ACE inhibitors. Reduce SVR. What does that
mean? Total peripheral resistance, systemic
vascular resistance, how? You don’t have as
much angiotensin II. Here we go. Reduces remodeling,
ACE inhibitors first line of therapy with
CHF because of the ability to reduce remodeling.
What does that mean? You do not introduce
the repair process and cause further harm.
Do not start if your patient has acute renal
failure. Is that understood? A lot of times
remember your instances in which the kidneys
require angiotensin II so that it can restore
GFR or maintain GFR. So please make sure that
you pay attention to renal status before you
do give your ACE inhibitor. We have talked
about this earlier when we did atherosclerosis
with renal arterial stenosis as well. Keep
that in mind. In addition, the side effect
that you are looking for is a dry cough. In
addition, you have the inability to properly
metabolize what component with ACE inhibitor
that results perhaps in cough? It is called
bradykinin. What kind of effect that the bradykinin
can have on your blood vessels? Increased
vascular permeability. So what do I sound
like? What does that mean? Angioedema. What
is happening? The blood vessels around my
oral mucosa undergo vasodilation, increase
capillary permeability. And it is how I talk,
you know that, which my impersonation of angioedema
is. Will you forget this? Never. So ACE inhibitors,
inability to properly handle bradykinin. Know
that, for any exam, you will be in good shape.
We talked about cough, angioedema, renal
failure. What about this hyperkalemia? Important
yeah. Remember, please. In addition, ACE
inhibitor with angiotensin II and bradykinin,
aldosterone does normally. What kind
of effect does aldosterone normally have on
potassium? It gets rid of it. If you have
ACE inhibitor, they don't produce aldosterone
from your glomerulosa. So, therefore, you are
going to retain your potassium, hyperkalemia.
Not good for whom? If hyperkalemia, EKG
T tenting. Next, more importantly, what happens?
The resting membrane potential and threshold.
So, the difference between those two, what
happens now? Is that resting membrane potential
going to become more positive or is it going
to become more negative? You answer that question.
Way back in basics, everyone loves this
question as you do. It is the fact that the
resting membrane potential gets closer to
threshold, it will depolarize. It gets
closer. It is not a good thing. Very scary,
especially for the heart.
ARBs. Angiotensin receptor blockers, pretty
straight forward. Very analagous. If your
patient is having dry cough and some of the
intolerance of ACE inhibitor, then you will
start thinking about using your
losartan and such.
Side effect. Hypotension, angioedema. You
see dry cough is not here.
Recently, the angiotensin receptor-neprilysin inhibitor, sacubitril-valsartan,
has been preferred over ACE inhibitor or ARB therapy.
In addition to the benefits of an angiotensin receptor blocker,
sacubitril inhibits the degradation of peptides that promote vasodilation and natriuresis.
However, neprilysin inhibitors alone are not effective, as they also increase angiotensin II levels.
Thus, it is used in combination with an ARB to mitigate that effect.
This combination has been shown to improve mortality and reduce hospitalizations
to a larger extent than ACE inhibitors or ARBs.
Beta-blockers. Metoprolol, carvedilol. You
knock out the beta-1 receptors, should not
be used in patients with CHF. It may blunt
the tachy. Be careful and so, therefore, remember
if you knock out the tachy, there might be
a compensatory mechanism that needs to be
taken place. So be careful.
Side effects. Brady, heart block, hypotension,
bronchospasms. Why? Especially be careful
even when they say selective beta-1 blocker
like metoprolol, you know is there such a
thing as a guarantee? No right. So just
because you say selective, yeah general scheme
of things and definition, sure. However, is
there a possibility that it might also have
beta-2 blocking effects? Sure. What are you
breathing in to relieve ashtma? Inhaler, beta-2
agonist. So there is every possibility that
by giving a beta-blocker to a patient that
has asthma you exacerbate the condition.
Please be careful.
And that tachycardia is huge as
well because there are times with the beta-blocker
that might mask the events that might be taking
place to who you win that your patient might
be going into hypglycemia with diabetes. Keep
that in mind. That is a huge pharmocologic
point. So, once again, if you want to review
some of you form, take a look at the conditions
or what conditions would then exercise caution
or great caution when using beta-blocker?
For sure bronchospasms and diabetes mellitus
are two big ones. Nitrates, We talked about
It is the fact that here you have your longer
acting causes vasodilation,
both the venal and the arterial, decrease
TPR and it also decreases your preload. In
addition, used in combination with hydralazine
in African Americans to decrease mortality.
Sodium-glucose cotransporter 2 (or SGLT2) inhibitors
have also now been added to guideline-directed medical therapy.
There is much that we are still learning about this class of drugs,
and many potential benefits in patients with heart failure.
These drugs are primarily known for their effects on the kidneys, where they reduce renal tubular glucose reabsorption.
This promotes diuresis and natriuresis, which reduces preload.
In addition, they appear to improve endothelial function and vasodilation, which can improve blood pressure and reduce afterload.
There is also a belief that these medications may work through multiple mechanisms
to improve energy metabolism and decrease oxidative stress on the heart.
While they were originally used in the management of diabetes, patients without diabetes also benefit from these cardiovascular effects.
Side effects to be aware of include an increased risk of genitourinary infections
and volume depletion (which can lead to acute kidney injury).
Additionally, diabetic ketoacidosis (even with normoglycemic levels) has been seen in patients with type 1 or 2 diabetes.
Spirinolactone, what do we do in here?
Here is your class III and IV heart failure. What
does that mean? Minimal exertion. Oh no,
I am having symptoms for even symptoms at
rest. "Hey doc, I can't even sleep on my bed.
I can't even sleep in a supine position." Well I
am not going to tell you that but I have to
go sleep where? On my recliner chair. Sad. III
and IV indicated spirinolactone. If you knock
out your aldosterone, you have hyperkalemia.
Hence, it is called potassium sparing drug
and not only that but spirinolactone has what
kind of effect? It is the other hormone that
it can also antagonize. Please
tell me what that hormone is. An androgen
antagonist, isn't it? Where does that come
in handy? Something like polycystic ovarian
syndrome. Here is a patient with polycystic ovarian
syndrome. She is a female, genotypiclly XX.
She walks in, but she has hirsutism, male-like
hair features. So there's a lot androgens in that
patient, polycystic ovarian syndrome and that
is clinically true because you are actually
looking for LH being greater than FSH. You
are with me here? If you don't, that is okay.
That is quite right because you will come in
to spirinolactone. Later on we will talk about
polycystic ovarian syndrome and how you want
to manage that? With there, we will talk about
spirinoloactone because it is an androgen
antagonist. But in the process may give you
There is something called ICD. You want to
make sure that you at least know what it
stands for. Implantable Cardioverter Defibrillator.
Nowadays you know that it is
pretty much found in everywhere. Thank goodnes.
Advanced heart failure because you are worried
about that arrhythmia. And well with these
hopefully you will be able to prevent from
arrhythmia kicking in. We talked about what
arrhythmia means. It just means that once
you disrupt the architecture of the heart, then
you are prone to whatever type of arrhythmia
it may be.
Now a couple of things here. Post MI 40 days,
implantable or nonimplantable with ejection
fraction less than 35? And here once again
class II and III, which means that you have
moderate exertion with symptoms and minimal
exertion. Please make sure you go back to take a look at
your New York Heart Association classes so
that you are familiar with the symptoms of
Side effects. Expenses obviously quite complications,
not all will benefit. And inappropriate shocks
which you might be feeling with a defibrillator
which your patient might then be complaining of.