Shock | Clinical Medicine

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what's up Ninja nerds in this video

today we're going to be talking about

shock this is a part of our clinical

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all right without further Ado let's talk

about shock there is a couple types of

shock that we got to go into a little

bit of depth on and that is hypovolemic

obstructive distributive and cardiogenic

shock out of all of these one of them

has like some subtypes that will kind of

like dive into a little bit we'll

actually have separate lectures on all

of those into more detail

so first one is hypovolemic shock

hypovolemic shock is super simple the

volume within your vascular system is

significantly reduced now when a patient

lose volume you can lose volume in two

ways one is you're losing volume from

sources such as the git what will be a

way that we could lose

some fluid from your Git it doesn't take

a genius to recognize if it's coming up

from the top tube vomiting

if it's coming from the bottom tube

diarrhea another thing could also be

like excessive NG tube suctioning as

well or very very poor po intake from a

decent amount of time this can cause

hypovolemia the reason why is is if it's

not getting absorbed across the GI tube

you're not absorbing the volume so this

is one particular reason why you drop

your blood volume

second one is excessive skin losses that

would also lead to it and renal losses

and again for skin losses it's again

straightforward this would be a patient

who has um usually excessive diaphoresis

in other words they are sweating up a

storm or and this could be from fevers

so usually that'd be a big thing to

think about so diaphoresis from fevers

or burns like third degree burns that

could be another big one and then Rhema

losses is usually from things such as

like diuretic abuse

these scenarios will cause the patient

not to be able to maintain a good blood

volume right now

if in these particular scenarios you

reduce the blood volume that way that's

going to lead to a problem you know

generally the systemic circulation right

you have the venous part and the

arterial part the venous part is

supposed to receive this volume if you

will and take it where into the heart

and allow for good venous return to

allow for a good preload a good stroke

volume cardiac output Etc

if you have this problem where you're

losing fluid this will lead to what a

decrease in this particular scenario

here a decrease

in the venous return

and if you decrease venous return

you will drop your stroke volume

and you will drop your cardiac output

right so these are the underlying

effects here because if you don't fill

the heart you don't have enough volume

of blood to pump out of the heart and

one beat and then in one minute and

that's the problem with this disease is

you're losing fluid this way another way

which is also catastrophic is it could

be from blood loss

if a patient has massive blood loss

what would be some particular scenarios

in this well we kind of talked about a

little bit a triple A rupture would be

pretty catastrophic I would say another

one would be a GI bleed these are very

very common or like a uterine bleed and

you also can't go wrong with thinking

about any type of trauma in that

particular situation where it's like an

external exanguination effect

right so blood loss

would be in this particular scenario and

it's the same exact concept my friends

where you're losing blood you're having

a reduction in venous return in other

words this process where blood is

supposed to be going into the ventricles

from the Atria

is being reduced if you're reducing this

process you're not having enough filling

your edv is going down your stroke

volume goes down cardiac output goes

down now if we follow that process the

amount of blood that's coming out of the

heart

is reduced

and in that particular scenario that

then drops as we said here your cardiac

output and then if you drop your cardiac

output what do you do to your your blood

pressure you're dropping your blood

pressure and so this will lead to a drop

in What's called the mean arterial

pressure which is the perfusion pressure

if that drops you can't give oxygen to

the tissues and this leads to something

called

organ malperfusion

when you have organ malperfusion then

this starts leading to organ dysfunction

if not reversed in other words multiple

organ systems can start to actually fail

that is the concept of shock is where in

this particular scenario the volume loss

or blood loss is leading to reduction in

venous return stroke volume cardiac

output map and not perfusing the

particular tissue and the organs such as

liver kidney heart brain start to fail

that's the concept there

all right next one is obstructive shock

in obstructive shock it's two particular

etiologies here one is you are massively

massively massively reducing the preload

on the heart or you are massively

increasing

the afterload on the heart so it's one

of the two there is a massive drop in

the preload or there is a massive

increase in the afterload so it's kind

of like similar because if you think

about a preload kind of goes with venous

return right if you have a reduction of

