Now we've got some pictures appear to kinda walk through the same concepts again that I just talked to you about.
Remember, no one learns anything just seeing it one time,
that’s why we repeat the concepts for you so it kinda help them sink in,
so if you’re getting to the point reading, ahh, I know this -- that’s awesome!
That means that you’ve done the work and the hard work of really focusing and understanding why these concepts are important.
So you have a normal vessel and what normally lives in our vessel you can see it should be wide open clear sailing.
You’ll see red cells and platelets and neutrophil which are white cells.
You see the endothelial cells that line the lining of our vessels and everything is happy,
everything is flowing, everything is smooth.
Now what the vessels look like in exertional angina?
As you can see we’ve got all those things but look how they’ve been pushed down and squished by plaque.
That’s the build up that comes in our vessels and it narrows the diameter of the vessels and therefore the blood supply,
so I still have the red cells, the white cells and the neutrophils, but look, they are all in this little tight compartment now
because you have that atherosclerotic plaque that’s squishing them,
so therefore, you don’t have as good a blood supply as you do in normal clear arteries.
Now vasospastic angina is like the worst kind of hug because what that does is those vessels just clamp down
so you have all these same players but it’s like trying to ride the subway in New York at rush hour,
you’re all tight, it’s just not getting the blood supply you need.
Unstable angina looks like exertional angina, right?
You’ve got the atherosclerotic plaque squishing that vessel
but the problem is you’ve got a clot or something that’s broken off and started to collect things.
Well, once that our body is responding to, hey, this doesn’t belong here
and it tries to deal with this extra things that are flowing by start sticking to it,
now we have a clot that moves from unstable angina to infarct
because we’re completely blocking off that blood supply and we’re gonna end up with, you got it, dead tissue.
So before we go on, see if that’s very clear to you.
I want you to pause the video and see if you quiz yourself what’s the difference and how a vessel looks.
See if you wanna draw this on your own.
What’s the difference between how a vessel looks in exertional angina and infarct?
How does a normal vessel look different than a vasospastic vessel?
How does a normal vessel look different than unstable angina?
So make sure you’re really solid on these concepts before we move through talking about the medications.
So let’s revisit that concept of oxygen supply versus oxygen demand.
Now look at that we’ve got a scale up here for you that when the supply of oxygen
is equal to the heart’s demand for oxygen everything is balanced and life is good.
So when I have enough oxygen supplied for the demand that my heart needs, everything is in balanced.
That’s the whole game that we’re playing in dealing with chest pain
because things that impact the amount of oxygen that you need could be heart rate,
but the amount of oxygen that you can supply is also impacted by the heart rate.
The oxygen content of the blood definitely impacts how good or effective the oxygen supply is.
Also the amount of coronary perfusion -- how open are those vessels?
So those are the things that we look at -- if we have a supply problem, well look at the patient’s heart rate,
what the oxygen content is of their blood, and what is the status of their coronary perfusion.
Are those vessels open, kind of open or completely closed?
In issues of demand, heart rate. So if I need more oxygen my body will increase my heart rate that’s how it works.
If I need more oxygen doing something like, say you're out there shovelling the driveway,
your heart rate is gonna get elevated, your heart’s gonna pump harder and faster, right,
contractility will increase, it will pump harder.
Now the impact of afterload is the workload the heart has to do to push blood out through the rest of the body, afterload.
Preload is the amount of blood that comes back to the body.
We will come back to those concepts so if they seem a little sketchy right now, it’s okay.
The most important concept in this slide is are you clear that we have to keep a balance
between how much oxygen is being supplied to the heart and how much oxygen the heart needs
or demands based on heart rate, activity, contractility and the amount of volume there in the body.
Now when this become unbalanced, when the heart needs or demands more oxygen than the body can supply it,
now we have problem which is why you’re slide just turned this way, to help you understand that concept.
So let’s look at some issues with supply.
If my heart rate is too faster or too slow, those can either way, can cause a decrease in oxygen supply.
Let me explain, if your heart rate is too fast, going like that, the heart chambers can't fill and completely empty out
because they just can't -- it’s not appropriate for the pumping system.
So if it’s way too fast, you're not getting adequate blood perfused throughout the body.
If it’s way too slow, you're also not getting enough oxygenated blood pumped to the body where you need it.
The oxygenated content of the blood might be too low.
Maybe there is something going on in your lungs.
You could have a pneumonia, you could have some type of clot on your blood, you could have -
you could be in what we call ARDS, a really significant respiratory lung problem,
well then it’s not gonna be able to exchange that CO2 for O2 very efficiently
so your heart maybe pumping enough blood initially,
but if we don’t have enough good solid oxygen content, your heart is gonna take a hit.
That’s why we watch hemoglobins.
When a patient’s hemoglobin, remember that’s the one that carries the oxygen in our blood,
is too low you can have a heart attack because of this, because there’s not enough oxygen being delivered to the heart.
Obviously if there's a blockage in coronary perfusion, we're not gonna be supplied enough.
And contractility, there's afterload and preload numbers are way off we're not gonna be able to supply enough.
So on this slide, this is all the reasons for you to keep in mind kind of an overview to consider
what are the reasons that one of our patient’s end up with not enough supply?
Now this is just isn’t a list for you to memorize, this is what the healthcare team does when someone presents with these symptoms.
We think through either it’s a supply or demand, so what is the issue?
What’s my patient’s heart rate? What is their sat telling me? That’s their oxygen content.
Do I think that there's some perfusion problems?
We can figure that out by going to cath lab and looking at their 12 lead. How’s contractility?
We've got some really cool ways to kinda measure those things.
So this is the framework that we use to think through. How can we best save this patient’s life?
Now what about increase demand?
Well, the heart’s gonna want more oxygen if the sympathetic nervous system is activated.
Now, this can happen for me if you make me do burpees which if you don’t know what burpees are, they’re horrible.
But anytime I go to the gym and I work out with my bootcamp friends, that’s one of the worst exercises the trainer has us do.
If you don’t know what it is, Google it, but just let me tell you, it takes a lot of energy to do that
and when I do a stressful physical energy action like that, whether I'm on the Stairmaster are doing burpees
which I still don’t know why I have to do those, that’s gonna cause me to having an increase oxygen demand for my heart.
I’ve stimulated my sympathetic nervous system because my body knows,
when I start to do something really strenuous, my adrenal glands they scoured out that norepinephrine, that adrenalin,
and it kicks in the sympathetic nervous system in my body.
The same thing would happen if I was standing in the street and I was about to be run over by a truck.
Fight or flight? That’s the one, that’s the system, the sympathetic nervous system that gets kicked in.
So demand is increased by anything that kicks in my sympathetic nervous system,
whether I chose to do a physical activity, if I'm emotional about something, or if someone made me mad,
if someone made me really upset or frightened, any of those things that kicked in the sympathetic nervous system
are what will increase my demand for oxygen.
Okay, we've talked about supply and we've talked about demand,
so you’ll often hear with demand, we can get the patient’s history or you’re doing something more -
that was more physically demanding than you’ve done before
or did some event happen that caused that demand in your sympathetic nervous system.