Septic Shock | Shock (Part 8)

Summary

This educational video, presented by Eddie Watson, delves into septic shock, the most common type of distributive shock. It explains the term 'septic', originating from the concept of body decay due to infection. The script covers the pathophysiology of septic shock, highlighting the systemic infection's role in triggering a cytokine release, leading to vasodilation, decreased blood pressure, and organ damage. It discusses the high mortality rate associated with septic shock and outlines the signs, symptoms, diagnostic tests, and treatment strategies, emphasizing the Surviving Sepsis Campaign's 'one-hour bundle' for prompt and effective care.

Takeaways

• 📚 The lesson focuses on septic shock, the final and most common type of distributive shock.
• 🔍 Septic shock originates from systemic infections, particularly those that enter the bloodstream.
• ⚠️ Septic shock has a high mortality rate, with statistics showing it's involved in one-third of hospital deaths.
• 🧬 The condition is triggered by a massive release of cytokines due to the body's response to a systemic infection.
• 🌡️ Early signs of septic shock include fever, warm skin, and increased respiratory rate, while late signs involve cold clammy skin and respiratory distress.
• 🩺 Diagnostic tests for septic shock include blood cultures, serum lactate levels, arterial blood gas assessments, and complete blood counts.
• 💊 The Surviving Sepsis Campaign emphasizes prompt treatment, including the 'one hour bundle' of interventions within the first hour of diagnosis.
• 🚑 Immediate treatment involves administering broad-spectrum antibiotics, fluid resuscitation, and the use of pressors to maintain blood pressure.
• 🩹 Supportive care for septic shock may include mechanical ventilation for respiratory support and treatments for failing organs.
• 💡 Steroids may be considered in treatment to reduce inflammation, especially if patients do not respond to pressors.
• 🔬 Understanding the pathophysiology of septic shock, its signs, symptoms, diagnostic methods, and treatment approaches is crucial for improving patient outcomes.

Q & A

What is the main focus of the eighth lesson in the series on shock?

The main focus of the eighth lesson is septic shock, which is the most common type of distributive shock that people encounter.

What does the term 'septic' originate from and what does it imply?

The term 'septic' originates from a word meaning 'rotten'. It implies a condition where the body is perceived as rotting from the inside out due to an infection.

What is the source of septic shock according to the lesson?

Septic shock arises from a systemic infection, specifically an infection or infectious agent within the bloodstream.

Why is it crucial to understand and treat septic shock promptly?

It is crucial because septic shock has a high mortality rate that can be as high as 50 percent, and timely treatment can significantly improve patient outcomes.

What is the significance of cytokines in septic shock?

Cytokines are released by white blood cells in response to an infection. In septic shock, a massive release of cytokines contributes to the dilation of blood vessels and a drop in systemic vascular resistance and blood pressure.

How does septic shock lead to relative hypovolemia?

Septic shock leads to relative hypovolemia as fluid from the intravascular space leaks out into the tissues (third space) due to increased permeability of blood vessels, resulting in decreased blood volume and blood pressure.

What is disseminated intravascular coagulopathy (DIC) and how is it related to septic shock?

Disseminated intravascular coagulopathy (DIC) is a condition where the body can no longer keep up with the amount of damage due to widespread clotting and bleeding. It is related to septic shock as the systemic infection can cause damage to blood vessels and endothelial cells, leading to clot formation and eventual DIC.

What complications can occur in the lungs as a result of septic shock?

Complications in the lungs due to septic shock include damage to lung vessels and alveoli, increased capillary permeability leading to fluid in the alveoli, respiratory distress, respiratory failure, and potentially acute respiratory distress syndrome (ARDS).

What are the early and late signs of septic shock?

Early signs (warm stage) include fever, warm skin, increased respiratory rate, and restlessness or anxiety. Late signs (cold stage) include cold clammy skin, respiratory distress or failure, altered mental status, and signs of organ damage like decreased urine output and absent bowel sounds.