venous Trend you have a reduction in

preload so just like you can see that in

hypovolemia you may see that here but it

has nothing to do with volume loss

there's something obstructing the heart

from filling because in this particular

scenario as you couldn't fill same thing

exists here

where I can't get blood

into the heart that same concept exists

so there is a reduction in preload

venous return

then because of that if you drop your

preload

you drop your stroke volume

and if I drop my stroke volume I'll also

drop my cardiac output and that'll drop

my mean arterial pressure

and then the same concept here exists

the difference in this scenario though

is that there's something else reducing

the filling one is you have the

pericardium pushing on the heart and

it's not allowing good filling of the

heart or you have a lot of the lung

pressing on the heart because the

pressure inside of the pleural cavity is

crazy high so it's either pericardial

pressures are high or plural pressures

are high what are the two diseases

this is actually pretty straightforward

one here would be a tension

pneumothorax that will cause the plural

pressures to go high and compress the

heart and prevent it from Philly the

second one would be tamponade

and that would be the pericardial

pressures are high compressing the heart

preventing it from filling and these two

scenarios these will massively drop your

preload drop your perfusion to the

tissue

and so subsequently the patient develops

organ

malperfusion and again we'll talk about

all the organs that can be malperfused

and what that looks like a little bit

later

but that's the concept of shock

now

other things actually do happen here

that not only does the heart actually

get compressed but it also does like

really quickly here cause something

called septal shift so you shift the

actual septum into the left ventricle

which impairs its fillingness process as

well but either way you're not filling

right

here's one with increased afterload

if you increase your afterload what do

you do to your stroke volume in your

cardiac output

you reduce it right

so the reason why is afterload is the

amount of pressure that you have to

exert to push Blood Out Of The ventricle

whether it's right or left into the

aorta or into the pulmonary artery if

it's too high can you get a lot of blood

out no

so your stroke volume and subsequently

your cardiac output will drop and so

will your map

so in this particular scenario it's the

exact same it's just a different

mechanism

but the question is coming what is

causing this massive afterload increase

look at that big chunky clot in the

right right in the pulmonary artery what

is that called

pulmonary embolism now I can't get blood

out of the heart why because the

afterload's high because something's

blocking that flow

and then because of that

if I can't fill the pulmonary arteries I

won't be able to fill the left atrium

and fill the left ventricle and if I

can't fill the left ventricle I can't

get a good stroke volume cardiac output

map drops I don't perfuse tissues

what in the heck did I just say it can

cause this

a pulmonary embolism

so a p e is one of the potential

etiologies that can really stimulate

this okay so we have these etiologies

here and these

etiologies here

that's obstructive shock

for distributive shock it's a little bit

different

this one's interesting so the whole

primary pathophysiology here

for all of these is the vessels

are vasodilated so let's actually put

that right here you see how these

vessels look at this one compared to

this one compared to this prior one

these suckers are huge right so these

patients have massive

vasodilation all right

when you have massive vasodilation of

your vessels now blood can easily flow

through here without very little with

very little resistance what happens to

the svr I just told you and I told you

the svr is going to drop right so

vasodilation occurs intensely

this drops your systemic vascular

resistance

when you drop your systemic vascular

resistance what does that do to your

blood pressure we already know

cardiac output is equal to heart rate

times stroke volume and blood pressure

is equal to cardiac output times svr so

if svr goes down blood pressure goes

down so then what happens

the map drops

you don't perfuse your tissues

and more organ malperfusion begins to

ensue

and that is the problem here

but the question then arises here

that we have to try to figure out

is what in the stink is causing

vasodilation massive vasodilation one

other thing

here's a big thing that's really really

important we'll talk a little bit more

get into the complications but whenever

your svr if you'll notice something

and this shock here this is the only one

out of all the shocks where the svr is

really low

and all of these other shocks the svr is

usually High

the reason why is cardiac output is low

cardiac output is low and in this one

cardiogenic shock cardiac output is low

remember the formula

we said blood pressure is equal to

cardiac output times svr if cardiac

output goes down what has to happen to

the svr it has to go up

and if svr goes down what has to happen

to the cardiac output it has to go up so

sometimes these patients will exhibit

