Congestive Heart Failure | Clinical Medicine
Summary
TLDRThis video script delves into the clinical aspects of heart failure, distinguishing between left and right heart failure and high-output failure. It discusses the pathophysiology, causes, and complications associated with each type, highlighting the importance of left ventricular ejection fraction and the role of systemic vascular resistance. The script also covers the diagnostic approach and treatment strategies, including medication therapy, device therapy, and potential transplant considerations for severe cases, aiming to reduce mortality and improve patient outcomes.
Takeaways
- π **Heart Failure Overview**: The script discusses heart failure, covering its types, pathophysiology, and clinical aspects within clinical medicine.
- π **Pathophysiology of Heart Failure**: It differentiates between left heart failure, right heart failure, and high-output failure, detailing the pathophysiological processes behind each type.
- π **Systolic vs. Diastolic Heart Failure**: The script explains the differences between systolic heart failure (reduced contractility and ejection fraction) and diastolic heart failure (difficulty filling the heart with preserved ejection fraction).
- π **Causes of Heart Failure**: It identifies common causes of heart failure, such as myocardial infarction, cardiomyopathies, and aortic stenosis, which affect the heart's ability to pump blood effectively.
- π **Ejection Fraction Importance**: The left ventricular ejection fraction (LVEF) is highlighted as a critical measure, with a reduced LVEF indicating systolic heart failure (HFrEF) and a preserved LVEF indicating diastolic heart failure (HFpEF).
- π‘οΈ **Compensatory Mechanisms**: The body's compensatory mechanisms, such as the renin-angiotensin-aldosterone system and sympathetic nervous system activation, are explained in response to reduced cardiac output.
- π **Complications of Heart Failure**: The script outlines complications of heart failure, including pulmonary edema, cardiogenic shock, and organ malperfusion due to decreased systemic perfusion.
- π©Ί **Diagnosis of Heart Failure**: It describes the diagnostic approach to heart failure, including the use of chest X-rays, BNP levels, echocardiograms, and right heart catheterization.
- π οΈ **Treatment Strategies**: The script covers the treatment of heart failure, emphasizing guideline-directed medical therapy, device therapy, and the use of inotropes and mechanical circulatory support in severe cases.
- π **Acute Decompensation**: It discusses the management of acute decompensated heart failure, including the use of diuretics, BiPAP, and the consideration of mechanical support such as ECMO and LVADs.
- π₯ **Patient Management**: The importance of a systematic approach to patient management in heart failure, from risk factor modification to advanced therapies like cardiac transplantation, is emphasized.
Q & A
What is the main focus of the video script?
-The main focus of the video script is to discuss heart failure, covering its types, pathophysiology, causes, and the different aspects of left and right heart failure.
What are the two primary subtypes of left heart failure mentioned in the script?
-The two primary subtypes of left heart failure mentioned are systolic heart failure and diastolic heart failure.
What is systolic heart failure?
-Systolic heart failure occurs when there is a reduction in the contractility of the left ventricular myocardium, often caused by conditions such as myocardial infarction, dilated cardiomyopathy, or myocarditis, leading to a drop in left ventricular ejection fraction (LVEF).
What does LVEF stand for and why is it important in systolic heart failure?
-LVEF stands for Left Ventricular Ejection Fraction, which is the amount of blood pumped out of the heart with each contraction. It is important in systolic heart failure because a reduced LVEF indicates poor contractility and is used to diagnose heart failure with reduced ejection fraction (HFrEF).
What are the common causes of diastolic heart failure?
-Diastolic heart failure is commonly caused by conditions that increase afterload, such as chronic hypertension and aortic stenosis, leading to left ventricular hypertrophy and difficulty in filling the ventricle.
How does high output heart failure differ from typical heart failure?
-High output heart failure is characterized by increased cardiac output due to systemic vasodilation, which, despite the high output, is not sufficient to meet the body's oxygen demands, leading to tissue hypoperfusion.
What are the potential complications of heart failure mentioned in the script?
-The potential complications of heart failure include pulmonary congestion, pulmonary edema, cardiogenic shock, organ malperfusion, and the development of conditions such as hypoxia, acute kidney injury (AKI), and lactic acidosis.
What is the role of the renin-angiotensin-aldosterone system (RAAS) in heart failure?
-The RAAS plays a significant role in the compensatory mechanisms during heart failure. Activation of the RAAS increases systemic vascular resistance (SVR) and promotes sodium and water retention, which can worsen heart failure by increasing preload and afterload.
What are some of the treatment strategies for heart failure discussed in the script?
-Treatment strategies for heart failure include the use of medications like ACE inhibitors, ARBs, beta-blockers, diuretics, aldosterone antagonists, and sglt2 inhibitors. Other treatments involve device therapies such as CRT, ICDs, and LVADs, and in severe cases, the use of inotropes or mechanical circulatory support like ECMO.
How does the body compensate for decreased cardiac output in heart failure?
-The body compensates for decreased cardiac output by increasing systemic vascular resistance (SVR) through the activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system, which can lead to vasoconstriction and fluid retention.
What diagnostic tools are used to assess heart failure according to the script?
-Diagnostic tools used to assess heart failure include chest X-ray, B-type natriuretic peptide (BNP) levels, echocardiogram, EKG, and in more severe cases, right heart catheterization to measure pulmonary capillary wedge pressure.
Outlines
π Introduction to Heart Failure
The video script begins with an introduction to heart failure, discussing its relevance in clinical medicine. The speaker encourages viewers to support the content through likes, comments, and subscriptions. Additional resources such as notes and illustrations are available on their website. An upcoming course for the USMLE Step 2 and merchandise are also promoted. The script then delves into the pathophysiology of congestive heart failure (CHF), distinguishing between left heart failure, right heart failure, and high-output failure, with a focus on the most common type, left heart failure, and its two subtypes: systolic and diastolic heart failure.
π Understanding Left Heart Failure
This paragraph delves deeper into left heart failure, explaining the difference between systolic and diastolic heart failure. Systolic heart failure occurs when there is a reduction in the contractility of the left ventricle, often due to myocardial infarction, dilated cardiomyopathy, or myocarditis. The decrease in contractility leads to a drop in the left ventricular ejection fraction (LVEF), causing forward flow issues. Diastolic heart failure, on the other hand, is characterized by difficulties in filling the left ventricle due to high afterload, often caused by chronic hypertension or aortic stenosis. The script also discusses the implications of these conditions on cardiac output and the compensatory mechanisms of the body.
π Compensatory Mechanisms and Their Effects
The script explains the body's compensatory mechanisms in response to decreased cardiac output, such as the activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system. These mechanisms aim to increase systemic vascular resistance (SVR) to maintain blood pressure, but they can exacerbate heart failure by causing vasoconstriction, increased afterload, and promoting ventricular hypertrophy. The release of atrial natriuretic peptide (ANP) by the heart in response to stretch is also discussed as a compensatory mechanism to counteract the effects of angiotensin II.
