April 4, 2023 • 50 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 1Hypoxia, hypoperfusion, and hypoglycemia are common patient presentations. Yet many providers weren’t taught in a depth to truly understand these conditions. This episode of 7 Things EMS will take you from memorization to truly understanding these conditions and relating them to assessment findings. Guest Joe Mistovich takes detailed pathophysiology and makes it interesting and understandable.
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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.
(00:33):
And welcome to another Seven Things EMS, I'm your host Dan Limmer from Limmer Education.
I am thrilled today for two reasons.
The first is that we're going to talk about pathophysiology, an important foundation for
everything we need to learn in EMS.
But the second part is that I get to do it with my longtime friend Joe Mistovich and
(00:54):
I will note longtime friend and competing EMT author Joe Mistovich.
Joe is a longtime professor at Youngstown State University.
He's published a bunch of books out there in EMS.
He's a prince among men.
And we don't spend a lot of time in the beginning of this audio series because we like to get
right down to business, right down to those seven things.
(01:17):
So I'll say welcome Joe and we'll get started.
Thanks Dan.
All right, number one.
Hypoxia affects the brain.
But the way it affects the brain provides clues that are important in the primary assessment.
Let's get right into it.
Okay.
And you know through our discussions and you know in our presentations together and
(01:42):
so forth.
And I'm a firm believer like you that pathophysiology is important to understand because it provides
so many clues to the EMS practitioner.
Whether you're an EMR, an EMT, advanced EMT or paramedic, it provides a lot of clues.
And a lot of times these are subtle clues that really will enhance your ability to assess
the patient and also trending of the patient's you know condition.
(02:07):
Whether they're improving, deteriorating or not.
A lot of these little signs and symptoms are things that you have to pay attention to.
I say a lot of times you know people will say like well I found the skins palcone clamia
and they document it and it's like oh I gotta remember to put that in my pre-hospital care
report but they really don't pay much attention to what it actually means about the patient.
And so as I said you know understanding these little you know little pearls of pathophysiology
(02:33):
are really important.
And so you know right hypoxia affects the brain, we know that the brain tissue is the
most sensitive to any insults of hypoxia.
And the hypoxia is coming from hypoxemia which obviously hypoxemia is an inadequate amount
of oxygen found in the blood because the blood we know is the number one carrier of the oxygen
(02:57):
to the brain.
So it's interesting you know in times people say like well you know they weren't cyanotic
and I say well you know when the patient becomes cyanotic you're so far behind the
ball at that point that it's going to be real tough to recover.
And so therefore you have to start looking for these very subtle signs and symptoms of
hypoxia or hypoxemia.
(03:19):
So we already know the brain is the most sensitive organ to hypoxia.
And because of that it is going to respond relatively quickly.
It's kind of like the heart when the heart gets irritable you start having you know
dysrhythmia as well.
When the brain gets irritable because it's hypoxic it starts sending out impulses.
Okay.
And what happens is so the brain gets hypoxic and one of the centers in the brain that's
(03:44):
extremely sensitive to this hypoxia is the medulla.
And we know that medulla houses the respiratory center, the cardiac center, and the vasomotor
center.
And the cardiac center has both the cardio inhibitory and the cardio acceleratory center.
So when the brain starts getting hypoxic what it does instantaneously and this is within
(04:06):
seconds it's sensing this hypoxia it triggers the medulla to start sending out impulses.
It's almost like a distress signal that the brain needs more oxygen.
And so its response by the medulla is to send out impulses from the cardio acceleratory
center, the vasomotor center, and the respiratory center.
(04:28):
And so you start looking at this so okay so that's great.
So clinically though when you apply it what you start to look at is what are the responses
from the medulla.
Well if the cardio acceleratory center is stimulated what you're going to see clinically
is the patient starts to exhibit some tachycardia.
(04:48):
Now initially the patient's resting heart rate might be 70 and you say well you know
what's normally heart rate well a lot of patients don't know that but if they do or if you've
had this patient before you might say or even just judging.
So you have a 32 year old patient and you say well I would speculate that the heart
rate probably resting heart rate would be in the 70s and now they're at 92.
(05:10):
And so although 92 is not considered tachycardia for that patient it is obviously a physiologic
response and the heart rate is higher.
And so suddenly you start looking at these things you start looking at this.
So the cardio acceleratory center triggers the heart it actually sends impulses to the
SA node to increase the speed of the heart rate.