what's called a reflexive increase in

cardiac output in other words their

hearts banging away it's important

remember we'll talk about a little bit

later

but let's come to the question what in

the heck is causing this vasodilation

one

is you're losing your sympathetic tone

the norepinephrine and epinephrine that

are supposed to naturally bind here to

your alpha-1 receptors and you've got

Alpha One receptors here

it's just not happening for some reason

there's some type of Disconnect there is

just this disconnect where they aren't

being released so there's like these

lower levels of norepinephrine

epinephrine they're not hitting the

alpha-1 receptor so this is inhibited

Alpha One respect receptors are supposed

to cause vasoconstriction if you don't

have them they'll produce

vasodilation

what is the reason why I'm having this

disconnect

usually the reason is some type of

spinal cord injury

it's usually a spinal cord injury

sometimes a spinal anesthetic and this

is called neurogenic shock

neuro

genic

shock and we usually see these and I'm

going to abbreviate this in spinal cord

injuries

all right

there's a lot of different reasons why

these can happen besides spinal cord

injuries but this is the big one

the other thing that's important to

remember just to add in here is that

these epinephrine epinephrine also hit

the

just as a little quick note a little

side note

it also has beta receptors on the heart

beta 1 receptors

so this may be the only type of shock

besides maybe cardiogenic shocks that

can also if there's less norepinephrine

epinephrine hitting these receptors the

heart rate will be a little bit lower so

remember neurogenic shock is a weird one

where they can have hypotension and

bradycardia but look for some type of

neurological catastrophe

all right let's come back here

neurogenic shock is one probably one of

the least common this is going to be by

far the most common type of distributive

shock and this is called septic shock

and this is usually due to a nasty type

of infection

so usually you have some type of

bacteria that has reached its way into

the bloodstream

when it gets into the bloodstream it's

called bacteremia but when the

bacteremia starts leading to effects

like hypotension fevers infectious types

of properties now we're talking about

septic shock

so what happens is the bacteria we're

not going to go through the entire

mechanism here we'll do this in the

pathology lectures but these bacteria

activate our immune system cells and

these bad boys release Bunches of

cytokines

and these cytokines some of the

interleukins and tumor necrotic factors

Etc

what they do is

they have the capability of

precipitating oh wow vasodilation

and that's going to cause this whole

downward Cascade

another thing is that they also do cause

the vessels to become super leaky so

fluid also leak is leaks out as well so

they get a little bit of volume

hypovolemic too

the last one here

is usually

anaphylaxis

okay with anaphylaxis this is usually

an allergic

reaction of some sort

by a bee ate something that they're

super super allergic to have a contrast

allergy they got contrast

what happens is that allergic reaction

causes them to activate the immune

system massive cytokines be released

causing vasodilatory shock

how do you differentiate these it's

usually in the context of some type of

spinal cord injury an obvious infection

leukocytosis fevers

whereas they have some type of

angioedema upper Airway obstruction

hives a recent exposure but that's some

of the big ways of differentiating these

from one another as a Distributive

shocky theology

all right we come down to the last one

this is preferably one of my favorite

ones in comparison to septic shock

Cartesian shock is really really

interesting in the sense that it can

happen in two different ways

one

is it can be mechanical

or it can be arithmogenic so let me

explain here let's say here we have a

patient who has cardiogenic shock they

have

some type of problem with their

myocardium

in other words they have a poor

contractility that is their disease

process let's say they have a reduction

in the contractility

and what's reasons why you can have a

reduction in contractility one

is you have an MI the second one is you

could have heart failure usually with a

reduced EF so an MI is one heart failure

with a reduced ejection fraction will be

another example right so this area is

damaged and you're losing the ability to

get blood out if contractility drops

I am going to now have a problem getting

blood out of the heart so what is that

called

stroke volume right in in one kind of

beat and then if that's the case I may

also over a process of a minute drop my

cardiac output

and so this is something that you could

potentially see is a drop in stroke

volume

and a drop in cardiac output due to a

drop-in contractility

another thing to think about is is there

a valvular damage

oftentimes when valves are super super

damaged and the one that I really would

want to point out here is if there is

damage to the aortic valve sometimes the

mitral valve as well

in acute let's say

acute

aortic regurgitation or mitral

regurgitation and these scenarios what

happens is is you have a constant