What is the Surviving Sepsis Campaign and why is it significant?

The Surviving Sepsis Campaign is an initiative by professionals aimed at improving the survival rates of sepsis patients. It is significant because it provides guidelines and protocols, including the 'one hour bundle' of treatments to be administered within the first hour of diagnosis for optimal patient outcomes.

What are the components of the 'one hour bundle' in the treatment of septic shock?

The 'one hour bundle' includes checking serum lactate levels, obtaining blood cultures before starting antibiotics, administering broad-spectrum antibiotics, fluid resuscitation, and the use of pressors to ensure normal hemodynamics.

Outlines

00:00

🦠 Introduction to Septic Shock

The video introduces the eighth lesson in a series about shock, focusing on septic shock, which is a distributive shock type and the most common. Presenter Eddie Watson explains that septic shock originates from systemic infections, often bacterial, in the bloodstream. It's critical to understand and treat septic shock due to its high mortality rate, which can reach up to 50%. The video will explore the pathophysiology behind septic shock, its symptoms, diagnostic tests, and treatment strategies.

05:01

🛠 Mechanisms Behind Septic Shock

This section delves into the biological mechanisms that lead to septic shock. It discusses how white blood cells respond to infections in the bloodstream by releasing cytokines and nitric oxide, causing blood vessels to dilate and leading to a drop in systemic vascular resistance and blood pressure. The process also includes the opening of endothelial cell junctions, allowing fluid to leak out and creating a state of relative hypovolemia. This fluid loss, combined with vasodilation, further decreases blood pressure and oxygen delivery to tissues, contributing to the shock state.

10:02

🏠 Systemic Effects and Complications

The script explains the systemic effects of septic shock, including the release of molecules and enzymes by white blood cells, which can damage blood vessels and endothelial cells. This damage can lead to fluid leakage and disseminated intravascular coagulopathy (DIC), a serious complication characterized by simultaneous clotting and bleeding throughout the body. Additionally, the lungs are affected, with enzymes and cytokines damaging lung vessels and causing fluid to accumulate in the alveoli, potentially leading to respiratory distress, failure, or acute respiratory distress syndrome (ARDS).

15:03

🌡 Signs, Symptoms, and Diagnostics

The video outlines the signs and symptoms of septic shock, differentiating between early 'warm' and late 'cold' stages. Early signs include fever, warm skin, increased respiratory rate, and restlessness or anxiety. Late signs may present as cold, clammy skin, respiratory distress, altered mental status, and disturbances in glucose regulation. Diagnostic tests suggested include blood cultures, serum lactate levels, arterial blood gas assessments, complete blood counts, and labs for C-reactive protein or cortisol levels to confirm septic shock.

20:06

🚑 Treatment Strategies for Septic Shock

Treatment for septic shock is emphasized as time-sensitive, with the Surviving Sepsis Campaign's 'one-hour bundle' being crucial for prompt restoration of normal hemodynamics. This includes checking serum lactate levels, obtaining blood cultures before administering broad-spectrum antibiotics, fluid resuscitation, and the use of pressors. The video also discusses the importance of adjusting antibiotic therapy based on blood culture results, using IV fluids and vasopressors to manage blood pressure, and supporting organ function with inotropes or dialysis. The potential use of steroids to reduce inflammation in non-responding patients is also mentioned.

📚 Conclusion and Future Lessons

The presenter summarizes the lesson, highlighting the importance of understanding septic shock for better patient outcomes. The video has covered the basics of septic shock, its pathophysiology, signs and symptoms, diagnostic tests, and treatment options. The Surviving Sepsis Campaign's one-hour bundle is reiterated as a key intervention. The presenter thanks viewers for watching and encourages them to like, comment, and ask questions. The channel's next lesson, focusing on identifying different types of shock, is also promoted.

Keywords

💡Septic Shock

Septic shock is a life-threatening condition arising from sepsis, which is a systemic infection. It is characterized by a very high mortality rate and is the focus of the video's educational content. The script explains that septic shock results from the body's response to infection, leading to a massive release of cytokines and causing a drop in blood pressure due to vasodilation and fluid leakage from the blood vessels.

