April 4, 2023 • 46 mins
Special Double Episode! Three things in EMS are deeply connected: pathophysiology, assessment, and differential diagnosis. If a provider can apply principles of pathophysiology to assessment, coming to an accurate diagnosis becomes much easier. This 7 Things EMS brings in Joe Mistovich. Paramedic, educator, author, and pathophysiology geek. Joe explains the presentation of common conditions like hypoxia, hypoglycemia, and more through the lens of pathophysiology Part 2The second episode in this series digs deeper into common patient presentations and makes them understandable. We know that abdominal pain can present vaguely, edema is bad, and altered mental status can indicate a serious condition. But do you know exactly why? This episode digs into these conditions and more to provide a deep understanding that will improve your patient assessment.
Get CE for listening! 2 hour CAPCE-approved F3 CE. Purchase here: https://lc-ready.com/store/details/96-7_things_pathophysiology_based_assessment
Mark as Played
Transcript
Episode Transcript
Available transcripts are automatically generated. Complete accuracy is not guaranteed.
(00:00):
Welcome to the Seven Things EMS Podcast, a continuing education offering of Limmer education.
(00:12):
Seven Things EMS Podcast is designed to give you what you need to succeed in EMS, it's
conversational, informational, and without the fluff.
And welcome to another episode of Seven Things EMS, this is a continuation of our Pathophysiology
(00:37):
and Assessment series with my friend and someone I consider an expert in this, Joe Mistovich.
In our last episode, we talked about hypoxia and hypoglycemia and provided some understanding
and we're going to continue with that one today.
So welcome back, Joe Misovich.
Thanks, Dan.
(00:57):
All right, number four.
Now people may have listened to the first one, but Joe is a textbook author, conference
speaker, professor, retired from Youngstown State University, certainly has the credibility
to be doing all these things that I want to not introduce you in this.
But it's our mantra to go right into it.
(01:19):
And let's go to our number four as we continue on to seven about peripheral edema.
It provides important clues to the diagnosis of a patient's condition.
And I think we see edema and we generally jump to one conclusion.
And I think you may change the way we think about that.
(01:41):
Yeah, and it's so true.
And I think what bothers me here the most is that you'll see that, and again, this is
not just EMTs.
It's advanced EMTs and paramedics will do this too sometimes in their assessment.
And they'll be doing their assessment and say, oh, look, the patient has some edema to
(02:03):
their ankles and to their feet.
And then they're like, okay.
All right, I'll note it.
And then that's as far as they go with it.
And they stop there and they just think like, okay, I'll note it.
Instead of saying, okay, why is that?
Again, in that possibilities to probabilities, this is huge.
And again, and you're right.
And I think if you had asked your typical paramedic and say, hey, you got a patient that presents
(02:27):
with dependent edema, what are you thinking?
They're going to go, heart failure.
Well, it's got to be heart failure.
You know, well, you know, that's one out of many things.
But again, in the big scheme of things, this edema could be providing huge clues to actually
what's going on with the patient.
And why do I think you're going to tell us those things?
(02:49):
And a little bit of pathophysiology to explain those.
So, you know, and so, you know, I say, you know, just this is not just the point for
you to note.
And one other thing I want to point out is edema, remember, they call it dependent edema
because it is gravity dependent.
And what that means is if your patient is sitting, the extra fluid, and this is lymphatic fluid,
(03:12):
this is interstitial fluid, it's going to collect in the feet, the ankles, and the hands
because they're dependent.
They're lower portions of the body.
And that's where that fluid based on gravity is going to collect.
If you have a patient who's a supine patient, somebody maybe who's bedridden, and they have
edema, it's not going to be in their feet and their hands.
(03:33):
You're going to find it primarily in the pre-sacral area in the posterior body.
So, you've got to get these patients up and you've got to look at their back and it's
pre-sacral.
So, it's like between the lumbar area and the sacral area of the body, and you start
looking for the edema there because that's where it's going to settle based on gravity.
So, when you find edema, you have to start thinking, you know, what, okay, so what are
(03:58):
the things that causes edema?
You say, well, there's four things primarily that will cause edema.
One is an increase in hydrostatic pressure.
Now, hydrostatic pressure is, all you got to remember is hydrostatic pressure is the
push factor inside the vessel.
And this is primarily inside capillaries, arterioles, and venals.
(04:22):
But hydrostatic pressure is primarily affecting the arterial and the beginning portion of
the capillary bed.
And so, this is right before the entrance into the capillary and it's a push pressure.
It's pushing, its force is being exerted on the inside of the vessel wall, trying to
push stuff out.
So, that's one, an increase in hydrostatic pressure.
(04:44):
So, that means if you have a dramatic increase in hydrostatic pressure, that pressure, the
higher it gets, it reaches a point where it overwhelms that vessel wall and that vessel
wall where these just cells lined up together can't hold it in any longer because the pressure
overcomes it and it pushes out more fluid than it can recover.
(05:06):
So, that's the one thing you think of peripheral edema is, do I have, well, what's going to
increase hydrostatic pressure?
Increase in blood volume is one, or a dramatic increase in blood pressure is another.
So, therefore, when you start getting the patient that you immediately think, heart
failure, you know, so funny because they've kind of gotten away from the term congestive,
(05:29):
although we keep saying congestive heart failure, you know, and they say, well, it's not necessarily
congestive because, hey, to say it, but when you turn 40, you now start on your journey
of heart failure, normal pathologic heart failure.
And so, it's not necessarily congestive, but the congestive piece is there's too much
volume now and there's higher pressure in the vessel and it's pushing the fluid out.
(05:53):
And I'll explain that.
And then the second one is a decreased oncotic pressure.
And when you say oncotic pressure, you're referring to proteins in the blood.
The biggest protein in the blood is a plasma protein that we know is albumin, okay?
And what albumin is, is we know two things attract water.
(06:14):
Charged particles like sodium and so forth where sodium goes, water falls it because
it's a charged particle.
It's an electrolyte.
And the other is large particles.
What's a large particle?
Albumin.
You know, it's another large particle?
Glucose.
Where glucose goes, water is going to follow it.
That's why we don't give any injured patients glucose because glucose gets crossed into
(06:35):
the brain cells and draws water and worsens the edema in the brain.
So this oncotic pressure, this big albumin molecule that's in plasma, exerts this, this
osmotic force where it's forcing water to be pulled in.
So the way that capillary works, and this is referred to as the Starling equation, its
(06:59):
net filtration is, as blood enters in the beginning of the capillary, it comes into the
arterial because the arterial was the most distal part of the artery.
And it enters into the arterial.
And in the arterial, because of the hydrostatic pressure, it's pretty high because the vessel
is so small that the hydrostatic pressure is pushing fluid out of the arterial.
(07:22):
The blood then gets into the capillary bed.
Then when it hits the venial, the beginning of the venial is where now you pushed out
a lot of fluid and it's plasma volume, right?
It's not whole blood, it's plasma volume.
You pushed it all out.
But what did you leave behind?
Albumin.
Those big particles.
(07:43):
And so when the blood enters the beginning of the venial, you got big particles.
And because of osmosis, where you have big particles, it's drawing the fluid and it draws
it back in.
And so what Starling equation says, there should be zero net filtration.
Net filtration should equal zero, meaning the forces, the hydrostatic pressure, the
(08:04):
push should be pushing out a certain amount of fluid.
And the pull factor, on caudic pressure is known as the pull factor, should be pulling
that same amount of volume in.
And when we have net filtration that equals zero, the amount being pushed out as being
pulled in, we have no edema.
The problem is now when we have a disturbance in either one of those.
(08:27):
So let's take our congestive heart failure patient.
Our congestive heart failure patient hasn't lost any albumin.
They haven't lost those big plasma proteins, it's still in the blood.
The problem is when their left ventricle can't eject all that blood volume, people say, well,
it backs up into the lungs.
Well, it doesn't really back up.
But what happens is the pressure starts to increase because the volume is increasing
(08:51):
in the pulmonary capillaries.
And so what do you increase?
You increase the hydrostatic pressure.
So I'm just going to use this arbitrarily.
Let's say just for numbers.
Let's say that in this pulmonary capillary, you normally would push out 10 mLs of interstitial
fluid of plasma volume.
And then you had the plasma proteins to pull back in 10 mLs.
(09:15):
But now because this patient is in heart failure and they have this dramatic increase in volume
in the pulmonary capillaries that are one cell thick, it pushes out 30 mLs of interstitial
fluid.
But you still only have enough albumin in the venial to pull 10 mLs back in.
(09:37):
So now you have 20 mLs of fluid that remains outside of the vessel around the cells.
Now you start developing edema.
So that's one way.
And that's your heart failure patient.
Anaphylaxis.
What's one major sign of an anaphylactic reaction?
(09:59):
Edema.
In a lot of it's dependent edema.
You start seeing the edema.
Why do you get so much edema to the tongue, to the face, to the neck?
Because it's a very vascular area.
The more vessels you have, the more it's going to be affected.
So what does the chemical mediators like histamine and prostaglandins and bradykinins and all
(10:19):
these chemical mediators do?
They increase capillary permeability, meaning that they make the spaces in the capillaries
wider.
So that means when the pressure, when the volume of blood is coming into the arterial,
they got out now wide spaces.
So what happens is when they're only supposed to push out 10 mLs, they're able to push out
20 because they have no longer kind of like the fence to keep it in.
(10:43):
But the same thing.
On the venial side, it only has enough albumin to pull 10 back in.
So that's why you're losing the volume.
Now you're actually losing the volume out of the vascular space.