backflow of blood right so you push

blood out but the blood comes right back

in and that can cause patients to go

into an acute heart failure so it's the

same kind of concept it kind of volume

overloads them in the heart but you

can't get blood out same concept so

think about a catastrophic mitral or

aortic regurgitation or recent Mi or do

they have acute heart failure

so usually this is heart failure where

they reduce ejection fraction but it's

usually acute not chronic in other words

they decompensated if they have chronic

or they developed acute heart failure or

something to that effect

in this particular scenario if you have

a reduction in cardiac output what do

you do to your map

you drop your map you don't perfuse the

tissues and what ensues my friends

organ

malperfusion so we're getting the

concept here that some problem is there

is a reduction of perfusion to the

tissue and the tissues start becoming

dysfunctional

and all of these reasons just occur

based upon the different

pathophysiological process all right

that's one way cardiogenic shock can

ensue acute valvular regurgitation or

reduction in contractility

and just remember acute aortic

regurgitation of mitral regurgitation

can be a factor that can cause heart

failure an acute heart failure

okay next one here the other scenario

that maybe causes us to get less blood

out of the heart so less stroke volume

and as a response

less cardiac output

and then if there's less cardiac output

there has a lower map

this concept here would be its

arithmogenic

so I have an arrhythmia that is

preventing me from getting blood out of

the heart there's two types of

arrhythmias it's not too hard right one

is the heart rate is going way too dang

fast or it's going way too dang slow

and this would be if you have a tachy

arrhythmia this has to be really fast

though guys I'm talking like a patient

who is going like 150 or greater

ventricular rate so we see this

particularly in vtac maybe v-fib or

atrial fibrillation sometimes SVT all

right that it can potentially do this

but I'd say it's more these top three

the concept behind this super high heart

rate

is that what you do is you impair

filling so what it's supposed to do is

this is you're supposed to have blood

coming into the heart

this will be inhibited in the situations

of tachycardia so this massive

tachycardia will actually do this

now bradycardia is really cool because

when the heart rate is super super low

such as in an AV block right

this is interesting because it directly

drags down the cardiac output

if you increase the heart rate you'd be

like oh well cardiac output is equal to

heart rate time stroke volume so if I

increase the heart rate I would increase

my cardiac output sex that doesn't make

sense

it's if your cardiac output is so high

it reduces diastolic filling then it can

drop your cardiac output

but in the other scenario cardiac output

is equal to heart rate times stroke

volume a heart rate drops so does

cardiac output that is direct

correlation relationship so these are

two particular scenarios here where you

can see heart rate driving a reduction

of stroke volume cardiac output map and

organ malperfusion

so with all of that being said we've

covered the different types of shock now

what I need is to really kind of

understand here is

how do we really look at the

complications and some other

differentiating factors for patients

with shock I'm reference so now we're

going to talk about shock particularly

the complications that can arise from

shock and that is usually multi-system

organ failure as the result of organ

malperfusion regardless of any etiology

of shock this is the problem

so to quickly recap again and those

patients who have cardiogenic shock

obstructive shock or

hypovolemic shock all of their problems

is a result of their cardiac output

being reduced so the problem is in these

particular patients is their cardiac

output is reduced again which types of

shocks would do this my friend this

would again be

just as an aside here this would be

cardiogenic 100 would be cardiogenic

the second one would be obstructive

and the last one would be

hypovolemic all of these via different

mechanisms reduce the cardiac output

right so that's what we know about these

particular shocks here is that these

very specifically reduce the cardiac

output

now if we reduce the cardiac output what

that tells me is that I am not getting

enough blood out of the heart right so

this process here is significantly

reduced right so I'm getting a reduction

in cardiac output which reduces my mean

arterial pressure leading to organ

malperfusion right

and that's the concept here

and we'll talk about those organs that

get malperfused

one thing that I want to also mention

here is when a patient has a low cardiac

output

some things happen you guys remember

this

formula here that BP is equal to cardiac

output time systemic vascular resistance

the cardiac output in this disease

is doing what it's dropping

which will drop your blood pressure all

right so the cardiac output is dropping

this will drop your blood pressure what

does your body have to do to compensate

here

increase the systemic vascular

resistance let's do this in a different