💡Cytokines

Cytokines are small proteins released by certain cells, particularly white blood cells, in response to an infection. In the context of septic shock, the script describes how the systemic infection leads to an overproduction of cytokines, which contributes to the dilation of blood vessels and subsequent drop in blood pressure.

💡Vasodilation

Vasodilation refers to the widening of blood vessels, which reduces systemic vascular resistance (SVR) and leads to a drop in blood pressure. The script illustrates this concept by explaining how the release of pro-inflammatory mediators and nitric oxide by white blood cells in response to infection causes vasodilation, contributing to septic shock.

💡Systemic Infection

A systemic infection is an infection that has spread throughout the body, typically via the bloodstream. The video script emphasizes that septic shock is a result of such an infection, which triggers a cascade of physiological responses leading to shock.

💡White Blood Cells

White blood cells, or leukocytes, are a crucial part of the immune system and play a central role in the body's response to infection. The script describes how white blood cells encounter the infectious material in the bloodstream and release cytokines, which is a key event in the development of septic shock.

💡Nitric Oxide

Nitric oxide is a molecule that can cause blood vessels to dilate. In the script, it is mentioned as one of the substances released by white blood cells during the immune response to infection, which contributes to vasodilation and the drop in blood pressure characteristic of septic shock.

💡Hypovolumia

Hypovolumia refers to a decrease in the volume of fluid in the body, particularly within the blood vessels. The script explains that fluid leakage from the intravascular space due to septic shock leads to relative hypovolemia, which further decreases blood pressure and perfusion.

💡Disseminated Intravascular Coagulopathy (DIC)

DIC is a serious condition characterized by the systemic activation of clotting mechanisms, leading to widespread clotting and bleeding. The script describes how the damage to blood vessels and endothelial cells during septic shock can trigger DIC, further complicating the patient's condition.

💡Acute Respiratory Distress Syndrome (ARDS)

ARDS is a severe lung condition characterized by widespread inflammation and fluid accumulation in the lungs, impairing gas exchange. The video script discusses how septic shock can lead to ARDS due to the inflammatory response and damage to lung vessels and alveoli.

💡Surviving Sepsis Campaign

The Surviving Sepsis Campaign is an international initiative aimed at improving the care for patients with sepsis and septic shock. The script mentions this campaign and its 'one-hour bundle' of treatments, which includes measures like blood cultures, antibiotics, fluid resuscitation, and pressor use, all to be administered within the first hour of diagnosis to improve patient outcomes.

💡Vasopressors

Vasopressors are medications that constrict blood vessels to increase blood pressure. The script discusses the use of vasopressors, such as Levophed, as part of the treatment for septic shock when patients remain hypotensive despite fluid resuscitation.

Highlights

Introduction to the eighth lesson in a series on shock, focusing on septic shock.

Septic shock is the most common type of distributive shock and originates from systemic infection.

The term 'septic' comes from the word meaning rotten, reflecting the historical perception of the body rotting from infection.

Septic shock has a high mortality rate, with statistics showing one in every three hospital deaths involve sepsis.

Explanation of the immune response to systemic infection, including the release of cytokines by white blood cells.

The process of vasodilation and drop in systemic vascular resistance leading to decreased blood pressure in septic shock.

Description of fluid leakage from blood vessels into the third space causing relative hypovolemia and decreased tissue perfusion.

The role of white blood cells releasing enzymes that can damage blood vessels and endothelial cells.

Formation of clots as a response to blood vessel damage, leading to disseminated intravascular coagulopathy (DIC).

Impact of septic shock on the lungs, causing fluid to shift into alveoli and potentially leading to ARDS.

Effects on the heart, including initial compensation with increased heart rate and cardiac output, followed by potential heart failure.

Signs and symptoms of septic shock, including fever, warm or cold skin, respiratory distress, and altered mental status.

