Physical examination. Left sided everything
is pulmonary. Crackles.
Where? On both sides bilateral. What are
you going to find on X-ray? You are going
to find pulmonary edema and you will find
opacity, both sides. Bibasilar crackles,
bibasilar opacities because that is what edema
looks like. What is this edema? It is transudate.
It is protein poor. Increased hydrostatic
pressure that causes pulmonary edema, you tell
me. Cardiogenic or noncardiogenic cause the
pulmonary edema? Obviously cardiogenic, is
that clear? Transudate. Increased hydrostatic
pressure. Obviously, there is a reason as
to why I asked you that question because later
on we will talk about noncardiogenic type
of pulmonary edema in pulmonology. And when
we do so, then we will refer to what is known
as increased capillary permeability. Therefore,
there would be exudate and protein rich. Now
it is transudate. S3 gallop, what does that
mean to you? CHF, large left ventricle. Blood
is gushing into left ventricle in
a hurry and you are going to create an S3.
Where? After S2. Come on bring these stuff together.
You got this or you? You have control of your education?
Doesn't that feel good? Right-sided
heart failure. Positive JVD, pitting lower
edema. What does pitting mean to you?
Transudate. Protein poor.
Perhaps ascites and hepatojugular reflux. What does
that mean? A touch upon the liver upon inspiration
comes a jugular. Not good. Right-sided
heart failure. Ask you a question. It is
typical question, which you can do this. Cor
pulmonale. No that is not what this is. Right-sided
heart failure secondary to left-sided heart
failure is a particular topic here. I will
just make sure we're clear. At some point
we'll go into cor pulmonale and then I will start talking
about pulmonary fibrosis, talk about pneumonia,
lobar type of consolidation
so on and so forth. At this juncture, not yet.
Chest X-ray, well here you have a large apex,
cardiomegaly. Talked about this a number of
times. Now the curly B lines represent? Well tell me
about lymphatics? When it rains, on the roads,
well you have the gutter system,
which is responsible for removing that excess
fluid. That is with the lymphatics or the lymphatics are
the gutter system of the roads. The lymphatics
are responsible for, in the interstitium to
remove the excess fluid. How can you confirm
this? What if your patient had lymphoma? What
if your patient had a tropical disease such
as elephantiasis secondary to which area of
Bancroft? What is that going to do? Block
off the lymph. When you block off the lymph,
my goodness you cannot drain out the fluid.
What do we call that? Lymphedema right. So
my point is this. When you have excess pulmonary
edema obviously the lymphatics are quite
active. Welcome to Kerley B lines.
The echo, what do you going to find? A systolic
ejection fraction that is decreased. Clear? What
do you want to do with this patient? Management.
Overall, improve quality of life,
increase comfort. How do you do that or maybe
something as simple as recommendation? A couple
of pillows. At all cost, you want to try to
reduce the amount of time this patient
spends in the hospital. Absolutely. Prolonged
life, treat with proven therapies that is
going to do what? Decreased mortality. What
does that bring us to? Neurohormonal blockade.
What kind of drugs are you thinking about?
How about spironolactone? How about ARBs?
How about ACE? Really. Spirinolactone what
does that knocking out? It is an
aldosterone receptor antagonist. You are not
using it for its potassium sparing effect or quality.
That is great, but really that
is not te point. It is the fact that you are
knocking out all those. What does remodeling
mean by the way? Remodeling is the fact that
the heart is trying to regenerate, but the
problem is it might then actually introduce
fibrosis. And when you do so during the repair
process, you might then actually end up creating
more harm than good. And if you are able to
slow down or perhaps even inhibits some of that
remodeling, then just may be you might be
able to increase the survival time of your
patient. Wonderful. You look for those type
of drugs. Neurohormononal, by that beta-blockers,
metoprolol. ACE inhibitors, you don't produce
aldosterone. You have ARBs. You block your
aldosterone. Aldosterone receptor antagonist.
Welcome to spironolactone. Is that clear?
Correct underlying cause absolutely. May be
this congestive heart failure was due to some
kind of valvular defect. Aortic stenosis,
mitral regurgitation. Revascularization if
needed. So, for example, if this particular
CHF was caused by MI, why not try to go in
there and do percutaneous type of intervention,
PCI, coronary artery bypass grafting if needed.
Treat hypertension, thyroid disease, autoimmune
all of the different causes of heart failure
that we have covered in this lecture series.
Stop offending medications. May be calcium
channel blockers and maybe perhaps NSAIDs.
Quality of life. Sodium, cut it down. May be
loop diuretic to improve, get rid of the pulmonary
edema. "I have a hard time breathing doc!"
Alright let's get rid of some of that fluid. Maybe you feel a little
bit better. Obviously you are not treating
the congestive heart failure. You are treating
the symptoms for the patient. What is a
symptom? The patient is expressing trouble.
What is sign? You as a clinician finding
the edema. Think PT and symptom that your
patient is expressing. The sign is you. You
are the sign. That is then going to find the
different clinical manifestations of a disease.
Reduce hospitalization. How are you going to go by doing this?
Maybe perhaps positive inotropic agent
if needed. What does it do? It blocks the
sodium-potassium ATPase pump on the basolateral
membrane. So therefore where is my sodium?
You tell me. You got this. Sodium is accumulating
where? Inside my myocardiocyte. If it is accumulating
within my myocardiocyte, it is not being pumped
out and so, therefore, no sodium is coming in
and calcium is not leaving. So indirectly
what are you doing? You increase your intracellular
amount of calcium. And that intracellular calcium
that you are increasing is then going to perhaps
bind to your troponin C or maybe perhaps even
increase the amount of calcium that is being
released from the sarcoplasmic reticulum. You see as to how
everything is being integrated. You see as to how by
learning your basics and you find in getting
digoxin digitalis and such that by increasing
calcium, then you might do what? You might
be increasing your positive inotropic affect.
Fantastic. Now the part that you want to worry
about is well there is every possibility
afib kicking in. So that you want to be careful
for a number of reasons. We prefer to warfarin
as being prophylactic. Now, treatments for neurohormonal.
do you want to do here? You want to try to
decrease the afterload. You can do so by giving
angiotensin type of inhibitors and so, therefore,
the less amount of angiotensin II, then you
have less vasoconstriction. You decrease your
afterload. Does that help with cardiac output?
Yeah. Does that ACE inhibitor also increases
quality of life because it inhibits remodeling?
The five class of medication. Pay attention.
The five classes of medication that have been
shown to reduce mortality by inhibiting remodeling
include ACE inhibitor, pro. Beta-blocker
metoprolol. Nitrates. ARBs. Losartan, tans. And we have
spironolactone, which is an aldosterone receptor
antagonist. The five classes. Look for these.
All depends as to what that
question is, what your attending is going for.
Are you trying to treat the pulmonary edema?
Please don't say ACE inhibitor there. You
will be a left out of your rotation. Pulmonary
edema, furosemide. Get rid of your fluid.
If you want to improve the quality of life,
then you start thinking about these drugs.
Is that clear? Yes.