So this could create a hypovelemic state with severe increases in capillary permeability.
So that's why.
Now here's a question I would pose to my students based on this.
(11:07):
Why is it if you have a patient who has a partial thickness or a full thickness burn,
let's say it's to the entire thorax of the body.
So let's say it's like a, I don't know, a 40% body surface area burn, but it's to the
thorax of the body.
(11:30):
Why is it that these patients, if you've never seen a burn patient who becomes severely
adeptus all over their entire body, why are they becoming adept?
We know there's immediate edema in the area of the burn.
We know that.
If you're listening to this podcast, you don't believe me, go upstairs, put on your stove,
(11:52):
heat it up, put your hand on it, hold it down as long as you could.
Hold it, hold it, hold it, pull it off and what's going to happen almost immediately?
Blister formation.
Better put this place.
Letters education and our sponsors don't recommend touching hot stove burners.
Well, what do we know?
We know immediately we started developing blisters.
That's how we develop blisters because it's from an increase or increase in capillary
(12:14):
permeability.
But you look at the burn patients, you say, but why are their legs swollen when they're
lying supine?
Why is their face so swollen when they're lying supine?
That's not dependent.
Gravity should be pulling it down.
One of the reasons is because in the burn area, if you have a big enough burn, and usually
it only takes a burn of greater than 30% body surface area, partial thickness, full thickness,
(12:38):
where you increase the capillary permeability in the burn area because you're destroying
those arterials and you leave such huge spaces that albumin is leaking out along with the
fluid.
So now hydrostatic pressure is pushing out 50 mL of fluid because you've got big spaces
in there because the capillaries are damaged from the burn.
(13:00):
Not only is the plasma volume going out, albumin is leaking out with it.
Now on the venial side, you have very little albumin, maybe only to pull five mLs in and
the albumin is collecting outside in the interstitial space.
So now when you get to unburned areas, the legs aren't burned, but when you come into
(13:20):
the capillary, the hydrostatic pressure that should be pushing out 10 is still pushing
out 10, but when it gets to the venial, it only has enough albumin to pull in three.
So you've got seven mLs left out there.
Forget the numbers.
Let's just try to explain.
But you have very little albumin because it's all wear in the burned area.
(13:40):
Pushing out in the interstitial space, you don't have enough albumin to pull that fluid
back in.
Now, we know one thing about burn patients, we have that first 24 hours, right?
We give them tons of fluid in the first 24 hours.
We use Parkland's formula and some of these patients were given 24, 30, 6, 48 liters of
fluid depending on the burn and the size of the patient, right?
(14:02):
But then we have what?
A reversal.
All of a sudden now, we're going to start giving them some type of like Lasix or something
to start getting rid of fluid because what happens is that albumin starts coming back
into the capillaries.
Now, all of a sudden, the albumin starts pulling all that fluid you gave the patient and all
(14:23):
that fluid hanging on it pulls it back in and all of a sudden we make our patient hypervolumic.
But that's how this works.
Now a patient that could have an albumin disturbance also could be a patient with some type of
kidney disease where the kidneys are actually dumping out albumin.
So the other is the lymphatic blockage or inability of the lymph system.
(14:43):
The lymph system takes the interstitial fluid and puts it back into the venous side.
So next time, you know, you go to a call and you got a patient with edema.
You just don't say, well, mark it on the PCR as edema.
You got to start thinking, does this patient have too much volume or high pressure?
Okay.
Here's another one.
(15:05):
Cocaine or vasoactive drugs.
Why is it that an 18 year old kid all hyped up on cocaine or crack could go into pulmonary
edema?
You remember, Dan, we worked in the days as paramedics where cocaine was the big drug.
And we would see these kids that are 18, 19, 21 year old kids in great physical shape doing
(15:26):
cocaine in pulmonary edema.
Well, if you think about it, what happens?
Pressure.
It's pressure.
Cocaine is a vasoactive substance.
Causes vasoconstriction.
What does it do?
Dramatically increases the hydrostatic pressure.
You're pushing out too much fluid then you can recover.
Happens in the lungs and they end up with pulmonary edema.
(15:46):
So you got to start thinking, this isn't just edema.
Why is there edema?
Because there's some underlying cause.
You know, that could be dramatically related to what you need to do with on the scene too.
I'm not saying you're trying to diagnose for the hospital.
You're not trying to determine they have kidney disease, but you need to know, do they have
a vasoactive drug on scene?
(16:08):
You know, on.
But also at the same time, somebody's been doing cracker cocaine, you better be listening
to their lungs because they could be in pulmonary edema from the increase in hydrostatic pressure.
All right.
I'm going to keep, I'm going to move on to number five.
And normally, normally I jump in and we'll say something, but I just think your explanations
(16:28):
are so incredible.
I think people at all levels can understand these.
I'll also add that we have some detailed show notes people can look at to find more information
on this.
Number five talks about pain.
Not all pain is the same.
Knowing different pain presentations in that medical patient is important.
It's going to tell you something.
(16:48):
Yeah.
And this is very similar to, to like the edema.
So when you get on the scene and the patient is complaining of pain, you know, there's
a big difference between your trauma patient and your medical patient.
If you have a trauma patient who has a fractured extremity or has a sprain or a tear or something
like that or a knife wound, that's all mechanical type of pain.
(17:09):
And that's pretty easy.
It's kind of like, well, yeah, I know why you haven't pain because look at the bone.
It's at a right angle of where it should be.
That's what's causing the pain.
And pain, you have no C receptors and these receptors are basically sensory fibers that
are picking up this stimulation, you know, and it's picking up the pain response.
And typically pain is caused by a thermal source, which is heater cold and mechanical
(17:33):
source was just going to be your crushing, your tearing, your sharing and chemical.
Good example of a chemical cause of pain is if you remember the old days, actually we
remember the, what was it?
Meachuricrome.
Meachuricrome.
Meachuricrome.
Meachuricrome.
That they, that, you know, you would get a cut and your parents will pour that in that
(17:57):
wound.
It was like, oh, it was like peroxide, the same thing.
That's a chemical type of pain.
And what you're doing is you're introducing a chemical and you're stimulating then those
no C receptors.
But what's, you know, and that's pretty obvious.
Okay.
So if you have a burn, it's going to cause pain.
Okay.
That's a thermal, thermal cause.
But now when you get on the scene and you have a medical patient who has no trauma
(18:21):
complaining of pain, again, it's not just something for you to document in the PCR.
It's for you to actually think about because you say in a medical patient, what's going
to cost pain?
Well, basically there's four major things.
It's ischemia or tissues, hypoxic.
It's inflammation.
Whereas as an inflammatory response, there's infection or they're stretching like there's
(18:47):
an obstruction.
The best example of pain by stretching gas.
When you have gas, when you build up gas in your intestinal system, what do you get?
A crampy abdominal pain.
And that's nothing more than those no C receptors being stimulated from the stretch of the intestine.
Okay.
(19:07):
But the key is if you have a pain.
You're saying you should let it out, Joe.
Let the gas out.
Absolutely.
And then you know, the funny thing is you let it out and all of a sudden the pain goes
away because what happens?
That colon is no longer being stretched.
And so those receptors are no longer being stimulated.
So if you had to station, just say it's an experiment.
You're validating what Mr. Vich said about that.
(19:28):
It is.
And it's a physiological relief thought.
This is what it is.
I mean, I think it's true.
But when you get on a scene and you have a patient complaining of pain and it's not related
to trauma, you have to start thinking, is it ischemia?
Is it infection?
Is it inflammation?
Or is it something, some stretch of a viscous?
(19:50):
And again, it's taking you from those possibilities to probabilities.
We look at chest pain in the patient having an MI.
Why is a patient having a heart attack having chest pain?
Well, because what's happening?
That cardiac muscle is ischemic.
Ischemia is causing the pain.
(20:11):
And so you say, well, okay.
So if that's the case, so if my liver is ischemic, they should have right upper quadrant pain.
You know, you know, infection is the same.
A patient having some type of infection will complain of pain.
If if, you know, they have an infection in their leg, typically they will have pain associated
(20:34):
with that.
Okay.
And the thing is, is not to just note that the patient has pain, but you start saying,
why is there pain?
If they're ischemic, do I need to fix a hypoxemic state?
You know, do I need to fix a ventilation or oxygenation state?
If it's inflammation, what's the inflammatory process?
(20:56):
You know, what is causing the inflammation to occur?
Maybe you can't, you know, and it's like a bee sting, right?
You get a bee sting and all of a sudden it becomes red and it becomes inflamed.
And it's what?
Painful.
Well, the pain is not from the venom or the pain.
The pain is from the inflammation occurring at that site.
(21:18):
That's what's triggering the nosy receptors.
So you know that.
So I'm just saying, if it's deeper in the body and you got a patient that says they're
having pain immediately, I say immediately, what should pop in your head is do they, do
they have some ischemia, inflammation, obstruction or infection going on?
Because those are going to be the causes of pain.
(21:39):
Makes you, again, makes you more thorough in your assessment because now you're paranoid,
you're looking for things.
All right.
So we talked about visceral structures and how they apply.
I think that's really where we're going next into this and why that causes problems.
(22:02):
It's pretty evasive, a little elusive for us to figure out.
Absolutely.
So visceral is basically referring to viscous and viscous not being like a substance of
viscous substance, but viscous is an organ.
So if you look, another name for an organ is viscous.
And so visceral structures is basically referring to organs.
(22:25):
Now organs, they're very sensitive to ischemia.
They're very sensitive to inflammation, not real sensitive to stretching your organs.