Diagnostic tests for septic shock, such as blood cultures, serum lactate levels, and arterial blood gas assessments.

Importance of prompt treatment to decrease mortality in septic shock, emphasizing the Surviving Sepsis Campaign's one-hour bundle.

Treatment strategies including broad-spectrum antibiotics, IV fluids, vasopressors, and support for failing organs.

Potential use of steroids in septic shock treatment to reduce inflammation, especially in non-responders to pressors.

Conclusion summarizing the lesson on septic shock, its pathophysiology, signs, symptoms, diagnostic tests, and treatment approaches.

Transcripts

you

[Music]

okay I want to welcome everybody to this

eighth lesson in our series on chalk in

this lesson we're going to talk about

our final type of distributive shock and

probably the most common type that most

people will run into is septic shock my

name is Eddie Watson I will be

presenting this series of lessons and as

always make sure and subscribe to our

channel below and don't forget to hit

that Bell icon in order to be notified

as we release our new lessons alright so

in this lesson this will be the last

lesson that does a breakdown on the

various causes or types of shock and

like I said this is also the last of the

types of distributive shock and so now

we're going to talk about septic shock

and again like with all the other ones

we're going to talk about the word

septic and what that means and really

this comes from the word meaning rotten

and going way back into our past that

this is how people used to describe this

as the body was rotting from the inside

out and this is all as a result of some

sort of infection and more importantly

in the case of septic shock this is

going to come from a systemic infection

or essentially an infection or an

infectious agent that is inside of our

bloodstream and so our patient can find

themselves in septic shock as a result

of that systemic infection or what we

refer to as sepsis and it's really

important that we really have an

understanding of what's going on with

septic shock as well as how we would

treat our patient with it because septic

shock comes with a very high mortality

rate depending on where you look the

mortality rates for septic shock can be

as high as 50 percent so in order to

really drive this point home it's

important to know this statistic that

one in every three patients that died in

the hospital have sepsis and so a person

with sepsis that just continues to

progress either not being treated or

unresponsive to treatment ultimately

leads to septic shock and this is as a

result of the systemic infection leading

to a massive release of cytokines

and so just like we did with

anaphylactic shock

let's go ahead and take a look inside

one of our blood vessels and take a look

and see what exactly is going on with

septic shock and so like we talked about

we have some sort of systemic infectious

material and this can be what is most

commonly are bacteria but this can also

be things like viruses fungus or even

parasites and for this bacteria this can

be either gram positive or gram negative

but like I said in most cases of sepsis

this is a result of some sort of

bacterial infection all right so let's

go ahead and say we have our bacteria

here and so now the bacteria has made

its way into our bloodstream and the

first thing that's going to happen is

it's going to encounter one of our white

blood cells and as we know our white

blood cells job is to clean up

throughout the body and so when they

first encounter some sort of infectious

material they're going to release

cytokines in order to recruit other

white blood cells to the area now one

important thing to know here is

typically we have infections that are

taking place outside of the vasculature

and usually these infections are

localized to certain locations but again

with sepsis and this infectious material

and the blood that this is happening all

throughout the entire body and so it's

important to remember that because what

happens next is all a part of a cascade

of events that are really meant to help

get white blood cells to a localized

infection in order to be able to fight

it off appropriately but since this is

happening systemically within the blood

vessels this response ends up actually

hurting us and so what's going to happen

is these white blood cells are going to

Reese release some pro inflammatory

mediators as well as they're also going

to be releasing nitric oxide and so now

as a result of these being released the

four

thing that we're going to see is a

dilation of these blood vessels so just

like in our anaphylaxis reaction we're

gonna see these these blood vessels get

larger again leading to a drop in our

systemic vascular resistance ultimately

meaning a drop in our blood pressure

because again think about that this is

happening systemically everywhere

throughout the body causing this

substantial drop in our SVR and

ultimately that substantial drop in our

blood pressure now in addition to that

again we're going to have the space in

between the cells of our endothelial

lining are going to open up and again

typically this process is to open up to