π Right Heart Failure and High Output Failure
The script moves on to describe right heart failure, which is often a result of reduced contractility due to conditions like right ventricular MI or increased afterload due to pulmonary hypertension. The consequences of these issues include dilated and hypertrophied right ventricles, leading to a decrease in right ventricular filling and cardiac output. High output heart failure is also introduced as a rare condition where systemic vascular resistance is low, leading to increased cardiac output that is still insufficient to meet the body's demands.
π¨ Complications of Heart Failure
This section outlines the complications associated with heart failure, focusing on left heart failure. Complications include pulmonary congestion, pulmonary edema, and the associated symptoms such as dyspnea, orthopnea, and paroxysmal nocturnal dyspnea. Severe cases can lead to acute decompensated heart failure, which may cause severe pulmonary edema, hypoxia, and increased work of breathing. The script also touches on cardiogenic shock as a critical complication of heart failure.
π Advanced Complications and Presentations
The script further discusses the advanced complications of heart failure, including the effects of decreased systemic perfusion on various organs. It mentions the potential for encephalopathy, myocardial infarction, acute kidney injury (AKI), and acute mesenteric ischemia. The development of lactic acidosis due to poor tissue perfusion is also highlighted. Additionally, the script describes the signs of right heart failure, such as jugular venous distension, pitting edema, hepatic congestion, and ascites.
π₯ Diagnosis and Treatment of Heart Failure
The final paragraph covers the diagnostic approach to heart failure, including the use of chest X-rays, B-type natriuretic peptide (BNP) levels, echocardiograms, and right heart catheterization. It emphasizes the importance of physical examination and the consideration of acute left heart failure in the presence of elevated BNP levels, pulmonary capillary wedge pressure, and suggestive chest X-ray findings. The treatment approach involves guideline-directed medical therapy, which includes the use of ACE inhibitors, ARBs, beta-blockers, diuretics, aldosterone antagonists, and sglt2 inhibitors. The script also mentions alternative therapies and device therapies such as CRT, ICDs, and LVADs, as well as the use of inotropes and mechanical circulatory support in cardiogenic shock.
Mindmap
Keywords
π‘Heart Failure
π‘Systolic Heart Failure
π‘Diastolic Heart Failure
π‘Ejection Fraction
π‘Cardiac Output
π‘Afterload
π‘Renin-Angiotensin-Aldosterone System (RAAS)
π‘Pulmonary Edema
π‘Cardiogenic Shock
π‘Compensatory Mechanisms
π‘Diuretics
π‘Cardiac Resynchronization Therapy (CRT)
π‘Left Ventricular Assist Device (LVAD)
Highlights
Introduction to the topic of heart failure within clinical medicine.
Discussion of different types of heart failure: left, right, and high-output failure.
Explanation of systolic heart failure, its causes, and the impact on left ventricular function.
Causes of systolic heart failure including myocardial infarction and dilated cardiomyopathy.
Importance of left ventricular ejection fraction (LVEF) in diagnosing systolic heart failure.
Description of diastolic heart failure, its causes, and the role of afterload in the condition.
Mention of chronic hypertension and aortic stenosis as common causes of diastolic heart failure.
Differences between systolic and diastolic heart failure in terms of ventricular changes and ejection fraction.
Compensatory mechanisms of the body in response to low cardiac output in heart failure.
Role of the renin-angiotensin-aldosterone system in heart failure and its therapeutic implications.
Potential complications of heart failure, including pulmonary edema and cardiogenic shock.
Diagnostic approach to heart failure, including the use of chest X-ray, EKG, and echocardiogram.
Treatment strategies for heart failure, focusing on guideline-directed medical therapy.
Use of device therapy such as CRT, ICD, and LVAD in advanced heart failure management.
Management of cardiogenic shock, including the use of inotropes and mechanical circulatory support.
Importance of patient education and support, as well as the development of course materials for medical students.
Transcripts
foreign
ERS in this video today we're going to
be talking about heart failure this is
going to be again within our clinical
medicine section if you guys really like
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yourself some swag all right let's start
talking a little bit about CHF or heart
failure congestive heart failure many
different terminologies there
we talk about heart failure the first
thing we want to talk about is the
pathophysiology behind it
and really there's a couple different
types of heart failure believe it or not
there's left heart failure right heart
failure and this weird one called high
output failure we're going to talk first
about left heart failure which is going
to be by far the most common type of
heart failure
now we talk about left heart failure we
want to think about two different types
or subtypes if you will of left heart
failure there's what's called systolic
heart failure and diastolic heart
failure now what would cause this
patient was a normal heart to start
diverting its way into developing
systolic heart failure the primary
reason why this would develop is a
patient would have a reduction
in their contractility so the
contractility of the left ventricular
myocardium is going down so there's a
drop in the contractility so then you
have to ask yourself the question what
is causing this left ventricular
myocardium to not contract what are the
disease processes which would lead to
this so here we're going to say that
this myocardium here this left
ventricular myocardium is damaged in
some way shape or form and the
contractility here is knocked down
what's some causes
one of the most common causes here by
far is going to be a myocardial
infarction if a patient had an MI it's
going to cause fibrosis of that tissue
do you lose you lose contractility there
that's one way
another one believe it or not is
cardiomyopathies you know which one
particularly is very very commonly
associated with this one it's called
dilated
cardiomyopathy because what happens is
the the actual ventricles get really
really thin and very weak that's another
one where the contractility goes down
another one could be myocarditis but
it's relatively uncommon but we'll put
that one down as well so another one
could be myocarditis so inflammation of
the myocardium but all of these things
would be stimulatory factors that could
lead to systolic heart failure where the
contractility is just not good if the
contractility of the heart is not good
particularly left ventricle can it push
blood out of the left ventricle and into
the aorta very well no and so this is
where the issue occurs is that the
patient has a hard time being able to
pump blood out of the heart
so it's a problem with forward flow
there's a very important kind of like
formula we're not going to go crazy into
it but it helps us determine something
called the left ventricular ejection
fraction and this is a very important
terminology so in this person who has
systolic heart failure sometimes what
happens is as you drop the contractility
as you drop the contractility you drop
What's called the left ventricular
ejection fraction which is basically the
amount of blood that you're able to pump
out of the heart right and so when this
happens a decrease in left the
contractility when that happens that
goes down you drop your left ventricular
ejection fraction
and now it's hard being able to get
blood out of the heart
when that happens
what we do is we have a very specific
terminology whenever the patient has a
reduced left ventricular ejection
fraction particularly particularly when
it's less than 40 percent you know we
call that we call that heart failure
with a reduced ejection fraction we call
this hefref and that's usually when it's
less than
40 percent so when the left ventricular
ejection fraction is less than 40 we
call that hefref which is a another way
of describing systolic heart failure
but the whole point here that I want you
to understand is can contractilities
down the amount of blood getting out of
the heart is down so what is that called
when the volume of blood that you're
supposed to be pumping out of the heart
and one minute goes down that's cardiac
output
so in these patients they will start to
experience a drop in there cardiac
output which we're going to abbreviate
Co
and that's the big highlighting Factor
here for systolic heart failure or
hefref heart failure where the reduced
ejection fraction their causes dropping
contractility due to these can diseases
now
when we come over here to the other