And so, like, again, if an organ, if the spleen is getting infected, if the spleen is getting
(22:46):
ischemic, if the spleen is being inflamed because of the infection, they're going to
have pain.
But if the spleen is being stretched, they don't have as much pain from the stretching,
just knowing how these visceral organs work.
The other thing too is visceral pain is very poorly localized.
(23:09):
It's crampy.
It's achy.
It's not the sharp stabbing pain.
It's like cramps and it comes and it goes.
It's intermittent pain and it's not real severe.
But then you have deep somatic pain.
And deep somatic pain is usually nocereceptors and ligaments, tendons, bones, blood vessels,
(23:30):
stash, muscles, and so forth.
And it's also a dull, achy and poorly localized pain too, like a sprain.
You know, it would be a good example.
A lot of times it's not like this burning unless it's torn, but it's usually a dull,
achy pain that's just there, comes and goes and so forth.
But then you have superficial somatic pain.
(23:50):
And now this is the stimulation of more peripheral nocereceptors.
And these now are interesting because when they get stimulated, they cause sharp pain,
constant pain, knife-like pain.
You know, so it's constant.
It's knife-like.
It's sharp.
And it hurts bad.
(24:11):
It's much more intense, excuse me, intense than the visceral pain.
And so again, the thing is more or less recognizing that there's a pain complaint and that pain
has to be being caused by a scheming inflammation, infection, or stretching.
But then when you say, you start asking about it and they start saying, well, you know,
(24:33):
it comes and goes.
It's not real bad.
It's kind of like this dull pain.
Then you got to start thinking it's the organ.
The best example of this is appendicitis.
Initially, when a patient's appendix is becoming inflamed or it's becoming infected, it's becoming
inflamed and it's stretching.
And so what happens?
That patient starts complaining of what?
It's some dull, achy pain, not severe.
(24:57):
They can't localize it.
They can't even point to it one finger.
You're like, where is it at?
And they rub their hand across their belly.
Like, well, it's kind of like here.
They can't really localize it.
Well, as that appendix continues to get worse and worse, well, the visceral pain does too,
but it's still not producing that sharp, knife-like pain.
However, when that appendix begins to leak and it starts leaking that perulent fluid
(25:21):
and it starts now hitting the peritoneal wall, suddenly now you're now triggering those superficial
somatic pain receptors.
And once those are triggered, what do we get?
Now the patient says, it hurts right here.
It's constant.
It feels like somebody's stabbing me.
It's really sharp because now we've transitioned from visceral pain to this parietal pain.
(25:45):
And that's the difference in those different types of pains.
But I mean, realistically, the takeaway point to this whole thing is, if you've got a patient
complaining of pain, you really need to not blow it off, but really say to yourself, do
I have ischemia, infection, inflammation, or stretching occurring, that there's something
(26:07):
that I need to be concerned about, that I need to find, that I need to treat.
Again, we're not trying to diagnose intraabdominal organ complaints and things like that.
But it's again, the pain, you just can't blow it off and say, well, it's pain.
They're having pain.
Get to try to figure out.
Dominal pain is really challenging.
I remember being told once that sometimes the most serious pain is the least critical,
(26:31):
but you can find that you have serious things going on with minor pain.
Now if you look at some of these things, I throw out ectopic pregnancy, bowel obstruction,
the alcoholic patient, and you say, well, we have a liver or a pancreatitis, and you
see these organs, and you put together the history, some of the pathophysiology we talk
(26:55):
about here.
And I think it's true that we really can't diagnose.
You get in and you have the ER doc as smart as they are.
They're thinking, okay, at some point we're going to get a CAT scan to try and give us
some answers here.
So we don't expect diagnosis per se, but identifying potential criticality when things could go
bad as well as being able to ask the right questions.
(27:19):
Have you pooped?
Right?
What does it look like?
And what's going on as well as could palpation and other things help put all this together
and make this pathophysiology relevant?
In one point that you brought up, Dan, is the ectopic pregnancy patient.
We know that ectopic pregnancy is truly a surgical emergency.
(27:42):
And in the fear I have today, and it seems like there's a lot more, and I'm not being
critical, it's just an observation of mine, there's a lot more no transports today than
I think ever before.
If the patient says, I don't know, maybe I don't want to go, then a lot of times the
MS crews are like, well, look, you really should go, but if you don't want to, and they're
(28:03):
signing them off and so forth.
And these are these little subtle things, and you bring up the ectopic pregnancy patient,
because again, that's the stretching of the fallopian tube that's causing the pain.
So that's a visceral pain.
So it's not going to be, it's going to be dull, it's going to be achy, it's going to
be poorly localized and so forth until it ruptures.
Now you've got the bleeding occurring into that peritoneal cavity, then suddenly, now
(28:29):
we have, or it's creating the parietal pain, now we have something that's much more significant.
But the fair mine is that you look at this, say, well, it's a dolly-key pain, you can't
really localize it.
All right, well, you promise me you're going to call your OBGYN or they don't even know
that yet.
Call your doctor and that's those things that you look at and you say, well, yeah, and then
(28:52):
she doesn't, and then two days later you go there and all of a sudden now you have a severely
apophilemic patient because you blew it because you blew off the pain.
And that point is so important, like you said, that ectopic pregnancy is a perfect example.
That is serious surgical emergency.
And again, it takes that diagnostic ability, that follow your intuition and some understanding
(29:17):
of pain is just not something that the patient is complaining of.
It means something, infection, inflammation, stretching or ischemia, inflammation, infection
or stretching.
All right, so as we go into six and seven, it almost seems to me that we are doing a
(29:39):
little bit of a recap and putting it all together.
So let's start with number six, metabolism, perfusion and mental status.
They're related.
I think this really kind of brings together a lot of the things we've talked about.
Yes, absolutely.
And we did talk about this in the previous session too.
(30:00):
And again, we teach EMTs at this point the difference between aerobic and anaerobic metabolism.
And the thing, so one thing I always say is which is so important to understand is we
know that aerobic metabolism is we take a glucose molecule, we put it into a cell and
that cell that metabolizes that glucose, it oxidizes it.
(30:22):
And initially in the process, it's called glycolysis.
You don't need oxygen for that process.
It's an anaerobic process.
It produces two molecules of ATP, very little energy.
It's producing a little bit of energy, but very little energy.
Then you create this pyruvate and it gets into the mitochondria.
And whether you remember that or not, it doesn't matter.
(30:43):
But all you know is you go to the next step in the mitochondria and that's where you
need to have the oxygen.
And if you have the oxygen available, then you're in an aerobic metabolism.
And in that aerobic metabolism state, it's very important to understand the byproducts.
One is a lot of energy.
And again, there's differences in opinions out there.
(31:04):
Some say 34 molecules, some say 36, some say 38, regardless.
You're producing a lot of molecules of ATP, meaning that cell has a lot of energy to actually
use for its function.
Without the energy, it can't function.
We said that earlier.
If you don't have the ATP, that cell doesn't function.
If it's a cell in the respiratory tract that's going to cause...
(31:28):
Here's a good example.
You have a patient having a severe asthma attack, right?
Severe asthma attack.
And you're wondering why these bronchodilators are not working any longer.
You can't get any movement in the bronchoconstriction with that bronchodilator.
Well, if those cells, those smooth muscle cells, are severely hypoxic and they're not
(31:50):
getting the oxygen to be in an aerobic state, they're only making two molecules of ATP.
That means what?
That cell wants to do what?
Cause dilation?
It can't because it doesn't have the energy to perform its function.
So therefore it stays...
He explains the downward spiral we see in patients.
(32:12):
Exactly.
And you say to yourself, well, how do I fix it?
You've got to fix the hypoxia.
Yeah.
But then you get in the vicious circle, you start chasing your tail saying, well, how
do I fix the hypoxia?
I got a bronchodilate.
But you've got to figure it out.
You've got to oxygenate.
You've got to fix it.
And that's until you do and you stay in that anaerobic state, you don't have the energy
for that cell to function.
(32:33):
So in the aerobic state, you produce a lot of energy.
You produce CO2.
CO2 is great, but CO2 is really bad.
CO2 is great because we could get rid of it so easily.
We blow it off.
We transport it to the lungs and we blow it off.
And if we produce more CO2, we breathe deeper, we breathe faster, we just blow it off.
(32:56):
So it's beautiful.
It's like this great relationship to have until it starts to collect.
And when CO2 starts to collect, because you have an injury in the lungs, you have a condition
where you can't offload the CO2 and it stays in the blood and it starts hanging around
and it starts collecting, well, when you take CO2 and you combine it with water, you farm
(33:18):
carbonic acid.
And carbonic acid is acid.
It's bad.
Any acid in the body is bad.
Although we know we have to have a certain amount, when you start accumulating acid,
it's bad.
It starts having effects.
Cell membrane starts to break down.
Nerve transmission doesn't go right.
Enzyme function doesn't work and so forth.
So we produce CO2, which is a good thing because we can easily get rid of it.
(33:40):
Again, a good example is, you know, you would see how it works is like, get up, run down,
run down the steps and run back up the steps.
And then you sit down, you're going, I'm breathing faster and deeper.
Why is that?
Because you had, you had, you needed, your muscles needed more energy to work to do that.
And in order to do that, they had to do more glucose into the cell.
(34:01):
And when you put more glucose into the cell and needed more oxygen in the byproduct was
a lot more energy for you to run up and down the steps.
But at the same time, it produced a lot more CO2.
What are you doing when you sit down?
Breathe heavier and deeper.
Okay.
So CO2 is a good byproduct.
Another byproduct is water, which water is so necessary in the cells because if we don't
(34:23):
have an adequate amount of water, we don't have normal enzyme function.
