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