allow those white blood cells to get

into that localized infection but again

now this is happening everywhere

throughout our body and so really a

couple things happen as a result of that

so here we have some sort of cells and

some sort of tissue that this blood

vessel is perfusing and so what's going

to happen now is fluid from within the

intravascular space is going to start

leaking out into that third space and so

as that fluid leaves the intravascular

space combined with our decrease in our

SVR this is further gonna work to

decrease our blood pressure and this is

as a result of something that we call a

relative hypovolemia and so if you think

about that we have a larger volume of

space to be filled due to that

vasodilation as well as a decreased

amount of fluid within the vasculature

leading to that hypovolemic type of

state and so ultimately this means we're

going to have less perfusion happening

which means less red red blood cells

coming through and as we know those red

blood cells are responsible for carrying

oxygen and so we're gonna be delivering

less oxygen to our tissues now in

addition to that we've now had

all of this fluid that has leaked out

into the third space and has surrounded

these these cells that normally don't

have all this fluid here and this oxygen

is going to have a really hard time

trying to get over to these cells

further adding to our shock state and

again I can't stress this enough just

remember that this is happening

everywhere throughout the entire body

and so now another thing that's also

going on is the white blood cell is

going to be releasing certain molecules

and lytic enzymes with the intention of

destroying this infectious material and

again normally this is taking place

localized here in the tissues and so

here we are again in the situation where

this is happening systemically inside of

the blood vessels and so this is going

on everywhere throughout our body and

these molecules and enzymes that they

can actually lead to damage to our blood

vessels in our endothelial cells so now

in addition to that increased

permeability from the nitric oxide and

the inflammatory mediators we're going

to start to have damage and death of

cells within our vasculature which is

again going to lead to more fluid

leaking out as well as if this becomes

large enough we're also going to begin

to see our blood coming out here as well

and so typically what's happening in our

body at this point is these damaged

cells are going to release what we call

platelet aggregation factor and so

what's going to happen is we have

coagulation factors within our our blood

naturally and this is going to lead to a

cascade in which we're going to start to

get a buildup of platelets in order to

try and stop the the bleeding that's

going on or the damage and these clots

can break off and continue traveling and

if large enough and in small enough

vessels can ultimately lead to decreased

blood flow or absent blood flow to

certain vessels ultimately impacting

whatever those those organs or tissues

are but again most notably again we're

having this

hold of clots systemically throughout

the entire body and the body only has so

much of these clotting factors available

and so while we're forming new clots

we're continuing to have more damage and

open up more areas and so ultimately we

find ourselves in a state where the body

can no longer keep up with the amount of

damage and has used up all of these

coagulation factors and so we find

ourselves in the state where we continue

to have bleeding but we also continue to

have this massive clotting throughout

the body and this is what we refer to as

disseminated intravascular coagulopathy

or di c for shorter now in addition to

all of this that's going on we also need

to talk about what's going on inside of

our lungs and so as we know we've got

our blood vessels coming out here into

the lungs and so all of this process

that we talked about happening

throughout the body is also happening

all throughout our lungs and these

enzymes and cytokines are going to

continue to cause damage to the vessels

in our lungs as well as the inflammatory

mediators and the nitric oxide leading

to that increased capillary permeability

which is going to cause fluid to shift

out into the alveoli and so now we find

ourselves in a state with damaged

vessels and alveoli which we normally

are using for our gas exchange is now

filled with fluid and this ultimately

can cause our patient to have

respiratory distress lead to respiratory

failure or ultimately lead to what we

call acute respiratory distress syndrome

or ARDS which is a very serious

complication as a result of septic shock

and really the last thing that I want to

talk about with this process is if we

take our our heart here and again we

know we have blood that's coming to our

heart all of this stuff is going to be

happening within the vessels within our

heart and so initially the heart is

going to be working to compensate for

that that decreased SVR and so initially

we're going to see in

crease in a heart rate and an increase

in our cardiac output but as that

hypoperfusion and damage to the cells

continues to take place eventually we're

