Atherosclerosis, the primary cause of impaired blood flow, narrows and obstructs blood vessels, leading

to ischemia or inadequate blood supply due to blockage. This can give rise to various conditions such
as angina, heart attack, stroke, and peripheral vascular disease.

Ineffective tissue perfusion describes the lack of oxygenated blood flow to areas of the body. Proper
perfusion is detrimental to the function of organs and body systems as organs and tissues that are not
perfusing will die.

2. Vasoconstriction the muscles around your blood vessels tighten or narrowing to make the space inside
smaller.

3. The increase in blood flow is presumed to be a result of the increased O2 requirements for efficient
digestion and absorption of ingested food.

4. The catecholamine hormones are epinephrine, norepinephrine, and dopamine. Epinephrine is also
called adrenalin. Catecholamines are made in the adrenal glands. They are released when you have
physical or emotional stress. These hormones have many functions in the body. These include sending
nerve impulses in the brain, narrowing blood vessels, and raising your heart rate.

one of the consequences of

atherosclerosis in the artery supply in

the heart

or the coronary arteries and that is

angina pectoris

so angina is chest pain caused by

reduced blood flow to the heart

secondary to coronary heart disease so

if we see in this image we have a

narrowing

of the coronary arteries here and this

will impede blood flow to the heart

muscle so usually this is not

life-threatening but it is a warning

sign of a future

heart attack so the difference there

between angina

and a heart attack is that in angina you

still get

blood flow to the heart so it's not a

complete occlusion of the coronary

arteries

and in a heart attack there's no blood

flow to the heart

and so you get myocardial infarction

so myocardial cell death so

the pain described in angina might be

similar to that in

a heart attack that is heavy tight

crushing pain and it may

radiate to the jaw neck left arm

stable angina and this is chest pain brought on by exertion so when you exercise start getting that chest
pain um that is that shows a decreased supply of blood uh to the heart because as we exercise there's an
increased oxygen demand by our heart muscle this often lasts around 15 to 30 minutes and it is relieved
by rest or nitroglycerin so nitroglycerin is a medication that once in your body it is converted to nitric
oxide which is a vasodilator so it will dilate those coronary arteries allowing more blood to go to the
heart muscle so a stable angina presents a stable pattern meaning exercise will bring on chest pain but
then if you rest the chest pain goes away so stable angina is confirmed by a stress test so essentially
you're trying to induce that angina in a patient by making them exercise and see if exercise is the cause
of that chest pain.

unstable angina which is a

more serious condition

here the attack is unpredictable so it's

not really caused by

exertion you can be just laying at rest

and start feeling uh chest pain

now there's an increase in the frequency

and severity of pain in unstable angina

and it is not relieved by rest so you

still get that chest pain

at rest now it is often developed from

stable angina so stable angina can

develop

into an unstable angina and it is often

caused by a thrombosis with incomplete

coronary artery occlusion

so as we mentioned in the other video as

the atherosclerotic plaque

grows there is a chance of rupture

and if there is rupturing of the plaque

you got a formation of

it thrombus and if there is

incomplete occlusion of the arteries you

get unstable angina

and if there is a complete occlusion of

the arteries

then you get a heart attack

so in unstable angina there will be some

degree of necrosis

but not a lot it's very variable it

might even be no necrosis present

and that is the different with a

myocardial infarction a myocardial

infarction will have

necrosis or a death of heart tissue

so here you'll also see an st depression

and you may even see t wave inversion on

the ecg

so here the difference between unstable

angina and myocardial infarction

is that in angina you will not see

raised cardiac enzymes so here we're

talking about troponin

and in myocardial infarction you will

see raised levels of cardiac

enzymes so if we have a look here at

this image it just shows the

mode of contraction of muscles

so our muscles are made up of myosin

filament which is this uh structure

right here

and then we have actin filaments which

are these structures right here

now for a muscle contraction to take

place

the myosin head attaches to the actin

filament

as you can see here and essentially

pulls on it

to contract the muscle and for that to

happen

we need tropomyosin which is this

long filament there to move out of the

way

so to clear that binding site and this

happens when

troponin uh binds to calcium and then

uh um there is a conformational change

that occurs

so triponin right here bound to calcium

and this allows

for the contraction of muscle so

if there is muscle death these

continents are
spilled into the bloodstream and mainly

we see troponins

in the bloodstream that is an indicator

of heart

muscle damage as i wrote here troponins

indicate cardio

cardiac muscle death and necrosis

so just to say that again you won't see

raised cardiac enzymes so you won't see

raised

troponin in angina.

vasospastic angina but you might have seen it called prinzmetal or

variant angina this is very different

from stable or

unstable in that it does not follow that

same pathogenesis

so it is a chest pain caused

by focal coronary artery spasms and not

by atrosclerosis so has no relation

there to atherosclerosis

so the cause of the spot this spasm is

unknown

but some triggers including cocaine

alcohol

tryptanes and smoking may lead to

a coronary artery spasm so

in this case instead of an st depression

you get transient st elevations on the

ecg
so as you can see here in this image we

have there the qrs complex

and then a very elevated st segment

and this is a spasm in one of these

arteries the coronary

artery supply and the heart muscle so

like the other types of angina there is

no elevation of cardiac enzymes so we do

not see

the raised troponin

now vasospastic angina will be present

in younger patients compared to

stable and unstable angina as we don't

have we

we're not dependent on that formation of

atherosclerosis

so here are some questions to make sure

you've understood everything we've been

talking about feel free to pause the

video

to think of your answers

what is the definition of angina

what is the main characteristic of

stable angina

what can be seen in the ecg of someone

with

stable angina

what is the difference between unstable

angina and
myocardial infarction

what can be seen in the ecg of someone

with vasospastic

angina

and what is a trigger for vasospastic

angina