section of the artery
is something like this
now this you know so we have a fatty plaque here that is partially
obstructing the lumen of the vessel and this has an impact on the amount of
blood that can flow through so this actually decreases the potential flow
through the vessel right so when the person is at rest and demand is low the
flow is not is not that high right but when the person exercises and demand
increases then they are going to start to have restrictions in this flow so if
we restrict potential flow and we asked for a high-flow then we may have an
actual decrease in flow during high demand states so what's
going to happen
well during those high demand States a person on the coronary artery disease
downstream of this area is going to is is not going to be able to keep up with
demand and we are going to air end up with an area of ischaemia ok so again
and ischemia means that there is tissue that is not receiving adequate
oxygenation now this ischemia - do not confuse the ischaemia with infarction
the tissue is not dying but because it has reduced oxygen flow it is causing
the cells to have to shift from aerobic metabolism to anaerobic metabolism which
causes the build-up of of acid lactic acid in the tissues in that is actually
what is causing the the chest pain so this ischaemia causes pain which is the
characteristic symptom chest pain
of angina - now why is it stable angina well stable because the plaque
actually stable so the stable plaque results in stable symptoms so
up the plaque is slowly increasing in size over time so it's not causing any
acute changes sure this picture here actually depicts on time as it as a
plaque sort of increases over time
ok now i want to kind of talk a little bit about the decreased flow potential
so this is sort of a lot of perfusion so this graph i'm going to draw a what I'd
call a perfusion curve and so here we have at the bottom the degree of
occlusion in the coronary artery so this is the degree of occlusion and this is
the myocardial oxygen oxygen demand so if we are at rest the myocardial oxygen
demand is at baseline or 1 times normal right
and as we go of the perfusion actually doesn't decrease at all until we get to
around eighty percent and then it decreases obviously down to zero by one
hundred percent but if we have someone working at maximal exercise so they're
really working out there going out for a jog or they're running up a flight of
steps myocardial oxygen demand can increase by six times and typically if
we have no occlusion of course demand-supply are equal
ok and what's interesting is demand and supply actually stay equal to around
sixty percent and then we have it curving down here so what does this mean
well typically people do not even notice symptoms until the artery is about
60-percent included
ok so so what does this mean
well I had talked before about how stable angina is characterized by a
decrease in potential flow so if we try to increase flow up to six times normal
when an artery is sixty to eighty percent
included we're going to bump up against the limits of this potential flow
because of the the atheroma is decreasing the amount of flow that can
go through the artery at that point as the atheroma continues to grow slowly
over time people are going to start to have the patient is going to start to
have symptoms at lower and lower levels of exercise right so you know so a
person initially is going to have chest pain when they are running up a flighter
to have steps but over time and I'm talking over periods of months to years
the amount of exercise that's required to cause symptoms is going to is going
to decrease so as and we're going to work our way down to baseline as this
atheroma grows in size over time so stable angina progresses slowly has
stable symptoms and it's characterized by reversible ischaemia that does not
lead to infarction
ok and this is all because of the underlying stability of this plaque that
grows and progresses slowly over time
okay thank you very much