gonna see death of cardiac cells which

is ultimately going to have an impact on

our hearts ability to function and we

could see a decreasing in our heart rate

and probably more more common would be a

decrease in our heart's ability to pump

leading to a decreased cardiac output

and so as you can see here this is a

very complicated cascading series of

events with multiple things that are

going on that are all contributing or

having apart and leading to our patient

being in that shock state and so with

that said let's go ahead and move on and

talk about some of the signs or symptoms

that your patient might be exhibiting

when they're in septic shock and so with

some of these signs and symptoms we are

going to discuss some variation that we

may see between both the early versus

the late stage and this sometimes you'll

hear referred to as the warm or the cold

stage and really we can just think about

this as our compensated versus our

uncompensated so the first of these that

we're going to see and that we're going

to talk about is an increase in our

temperature or fever

now this often times can be a pretty

good indicator of what type of shock

your patient is in but in addition to

this when your patient is in that that

early stage of shock they're also going

to have warm skin and this is

essentially where the term warm stage of

shock comes from but ultimately as the

shock state progresses and continues to

go on we are going to have that systemic

response and vasoconstriction and so

that will lead to our cold clammy skin

which is what we typically would expect

to see in a patient in shock now again

in our early stage we're gonna see an

increase in our respiratory rate of our

patient but ultimately as this

progresses we're going to see our

patients enter into respiratory distress

respiratory failure

or even ard s often early on you may

find them to be either Restless or

anxious but again as we progress into

the late stages this can lead to our

altered mental status or even being

obtunded or in a coma

now another thing that we're also going

to find in our patient is disturbances

in our glucose regulation and so I'm not

going to go too deep into this here for

this lesson but this is a result of a

hyper metabolic state that the patient's

going to find themselves in a lot of it

having to do with this inflammatory

process and so you may find your

patients with profound hypoglycemia or

even hyperglycemia in addition to this

hyper metabolic state the cells and

throughout the body are going to be

initially using up a lot more oxygen

than we normally would also partially

contributed by the fact that our our

perfusion has now decreased and so

initially early on we'll see a decrease

in our venous oxygen saturation but as

things progress and we begin to really

build up that fluid we start to lose the

ability for that oxygen to diffuse over

to the cells and over time this can

actually lead to an increase in our

venous oxygen saturation because our

cells are just unable to use the oxygen

that's delivered now also along with

this partially due to fever as well as

the body's compensation mechanisms we're

gonna see that elevated heart rate and

initially that elevated cardiac output

but as things go on like we talked about

we will see that drop down and finally a

couple more things to look out for would

be decreased urine output as well as

decreased or absent bowel sounds and

again we talked about this within our

first lesson on shock but this is again

as a result of that decreased perfusion

and organ damage

so now along with these signs that you

would see there's also going to be some

diagnostic tests that you're going to

want to do or perform and

to see what's going on with your patient

and really our gold standard for septic

shock it's gonna be our blood cultures

you're also going to want to check your

serum lactate level or your lactic acid

again checking to see if your patient

has switched into that anaerobic process

or if the state of shock is

progressively getting worse

you're also going to want to assess an

arterial blood gas in order to assess

your patients oxygenation you could also

check a complete blood count or a CBC

and here you're really looking for

either elevated or decreased white blood

cells which would be a sign of infection

and finally you also may want to check

labs for things such as C reactive

protein or cortisol level in which an

elevation of these can be indicative of

septic shock as well alright so we have

talked about quite a bit so far and so

we're going to move on to the last part

of this lesson which is going to be

talking about the treatment and really

an important thing to note to start off

here is the sooner we can have treatment

the better the decrease in mortality and

so really the whole point of this is to

have a prompt restoration of our normal

hemodynamics

and due to this fact there was the

formation of a group of people working

to really help the survival of sepsis

and they formed what they call the

surviving sepsis campaign and with this

there's a lot of really great

information out there for practitioners

really of all levels but one of the most