flavor of left heart failure diastolic
heart failure this is another really
really common one
the problem here is something different
in the sense that it is really hard to
get blood out of the heart
and there's a couple ways that blood
leaves the heart right so we call that
like stroke volume the amount of blood
that you're kind of getting out of the
heart and one heartbeat that's dependent
upon preload contractility and what's
the last one afterload
when the afterload is crazy high in
these patients it's hard for them to get
blood out of the heart and that's
usually the problem here is that these
patients develop a massive
increase in their afterload
what are diseases
that would really kind of increase the
afterload and cause these particular
types of problems
chronic hypertension can't say how
common that particular etiology is that
is probably going to be by far one of
the most common causes so this would be
a chronic
hypertension we'll put chronic here
what's another one you know there's a
valve right here right there's a valve
right here called the aortic valve
aortic semilunar valve what if that
valve is super super stonotic and
because it's crazy crazy snotic it's
almost hard it's kind of obstructing the
forward flow that would also cause a lot
of afterload aortic stenosis is another
really common cause here so another
disease would be called aortic
stenosis this is another very very
common cause for an increase in
afterload it's basically anything that's
going to make it harder for the blood to
get out of the left ventricle these two
things
by far are going to be the most common
thing that will cause diastolic heart
failure now in systolic heart failure
what do you notice about The ventricle
Cooper dilated right so let's actually
write that over here so this is a very
dilated
enlarged ventricle
what you're going to notice here is that
this is super hypertrophied this
ventricle is very
hypertrophied so you have what's called
hypertrophy
it's a very thick and large left
ventricle we call that left ventricular
hypertrophy or sometimes abbreviated LVH
now the reason why is think about this
if the pressure in the actually aorta is
so high that you have to overcome it
what what's one way that you can do that
get stronger and thicken up the left
ventricle but when you do that when you
thicken up this left ventricle and you
make it to where you're actually able to
generate higher stroke volumes the
problem is now is that you decrease the
actual space of the left ventricle and
now
my problem is that I can't get the damn
blood into the left ventricle I can't
fill it properly and so this issue is a
filling issue this was a forward flow
issue
so what do I notice here in this
particular disease process the problem
with diastolic heart failure
is that they have a reduction in their
filling process
so there's a decrease in there left
ventricular filling
and because I can't fill the ventricles
very well that's going to cause a
problem
now here's the thing they're left
ventricular ejection fraction is
completely fine it's usually completely
preserved so this filling process won't
affect the ejection fraction so their
left ventricular ejection fraction is
usually what we refer to in this case as
normal
or let's use the term preserved
and so that's where we get this term a
heart failure with a lowercase p
preserved ejection fraction where if we
were to give it a particular number it's
at least greater than 40 percent so in
these patient populations of diastolic
heart failure their filling is reduced
because their ventricle is super super
hypertrophied that causes their left
ventricular ejection fraction to be
preserved and they have what's called a
half path but here's the question
this has a low cardiac output because of
low contractility
this will also have a low cardiac output
you guys know why why this one will have
a low cardiac output
this will have a low cardiac output
because again think about your
physiology guys it's very very important
to understand physiology here
if I have a decreased filling I'm not
going to load my ventricle very well so
I have preload is going to drop if my
preload drops what happens to my stroke
volume that goes down if stroke volume
goes down what happens to my cardiac
output that goes down so both of these
patients will have a low cardiac output
but the primary difference here is that
this is a preserved EF because they have
no problem with the rejection fraction
no contractility problem this one has a
reduced ejection fraction because they
have a contractility problem dilated
ventricle hypertrophy ventricle super
high yield can't forget these things
understanding the causes high afterload
understanding the causes contractility
problem
okay now we get into something that I
think is really really important and I
think can often be overlooked
when patients develop heart failure
because of these issues it can continue
to get worse and worse and worse if not
treated let me explain why when cardiac
output goes down
this is going to go back a little bit to
your physiology here
when cardiac output goes down
what we know is
there's always that formula do you guys
remember the formula uh for blood
pressure
the formula for blood pressure
is you have this one here
that blood pressure is equal to cardiac
output times systemic vascular
resistance
in patients who have heart failure
what's the problem here
their cardiac output drops
and then if you were to say keeping this
normal or constant what would happen to
their blood pressure that would also
drop
so then what's the general compensatory
mechanism that our body tries to create
we'll do this in pink
svr has to go up
and so this is usually what ends up
happening to the body is the body
creates this weird mechanism to try to
increase your systemic vascular
resistance which causes a lot of
problems let's see what that looks like
so the reason why you may be like Zach I
really don't want to know this this is
kind of like foundational stuff it's
very helpful for your pharmacology and
understanding I promise
so here critic output is low
normally what this will do is a couple
different things you know there's a
those Barrel receptors
and bear receptors are located in like
your your carotids like right at the
bifurcation or the aorta
and they sense
changes in cardiac output and blood
pressure
and so what happens is
you're going to stimulate these things
called Barrow receptors
and they're going to go and they're
going to activate
your sympathetic nervous system
when your sympathetic nervous system
becomes crazy activated it's thinking to
jack up all your epinephrine and
norepinephrine release so then what
you're going to see is you're going to
see a lot of epinephrine and you're
going to see a lot of norepinephrine
increasing why is that a problem well
the reason why that's a problem is is
that these little chemicals here they
love to go to the heart and to your
vessels and cause some problems
they go to the heart and they say hey
why don't you speed up the heart rate
because if you speed up the heart rate
that'll increase the stroke volume
hopefully increase the critic output but
it's not good for a patient's heart rate
to be super high but that's one of the
potential compensations is you're going
to increase the patient's heart rate
oops sorry guys
you're going to increase the heart rate
and again this is because it acts on
what's called beta 1 receptors this is
going to become helpful I promise
the other thing is it acts on other
types of receptors like alpha-1
receptors on your vasculature and causes
it to constrict
and if you constrict these vessels what
happens to the diameter of them they get
smaller what happens to the resistance
it goes up
so my svr will go up
and if that happens on the artery side
what's that going to do in my afterload
it's going to go up
and so it increases the afterload
now you're like that sounds like a
terrible thing it is terrible because
think about this
if a patient has
diastolic heart failure and you increase
their afterload what are you going to do
you're going to worsen their diastolic
heart failure because now if their
afterloads High what does their body try
to do to compensate it hypertrophes and
it's going to worsen their already
present heart failure so this is going
to be it's going to trigger hypertrophy
and guess what that's going to do that's
going to worsen their heart failure and
they're going to get sicker and their
heart failure is going to get worse
the other thing it's going to do is it's
going to constrict the veins because
there's alpha 1 receptors on both the
arteries
and there's Alpha interceptors on both
the veins so it's going to squeeze the
veins and try to push a lot of blood
back to the heart
and that's going to try to increase the
preload
but then if you increase the preload now
the ventricles have to dilate to
accommodate for that volume
and if the ventricle dilates