colors do the pink

so this will have to increase

now what that will look like is super

super interesting when you increase your

systemic vascular resistance you clamp

down on those vessels like you squeeze

the living heck out of them so you have

intense Vaso constriction

what that will do is is that will reduce

the blood flow through the arteries in

your extremities

and when you go and look at these

patients on exam what you will know is

is they will have cold

extremities

pale extremities and they will have

modeling

of the extremities so this is what you

will notice cold extremities pale

extremities and modeling of their

extremities all because their vessels

are super super constricted that's super

common cold pale modeled extremities

very common in cardiogenic obstructive

and hypovolemic shocks because of this

mechanism here right

so this is one thing I want you to

understand

the other thing is that whenever your

cardiac output drops there's another

formula that you want to remember and

this is

cardiac output is equal to heart rate

times the stroke volume

well in all of these types of shocks

with the exception of cardiogenic shock

which is the bradycardia related

if your cardiac output

is dropping what should be the reflexive

reaction to your heart rate it should go

up and so oftentimes

these patients will develop what's

called a

reflex tachycardia so we call this a

reflex

tachycardia

and this is common in all of these

shocks there is an exception AV blocks

would be one particular exception

uh and and anything that a bradycardia

so AV blocks or like a beta blocker

overdose and this would all be related

to Beta like a braided cardio

all right so these are the concepts that

I want you guys to understand here and

low cardiac output related shocks your

body increases resistance and increases

your heart rate

super important

the other scenario here is we have the

vessels that are jacked up so the

systemic vascular resistance is the

problem and the other types of shocks so

whenever we have the systemic vascular

resistance is really low what does that

do to your mean arterial pressure

that also will lower your mean arterial

pressure

and what are the shocks that lower your

systemic vascular resistance my friends

you should already know this once so

again it's going to be

which type of shock here

oh son of a gun

this will be

distributive shocks

distributive

and so when a patient has distributive

shock their systemic vascular resistance

is massively going to be reduced

this would be septic shock this would be

neurogenic shock and this would be

anaphylactic shock now

what happens here is when a systemic

vascular resistance is low think about

the equation so BP is equal to cardiac

output times systemic vascular

resistance

if we think about this formula when the

systemic vascular resistance

is going to be low

then we know that the blood pressure

will be low and so your body will have

to increase

its cardiac output so it'll beat harder

and beat faster

but here's the other concept what's the

svr it's low

so if you have a low svr your vessels

are what we call dilated

so that's why we call this a

vasodilatory shock

or a Distributive shock are they going

to have good blood flow through them

yeah because they're going to be pump

and plump and leaky

so they should have

warm

and they should have it should not be

pale

and it should not be modeled and in fact

we should actually use this term there

should be warm

and pink slash red so warm and well

perfused which means that they're pink

and red so it should be warm

pink and red and not modeled

this is going to be your distributive

shocks

okay

the last thing here is whenever your

systemic vascular resistance drops your

map drops

your cardiac output has to increase the

only other thing to remember here is

is that whenever the svr reduces and as

happens it also will try to create a

reflex

tachycardia

the only exception to this process here

is going to be neuro

genic shock

all right that is the only type of

exception so all of these you should

have a reflexive tachycardia a reflex

increase in cardiac output

that is the big Concepts that I need you

guys to understand so neurogenic shock

will have bradycardia

and AV blocks or beta blocker overdose

we'll have bradycardia

all right now that we have a good

understanding of that

when your map's low you stop perfusing

organs

so I lead to a lot of problems here I

don't perfuse generalized tissues when

tissues don't get perfused they produce

something called lactic acid

and lactic acid what it will do is is it

will actually drop your pH

and when it drops your pH

that is going to create a metabolic

acidosis

that then does something really

interesting

it triggers your lungs to have to

breathe faster and so one of the ways

that you can see disease in these

patients is their respiratory rate is

increased look for that in shock

another one

is they don't perfuse the brain and they

can it can actually start to experience

things like encephalopathy

they also don't perfuse their coronaries

and if you can't perfuse your coronaries

enough guess what this heart starts to

become a little bit sad and becomes a

little bit ischemic