And the fourth is heat.
50% of the oxidation of glucose, 50% of the breakdown of glucose results in the form of
heat that produces our heat load.
You know, you have to wonder and say, well, how do I stay warm?
(34:45):
I don't stay warm because of the atmosphere because right now I'm in my office in the
basement and it's probably 70 degrees.
Well if it's 70 degrees out here, I'm giving off heat from my, so it's surely not my basement
that's keeping me warm.
It's my aerobic metabolism that's generating the heat, you know?
And so again, you say, well, febrile patients, what happens?
(35:08):
Why is it?
What happens to your febrile patient?
You know, when you get a fever, what happens to your heart rate?
Goes up.
Matter of fact, for every one degree increase in Fahrenheit or.6 in Celsius, you get a
responding increase of your heart rate by about 10 beats per minute.
Well, we all know this.
You get a fever, boom, boom, boom, boom.
(35:30):
You're tacking up.
Well, why are you tacking up?
Because your metabolism has gone up.
And you got to deliver that glucose to those cells.
And why are you, why do you have a fever?
Because metabolism to fight off this infection and so forth is producing a lot more heat.
Okay.
Now we got to figure out how to get rid of it.
So that's normal in the aerobic metabolism.
So for byproducts that you want, lots of energy, CO2 that we could blow off, water that we
(35:55):
need for enzymatic reactions and for the cells, and lots of heat.
So what happens now when we go to a patient that goes to aerobic?
Well, aerobic, you put a glucose molecule into the cell.
You still produce two molecules of ATP.
But what happens when it goes into the mitochondria?
(36:18):
Well, it really can't get into the mitochondria because you don't have oxygen.
And so you have pyruvate.
And because the pyruvate can't get into the mitochondria, it starts forming lactic acid.
And this is anaerobic?
This is anaerobic metabolism.
So when you should switch over to anaerobic metabolism, you produce two molecules of ATP
(36:40):
because the majority of your ATP production is an oxygenated mitochondria.
Now you're producing two molecules of ATP.
You're really not, you're producing not large amounts of CO2, but lactic acid.
And you're producing no heat or very little heat, very little heat.
(37:01):
So very little energy.
Your CO2 production is really gone to lactic acid production.
You start producing mass amounts of acid and very little heat.
You know what somebody says?
Well, if that's the case in anaerobic metabolism, why is the patient, why are they breathing
faster and deeper?
Well, if you think about it, you say, well, because there's that equilibrium.
(37:25):
You know, CO2 in water forms carbonic acid, right?
And we say, well, how do we, how do we get rid of carbonic acid?
Well, if we blow off CO2, we don't have the CO2 to combine with water form carbonic acid.
So if we could get rid of CO2, our carbonic acid level is going to fall.
(37:45):
So if we can't keep up with that.
What's that?
We can't keep up.
No.
Just the rest of the time.
Because of our lactic acid levels going up, we're trying to lower our carbonic acid.
So that's why the patient is breathing faster and deeper.
We're trying to actually create an equilibrium by lowering the carbonic acid to allow their
lactic acid levels to go up.
(38:06):
And it's, and again, it's all still bad because they're really just, they're playing a game.
It's kind of like the shell game, you know?
So we go back to then mental status and you say, okay.
So now you say, okay, Swiss definition is shock.
You know, it's to say, well, it's inadequate tissue perfusion.
(38:26):
Great.
And that's the definition of shock.
It is the definition of shock.
But what is inadequate tissue perfusion?
And basically what that means is you're not delivering enough glucose or oxygen to cells.
And if you have inadequate tissue perfusion, you're saying out loud, I now have a state
where I'm going to start shifting from aerobic to anaerobic metabolism.
(38:47):
And if I go to anaerobic metabolism, then suddenly I no longer have the energy.
I no longer have the mass amounts of CO2, but I have mass amounts of acid.
I'm not producing the water and I don't have the heat.
So here's my, here's my example.
You have a patient involved in a car crash.
(39:08):
Again, you got it.
You got two guys on a fishing trip.
They're coming home from their fishing trip.
They're tired, driving 70 miles an hour on the turnpike.
Suddenly he loses control.
He falls asleep.
Bam, hits head on into the concrete barrier.
You get on the scene, you and your partner, and you got two patients and you got the driver
(39:30):
of the vehicle.
You got the passenger vehicle and the driver of the vehicle is screaming and yelling and
screaming because he has an open humorous fracture.
And he's screaming and yelling that his arm hurts.
It's so bad.
I'm bleeding to death.
Oh my gosh.
Help me.
Help me.
Okay.
(39:50):
And you think, wow, this is pretty dramatic too, right?
Open humorous fracture, bone sticking out at the right angle.
This is dramatic.
You focus on that drama.
But yet the passenger vehicle, you look, you poke your head and say, how you doing, buddy?
He goes, okay.
You doing all right?
I think so.
Are you injured?
(40:11):
And all of a sudden you start saying, who's worse?
Who probably has a much poorer hemodynamic state?
You say, well, the patient who's sitting there yelling and screaming and grabbing you and
pulling you into the car to help him, help him, help him has a ton of energy.
(40:35):
In order to have a ton of energy, you got to have what?
Good profusion and good aerobic metabolism.
But the guy sitting in the passenger seat has a very low energy state.
And what do you have to assume?
He's got a poor profusion state.
He's not producing the ATP.
Who am I going to go to first?
(40:56):
The passenger.
There you go.
I think it might be that he's just tired and he doesn't really care.
Maybe he had a food beard.
Tough day of fishing.
Yeah.
But again, clinically, that's how you put this together.
It's like, if you've got a patient sitting, they're screaming and yelling and walking
around versus the patient that's very quiet, very low key, you got to think.
(41:20):
It takes energy to do what they're doing.
But this guy over here doesn't look like he has a lot of energy.
That's related to profusion.
And the methods of that.
I think we've talked about number seven.
So we finished this up on time.
We talked about cold being bad.
That one patient is cold.
So I think we've covered that a little bit, especially in talking about the heat in number
(41:42):
six.
We now know another reason why cold is bad.
Let's wrap this up a little quickly so we finish on time and bring it home.
Yep.
Exactly.
As you said, Dan, we did.
As you said, we mentioned it.
50% of the heat production in an aerobic state is from glucose metabolism.
(42:02):
You're producing tons of heat.
Here's a funny, I always ask you, how many of you have gone through a Boy Scout first
aid class or a Red Cross first aid class when you were in elementary school?
A lot of people raise their hand and say, what's one thing that I taught you?
Even today, what's one thing that tells you if you're a layperson, you find somebody on
the ground and you think they're bleeding and you think they're in shock.
(42:25):
You always do what?
Cover them with a blanket.
Keep them warm.
Right?
Well, hell, it's 90 degrees outside.
Why am I covering a patient with a blanket and keeping them warm?
Well, if we shift from an aerobic to an anaerobic state, we lose that heat production.
Suddenly now, my body is no longer able to produce those mass amounts of heat.
(42:47):
What happens?
They start becoming hypothermic.
This is so important for EMS crews.
It could be 90 or 88 degrees, let's say outside.
Your skin temperature is typically about 90 degrees Fahrenheit, the temperature of your
skin.
Once you have an ambient temperature less than 90, you start losing the heat from your
body out to the ambient atmosphere.
(43:10):
That means if it's less than 88 degrees, you're going to start transmitting heat out of your
body out into the ambient atmosphere and the patient is going to have a tendency to become
hypothermic.
What does that mean?
Cover the patient.
It doesn't matter if it's 90 degrees outside, you cover the patient.
You put them in the back of the ambulance.
You turn on the heat.
(43:32):
You're sweating like crazy.
You got sweat rolling everywhere, but yet you turn on the heat because you're patient.
If it's not 90 degrees ambient temperature, they're losing heat.
We know what does cold do to bleeding and clotting?
Creates coagulopathies.
Cold trauma patients can't clot.
They continue to bleed and bleed and bleed.
(43:53):
It's so funny, that most basic thing that everybody is told.
If you've got a patient who's bleeding, keep them warm.
If you think they're in shock, keep them warm.
All goes back to because you think they're in an anaerobic metabolism and they lost the
ability to heat production and it's being conducted away.
Put them on a cold backboard that you keep in the side compartment of the ambulance and
(44:15):
your bay is 68 degrees.
Pull that backboard out, strip them down, put them on it.
They're conducting that heat so fast, becoming hypothermic from that conduction of heat from
their body to the board.
You just got to think about it.
That's where that heat production is coming from.
It's so important yet we always think of the big things first.
What we think are the big things, the IVs and the...
(44:39):
But maintaining body temperature is so simple yet so important.
It is something that we often overlook.
I think it's a really great point to end this with.
We did it, Joe.
It's not what makes you comfortable, it's what's right for the patient.
This is going to play a big end.
(44:59):
It really is.
I think we've covered a lot of stuff.
Well, I can't see people listening to this.
I can feel light bulbs coming on as a result of this.
You and I have always taught, especially at the EMT level, you mentioned EMRs and even
paramedics.
Paramedics should have gotten this in their EMT class and be able to understand and make
(45:20):
these decisions.
They are so foundational that understanding is just so important.
I think when these two episodes, part one and part two, we've done that.
And I offer my sincere thanks for the way you explain things.
A good man, a good friend, and very good for EMS.
Thank you, Joe.
(45:41):
Thanks, Dan.
Appreciate it.
Thank you for listening to another Limer Education Continuing Education podcast.
For more podcasts that are relevant to your practice of EMS, limereducation.com, slash
seven things.