what does that sound like
systolic heart failure so it's going to
worsen the patient's systolic heart
failure so this is why it sounds like
these things are kind of like a good
mechanism to try to increase your svr
that's what it's trying to do
is increase the svr to increase your
blood pressure right
but unfortunately it worsens the
patient's heart failure
and their heart rate another thing if
that wasn't enough
is this cardiac output is going to
stimulate these like weird cells in the
kidney called juxtaglomerular cells and
these juxtapoor cells are very sensitive
to blood pressure
and what they'll do is they'll release a
molecule called
you guys already know this right ran in
all right so it's going to release a
molecule called renin now renin will
then do what
it'll then lead to the formation of
angiotensin one Angiotensin one will
then lead to the formation of
angiotensin two what's the enzyme that
stimulates that process Ace don't forget
that
Angiotensin II can do a couple things
but one of those things
is it increases aldosterone release from
the adrenal gland
and it also increases ADH release from
the poster pituitary
now with all of this being said
what's the overall effect of all of this
I'll show you
Angiotensin II
works on your vessels
you get a lot of Angiotensin II
receptors on your your vessels so here
let's say we have what's called a
Angiotensin II receptor here in your
vessels guess what it does squeezes the
heck out of them
what'd that do svr goes up because
that's the compensatory mechanism if svr
goes up then what happens to your
afterlook
that goes up what happens if you have
diastolic heart failure you worsen the
hypertrophy patient's getting sicker
that's not helpful
what happens if you do the preload
you're going to cause more blood to get
returned to the actual heart preload
goes up but in a patient who has
systolic heart failure what is it going
to do it's going to dilate their heart
even more and worsen it so you guys get
the concept here is that this is another
potential problematic issue that can
worsen the patient's heart failure and
that's why we have drugs that we'll talk
about a little bit later that I'm going
to kind of preemptively kind of covering
here that this will help to treat
because we just don't want to have these
high angiotensin two levels the high
sympathetic nervous system activity and
just to complete this concept
aldosterone ADH will be higher and you
know what this does this increases
your reabsorption now the patient's
reabsorbing lots of sodium and water
and if you reabsorb sodium and water
what is that going to do it's going to
cause the patient to retain a lot of
this fluid and they're going to start
developing edema they'll have more
preload so the hot ventricles will have
to dilate more but one of the problems
that you'll see here is they'll start
developing a lot of Edema
because of this
so this is the concept that I really
really want you guys to be able to
understand here with this nasty disease
process
there's one more thing which is actually
super cool though
so this system here is called the renin
angiotensinaldastrin system right you
know whatever your heart your critic
output is really really low
another really interesting thing that
happens is
is that your heart whenever it's like
really low cardiac output the hearts
actually kind of get filled with blood
and so they can release this molecule
in response to a lot of stretch so let's
say that the heart is really really
being stretched it's being stretched a
lot
when the heart is being stretched a lot
it makes a molecule called atrial
natureuretic peptide and it makes a lot
of it and the whole point of increasing
this atrial nitritic peptide is it wants
to go and inhibit
the hope is that it inhibits Angiotensin
II
and if I inhibit Angiotensin II I
prevent this whole disastrous process
from occurring well that's cool I would
really like drugs that increase amp then
I would really like drugs that decrease
Angiotensin II block aldosterone and
block the sympathetic nervous system and
that's we'll talk about in the treatment
section but this is what I want you guys
to understand about left heart failure
now let's quickly go through right heart
failure and high output failure bye my
friend so now we got to talk about right
heart failure so we talk about the left
heart failure the right heart failure is
actually a lot easier when we talk about
right heart failures the same kind of
concept
we take this normal heart and we jack it
up to cause systolic heart failure now
when we talk about this it's again
you're dropping what the contractility
so what generally drops contractility on
that right heart
well in the left heart the most common
cause was an MI
guess what it would be here in mi okay
so generally a right ventricular
Mi is going to be the most common cause
generally of this systolic right heart
failure so you're dropping the
contractility here
and that's leading to the formation of
the systolic heart failure now again
what you're going to notice is that this
puppy's going to start be getting super
dilated all right so what you're going
to notice is this dilated type of right
ventricle
now
another concept here
with this dilated right ventricle here
is that your right ventricle the
contractility is reduced right so this
whole right ventricle let's say is
really really messed up
because it's messed up it's going to
have a hard time being able to pump
blood out into the pulmonary artery
right so it's going to have a hard time
with forward flow
so what you'll notice out of these
patients is that they're going to have a
low right ventricular cardiac output
right because of the contractility
and so because of that they're going to
have this low contractility
this is going to lead to a decrease in
their right ventricular ejection
fraction
now we don't generally give these you
know as we compared prior the heart
failure with the reduced ejection
fraction that's primarily only
consistent with left heart failure but
again you can think about it in this
particular way but again
a reduction in contractility will lead
to a reduction in the right ventricular
ejection fraction and the problem is
that these patients are going to have a
hard time generating a good cardiac
output out of the right ventricle and so
that's the concept here it's pretty
straightforward something is decreasing
contractility because you infarcted the
right ventricle
in the other aspect over here you have
something increasing the afterload right
so if I have something increasing the
afterload
in the example for left ventricle it was
hypertension it was aortic stenosis
for this one it's anything that
increases I'm going to put a little
parentheses here anything that increases
the pulmonary vascular resistance so for
the art systemic circulation was called
systemic vascular resistance that was
hypertension oreatics aortic stenosis
and this thing it's anything that causes
pulmonary hypertension so we say this is
pulmonary
hyper
tension and there is different types
we'll talk about this in poem when we go
over pulmonary hypertension but there's
type 1 which is idiopathic type 2 which
is due to left heart failure type 3 due
to some type of like lung disease like
COPD or interstitial lung disease Type 4
due to some type of chronic pulmonary
emboli and then type 5 is there's
usually something like sarcoidosis like
something compressing the pulmonary
vascular but this is the concept I want
you to understand pulmonary hypertension
for right heart failure systemic
hypertension for left heart failure for
that diastolic type
now what do you notice here about this
right ventricle is thick right so they
have some hypertrophy generally of that
right ventricle so we could say a right
ventricular
hypertrophy and this is usually because
that ventricle is going to have to
thicken to be able to accommodate the
high pressure of the pulmonary
vasculature that's the only way it can
do it
and so because of that it's going to
have a hard time being able to fill with
blood so the problem with this situation
here is the same concept they have a
reduction and right ventricular filling
which caused them to have a again a
normal ejection fraction they don't have
a problem with their ejection fraction
so they have a normal
right ventricular ejection fracture so
again decreased filling process
but normal right ventricular ejection
fraction that's the big kind of thing
that I want you guys to understand here
now again remember both of these are
going to have a reduction in right
ventricular cardiac output it's just
again the mechanism behind them
developing this
all right that covers this one for right
heart failure the pathophysiology and
the causes
what about this weird one there's this
weird entity called high output heart
failure and generally high output heart
failure is particularly only consistent
with generally left so the left heart
