Congestive Heart Failure | Clinical Medicine

Summary

This 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

• 🚑 **Heart Failure Overview**: The script discusses heart failure, covering its types, pathophysiology, and clinical aspects within clinical medicine.
• 📈 **Pathophysiology of Heart Failure**: It differentiates between left heart failure, right heart failure, and high-output failure, detailing the pathophysiological processes behind each type.
• 🔍 **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).
• 💊 **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.
• 📉 **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).
• 🌡️ **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.
• 💔 **Complications of Heart Failure**: The script outlines complications of heart failure, including pulmonary edema, cardiogenic shock, and organ malperfusion due to decreased systemic perfusion.
• 🩺 **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.
• 🛠️ **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.
• 🛑 **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.
• 🏥 **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

00:00

📚 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.

05:02

💓 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.

10:02

🔄 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.

15:04

👉 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.

20:05

🚨 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.

25:06

🛑 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.

30:07

🏥 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.

Keywords

💡Heart Failure

Heart failure is a chronic condition where the heart is unable to pump blood effectively, meeting the body's needs for circulation. It is central to the video's theme, as the script discusses various types, causes, and consequences of heart failure. The video differentiates between left and right heart failure, as well as high-output heart failure, providing examples such as reduced contractility and increased afterload.

💡Systolic Heart Failure

Systolic heart failure refers to a condition where the heart's ability to contract is compromised, often due to a decrease in left ventricular contractility. It is a key concept in the script, used to explain scenarios like myocardial infarction leading to fibrosis and reduced ejection fraction, exemplified by the term 'HFrEF' (Heart Failure with Reduced Ejection Fraction).

💡Diastolic Heart Failure

Diastolic heart failure is characterized by difficulty in the heart's filling phase, not its pumping phase. The script explains it as a common type where the left ventricle becomes hypertrophied, reducing its ability to fill with blood. This concept is integral to understanding heart failure with preserved ejection fraction.

💡Ejection Fraction

Ejection fraction is a measure of how efficiently the heart pumps blood with each beat. The script discusses its importance in diagnosing heart failure, mentioning that a reduced left ventricular ejection fraction (less than 40%) is indicative of systolic heart failure.

💡Cardiac Output

Cardiac output is the volume of blood pumped by the heart per minute. The video script explains how a decrease in cardiac output is a central issue in systolic heart failure, while in diastolic heart failure and high-output heart failure, the cardiac output is affected differently due to various pathophysiological mechanisms.

💡Afterload

Afterload refers to the resistance against which the heart muscle must contract to eject blood. In the context of the script, it is a critical factor in diastolic heart failure, where conditions like aortic stenosis or chronic hypertension increase afterload, making it difficult for the heart to pump blood.

💡Renin-Angiotensin-Aldosterone System (RAAS)

The renin-angiotensin-aldosterone system is a hormone system that regulates blood pressure and fluid balance. The script describes how in heart failure, activation of the RAAS system can lead to increased systemic vascular resistance and fluid retention, exacerbating the condition.

💡Pulmonary Edema

Pulmonary edema is the buildup of fluid in the lungs, often a complication of heart failure. The script discusses how it occurs due to high pressure in the pulmonary veins and capillaries, leading to fluid leakage into the lung tissue, which is a critical sign of left heart failure.

💡Cardiogenic Shock

Cardiogenic shock is a severe form of heart failure where the heart cannot pump enough blood to meet the body's needs. The script mentions it as a potential complication of both left and right heart failure, characterized by low cardiac output and systemic hypoperfusion.

💡Compensatory Mechanisms

Compensatory mechanisms in the script refer to the body's responses to maintain blood pressure and perfusion when cardiac output is reduced. These include increased systemic vascular resistance and activation of the sympathetic nervous system, which can have adverse effects in heart failure.

💡Diuretics

Diuretics are medications that increase urine production, helping to reduce fluid buildup and lower blood pressure. The script discusses their use in treating heart failure to alleviate symptoms of congestion and edema by promoting the excretion of excess fluid.

💡Cardiac Resynchronization Therapy (CRT)

Cardiac resynchronization therapy, mentioned in the script, is a treatment for heart failure that uses a pacemaker to improve the coordination of the heart's pumping action. It is particularly beneficial for patients with a left ventricular ejection fraction below a certain threshold and a specific type of heart conduction delay.

💡Left Ventricular Assist Device (LVAD)

An LVAD is a mechanical device that helps a failing heart pump blood. The script discusses it as a potential therapy for patients with severe heart failure who are not responding to other treatments, possibly serving as a bridge to a heart transplant.

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

this video and this helps you please

support us by hitting that like button

comment down the comment section and

most importantly subscribe also if you

guys want some great notes some great

illustrations to follow along with go

down the description box below check out

our link it'll take you to our website

we have a lot of great stuff there also

if you guys are interested we are

actually developing a course for the US

Emily Step 2 and pants that'll cover all

of this in great detail go check that

out as well and check out the merch we

got some great stuff please go to our

website check out all this stuff get

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