Welcome to the Seven Things EMS Podcast, a continuing education offering of Limmer education.
(00:12):
Seven Things EMS Podcast is designed to give you what you need to succeed in EMS, it's
conversational, informational, and without the fluff.
And welcome to another episode of Seven Things EMS, this is a continuation of our Pathophysiology
(00:37):
and Assessment series with my friend and someone I consider an expert in this, Joe Mistovich.
In our last episode, we talked about hypoxia and hypoglycemia and provided some understanding
and we're going to continue with that one today.
So welcome back, Joe Misovich.
Thanks, Dan.
(00:57):
All right, number four.
Now people may have listened to the first one, but Joe is a textbook author, conference
speaker, professor, retired from Youngstown State University, certainly has the credibility
to be doing all these things that I want to not introduce you in this.
But it's our mantra to go right into it.
(01:19):
And let's go to our number four as we continue on to seven about peripheral edema.
It provides important clues to the diagnosis of a patient's condition.
And I think we see edema and we generally jump to one conclusion.
And I think you may change the way we think about that.
(01:41):
Yeah, and it's so true.
And I think what bothers me here the most is that you'll see that, and again, this is
not just EMTs.
It's advanced EMTs and paramedics will do this too sometimes in their assessment.
And they'll be doing their assessment and say, oh, look, the patient has some edema to
(02:03):
their ankles and to their feet.
And then they're like, okay.
All right, I'll note it.
And then that's as far as they go with it.
And they stop there and they just think like, okay, I'll note it.
Instead of saying, okay, why is that?
Again, in that possibilities to probabilities, this is huge.
And again, and you're right.
And I think if you had asked your typical paramedic and say, hey, you got a patient that presents
(02:27):
with dependent edema, what are you thinking?
They're going to go, heart failure.
Well, it's got to be heart failure.
You know, well, you know, that's one out of many things.
But again, in the big scheme of things, this edema could be providing huge clues to actually
what's going on with the patient.
And why do I think you're going to tell us those things?
(02:49):
And a little bit of pathophysiology to explain those.
So, you know, and so, you know, I say, you know, just this is not just the point for
you to note.
And one other thing I want to point out is edema, remember, they call it dependent edema
because it is gravity dependent.
And what that means is if your patient is sitting, the extra fluid, and this is lymphatic fluid,
(03:12):
this is interstitial fluid, it's going to collect in the feet, the ankles, and the hands
because they're dependent.
They're lower portions of the body.
And that's where that fluid based on gravity is going to collect.
If you have a patient who's a supine patient, somebody maybe who's bedridden, and they have
edema, it's not going to be in their feet and their hands.
(03:33):
You're going to find it primarily in the pre-sacral area in the posterior body.
So, you've got to get these patients up and you've got to look at their back and it's
pre-sacral.
So, it's like between the lumbar area and the sacral area of the body, and you start
looking for the edema there because that's where it's going to settle based on gravity.
So, when you find edema, you have to start thinking, you know, what, okay, so what are
(03:58):
the things that causes edema?
You say, well, there's four things primarily that will cause edema.
One is an increase in hydrostatic pressure.
Now, hydrostatic pressure is, all you got to remember is hydrostatic pressure is the
push factor inside the vessel.
And this is primarily inside capillaries, arterioles, and venals.
(04:22):
But hydrostatic pressure is primarily affecting the arterial and the beginning portion of
the capillary bed.
And so, this is right before the entrance into the capillary and it's a push pressure.
It's pushing, its force is being exerted on the inside of the vessel wall, trying to
push stuff out.
So, that's one, an increase in hydrostatic pressure.
(04:44):
So, that means if you have a dramatic increase in hydrostatic pressure, that pressure, the
higher it gets, it reaches a point where it overwhelms that vessel wall and that vessel
wall where these just cells lined up together can't hold it in any longer because the pressure
overcomes it and it pushes out more fluid than it can recover.
(05:06):
So, that's the one thing you think of peripheral edema is, do I have, well, what's going to
increase hydrostatic pressure?
Increase in blood volume is one, or a dramatic increase in blood pressure is another.
So, therefore, when you start getting the patient that you immediately think, heart
failure, you know, so funny because they've kind of gotten away from the term congestive,
(05:29):
although we keep saying congestive heart failure, you know, and they say, well, it's not necessarily
congestive because, hey, to say it, but when you turn 40, you now start on your journey
of heart failure, normal pathologic heart failure.
And so, it's not necessarily congestive, but the congestive piece is there's too much
volume now and there's higher pressure in the vessel and it's pushing the fluid out.
(05:53):
And I'll explain that.
And then the second one is a decreased oncotic pressure.
And when you say oncotic pressure, you're referring to proteins in the blood.
The biggest protein in the blood is a plasma protein that we know is albumin, okay?
And what albumin is, is we know two things attract water.
(06:14):
Charged particles like sodium and so forth where sodium goes, water falls it because
it's a charged particle.
It's an electrolyte.
And the other is large particles.
What's a large particle?
Albumin.
You know, it's another large particle?
Glucose.
Where glucose goes, water is going to follow it.
That's why we don't give any injured patients glucose because glucose gets crossed into
(06:35):
the brain cells and draws water and worsens the edema in the brain.
So this oncotic pressure, this big albumin molecule that's in plasma, exerts this, this
osmotic force where it's forcing water to be pulled in.
So the way that capillary works, and this is referred to as the Starling equation, its
(06:59):
net filtration is, as blood enters in the beginning of the capillary, it comes into the
arterial because the arterial was the most distal part of the artery.
And it enters into the arterial.
And in the arterial, because of the hydrostatic pressure, it's pretty high because the vessel
is so small that the hydrostatic pressure is pushing fluid out of the arterial.
(07:22):
The blood then gets into the capillary bed.
Then when it hits the venial, the beginning of the venial is where now you pushed out
a lot of fluid and it's plasma volume, right?
It's not whole blood, it's plasma volume.
You pushed it all out.
But what did you leave behind?
Albumin.
Those big particles.
(07:43):
And so when the blood enters the beginning of the venial, you got big particles.
And because of osmosis, where you have big particles, it's drawing the fluid and it draws
it back in.
And so what Starling equation says, there should be zero net filtration.
Net filtration should equal zero, meaning the forces, the hydrostatic pressure, the
(08:04):
push should be pushing out a certain amount of fluid.
And the pull factor, on caudic pressure is known as the pull factor, should be pulling
that same amount of volume in.
And when we have net filtration that equals zero, the amount being pushed out as being
pulled in, we have no edema.
The problem is now when we have a disturbance in either one of those.
(08:27):
So let's take our congestive heart failure patient.
Our congestive heart failure patient hasn't lost any albumin.
They haven't lost those big plasma proteins, it's still in the blood.
The problem is when their left ventricle can't eject all that blood volume, people say, well,
it backs up into the lungs.
Well, it doesn't really back up.
But what happens is the pressure starts to increase because the volume is increasing
(08:51):
in the pulmonary capillaries.
And so what do you increase?
You increase the hydrostatic pressure.
So I'm just going to use this arbitrarily.
Let's say just for numbers.
Let's say that in this pulmonary capillary, you normally would push out 10 mLs of interstitial
fluid of plasma volume.
And then you had the plasma proteins to pull back in 10 mLs.
(09:15):
But now because this patient is in heart failure and they have this dramatic increase in volume
in the pulmonary capillaries that are one cell thick, it pushes out 30 mLs of interstitial
fluid.
But you still only have enough albumin in the venial to pull 10 mLs back in.
(09:37):
So now you have 20 mLs of fluid that remains outside of the vessel around the cells.
Now you start developing edema.
So that's one way.
And that's your heart failure patient.
Anaphylaxis.
What's one major sign of an anaphylactic reaction?
(09:59):
Edema.
In a lot of it's dependent edema.
You start seeing the edema.
Why do you get so much edema to the tongue, to the face, to the neck?
Because it's a very vascular area.
The more vessels you have, the more it's going to be affected.
So what does the chemical mediators like histamine and prostaglandins and bradykinins and all
(10:19):
these chemical mediators do?
They increase capillary permeability, meaning that they make the spaces in the capillaries
wider.
So that means when the pressure, when the volume of blood is coming into the arterial,
they got out now wide spaces.
So what happens is when they're only supposed to push out 10 mLs, they're able to push out
20 because they have no longer kind of like the fence to keep it in.
(10:43):
But the same thing.
On the venial side, it only has enough albumin to pull 10 back in.
So that's why you're losing the volume.
Now you're actually losing the volume out of the vascular space.
So this could create a hypovelemic state with severe increases in capillary permeability.
So that's why.
Now here's a question I would pose to my students based on this.
(11:07):
Why is it if you have a patient who has a partial thickness or a full thickness burn,
let's say it's to the entire thorax of the body.
So let's say it's like a, I don't know, a 40% body surface area burn, but it's to the
thorax of the body.
(11:30):
Why is it that these patients, if you've never seen a burn patient who becomes severely
adeptus all over their entire body, why are they becoming adept?
We know there's immediate edema in the area of the burn.
We know that.
If you're listening to this podcast, you don't believe me, go upstairs, put on your stove,
(11:52):
heat it up, put your hand on it, hold it down as long as you could.
Hold it, hold it, hold it, pull it off and what's going to happen almost immediately?
Blister formation.
Better put this place.
Letters education and our sponsors don't recommend touching hot stove burners.
Well, what do we know?
We know immediately we started developing blisters.
That's how we develop blisters because it's from an increase or increase in capillary
(12:14):
permeability.