and what I want to do quickly is talk
about this one so for the most part what
you've noticed is that when we talk
about left heart failure before is that
there was a low cardiac output and then
would you talk about right heart failure
there's a low cardiac output
there's this weird entity in the world
where this is called a high cardiac
output heart failure like what that
seems odd
it is weird but here's let me let me
kind of explain why this happens
and this patient here we see that their
vessels are super dilated
so they have extremely super vasodilated
blood vessels so what you'll notice here
out of these patients is they have a
massive
vasodilation all right and when you
vasodilate vessels that's a big ding
we'll talk about what causes this but
this is massive
vasodilation right so there is massive
vasodilation here
the question that you have to ask
yourself is what's causing these vessels
to become super super dilated and
there's a bunch of different things
one reason is very common is sepsis
sepsis will cause massive vasodilation
another one which is an odd one is when
you have thymine deficiencies such as
berry berry this will for some reason
cause massive vasodilation
thyrotoxicosis so when patient has
thyroid storm this can also cause
massive acetylation
other kind of interesting things could
be things like AV fistulas
as well as severe and I mean really
really severe anemia these are
particular things that in these diseases
but I would say sepsis being kind of one
of the most common ones these will cause
massive vasodilation
when you massively visually dilate these
vessels what happens to the systemic
vascular resistance now soccer's huge
resistance has got to be low
so now there's systemic vascular
resistance
is crazy crazy low
now go back to that formula what was the
formula called
for everything with low or how output
heart failure we said that we have blood
pressure is equal to cardiac output time
systemic vascular resistance and all the
ones that we talked about cardiac output
was low which dropped the blood pressure
now in this disease process
the systemic vascular resistance is low
which will cause the blood pressure to
be low what has to compensate the
cardiac output and that's why we call
this high output heart failure
so then what happens is when your
systemic vascular resistance drops what
it does is it creates a reflex kind of
situation here so what it does it'll
drop the blood pressure
So the patient's blood pressure may drop
when you drop the patient's blood
pressure what that's going to do is it's
going to activate the sympathetic
nervous system and the renin
angiotensinaldosterone system
and that is going to increase the
sympathetic nervous system
now look at this
if I increase the sympathetic nervous
system that's then going to go in work
on the heart
and when it goes and works on the heart
it's going to work on a bunch of
different components here
one is you have your SE node your AV
node your bundles of hiss and bundle
branches that's all going to be
activated and your heart rate
is going to try to go up because it's
going to hopefully try to increase your
cardiac output
and you're going to contract your heart
like a son of a gun so then on top of
that you're going to try to cause the
heart to really really contract in the
stroke volume will go up
and both of these are going to be an
attempt to try to push as much blood
possible out of the heart
so what you'll notice here is that these
patients will have a massive increase in
their heart rate and a massive increase
in their stroke volume
but here's what's really odd
you would think okay these guys are
pumping and I mean pumping
blood out of their heart into the
coronary I mean into the systemic
circulation so the cardiac output has to
be high enough right it's got to be good
enough to be able to meet the actual
tissue demands
it's not
and that's where the problem here in the
cycle occurs this disease causes
vasodilation leads to this whole process
tries to increase the cardiac output but
no matter what it's not enough to meet
the body's demands and so what happens
here is it's not
enough
and that's the issue so you see how we
talk about heart failure
it's the inability
to perfuse the tissues and meet their
demands
that would be a definition then so high
output heart failures the cardiac
output's high but it's not high enough
to overcome this massive vasodilatory
effect to meet the tissue's oxygen
demands and that is heart failure so so
far we've gone over left heart failure
low output right heart failure low
output and the Rarity of high output
heart failure now let's go over what are
the complications of a patient
developing heart failure all right my
friends so now if a patient has left
heart failure whether that's diastolic
or systolic heart failure or right heart
failure whether it's systolic or
diastolic heart failure we have to
understand the particular complications
that can arise
when a patient has left heart failure
one of the big things that you'll see
with these patients is features of
pulmonary congestion so either way the
patient's cardiac output stinks they're
not able to not get enough blood out of
their left ventricle
so what happens is because they have a
cardiac output that is being reduced if
you will in other words and these
patients it's hard to get the blood out
of the heart because of why because they
have a reduced cardiac output
now because of that
if the blood can't get out of the heart
where is it going to go it's going to
start backing up into the left atrium
when it backs up into the left atrium it
goes into all of these like cute little
pulmonary veins here you see it starts
moving into the pulmonary veins and then
what happens is it starts kind of like
congesting these pulmonary veins
intensely now when the pulmonary veins
start coming very very filled with all
of this Blood the pressure in those go
up
and we specifically use a terminology
here called pulmonary capillary wedge
pressure so we'll use that on both of
these here and this will go up and the
pulmonary capillary wedge pressure is a
measure of left heart pressures so if
the left heart pressure is high the
pulmonary capillary wedge pressures will
also be high
when that happens the pressure in the
pulmonary capillaries rise enough that
guess what starts leaking out of these
actual vasculature fluid so you're going
to have fluid leaking out of this
vasculature and into the interstitial
spaces
and into the alveoli so now this alveoli
is going to become filled with fluid
you're going to develop some edema here
in the interstitial spaces and now these
patients have pulmonary edema and so
this is one of the potential
complications is they get a little bit
of pulmonary edema
now why is that bad when you have
pulmonary edema some patients can
present a couple different ways
one is they particularly present with
what's called
dyspnea now dyspnea it may just be a
generalized Disney this may be with
exertion this may be at rest and that
depends upon the severity of their CHF
but another very interesting
presentation is that whenever these
patients lie flat the fluid tends to
kind of like kind of separate out into
multiple parts of the lungs normally
they'll be in the dependent inferior
portions but as you lay flat this edema
can become worse and spread throughout
multiple alveoli and this can worsen
their actual shortness of breath when
they're laying flat and so there's two
terminologies one is called proximal
nocturnal dyspnea this is whenever
they're at their sleep and they're
laying flat they're super short of
breath or just in general maybe they're
not sleeping they're laying down flat or
laying on a recliner and they have some
shortness of breath there it's the same
concept it's called orthopnia These are
big big common features that we see with
pulmonary edema one is just dyspnea
whether it be exertion or rest or the
other one is when they're laying flat
proximal nocturnal dyspnea orthopnia
another potential problem here
is that whenever these patients let's
say they really really have a massive
reduction so let's say that their
cardiac output massively reduces maybe
for whatever reason common triggers for
patients to develop what's called acute
decompensated heart failure
is they have an MI or they have a
massive tachyarrhythmia or they stop
taking their their medications they're
supposed to be taking and what this does
is this massively drops the cardiac
output massively increases the pulmonary
capillary wedge pressure and worsens
their pulmonary edema like terribly and
sometimes this pulmonary edema can be
severe I'm talking severe
pulmonary edema
and this is something that we would
generally see when a patient has what's
called acute decompensated heart failure
and what happens is is this fluid
will really start kind of like like all
over multiple different alveoli and
interstitial spaces will become filled
