Let's take a look at a very common medication group, hypertension.
What drugs do we use to treat hypertension?
Well, a good way to organize them is looking at the RAAS, right?
The renin-angiotensin-aldosterone system.
You end up with angiotensin II which causes very potent vasoconstriction and volume expansion.
So with vasoconstriction and volume expansion,
you end up with elevated blood pressure that's why we can use medications
that interact in that RAAS in multiple stages.
So let's take a look at these. I know you're familiar but I just wanna quick review.
The RAAS stands for renin so when that gets squirted out of my kidneys,
it hooks up with circulating angiotensinogen.
Okay, so renin hooks up with circulating angiotensinogen and we end up with angiotensin I.
Then angiotensin I connects with ACE known as angiotensin-converting ezyme.
Then we end up with the baddest mama jama, right?
Because angiotensin II is a super potent vasoconstrictor
and it causes -- also stimulates the release of aldosterone which causes volume expansion.
So we got them both. More volume on board and vessels that are clamped down in my body.
In the right balance, this is brilliant that this works.
We need this but when somebody has sustained high blood pressure,
chronic high blood pressure, we use medication to treat it.
Now, we can do things that interact in different sections of this process
and that's what drugs that interact with the RAAS do.
Alright, so we've got this quick review of the RAAS,
because we know that the blood pressure elevates due to 2 things:
volume expansion and vasoconstriction.
In the volume expansion, the adrenal cortex releases aldosterone.
So we know when that happens, the body hangs on the sodium,
where ever sodium goes, water follows.
Now, the vasoconstriction is due to the angiotensin II.
It is, when I say a bad mama jama, it is very bad.
It's a super potent vasoconstrictor, 4-8 times as active as norepinephrine.
So it is even stronger than anything I can hang in an IV bag for a patient in shock.
So this is the coolest part of how the RAAS works when I need it.
When it's chronically there, I'm in trouble.
Because blood pressure is impacted by my cardiac output or the SVR.
So cardiac output and SVR, preload, afterload, contractility,
all those words that we talk about in cardiac care.
So if I'm gonna maintain a blood pressure, I've got these 5 players, right?
The arterioles, the baroreceptors, the medulla oblongata, the hormones, and the RAAS.
All 5 of these are really important players in helping maintain a healthy blood pressure.
However, when we're out of balance,
we can also use medications that impact those different areas to help us deal with hypertension.
Now, I put the normals up here just to remind you.
Normal has to be less than 120/80 now.
And I've got it also listed there,
those are key numbers that you need to make sure that you're familiar with.
Now, we're talking about how we treat hypertension.
First step, diet and exercise. If that works, awesome blossom.
That's a cool deal.
But if it doesn't, and often times it doesn't because it's really hard to change diet and exercise,
but if you can do, that's the best.
If not, then we're gonna look at adding another first line drug.
Usually that's considered to be thiazide diuretics or a diuretic.
Thiazide is a relatively gentler one than a loop diuretic like furosemide
so after we've tried diet and exercise and it doesn't work,
we may try a diuretic to see if that works.
Our target blood pressures are there and I just really wanna underscore this is where they came from
so this is why it's a little different.
If you wanna have a normal blood pressure, it's gotta be less than 120 so make sure,
again, I know I'm repeating myself,
but because this is really important that you recognize that's our goal.