But you look at the burn patients, you say, but why are their legs swollen when they're
lying supine?
Why is their face so swollen when they're lying supine?
That's not dependent.
Gravity should be pulling it down.
One of the reasons is because in the burn area, if you have a big enough burn, and usually
it only takes a burn of greater than 30% body surface area, partial thickness, full thickness,
(12:38):
where you increase the capillary permeability in the burn area because you're destroying
those arterials and you leave such huge spaces that albumin is leaking out along with the
fluid.
So now hydrostatic pressure is pushing out 50 mL of fluid because you've got big spaces
in there because the capillaries are damaged from the burn.
(13:00):
Not only is the plasma volume going out, albumin is leaking out with it.
Now on the venial side, you have very little albumin, maybe only to pull five mLs in and
the albumin is collecting outside in the interstitial space.
So now when you get to unburned areas, the legs aren't burned, but when you come into
(13:20):
the capillary, the hydrostatic pressure that should be pushing out 10 is still pushing
out 10, but when it gets to the venial, it only has enough albumin to pull in three.
So you've got seven mLs left out there.
Forget the numbers.
Let's just try to explain.
But you have very little albumin because it's all wear in the burned area.
(13:40):
Pushing out in the interstitial space, you don't have enough albumin to pull that fluid
back in.
Now, we know one thing about burn patients, we have that first 24 hours, right?
We give them tons of fluid in the first 24 hours.
We use Parkland's formula and some of these patients were given 24, 30, 6, 48 liters of
fluid depending on the burn and the size of the patient, right?
(14:02):
But then we have what?
A reversal.
All of a sudden now, we're going to start giving them some type of like Lasix or something
to start getting rid of fluid because what happens is that albumin starts coming back
into the capillaries.
Now, all of a sudden, the albumin starts pulling all that fluid you gave the patient and all
(14:23):
that fluid hanging on it pulls it back in and all of a sudden we make our patient hypervolumic.
But that's how this works.
Now a patient that could have an albumin disturbance also could be a patient with some type of
kidney disease where the kidneys are actually dumping out albumin.
So the other is the lymphatic blockage or inability of the lymph system.
(14:43):
The lymph system takes the interstitial fluid and puts it back into the venous side.
So next time, you know, you go to a call and you got a patient with edema.
You just don't say, well, mark it on the PCR as edema.
You got to start thinking, does this patient have too much volume or high pressure?
Okay.
Here's another one.
(15:05):
Cocaine or vasoactive drugs.
Why is it that an 18 year old kid all hyped up on cocaine or crack could go into pulmonary
edema?
You remember, Dan, we worked in the days as paramedics where cocaine was the big drug.
And we would see these kids that are 18, 19, 21 year old kids in great physical shape doing
(15:26):
cocaine in pulmonary edema.
Well, if you think about it, what happens?
Pressure.
It's pressure.
Cocaine is a vasoactive substance.
Causes vasoconstriction.
What does it do?
Dramatically increases the hydrostatic pressure.
You're pushing out too much fluid then you can recover.
Happens in the lungs and they end up with pulmonary edema.
(15:46):
So you got to start thinking, this isn't just edema.
Why is there edema?
Because there's some underlying cause.
You know, that could be dramatically related to what you need to do with on the scene too.
I'm not saying you're trying to diagnose for the hospital.
You're not trying to determine they have kidney disease, but you need to know, do they have
a vasoactive drug on scene?
(16:08):
You know, on.
But also at the same time, somebody's been doing cracker cocaine, you better be listening
to their lungs because they could be in pulmonary edema from the increase in hydrostatic pressure.
All right.
I'm going to keep, I'm going to move on to number five.
And normally, normally I jump in and we'll say something, but I just think your explanations
(16:28):
are so incredible.
I think people at all levels can understand these.
I'll also add that we have some detailed show notes people can look at to find more information
on this.
Number five talks about pain.
Not all pain is the same.
Knowing different pain presentations in that medical patient is important.
It's going to tell you something.
(16:48):
Yeah.
And this is very similar to, to like the edema.
So when you get on the scene and the patient is complaining of pain, you know, there's
a big difference between your trauma patient and your medical patient.
If you have a trauma patient who has a fractured extremity or has a sprain or a tear or something
like that or a knife wound, that's all mechanical type of pain.
(17:09):
And that's pretty easy.
It's kind of like, well, yeah, I know why you haven't pain because look at the bone.
It's at a right angle of where it should be.
That's what's causing the pain.
And pain, you have no C receptors and these receptors are basically sensory fibers that
are picking up this stimulation, you know, and it's picking up the pain response.
And typically pain is caused by a thermal source, which is heater cold and mechanical
(17:33):
source was just going to be your crushing, your tearing, your sharing and chemical.
Good example of a chemical cause of pain is if you remember the old days, actually we
remember the, what was it?
Meachuricrome.
Meachuricrome.
Meachuricrome.
Meachuricrome.
That they, that, you know, you would get a cut and your parents will pour that in that
(17:57):
wound.
It was like, oh, it was like peroxide, the same thing.
That's a chemical type of pain.
And what you're doing is you're introducing a chemical and you're stimulating then those
no C receptors.
But what's, you know, and that's pretty obvious.
Okay.
So if you have a burn, it's going to cause pain.
Okay.
That's a thermal, thermal cause.
But now when you get on the scene and you have a medical patient who has no trauma
(18:21):
complaining of pain, again, it's not just something for you to document in the PCR.
It's for you to actually think about because you say in a medical patient, what's going
to cost pain?
Well, basically there's four major things.
It's ischemia or tissues, hypoxic.
It's inflammation.
Whereas as an inflammatory response, there's infection or they're stretching like there's
(18:47):
an obstruction.
The best example of pain by stretching gas.
When you have gas, when you build up gas in your intestinal system, what do you get?
A crampy abdominal pain.
And that's nothing more than those no C receptors being stimulated from the stretch of the intestine.
Okay.
(19:07):
But the key is if you have a pain.
You're saying you should let it out, Joe.
Let the gas out.
Absolutely.
And then you know, the funny thing is you let it out and all of a sudden the pain goes
away because what happens?
That colon is no longer being stretched.
And so those receptors are no longer being stimulated.
So if you had to station, just say it's an experiment.
You're validating what Mr. Vich said about that.
(19:28):
It is.
And it's a physiological relief thought.
This is what it is.
I mean, I think it's true.
But when you get on a scene and you have a patient complaining of pain and it's not related
to trauma, you have to start thinking, is it ischemia?
Is it infection?
Is it inflammation?
Or is it something, some stretch of a viscous?
(19:50):
And again, it's taking you from those possibilities to probabilities.
We look at chest pain in the patient having an MI.
Why is a patient having a heart attack having chest pain?
Well, because what's happening?
That cardiac muscle is ischemic.
Ischemia is causing the pain.
(20:11):
And so you say, well, okay.
So if that's the case, so if my liver is ischemic, they should have right upper quadrant pain.
You know, you know, infection is the same.
A patient having some type of infection will complain of pain.
If if, you know, they have an infection in their leg, typically they will have pain associated
(20:34):
with that.
Okay.
And the thing is, is not to just note that the patient has pain, but you start saying,
why is there pain?
If they're ischemic, do I need to fix a hypoxemic state?
You know, do I need to fix a ventilation or oxygenation state?
If it's inflammation, what's the inflammatory process?
(20:56):
You know, what is causing the inflammation to occur?
Maybe you can't, you know, and it's like a bee sting, right?
You get a bee sting and all of a sudden it becomes red and it becomes inflamed.
And it's what?
Painful.
Well, the pain is not from the venom or the pain.
The pain is from the inflammation occurring at that site.
(21:18):
That's what's triggering the nosy receptors.
So you know that.
So I'm just saying, if it's deeper in the body and you got a patient that says they're
having pain immediately, I say immediately, what should pop in your head is do they, do
they have some ischemia, inflammation, obstruction or infection going on?
Because those are going to be the causes of pain.
(21:39):
Makes you, again, makes you more thorough in your assessment because now you're paranoid,
you're looking for things.
All right.
So we talked about visceral structures and how they apply.
I think that's really where we're going next into this and why that causes problems.
(22:02):
It's pretty evasive, a little elusive for us to figure out.
Absolutely.
So visceral is basically referring to viscous and viscous not being like a substance of
viscous substance, but viscous is an organ.
So if you look, another name for an organ is viscous.
And so visceral structures is basically referring to organs.
(22:25):
Now organs, they're very sensitive to ischemia.
They're very sensitive to inflammation, not real sensitive to stretching your organs.
And so, like, again, if an organ, if the spleen is getting infected, if the spleen is getting
(22:46):
ischemic, if the spleen is being inflamed because of the infection, they're going to
have pain.
But if the spleen is being stretched, they don't have as much pain from the stretching,
just knowing how these visceral organs work.
The other thing too is visceral pain is very poorly localized.
(23:09):
It's crampy.
It's achy.
It's not the sharp stabbing pain.
It's like cramps and it comes and it goes.
It's intermittent pain and it's not real severe.
But then you have deep somatic pain.
And deep somatic pain is usually nocereceptors and ligaments, tendons, bones, blood vessels,
(23:30):
stash, muscles, and so forth.
And it's also a dull, achy and poorly localized pain too, like a sprain.
You know, it would be a good example.
A lot of times it's not like this burning unless it's torn, but it's usually a dull,
achy pain that's just there, comes and goes and so forth.
But then you have superficial somatic pain.
(23:50):
And now this is the stimulation of more peripheral nocereceptors.
And these now are interesting because when they get stimulated, they cause sharp pain,
constant pain, knife-like pain.