with fluid
and this can cause a massive VQ mismatch
when you fill up multiple alveoli with
fluid that causes a VQ mismatch decrease
in ventilation normal perfusion there's
a mismatch and that leads to hypoxemia
so watch out for a VQ mismatch here
and what will happen is the patient's
spo2 will be very low and they can
exhibit features of what's called
hypoxia
the other thing is that this fluid that
leaks into the interstitial spaces
when it actually does leak there
sometimes it may just cause the patient
to have generalized dyspnea or increased
work of breathing so they may be working
hard to breathe or they may have a
higher respiratory rate so that's
another kind of thing that you want to
watch out for is watch out for
an increased work of breathing
or
an increased respiratory rate
so these are some of the big findings
that you want to watch out for so again
watch out for a stimulation of VQ
mismatch
because of all of these alveoli being
filled with fluid and then hypoxia so
watch their O2 sat to see if they have
desaturations
this is super super common in left heart
failure so big things to look out for is
go to the patient see if they have any
respiratory distress or hypoxia on their
O2 saturation ask them if you have any
shortness of breath at rest exertion or
they're laying down flatter when they're
sleeping the other thing get your
stethoscope that you paid so much money
for and go and listen and see if you
hear any rails or crackles all of these
are potential signs of pulmonary edema
this is very common in left heart
failure
the scariest complication that I say
that you would potentially see in a
patient who has left heart failures
cardiogenic shock and this is definitely
the scariest one generally again a very
common trigger here
that can happen is an MI a massive tachy
arrhythmia or you stop taking your
medications these are very very common
triggers now again same concept the
patient has a massive drop in their
cardiac output
if you drop their cardiac output you're
not going to be getting enough blood
flow
out of their heart
when you don't get enough blood flow out
of the heart particularly enough volume
you drop that cardiac output what
happens to their perfusion oh that's
stinky that systemic perfusion goes down
so not only whenever you have a low
cardiac output do you have a hard time
getting blood out of the heart and it
backs up into the lungs but you have a
hard time getting it out of the heart
and delivering it to multiple tissues
when you have a decrease in systemic
perfusion
the problem with this is
that your body kind of says okay
perfusion is kind of stinky right now
the credit that's because the cardiac
output is really low
you know what the body tries to do is it
says okay what I'm going to do is if the
cardiac output is low what's that
formula BP is equal to cardiac output
times the systemic vascular resistance
let's write that out so BP is equal to
cardiac output times the systemic
vascular resistance and these patients
who are in cardiogenic shock this is low
causing this to be low what has to
compensate my friends
svr and this will shoot through the roof
and when svr goes up it's clamps down on
your vessels squeezes them and now you
have very little blood flow going to
your extremities you know what this is
going to do this is going to cause these
patients to have very cold
or pale
extremities
another really really terrifying sign
here is they have like modeling this is
really really kind of scary it's where
they have this weird kind of
discoloration usually at the knees and
that's a very sign of that's a very poor
sign of perfusion and this is usually
because you're clamping down on those
vessels to compensate
another thing is that when you have
decreased systemic perfusion not only do
you create this reflexive
vasoconstriction
but you also get organ malperfusion
right if I have organ malperfusion oh
man that ain't good because now I'm not
perfusing various tissues what are some
of these tissues that actually become
effective because of an increase in more
organ malperfusion one is the brain the
brain is super sensitive to blood
pressure the coronary circulation which
supplies The myocardium of the heart
well it's going to make things a lot
worse it becomes very susceptible
the kidneys become susceptible and the
git would probably be the last one of
the line but it's also super susceptible
if I don't perfuse the actual brain you
know then I can develop encephalopathy
and this is probably going to be one of
the most common causes sometimes if the
actual mouth perfusion is severe enough
it's possible it could cause a TIA CVA
all right that's another thing you want
to watch out for
the other thing is that if you don't
profuse the actual myocardium well
enough it may cause a myocardial
infarction
so you may see things like an n stand me
or a stemi potentially so these are
things that I think are really really
important to remember
the other thing is it may stimulate son
of a gum it may stimulate injury to the
kidneys this is called an Aki there is a
very common terminology that you may
hear here when patients have very severe
left heart failure and they don't
perfuse their kidneys very well because
of decreased systemic perfusion but also
their cvps are really high so it's hard
to get blood out of the kidney they can
develop kind of something called
cardiorenal syndrome very common trigger
of Aki so don't forget that one and the
last one is they may cause
acute mesenteric ischemia this is
another really really big one or
ischemic colitis and this is another big
trigger so you're going to want to watch
out for any kind of like bowel ischemia
and abdominal pain
the last thing that's always a feature
of systemic perfusion that's being very
very poor is your tissues whenever
there's very little oxygens being
delivered to the tissues so here this
tissue is supposed to be getting oxygen
if it's getting very very little oxygen
they do not like that and what they do
is they trigger the production of a
molecule that's usually a sign of poor
perfusion you guys know what that's
called lactic acid but lactic acid gets
broken down into lactate
and so you want to watch out for this
because one of the things that this will
do is this will really cause the pH to
drop and it'll trigger an acidosis so
watch out for acidoses that can occur in
the setting of cardiogenic shock
so again
when a patient has heart failure it can
kind of look a little bit different the
patient may have chronic CHF where their
primary symptom may just be dyspnea
peroxism nocturnal dyspnea orthopnia
but if they develop an acute
decompensated heart failure from those
triggers Mi tachyarrhea is medication
non-compliance they can develop severe
pulmonary edema hypoxia respiratory
distress
and most patients who have
chronic CHF they may just have minimal
decreased systemic perfusion and the way
that they compensate is an increase in
systemic vascular resistance so they may
have cold kind of pale modeled
extremities
but whenever it's really bad to where
there is an acute decompensated heart
failure due to an MI tachyarrhythmias
medication non-compliance now they don't
perfuse multiple organs and they can
develop things like encephalopathy Mi
Aki and acute mesenteric ischemia and
lactic acidosis these are big things to
think about my friends
all right we come to the last one here
patient has right heart failure all
right so the patient is Right heart
failure was because they had something
wrong with the contractility or the high
after the pulmonary hypertension this
one's super easy thank goodness
whenever the right heart is Damaged
what happens is again the whole concept
here is that it's either you can't fill
it or you can't get blood out of it
right so that's either one of those
Concepts you can't get blood in or you
can't get blood out of it
when that happens
what happens is the pressure in the
right heart increases and we use a
terminology to really describe that and
that's called your central venous
pressure so your central venous pressure
becomes very high
when your central venous pressure is
high what happens is the blood is is
kind of a measure of the blood backing
up into your superior vena cava
and blood backing up into your
inferior vena cava and what this will do
is this will kind of present in two
different ways that you want to try to
look for
one is it'll present with a patient
having a lot of jugular venous
distension so they'll have a plump
jugular vein
and the other one is they'll have some
edema of their lower extremities usually
what's called pitting edema so when you
press on it it kind of really dips in
and gives this kind of deformity there
this is super common in right heart
failure
another common presentation again
regardless of the type whether it's
problem filling or problem getting out
the concept is the same is that you have
a very high
central venous pressure