important things that we're gonna be

looking at specifically within the

hospital setting is that one hour bundle

and these are the the things that need

to be done within the first hour in

order to have the best possible outcomes

and these are going to be checking a

lactate getting blood cultures and it's

important that we get these blood

cultures before the next step which is

our broad-spectrum antibiotics ensuring

that we fluid resuscitate our patients

and finally the use of pressors to

ensure normal high mo dynamics and so

we've already covered the lactate the

serum lactate level as well as drawing

the blood blood cultures like I said the

most important thing is to make sure

that we get those blood cultures before

we start any antibiotics but really that

first line of treatment is going to be

that antibiotic treatment and so with

this we're going to be starting like we

talked about with those broad-spectrum

and essentially this is to cover all

areas with common broad covering

antibiotics to hopefully work to start

attacking whatever organism is going on

but eventually when your blood cultures

come back and you're able to do a

sensitivity test and determine what

organism you're dealing with then you're

gonna work to really adjust that

antibiotic their therapy in order to

specifically target and ultimately if

your blood cultures don't come back

positive or the patient is not

responsive to any of this antibiotic

treatment you may also consider

alternative treatments things with

antifungals antivirals or other sorts of

treatment and so our next line of

treatment which again often a lot of

this stuff is going on

at the same time but our next main line

of treatment is going to be our IV

fluids and with this we're really going

to want to make sure that we are using

our crystalloids but for IV fluids we

want to make sure that we are initiating

this if either our patients are

hypotensive or they have a serum lactate

level that's greater than four and when

we do this we're gonna be giving 30 MLS

of fluid per kilogram of body mass that

our patient has now while we're giving

this fluid to our patients if they're

either remaining hypotensive

during the fluid administration as well

as staying hypotensive after we've given

them this volume of fluid then our next

line of treatment is we are going to

look at our vasopressors and what this

typically Levophed is our first line of

choice and ideally we want to be

shooting for a map greater than 65 in

addition to this we also need to support

our patient's oxygenation

and this can perhaps mean our intubation

or our mechanical ventilation and in

addition to this we also need to make

sure that we are supporting our failing

organs and this could really cover a

whole host of different things but you

know this could be things like our

inotropes to help with our cardiac

contractility or even dialysis or

continuous renal replacement therapy in

the case of failing kidneys and note

that this one is particularly common

especially with septic shock and so

finally one of the last things that

we'll talk about when we look at

treatment for our patients is going to

be possibly the use of steroids and

really we're going to be looking at

these to try and decrease that

inflammation that's going on as a result

of the immune system reaction especially

in the case where your patients are not

responding to pressors okay well we

covered quite a bit in this lesson and

specifically talking about septic shock

we work to cover the the basics of what

septic shock is and what it may

and so really we talked through that

whole pathophysiological response when

your patient has sepsis or goes into

septic shock and what are some of those

factors that are contributing to that we

talked about the signs and symptoms that

you would look to see making sure and

differentiate between those early or

warm signs versus those late or cold

signs we also talked about some of the

tests that you would be looking to do

for your patient and finally went

through the various treatment modalities

including covering the very important

one our bundle that's included within

the surviving sepsis campaign I know

this was a lot of information but

hopefully this was presented in a way

that really would be helpful for you or

informative for you to be able to take

this be able to apply this information

into your practice and ultimately

towards better outcomes for your

patients and so with that said again I

want to thank you for for watching this

lesson and I really hope that you found

this informative if you did like it and

you did find it useful make sure and hit

that like button below as it really

helps to spread the word about our

channel in the comments below make sure

and tell us your favorite part of this

lesson as well as feel free to ask any

questions that you might have and

finally make sure and check out what's

going to be our last lesson in this

series on shock and in this lesson we're

going to be talking about identifying

the different types of shock that your

patient is in or make sure and check out

one of our other great lessons on

hemodynamics as always thank you for

watching and we'll see you in the next

lesson