Hello and welcome to Nursing School Explained. Today I'll go over the RAAS
system and how it pertains to fluid balance in the body.
I'll also cover other mechanisms that are important for blood pressure regulation
as well as RAAS antagonists so let's get started. So RAAS
stands for renin-angiotensin and aldosterone system basically what that
means if the blood pressure for some reason drops. This is all in response to
low blood pressure. The liver will excrete a hormone called
angiotensinogen. Angiotensinogen then also works on the kidney and the kidney
will release renin. Both of them will combine to angiotensin I. And think
about angiotensin - a lot of the words that we use in physiology are very kind
of intuitive, so angio meaning blood vessel, tensin meaning tense. So it causes
vasoconstriction. If the blood vessel gets really tight, it
will cause an increase in blood pressure. So now if the blood pressure is
normalized every organ, liver and kidney have normal perfusion again, everything
goes back to normal. However, if the blood pressure remains
low and just by secreting the angiotensin I the low blood pressure problem
hasn't been resolved, angiotensinogen then will cause the lungs to release
ACE, angiotensin converting enzyme, these two will combine and form
angiotensin II. So just think about angiotensin I being potent, angiotensin
2 being more potent, again angiotense, make the blood vessels tense, vaso
constriction therefore causing an increase in blood pressure. If the blood
pressure now is back to normal every organ that's involved here gets
nicely perfused, homeostasis is back in balance,
everything is good and the RAAS will kind of go back to sleep until it's
needed again. If the blood pressure here again remains low, then the angiotensin II
works on the adrenal gland on top of the kidney, and then the kidney will release
aldosterone. And aldosterone works again on the kidney but this time it
helps to increase the absorption of sodium and water, and we know if we have
more fluid in our system, the blood pressure will be increased. Then again
that mechanism kicks in and that feedback loop is restored so now if there's a normal
blood pressure the RAAS again, all these hormones, go back to normal and
everything is, homeostasis is reestablished. So a very, very potent
sequence of events here that takes place just to make sure our blood pressure is
normal. Now besides the RAAS we also have other mechanisms that help us regulate blood pressure.
So inside our two cerebral hemispheres we have the pituitary gland that
releases antidiuretic hormone, which the name kind of gives it away, it anti-
diuresis. So what does, ADH works on the kidney and it decreases sodium and water
excretion, therefore holding on to more fluid in the intravascular space and
blood pressure is increased. So that's another mechanism that helps us
regulate our blood pressure. Now then we have the RAAS antagonists and whenever
you think about antagonists, think about something that counteracts the effect of
something else. So in this case the RAAS antagonist ANP and BNP counteract
the RAAS system. So now if the problem is not low blood pressure but high blood
pressure, now we have too much fluid in our intravascular space. And ANP is
located in the atria, where BNP is located in the ventricles of the heart,
and both of those will be released in response to an increased stretch of the
heart muscles in the atria and ventricles because of fluid volume excess. So
if the blood pressure is too high and sodium is high, these hormones will
be released from their locations in the heart. They are natural antagonist to the
RAAS system and therefore suppress renin, angiotensin I, angiotensin II
and aldosterone. So this whole mechanism of increasing blood pressure
here is basically negated because we already have too much volume and too
high of a blood pressure in our system. And it does that and then it increases
the excretion of water and sodium and therefore less water, less sodium in the
system, decreases the blood volume, therefore it decreases blood pressure. So
a very important counteracting mechanism here and in a normal healthy individual
these systems really work together to balance each other out. Important to note
the kidneys are basically the major regulators here of our fluid balance as
well as our pituitary gland that plays a role with the antidiuretic hormone. Now
here's an extra caveat: so there are certain medications that we can use for
patients who have high blood pressure so this whole system will basically not
work.
So this is the typical mechanism, the usual mechanism of our RAAS. Now there are
medications called ACE inhibitors, which are very frequently used medications and
what ACE inhibitors do - they just inhibit this angiotensin converting enzyme
from being produced. And so then since we can't produce the angiotensin converting
enzyme the RAAS system basically as far as it can go is the angiotensin I.
Therefore this whole following mechanism is blocked and all these attempts to
increase blood pressure are negated. And this is for patients who have
hypertension, which is a very common problem in today's population. Now very
important to note that ACE inhibitors usually end in -pril. So I highly
encourage you to note the endings of classes of medications because they will
all have the same mechanism of action, the same side-effects, the same nursing
interventions. So ACE inhibitors are -pril medications and that would be
something like the lisinopril, captopril and so forth. So if you see a
patient is on lisinopril, for example, you already know it's an ACE inhibitor, it
works on the RAAS and all the different organ that it can affect and then you have to
kind of assess your patient accordingly. Now another class of medications that
work here on the RAAS are called a ARBs - angiotensin receptor blockers.
And they end in -tan.
So ARBs basically prevent the angiotensin II from working on the kidney,
from binding here with the adrenal gland and causing that release of the
aldosterone. So they basically, the mechanism here can go as far as the
angiotensin II and then the ARBs halt the whole following mechanism. Angiotensin
receptor blockers, so therefore aldosterone is not produced and the sodium and water
reabsorption that we have there is is negated. Now other medications, which are kind
of pretty self-explanatory, are diuretics. here. And diuretics will basically work
on counteracting the antidiuretic hormone. So now we give the patient's diuretics
and there are three different types of diuretics, which are the thiazide
diuretics, the loop diuretics,
and the potassium sparing diuretics.
And they basically just work on different parts of the kidney to help
decrease the sodium and water reabsorption and increase the excretion
of sodium and water therefore to decrease the blood pressure. So thiazide
diuretics, very easy, end in -thiazide. And probably the most prominent one would be
hydrochlorothiazide. You'll see that very often abbreviated as Hctz. Now loop
diuretics work on the loop of Henle in the kidney and they are typically
potassium wasting diuretics and that is something like furosemide. So they end in
-ide, which is also called lasix. You've probably heard of lasix or furosemide
before. And then we have the potassium sparing diuretics, which basically also
work on the kidney, again to help excrete more sodium and water but they they hold
on to more potassium. Therefore we have to also watch what's happening with our
potassium and this will be something like aldactone or spironolactone,
and they will end in -one.
Very important to notice here that all the different blood ressure medications
that we just discussed: ACE inhibitors, angiotensin receptor blockers as well as
the different types of diuretics, they all have something to do with the kidney.
The kidney are plays a big role in fluid and electrolyte balance, therefore
whenever a patient is on these medications we have to watch
kidney function, so sodium, sorry, so creatinine and BUN,
as well as our electrolytes, because we know that the kidney exchanges these
electrolytes for others. And so if the patient is taking a potassium wasting
diuretic, we have to keep a close eye because they're at risk for hypokalemia.
Many times patients who are on a loop diuretic will be on a potassium
replacement that they'll take on a daily basis. So when patients are on any kind
of blood-pressure medication, specifically ACE inhibitors, ARBs or
diuretics, we have to monitor kidney function and their electrolytes,
specifically if the patient has this medication that's new to them. So because
we don't know the effect that it's going to have on their kidney, so it's very
important to monitor these lab values to ensure that the patient is taken care of
and has no adverse effects on their kidneys or electrolyte balance. So thank
you for watching the summary of this RAAS system with it's antagonists as
well as other mechanisms for blood pressure control. I hope it has helped
you understand the mechanisms more. Please feel free to leave comments in
the section below, I'll be happy to also help you review any other topics that
you might want me to go over in the future and thank you for watching again,
thank you for watching Nursing School Explained.