You know, so it's constant.
It's knife-like.
It's sharp.
And it hurts bad.
(24:11):
It's much more intense, excuse me, intense than the visceral pain.
And so again, the thing is more or less recognizing that there's a pain complaint and that pain
has to be being caused by a scheming inflammation, infection, or stretching.
But then when you say, you start asking about it and they start saying, well, you know,
(24:33):
it comes and goes.
It's not real bad.
It's kind of like this dull pain.
Then you got to start thinking it's the organ.
The best example of this is appendicitis.
Initially, when a patient's appendix is becoming inflamed or it's becoming infected, it's becoming
inflamed and it's stretching.
And so what happens?
That patient starts complaining of what?
It's some dull, achy pain, not severe.
(24:57):
They can't localize it.
They can't even point to it one finger.
You're like, where is it at?
And they rub their hand across their belly.
Like, well, it's kind of like here.
They can't really localize it.
Well, as that appendix continues to get worse and worse, well, the visceral pain does too,
but it's still not producing that sharp, knife-like pain.
However, when that appendix begins to leak and it starts leaking that perulent fluid
(25:21):
and it starts now hitting the peritoneal wall, suddenly now you're now triggering those superficial
somatic pain receptors.
And once those are triggered, what do we get?
Now the patient says, it hurts right here.
It's constant.
It feels like somebody's stabbing me.
It's really sharp because now we've transitioned from visceral pain to this parietal pain.
(25:45):
And that's the difference in those different types of pains.
But I mean, realistically, the takeaway point to this whole thing is, if you've got a patient
complaining of pain, you really need to not blow it off, but really say to yourself, do
I have ischemia, infection, inflammation, or stretching occurring, that there's something
(26:07):
that I need to be concerned about, that I need to find, that I need to treat.
Again, we're not trying to diagnose intraabdominal organ complaints and things like that.
But it's again, the pain, you just can't blow it off and say, well, it's pain.
They're having pain.
Get to try to figure out.
Dominal pain is really challenging.
I remember being told once that sometimes the most serious pain is the least critical,
(26:31):
but you can find that you have serious things going on with minor pain.
Now if you look at some of these things, I throw out ectopic pregnancy, bowel obstruction,
the alcoholic patient, and you say, well, we have a liver or a pancreatitis, and you
see these organs, and you put together the history, some of the pathophysiology we talk
(26:55):
about here.
And I think it's true that we really can't diagnose.
You get in and you have the ER doc as smart as they are.
They're thinking, okay, at some point we're going to get a CAT scan to try and give us
some answers here.
So we don't expect diagnosis per se, but identifying potential criticality when things could go
bad as well as being able to ask the right questions.
(27:19):
Have you pooped?
Right?
What does it look like?
And what's going on as well as could palpation and other things help put all this together
and make this pathophysiology relevant?
In one point that you brought up, Dan, is the ectopic pregnancy patient.
We know that ectopic pregnancy is truly a surgical emergency.
(27:42):
And in the fear I have today, and it seems like there's a lot more, and I'm not being
critical, it's just an observation of mine, there's a lot more no transports today than
I think ever before.
If the patient says, I don't know, maybe I don't want to go, then a lot of times the
MS crews are like, well, look, you really should go, but if you don't want to, and they're
(28:03):
signing them off and so forth.
And these are these little subtle things, and you bring up the ectopic pregnancy patient,
because again, that's the stretching of the fallopian tube that's causing the pain.
So that's a visceral pain.
So it's not going to be, it's going to be dull, it's going to be achy, it's going to
be poorly localized and so forth until it ruptures.
Now you've got the bleeding occurring into that peritoneal cavity, then suddenly, now
(28:29):
we have, or it's creating the parietal pain, now we have something that's much more significant.
But the fair mine is that you look at this, say, well, it's a dolly-key pain, you can't
really localize it.
All right, well, you promise me you're going to call your OBGYN or they don't even know
that yet.
Call your doctor and that's those things that you look at and you say, well, yeah, and then
(28:52):
she doesn't, and then two days later you go there and all of a sudden now you have a severely
apophilemic patient because you blew it because you blew off the pain.
And that point is so important, like you said, that ectopic pregnancy is a perfect example.
That is serious surgical emergency.
And again, it takes that diagnostic ability, that follow your intuition and some understanding
(29:17):
of pain is just not something that the patient is complaining of.
It means something, infection, inflammation, stretching or ischemia, inflammation, infection
or stretching.
All right, so as we go into six and seven, it almost seems to me that we are doing a
(29:39):
little bit of a recap and putting it all together.
So let's start with number six, metabolism, perfusion and mental status.
They're related.
I think this really kind of brings together a lot of the things we've talked about.
Yes, absolutely.
And we did talk about this in the previous session too.
(30:00):
And again, we teach EMTs at this point the difference between aerobic and anaerobic metabolism.
And the thing, so one thing I always say is which is so important to understand is we
know that aerobic metabolism is we take a glucose molecule, we put it into a cell and
that cell that metabolizes that glucose, it oxidizes it.
(30:22):
And initially in the process, it's called glycolysis.
You don't need oxygen for that process.
It's an anaerobic process.
It produces two molecules of ATP, very little energy.
It's producing a little bit of energy, but very little energy.
Then you create this pyruvate and it gets into the mitochondria.
And whether you remember that or not, it doesn't matter.
(30:43):
But all you know is you go to the next step in the mitochondria and that's where you
need to have the oxygen.
And if you have the oxygen available, then you're in an aerobic metabolism.
And in that aerobic metabolism state, it's very important to understand the byproducts.
One is a lot of energy.
And again, there's differences in opinions out there.
(31:04):
Some say 34 molecules, some say 36, some say 38, regardless.
You're producing a lot of molecules of ATP, meaning that cell has a lot of energy to actually
use for its function.
Without the energy, it can't function.
We said that earlier.
If you don't have the ATP, that cell doesn't function.
If it's a cell in the respiratory tract that's going to cause...
(31:28):
Here's a good example.
You have a patient having a severe asthma attack, right?
Severe asthma attack.
And you're wondering why these bronchodilators are not working any longer.
You can't get any movement in the bronchoconstriction with that bronchodilator.
Well, if those cells, those smooth muscle cells, are severely hypoxic and they're not
(31:50):
getting the oxygen to be in an aerobic state, they're only making two molecules of ATP.
That means what?
That cell wants to do what?
Cause dilation?
It can't because it doesn't have the energy to perform its function.
So therefore it stays...
He explains the downward spiral we see in patients.
(32:12):
Exactly.
And you say to yourself, well, how do I fix it?
You've got to fix the hypoxia.
Yeah.
But then you get in the vicious circle, you start chasing your tail saying, well, how
do I fix the hypoxia?
I got a bronchodilate.
But you've got to figure it out.
You've got to oxygenate.
You've got to fix it.
And that's until you do and you stay in that anaerobic state, you don't have the energy
for that cell to function.
(32:33):
So in the aerobic state, you produce a lot of energy.
You produce CO2.
CO2 is great, but CO2 is really bad.
CO2 is great because we could get rid of it so easily.
We blow it off.
We transport it to the lungs and we blow it off.
And if we produce more CO2, we breathe deeper, we breathe faster, we just blow it off.
(32:56):
So it's beautiful.
It's like this great relationship to have until it starts to collect.
And when CO2 starts to collect, because you have an injury in the lungs, you have a condition
where you can't offload the CO2 and it stays in the blood and it starts hanging around
and it starts collecting, well, when you take CO2 and you combine it with water, you farm
(33:18):
carbonic acid.
And carbonic acid is acid.
It's bad.
Any acid in the body is bad.
Although we know we have to have a certain amount, when you start accumulating acid,
it's bad.
It starts having effects.
Cell membrane starts to break down.
Nerve transmission doesn't go right.
Enzyme function doesn't work and so forth.
So we produce CO2, which is a good thing because we can easily get rid of it.
(33:40):
Again, a good example is, you know, you would see how it works is like, get up, run down,
run down the steps and run back up the steps.
And then you sit down, you're going, I'm breathing faster and deeper.
Why is that?
Because you had, you had, you needed, your muscles needed more energy to work to do that.
And in order to do that, they had to do more glucose into the cell.
(34:01):
And when you put more glucose into the cell and needed more oxygen in the byproduct was
a lot more energy for you to run up and down the steps.
But at the same time, it produced a lot more CO2.
What are you doing when you sit down?
Breathe heavier and deeper.
Okay.
So CO2 is a good byproduct.
Another byproduct is water, which water is so necessary in the cells because if we don't
(34:23):
have an adequate amount of water, we don't have normal enzyme function.
And the fourth is heat.
50% of the oxidation of glucose, 50% of the breakdown of glucose results in the form of
heat that produces our heat load.
You know, you have to wonder and say, well, how do I stay warm?
(34:45):
I don't stay warm because of the atmosphere because right now I'm in my office in the
basement and it's probably 70 degrees.
Well if it's 70 degrees out here, I'm giving off heat from my, so it's surely not my basement
that's keeping me warm.
It's my aerobic metabolism that's generating the heat, you know?
And so again, you say, well, febrile patients, what happens?
(35:08):
Why is it?
What happens to your febrile patient?
You know, when you get a fever, what happens to your heart rate?
Goes up.
Matter of fact, for every one degree increase in Fahrenheit or.6 in Celsius, you get a
responding increase of your heart rate by about 10 beats per minute.
Well, we all know this.
You get a fever, boom, boom, boom, boom.
(35:30):
You're tacking up.
Well, why are you tacking up?
Because your metabolism has gone up.