when your central venous pressure is
high the blood is going to back up into
the inferior vena cava and what it does
is it causes one particular problem
which leads to hepatic
congestion
so you know the liver I'm kind of
zooming in on a basic model of the liver
let's say this is a liver cell this is
an artery this is the hepatic veins
which empty into the IVC and this is a
biliary duct
whenever this hepatic vein is congested
and it can't get blood to go up it
congests in the liver and causes the
liver to become injured and damaged and
you know what this could potentially
present as this could cause a patient to
develop liver failure more specifically
I would say you see this more commonly
as a serotic kind of presentation but
you can see this as a potential trigger
of liver failure because of the
increased hepatic congestion
all right the other thing that it can do
is it can increase your portal pressure
so what happens is your hepatic veins
what happens it can actually cause this
to really cause the portal pressure
within the venous circulation the
hepatic portal circulation to become
very very high
so if you increase your portal
pressure what this does is this causes
the hydrostatic pressure in the portal
veins and the peritoneal capillaries to
be super high and leak fluid into the
abdomen and when you leak this fluid
into the abdomen what do we call this
type of fluid that leaks into the
abdomen ascites and so that's another
very very common presentation here is
ascites
so watch out if a patient develops liver
failure and they have a history of right
heart failure think about that if they
have ascites and they have a history of
right heart failure think about that and
again if they have very plump jugular
veins and pitting edema think about a
right heart failure
and the last one
it's not commonly thought of but it can
happen left heart failure we talked
about cardiogenic shock right heart
failure can also get cardiogenic shock
so think about this this concept is
super interesting
in this situation here you're having
let's say blood difficulty this is more
common in the systolic types where the
right ventricle is super dilated in this
situation you have problem getting blood
out of the right heart
and because of that
now this right ventricle has a hard time
if it becomes super dilated maybe it
can't fill properly or it just can't get
blood out of the heart
when that happens
because you can't get blood out of the
heart the right ventricle
dilates even more so if it's dilated
before it dilates more
all right
so now this sucker is huge so whenever
this happens you can't get blood out of
the heart it's going to stimulate the
right ventricle to dilate even more
when the right ventricle dilates more
the next thing it does is is it causes
the septum
to Bow over into the left ventricle and
now look at the space of the left
ventricle it's smaller so then it causes
it's called a septal shift so a septal
shift and we'll say that this septal
shift is occurring from right to left
from the right side to the left side
what that does is
it makes it hard for the left ventricle
to fill with blood because now it's much
smaller
if it can't fill with blood what happens
to the left ventricular cardiac output
it drops
so now you have a septal shift and
that's going to cause a decrease in the
left ventricular
filling
if you decrease the left ventricular
filling
that is going to then do what
that is going to decrease the left
ventricular cardiac output
and if you decrease the left ventricular
cardiac output oh son of a gun
that can potentially lead to systemic
malperfusion and then if we go on
further
cardio
genic
shock
so this is a pretty scary one I'm
actually usually we don't see this one
too often right heart failure causing
cardiogenic shock but when you do it's
pretty terrifying because it's a really
really bad one
but this is another potential one that I
want you to think about but you really
primarily only see this one
with right ventricular Mi as the
particular etiology here not so much the
pulmonary hypertension causes
all right my friends that covers the
issues or complications if you will of
heart failure it's a pretty disastrous
thing if it gets really really bad what
I want to do now is I want to take you
through how to diagnose heart failure
first thing is get a chest x-ray this
will help you because if they have
cardiomegaly that's somewhat helpful do
they have pleural effusions pulmonary
edema and curly B lines that's all
suggestive of left heart failure for the
most part
now
with that being said if a patient has
these findings that doesn't Define or
determine that they have heart failure I
want to combine oh they have pulmonary
edema pleural effusions is their left
heart not doing a good job
well one way I could say if their heart
is not doing a good job is I can check
BMP this is not a good test though it's
usually used in the emergency department
to kind of quickly exclude a CHF
exacerbation because if BNP levels are
really low then you can say Okay their
Disney is probably not from a CHF
exacerbation if it is really high then
you can't rule that out the better test
as an echocardiogram because it's going
to look directly at the heart and it's
going to look to say hey what's the
rejection fraction is it less than 40
percent their left ventricle doesn't
look like it's moving at all that's
systolic heart failure or does it look
like the left ventricle is Contracting
and pumping but it's not filling
properly oh that's diastolic heart
failure in combination with the chest
x-ray that can be very beneficial also
do your physical exam if you don't see
anything on the chest x-ray look at the
jvd look at the legs look at the abdomen
to look to see if they have any features
of systemic congestion and combine that
with their Echo
after you've done that you should be
able to determine is it right versus
left that's pretty straightforward
now the most definitively diagnostic
test to determine if the patient is in
acute left heart failure or in left
heart failure in general is to do a
right heart catheterization also
referred to as a swan guns catheter you
take a catheter you run it down the IJ
you run it into the pulmonary into the
right atrium into the pulmonary artery
and up into these like pulmonary artery
capillary areas inflate the balloon and
then measure the pressures
I told you that the pulmonary capillary
wedge pressure if it's really high
that's very suggestive of failure of the
left heart
and if it's greater than 18 millimeters
of mercury that's a very suggestive
number of left heart failure so if a
patient has elevated B and P levels and
Echo and a pulmonary capillar wedge
pressure greater than 18 in combination
with a chest x-ray suggestive of
pulmonary edema I can really be
confident in them having left heart
failure
now with that being said if a patient
has acute left heart failure it's
important to go through their medication
list and look to see what their heart
rate is and look to see if they have any
valvular disturbances but one of the big
ones that I have to do is get an EKG and
also consider a left heart cath if I
think they're having an MI because
that's going to find the occlusion and
then treat that and that might be the
thing that knocks them out of this acute
heart failure potentially
all right how do we treat heart failure
this is a really really important topic
when I treat them I specifically went
into this for a reason I want to reduce
sympathetic nervous system activity
reduce Razz activity and increase amp
activity and if you remember increasing
amp activity did what decrease Razz so
my goal is to decrease sympathetic
increase decrease sympathetic and
decrease Razz how do I do that
well if I decrease my sympathetic
nervous system I have to use things like
beta blockers and sglt2 Inhibitors so
metoprolol Carvedilol or impact of
losing usually these sglt2 Inhibitors
are very very important patients with
diabetes but if they have cardiovascular
disease it's also beneficial and what
happens is they reduce the sympathetic
nervous system that reduces the heart
rate and that also reduces the systemic
vascular resistance I don't constrict
the veins I don't constrict the arteries
as much I don't reduce I don't actually
cause changes in preload and afterload
and I don't cause ventricular remodeling
that improves ventricular function
that's mortality beneficial right there
the other thing is that sglt2 Inhibitors
also cause aquauresis they Cause you to
pee out of tons of water and so that can
help with a lot of the edema if the
patient is edematus
the next concept is I want to reduce
Razz activity so the reason why is one
of our low cardiac output again we said
increased sympathetic and low credit
output activate renin
so renin leads to eventually Angiotensin
II but if I give them a drug called an
Ace inhibitor that blocks Angiotensin 1
from being converted into Angiotensin II
