Now, what this basically means with
ECF volume is the following. What
if we have too much or too little, what kind
of signs meaning you the clinician, are going
to find in your patient? If that patient has
lost too much sweat, what does the skin do?
You decrease skin turgor, what does that mean?
Well right now, you won't be able to see that in me
because I am pretty well hydrated, in fact
I am kind of a camel. I keep drinking and
drinking and drinking and I will never,
well as far as the lecture series are
concerned, you will not find decreased skin
turgor in me. However, say that I wasn't drinking
water and I am going 8 to 10 hours of just
lecturing. That is a lot of perspiration is
taking place through evaporation. And maybe
perhaps I am feeling a little dehydrated, but
anyhow point being is I am being dramatic
here. What if your patient has lost quite
a bit of sweat and their blood pressure has
decreased and then their skin is able to then
tent. You pull it up and then it remains as
such. That is called decreased skin turgor,
why? Because here literally you have lost
the plasma compartment. So, therefore, the
ECF has diminished in terms of its size or
its contraction process versus if you had
hypervolemia. If there is hypervolemia obviously,
you wouldn't have decreased skin turgor.
That becomes important in terms of being too
little. Decreased skin turgor equates to skin
tenting. Look for that description, understand
as to what we're describing. On the opposite
end of the spectrum, if you had too much ECF,
though not only might you have too much in
the plasma, but at some point maybe it is leaking
out into the interstitium. Give me examples.
Congestive heart failure, would mean what?
What do I mean by that? What am I asking
you? Well, what is it that is causing increased
fluid in the ECF in congestive heart failure
when you have decreased cardiac output? It
is the increase in which Starling's force?
Hydrostatic pressure. Good. You are pushing
the fluid into the interstitium. Is that too
much or too little in the ECF?
That is too much.
We will talk about the feedback mechanism
further where you should know that in congestive
heart failure because the fluid is escaping
the vasculature or in other words the plasma
compartment is going into the interstitium. Guess
what is going on the kidneys. Decreased perfusion
and you are releasing renin and this viscous
cycle of RAAS especially the aldosterone and
pushing that fluid into the interstitium.
We will continue unless you crack the underlying
issue of a dysfunctional heart. What is my
topic? Too much. But you see as to how much
detail we have just gone into so that you get
the full clinical picture. You are not just
memorizing this. What if there was a protuberance
stomach in a patient maybe perhaps
I am giving you a couple of stereotypical
situations and that is what medicine is, isn't
it? Where is your patient coming from? Developing
country, developed country. What kind of
exposure has your patient had? Did they live
in an apartment where maybe there was fire
mean to say gas is escaping? All of this becomes
very relevant, why? Because everything that
we are doing ladies and gentleman, most common
presentations. If you find a patient, you
might be from a developing country where just
perhaps, the child may not have had access
to food properly, malnutrition specifically
protein. Are you with me? So if there're lack of
proper protein consumption in this child.
Wow! What is this called? Kwashiorkor. Why
did I emphasize the -orkor? Kwashiorkor is lack
of proper protein consumption whereas if it
is marasmus, it is total caloric malnutrition.
Let us go back to Kwashiorkor. If your child
is not consuming proper amounts of protein,
then what then happens? You lose the oncotic pressure.
Are you with me? So now you have lost oncotic
pressure, so you are not able to properly do
what? Maintain and contain your fluid in the
vasculature. Now for a different reason, we
have now lost fluid from the plasma compartment
and has now gone into the interstitium. Interesting.
So this is Kwashiorkor or let us say that
there is Northan Africa where in Egypt,
in microbiology, you have learned that there
is a common organism that then cause damage
to the liver. Schistosomiasis you have heard
of before. That schistosomal organism has
a propensity of affecting and injuring the
liver to the point where the liver gets damaged.
What happens? You cannot produce proper amounts
of what? Albumin. Same concept. What happens?
Decreased oncotic pressure and your patient
may have a protuberance stomach. What
is this? This is ascites. Do you get my points
now? We talked about too little with decreased
skin turgor because of loss of fluid or there
might be accumulation of too much fluid
in the ECF and I have given you congestive
heart failure and I have also given you an
example such as liver damage or maybe perhaps
Kwashiorkor. Let us continue. Everything that
you do in physiology, any subject as you
can see here immediately give it a clincial
tag, you cannot go wrong and this information