And you got to deliver that glucose to those cells.
And why are you, why do you have a fever?
Because metabolism to fight off this infection and so forth is producing a lot more heat.
Okay.
Now we got to figure out how to get rid of it.
So that's normal in the aerobic metabolism.
So for byproducts that you want, lots of energy, CO2 that we could blow off, water that we
(35:55):
need for enzymatic reactions and for the cells, and lots of heat.
So what happens now when we go to a patient that goes to aerobic?
Well, aerobic, you put a glucose molecule into the cell.
You still produce two molecules of ATP.
But what happens when it goes into the mitochondria?
(36:18):
Well, it really can't get into the mitochondria because you don't have oxygen.
And so you have pyruvate.
And because the pyruvate can't get into the mitochondria, it starts forming lactic acid.
And this is anaerobic?
This is anaerobic metabolism.
So when you should switch over to anaerobic metabolism, you produce two molecules of ATP
(36:40):
because the majority of your ATP production is an oxygenated mitochondria.
Now you're producing two molecules of ATP.
You're really not, you're producing not large amounts of CO2, but lactic acid.
And you're producing no heat or very little heat, very little heat.
(37:01):
So very little energy.
Your CO2 production is really gone to lactic acid production.
You start producing mass amounts of acid and very little heat.
You know what somebody says?
Well, if that's the case in anaerobic metabolism, why is the patient, why are they breathing
faster and deeper?
Well, if you think about it, you say, well, because there's that equilibrium.
(37:25):
You know, CO2 in water forms carbonic acid, right?
And we say, well, how do we, how do we get rid of carbonic acid?
Well, if we blow off CO2, we don't have the CO2 to combine with water form carbonic acid.
So if we could get rid of CO2, our carbonic acid level is going to fall.
(37:45):
So if we can't keep up with that.
What's that?
We can't keep up.
No.
Just the rest of the time.
Because of our lactic acid levels going up, we're trying to lower our carbonic acid.
So that's why the patient is breathing faster and deeper.
We're trying to actually create an equilibrium by lowering the carbonic acid to allow their
lactic acid levels to go up.
(38:06):
And it's, and again, it's all still bad because they're really just, they're playing a game.
It's kind of like the shell game, you know?
So we go back to then mental status and you say, okay.
So now you say, okay, Swiss definition is shock.
You know, it's to say, well, it's inadequate tissue perfusion.
(38:26):
Great.
And that's the definition of shock.
It is the definition of shock.
But what is inadequate tissue perfusion?
And basically what that means is you're not delivering enough glucose or oxygen to cells.
And if you have inadequate tissue perfusion, you're saying out loud, I now have a state
where I'm going to start shifting from aerobic to anaerobic metabolism.
(38:47):
And if I go to anaerobic metabolism, then suddenly I no longer have the energy.
I no longer have the mass amounts of CO2, but I have mass amounts of acid.
I'm not producing the water and I don't have the heat.
So here's my, here's my example.
You have a patient involved in a car crash.
(39:08):
Again, you got it.
You got two guys on a fishing trip.
They're coming home from their fishing trip.
They're tired, driving 70 miles an hour on the turnpike.
Suddenly he loses control.
He falls asleep.
Bam, hits head on into the concrete barrier.
You get on the scene, you and your partner, and you got two patients and you got the driver
(39:30):
of the vehicle.
You got the passenger vehicle and the driver of the vehicle is screaming and yelling and
screaming because he has an open humorous fracture.
And he's screaming and yelling that his arm hurts.
It's so bad.
I'm bleeding to death.
Oh my gosh.
Help me.
Help me.
Okay.
(39:50):
And you think, wow, this is pretty dramatic too, right?
Open humorous fracture, bone sticking out at the right angle.
This is dramatic.
You focus on that drama.
But yet the passenger vehicle, you look, you poke your head and say, how you doing, buddy?
He goes, okay.
You doing all right?
I think so.
Are you injured?
(40:11):
And all of a sudden you start saying, who's worse?
Who probably has a much poorer hemodynamic state?
You say, well, the patient who's sitting there yelling and screaming and grabbing you and
pulling you into the car to help him, help him, help him has a ton of energy.
(40:35):
In order to have a ton of energy, you got to have what?
Good profusion and good aerobic metabolism.
But the guy sitting in the passenger seat has a very low energy state.
And what do you have to assume?
He's got a poor profusion state.
He's not producing the ATP.
Who am I going to go to first?
(40:56):
The passenger.
There you go.
I think it might be that he's just tired and he doesn't really care.
Maybe he had a food beard.
Tough day of fishing.
Yeah.
But again, clinically, that's how you put this together.
It's like, if you've got a patient sitting, they're screaming and yelling and walking
around versus the patient that's very quiet, very low key, you got to think.
(41:20):
It takes energy to do what they're doing.
But this guy over here doesn't look like he has a lot of energy.
That's related to profusion.
And the methods of that.
I think we've talked about number seven.
So we finished this up on time.
We talked about cold being bad.
That one patient is cold.
So I think we've covered that a little bit, especially in talking about the heat in number
(41:42):
six.
We now know another reason why cold is bad.
Let's wrap this up a little quickly so we finish on time and bring it home.
Yep.
Exactly.
As you said, Dan, we did.
As you said, we mentioned it.
50% of the heat production in an aerobic state is from glucose metabolism.
(42:02):
You're producing tons of heat.
Here's a funny, I always ask you, how many of you have gone through a Boy Scout first
aid class or a Red Cross first aid class when you were in elementary school?
A lot of people raise their hand and say, what's one thing that I taught you?
Even today, what's one thing that tells you if you're a layperson, you find somebody on
the ground and you think they're bleeding and you think they're in shock.
(42:25):
You always do what?
Cover them with a blanket.
Keep them warm.
Right?
Well, hell, it's 90 degrees outside.
Why am I covering a patient with a blanket and keeping them warm?
Well, if we shift from an aerobic to an anaerobic state, we lose that heat production.
Suddenly now, my body is no longer able to produce those mass amounts of heat.
(42:47):
What happens?
They start becoming hypothermic.
This is so important for EMS crews.
It could be 90 or 88 degrees, let's say outside.
Your skin temperature is typically about 90 degrees Fahrenheit, the temperature of your
skin.
Once you have an ambient temperature less than 90, you start losing the heat from your
body out to the ambient atmosphere.
(43:10):
That means if it's less than 88 degrees, you're going to start transmitting heat out of your
body out into the ambient atmosphere and the patient is going to have a tendency to become
hypothermic.
What does that mean?
Cover the patient.
It doesn't matter if it's 90 degrees outside, you cover the patient.
You put them in the back of the ambulance.
You turn on the heat.
(43:32):
You're sweating like crazy.
You got sweat rolling everywhere, but yet you turn on the heat because you're patient.
If it's not 90 degrees ambient temperature, they're losing heat.
We know what does cold do to bleeding and clotting?
Creates coagulopathies.
Cold trauma patients can't clot.
They continue to bleed and bleed and bleed.
(43:53):
It's so funny, that most basic thing that everybody is told.
If you've got a patient who's bleeding, keep them warm.
If you think they're in shock, keep them warm.
All goes back to because you think they're in an anaerobic metabolism and they lost the
ability to heat production and it's being conducted away.
Put them on a cold backboard that you keep in the side compartment of the ambulance and
(44:15):
your bay is 68 degrees.
Pull that backboard out, strip them down, put them on it.
They're conducting that heat so fast, becoming hypothermic from that conduction of heat from
their body to the board.
You just got to think about it.
That's where that heat production is coming from.
It's so important yet we always think of the big things first.
What we think are the big things, the IVs and the...
(44:39):
But maintaining body temperature is so simple yet so important.
It is something that we often overlook.
I think it's a really great point to end this with.
We did it, Joe.
It's not what makes you comfortable, it's what's right for the patient.
This is going to play a big end.
(44:59):
It really is.
I think we've covered a lot of stuff.
Well, I can't see people listening to this.
I can feel light bulbs coming on as a result of this.
You and I have always taught, especially at the EMT level, you mentioned EMRs and even
paramedics.
Paramedics should have gotten this in their EMT class and be able to understand and make
(45:20):
these decisions.
They are so foundational that understanding is just so important.
I think when these two episodes, part one and part two, we've done that.
And I offer my sincere thanks for the way you explain things.
A good man, a good friend, and very good for EMS.
Thank you, Joe.
(45:41):
Thanks, Dan.
Appreciate it.
Thank you for listening to another Limer Education Continuing Education podcast.
For more podcasts that are relevant to your practice of EMS, limereducation.com, slash
seven things.
Popular Podcasts
Crime Junkie
Does hearing about a true crime case always leave you scouring the internet for the truth behind the story? Dive into your next mystery with Crime Junkie. Every Monday, join your host Ashley Flowers as she unravels all the details of infamous and underreported true crime cases with her best friend Brit Prawat. From cold cases to missing persons and heroes in our community who seek justice, Crime Junkie is your destination for theories and stories you won’t hear anywhere else. Whether you're a seasoned true crime enthusiast or new to the genre, you'll find yourself on the edge of your seat awaiting a new episode every Monday. If you can never get enough true crime... Congratulations, you’ve found your people. Follow to join a community of Crime Junkies! Crime Junkie is presented by audiochuck Media Company.
24/7 News: The Latest
The latest news in 4 minutes updated every hour, every day.
Stuff You Should Know
If you've ever wanted to know about champagne, satanism, the Stonewall Uprising, chaos theory, LSD, El Nino, true crime and Rosa Parks, then look no further. Josh and Chuck have you covered.