if I also give them a drug like an AR
and I that increases amp it prevents amp
from being degraded if amp builds up it
shuts down Angiotensin II and then if I
also give an ARB our blocks Angiotensin
II from binding to receptors all three
of these drugs will help to decrease
Angiotensin II if I decrease Angiotensin
2 I reduce the constrictions of the
arteries in the veins and I have reduced
ventricular modeling and that's a
mortality benefit
another thing is Angiotensin II if
there's less of it there's less
aldosterone and also ADH but
particularly aldosterone because now
there's less sodium and water retention
if I don't retain as much sodium in
water I don't have as much edema but I
also don't have as much preload and I
don't cause ventricular remodeling
that's where aldosterone antagonists
would be really really beneficial in
shutting down aldosterone production
this is the concept and these are the
drugs that we have to incorporate in
patients who have heart failure because
they have mortality reducing benefits
okay that's a part of our guideline
directed medical therapy
other things that we can add on with
guideline directed medical therapy is
Alternatives so if patients
African-American they can't tolerate an
ace inhibit or an ARB hydralazine and
isosorbide nitrate is a good combo to
add because they're good vasodilators
the other one is an alternative to a
beta blocker if they're maxed on a beta
blocker and they are a normal sinus
rhythm I have a braiding can be
considered
if you want to help them to get rid of a
lot of the sodium and water retention
you can make them pee it out by giving
them diuretics Loop Diuretics and
thiazide diuretics
and then the next thing is if a patient
has the need for device therapy
so what I mean by this is if a patient
has heart failure especially left heart
failure it stretches out the left
ventricle and kind of causes left bundle
branch blocks and then that alters the
synchrony of the ventricles if I give
them what's called a CRT cardiac
resynchronization therapy it'll make
sure that the ventricles are Contracting
kind of in Tandem and improve
potentially the left ventricular
ejection fraction I should definitely be
instituting that in patients with an
lvef less than 35 percent in an lbb B
all right that's a CRT
if a patient has a left ventricular
ejection fraction less than 35 percent
and they have ventricular arrhythmias
they need to get an aicd this will shock
them if they go into vtac or into v-fib
and prevent them from going into cardiac
arrest
the next thing is if a patient is on all
these medications they have device
therapy their left ventricular ejection
fractions less than 25 percent they're
not looking good and they look like
they're going to need a transplant
sometimes we will play something called
an lvat a left ventricular assist device
which will take blood from their left
ventricle and shunt in a different
direction into the aorta to give that
left ventricle some time to rest
now
and patients who are in cardiogenic
shock all right they're systemic
perfusion stinks I want to have one
primary goal which is to increase
systemic perfusion so increasing
systemic perfusion is very beneficial in
patients who are in cardiogenic shock so
what could I do ionotropes or mechanical
circulatory support
one way I can do that is I give them
things like dobutamine or melanoma these
are commonly used in acute decompensated
heart failure cardiogenic shock
the benefit of these is that they reduce
afterload and increase contractility
which combined increased cardiac output
the downside is that evidence has shown
no reduction in mortality
the other drug is digoxin this is an
oral and IV drug so you can take this
outpatient you can't take these
outpatient
this you can give to the patient and
it's been shown to increase
contractility and decrease AV node
conduction so it's good in atrial
fibrillation as well
it is not shown to reduce mortality but
it may reduce the actual
hospitalizations so there's a potential
benefit to digoxin and increasing
perfusion especially in patients with
cardiogenic shock and even as an
outpatient continuing that drug
if the patient is failing these
inotropes and they're continuing to
decompensate and showing signs of
potential failure then we go to device
therapy and there's two ways that we
could go here an intraoric balloon pump
has been shown to at least preserve
coronary perfusion so this sucker
deflates during systole to get blood to
go forward and then it actually inflates
during diastole so here during diastole
it inflates and it keeps the pressure
all here and they order really high and
what that does is guess what comes right
off the aorta here the coronary arteries
so if the pressure is high in the order
during diastole it's going to improve
coronary perfusion and improve
myocardial contractility and that's the
benefit of this
most times patients who end up on
cardiogenic shock refractory to a lot of
medications such as dobedamine mil
Renown androtic balloon pumps may
require something called VA ECMO this is
called venal arterial extracorportal
membrane oxygenation we take a catheter
we run it into one of their veins we run
it out of the vein and into a pump from
there we run it through an oxygenator
and then we put it in a catheter that
runs right into their artery these are
Big stinking catheters and they are
designed to be able to help to maintain
a decent amount of flow and augment the
cardiac output and also oxygenate the
blood so this is a potential beneficial
therapy that could be used as a patient
refractory cardiogenic shock
the other thing I think that's important
to remember in a patient who's in
cardiogenic shock or having any signs of
cardiogenic pulmonary edema is what's
called BiPAP using diuretics to help to
get rid of some of the sodium and water
which will help to reduce some of that
actual pulmonary edema but BiPAP has
been shown to potentially increased
answer thoracic pressure and that will
help to reduce right ventricular preload
so you don't have as much blood going to
the right heart and you don't have as
much blood going out of the right heart
so now less blood is going through the
pulmonary circulation and going to the
left heart if there's left blood less
blood going that way that's going to
have less blood leaking out into the
pulmonary interstitium less pulmonary
edema
the other concept is it drops your left
ventricular afterload so the pressure in
the orders drops so it's easier to get
blood out of the left ventricle into the
aorta so you have less blood coming to
the left heart and you have more blood
going out of the left heart that's going
to improve your cardiac output and
reduce pulmonary edema but more
particularly reduce pulmonary edema and
that's one of the benefits of this drug
in patients who are in acute heart
failure or potentially cardiogenic shock
all right I know this is a lot let's go
through this in a systematic approach a
patient comes in they have heart failure
you've changed their modifiable risk
factors after that you start them on an
Ace inhibitor or an ARB all right plus a
beta blocker they're still symptomatic
give them diuretics to reduce venous
congestion whether systemic or pulmonary
they're still symptomatic add-on
aldosterone antagonist and an sglt2
inhibitor
they're still symptomatic
and they're potentially unable to
tolerate an Ace inhibitor in ARB well
switch them switch to an AR and I if
possible so an Angiotensin receptor
neprolysin inhibitor
so this would be things where you put
them on like succubutril
um valzartan so these are very good
drugs that have been shown to be very
beneficial
the other thing is if they can't do that
one or if they're African-American
consider hydralazine and isosorbide
nitrate it actually has a mortality
benefit
if the patients are symptomatic on all
these therapies and in normal sinus
rhythm maxed out on a beta blocker give
them either braiding
if the patient has a left ventricular
ejection fraction less than 35 percent
and a left bundle branch block or a QRS
greater than 120 give them cardiac
resynchronization therapy
if despite all of these measures they
remain symptomatic
try to increase their perfusion usually
inotropes would be the next step here so
digoxin would probably be the one that
you'd want to continue outpatient if
they're an overt cardiogenic shock male
Renown or dobutamine
and then from there if you have to
Mechanical circulatory support if
they're an overt cardiogenic shock
intriotic Bloom pumps via ECMO hopefully
they recover and then the thing that you
would need to put them on to bridge them
to a transplant is an lvad and hopefully
they would get a cardiac transplant and
improve
all right my friends that covers heart
failure I hope it made sense I hope that
you guys enjoyed it and as always until
next time
[Music]
thank you
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