and this is called an N stami this is

super common

the other one and you know what's

interesting encephalopathy obviously

they're present with confusion lactic

acidosis they can present with a low PH

if you check a gas but they'll also have

tachypnea for in stemi they may present

with chest pain but sometimes the way

that this is found is some

numbskull checks a troponin

and these troponins will be

elevated

and the other thing is they may have an

EKG that gets worked up for because

they're in shock and they can have St

depressions or T wave

inversions they may not present with

chest pain just remember that

the other thing here

is that they don't perfuse the kidneys

and when you don't profuse the kidneys

these poor kidneys they can develop

what's called an acute kidney injury and

acute kidney injury is usually the way

that you'll see this is the urine output

will drop off and their creatinine will

rise

and that is the big things to look for

with an acute kidney injury

the next thing is if you I mean it is

multi-system right my friends is you

don't perfuse the git

and if you don't perfuse the git this

can lead to what's called acute

mesenteric ischemia and this will

precipitate terrible

abdominal pain usually out of proportion

to what your exam is so watch out for

this potential finding

and lastly you may not perfuse the liver

and these patients can develop what's

called ischemic

hepatitis

and and these particular scenarios when

I've seen them these patients usually

have lfts that are through the roof like

into the thousands

and so this is another way that you'll

be able to see this is because you just

don't profuse the liver as well

in these scenarios we see how if a

patient develops any shock cardiogenic

obstructive hypovolemic shock

distributive shock they don't perfuse

these tissues these are the

complications that ensue

we also understand that in patients with

distributive shock they're vasodilated

they're warm pink red not modeled and

those with cardiogenic obstructive

hypovolemic they're vasoconstricted

they're cold they're pale they're

modeled both can have reflex tachycardia

with the exception and these AV blocks

beta blocker overdose and here

neurogenic shock let's now go into the

Diagnostics of shock how do we

diagnostically approach shock well first

thing is calculate the shock index and

the way that you can do that is by

taking the heart rate and dividing them

by the systolic blood pressure in all

shocks with the exception of a

bradycardic shock or neurogenic shock

the heart rate should be high and the

systolic blood pressure should decrease

so if you think about that if that shock

index is greater than one that supports

shock what else supports shock lactate

if lactate is super elevated that means

that you're not perfusing organs

potentially and that could also support

shock

and then ask yourself okay are there any

features of decreased organ perfusion in

other words do they have any

encephalopathy is there any evidence of

acute kind of changes in their EKG or

troponins is their abdominal pain is

there any features of acute kidney

injury like an increase in creatinine

and decrease in their urine output is

there any bump in their lfts if that is

the case that supports shock as well

now the question is how do we determine

which shock it is we do not do this in

every patient but on your boards you

will have to determine this based upon a

swan guns catheter or a right heart calf

you place this catheter into the jugular

vein run it down into the right atrium

right ventricle pulmonary artery into

the pulmonary capillary area and inflate

the balloon and it'll give you some

pressures

what it'll do is it'll give you these

different numbers that'll help you to

differentiate the type of shock so the

first one is hypovolemic I want you to

remember that this was a cardiac output

low so the way that we look at cardiac

output is cardiac index and svo2 these

should both be low

the next thing is svr in any shock

except for distributive should always be

high what's the only things that aren't

kind of like we didn't talk about CVP

and Pulmonary capillary wedge pressure

this means that the actual heart is

usually in some way shape or form

having a hard time getting blood out of

it

and so in this it's usually kind of

scenarios of obstructive shock or

cardiogenic shock so we would expect

these numbers to be low and patients

with hypovolemic shock so again low

cardiac output based upon these two

numbers High svr present in all of these

other types of shocks generally okay the

only difference is CVP and Pulmonary

capillary wet pressure should be low

obstructive shock CVP should be high

because you're not going to have good

filling into the right heart

and the reason why you're not going to

have good filling into the right heart

is because you have something pushing on

it like attention or a tamponade or you

have no blood leaving the right heart

because they have a pulmonary embolism

so in those scenarios the CVP should be

high but again if it's an obstructive

hypovolemic or cardiogenic cardiac

output should be low so that's based

upon these two numbers here their svr

should be high as the compensation and

their CVP will be high the only thing

that is different here is their

pulmonary capillary wedge pressure

should be low there's only one exception

in obstructive shock where the pulmonary

capillary wedge pressure is high and

that is tamponade otherwise that is the

big defining difference here between

obstructive and hypovolemic is this CVP

is high low here these should be the

same The Only Exception is cardiac

tamponade

cardiogenic shock

the problem is getting blood out of the

heart okay you can't get blood out of

the heart so the CVP and it's actually

hard again and these patients they have

problems with being able to get blood

out of the heart and they can't actually

get blood out of the heart and so they

kind of call them become overfilled and

congested so CVP should generally be

high in cardiogenic shock

pulmonary capillary wedge pressure is a

measure of left atrial pressures left

atrial pressures are usually always high

in patients with cardiogenic shock

so you see how that's the big defining

feature here between these is pulmonary

capillary wedge pressure is high that's

super suggestive of cardiogenic shock

and again these shocks all have a low

cardiac output so cardiac index should

drop and svo2 should drop

svr should always be high in all three

of these shocks but the only defining

features between these is cvp's low CVP

is high pulmonary capillary wedge

pressure is low pulmonary capillary

wedge pressure is high The Only

Exception here is cardiac tamponade

last one is distributive

so in this one we already know that

their svr should be super low

that's the defining feature of this

shock and then what's the compensatory

response an increase in cardiac output

so these should be high

and then pulmonary capillary wedge

pressure and CVP are low because you're

having an easy time filling the heart

it's not a problem of filling the heart

okay so you should be low and that's the

ways that I want you guys to

differentiate the types of shock based

upon the swan guns catheter

okay now we move into the next step

which is how do we treat Chaka depends

upon the type of shock the type of

bulimic you have to ask is it fluid loss

give them fluid is it blood loss give

them blood how do I do that give them IV

fluids if they're losing fluids give

them blood if they're losing blood

simple as that obstructive treat the

cause

it was tamponade stick a needle in pull

that fluid off

pericardiocentesis is it attention

pneumothorax chest tube relieve the air

there

is it a PE TPA or embulectomy if they're

hemodynamically unstable

cardiogenic you have to treat the cause

it is a reduction in contractility due

to myocardial infarction they have to go

to the cath lab is it an aortic valve

that's acutely blown or a mitral that's

acutely blown then you've got to give

them a valve replacement is it

bradycardia that second degree mode is

two or third degree okay then we need to

do a pacemaker is it a need potentially

because of beta blockers and calcium

channel blockers that have caused this

patient to go into a bradycardic rhythm

okay then we need to reverse that beta

blockers with glucagon calcium channel

blockers with calcium

and then is it because they're going way

too fast then we need to give them a

cardioversion if they're an afib or if

they're in vtac

next concept here is if a patient's in

cardiogenic shock and we've tried to

treat the underlying cause but their

perfusion is still being reduced and the

examples of that is usually myocardial

infarction and sometimes you may need to

initiate inotropes things like

dobutamine or mil Renown and if that

doesn't work sometimes mechanical

circulatory support so things like an

aorta interrated balloon pump or VA ECMO

we talked about that again in CHF and we

talked about that a little bit in mi

distributive shock is another one so

this one is again the different types so

anaphylactic shock is the systemic

allergic reaction usually the best

treatment for these patients is

epinephrine give it to them as soon as

you possibly can then after that you can

do things like antihistamines and

steroids

for septic shock it's all about

antibiotics you've got to get them on

antibiotics you can give them a 30cc per

kg slug of fluid initially but it's

antibiotics and Source control of the

infection that's going to prevent them

from continuing to be in shock one thing

that's important to remember is

and patients with distributive shock you

want to really support their blood

pressure any type of shock you want to

support the blood pressure but

distributed most commonly they need a

lot of vasoconstriction and so when you

vasoconstrict the blood vessels you

increase their svr which increases their

blood pressure and increases their

perfusion so you want to give drugs that

squeeze the heck out of the blood

vessels things like phenylephrine things

like norepinephrine things like

epinephrine or things like vasopressin

so this will help to keep their blood

pressure up long enough for the primary

cause to be treated which is treating

the anaphylaxis treating the sepsis okay

all right my friends in this lecture we

talk about shock I hope it made sense I

hope that you guys enjoyed it and as

always until next time

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