(05:34):
And then also what it does is it sends impulses to increase the force of conduction okay in
which again we know that is inotropy we know that the increasing this speed at which the
heart is beating is the chronotropy.
And then also the dromotropy if you want to increase how fast the heart beats you have
to increase the speed at which the impulse gets through the conduction system.
(05:57):
So we have an increase in inotropy which is contractility and increase in chronotropy
which is an increase in heart rate and increase in dromotropy which is the speed through the
conduction system.
Now this makes sense you know in a second here is why the brain is doing this there's
a reason for it.
And the other thing that gets stimulated is the vasomotor center and the vasomotor center
(06:20):
controls the vessel size and it changes the resistance in the vessels primarily in the
arterioles you know in the distal end of the artery right before it enters into the capillary
and in the small arteries it's not the large arteries but it's the arterioles and also
the smaller arteries.
And so what happens there is well the vasomotor center actually increases the systemic vascular
(06:46):
resistance through vasoconstriction.
And so clinically say so what are we seeing there?
Well when you start vasoconstricting the first organ obviously that's going to be affected
is going to be the skin.
So when you start squeezing that nice warm red blood out of the skin that skin starts
becoming pale because the red blood is not out there.
(07:06):
It starts becoming cool because the nice warm red blood is not out there.
And also you start to feel this you know diaphoresis this claminess and that actually is from stimulation
of the sweat glands by the nervous system.
(07:27):
And you know one has to wonder so why is the brain, why is the medulla increasing the heart
rate and trying to increase systemic vascular resistance when it's hypoxic?
Well the bottom line is this the brain thinks if I can get more blood because blood carries
oxygen I'm going to get more oxygen.
And so its intent is to increase the blood flow to the brain.
(07:52):
And the only way to increase blood flow to the brain is to increase blood pressure.
And so if we go back and we say well so what's the equation for blood pressure?
Well blood pressure equals cardiac output times systemic vascular resistance.
And we know that if we can increase cardiac output we could increase blood pressure.
If we increase blood pressure we increase oxygenation of the brain in theory.
(08:14):
That's what the body is hoping.
And at the same time we say well systemic vascular resistance is part of that equation
too.
If we increase systemic vascular resistance through a phase of constriction we can increase
blood pressure.
We increase blood pressure, we increase oxygenation of the brain.
And this is the brain's theory.
And so what does the body do?
What does the medulla intend to do?
(08:36):
And it tends to increase cardiac output.
Well how do you increase cardiac output?
Well we know cardiac output is determined by heart rate and stroke volume.
So if I can increase heart rate I can increase cardiac output.
If I increase cardiac output I increase blood pressure and hopefully get more oxygen to
the brain.
Therefore that's why the heart rate's increasing.
(08:56):
The body's trying to increase the heart rate in an attempt to give more blood flow to the
brain.
To the stroke volume now the only way to increase stroke volume is you've got to put more volume
which in this patient they don't have the ability to increase their volume.
They have their normal volumic.
They have a normal blood volume.
Unless it's a hypolumic patient but that's a whole different case.
(09:18):
But one other way to increase stroke volume is to increase the force of contraction.
So therefore that's your inotropy by increasing the force of contraction you might be able
to increase stroke volume.
If you increase stroke volume you increase cardiac output, you increase cardiac output,
you increase blood pressure and hopefully get more blood to the brain.
So clinically you-
Alright I'm going to stop you for one second.
(09:40):
I think that we've just had about seven or eight minutes of what some people are probably
thinking is some heavy duty pathophysiology.
But the truth is this is stuff that should be taught in every EMT class but it's not.
This concept of understanding is something we've lost with the EMTB curriculum and we're
(10:03):
trying to bring back and that this stuff is so important.
The concept of not memorizing signs and symptoms versus understanding what goes on is what
we're getting here.
So I just wanted just to stop and say as you started this section with is that you need
to understand and that this is the stuff that many people probably should have been taught
(10:28):
in class.
I would even venture to say there's some medics out there that never got this.
So this is just really important stuff and when we look at skin changes in color, temperature
and condition we say oh it's shock but now we're saying even hypoxia can do that.
(10:50):
Right.
You know it's so true Dan and then I'll tell you this you know just this little story and
you're so right is I'm teaching an EMR refresher an emergency medical responder refresher right
now and I'm presenting this stuff to these firefighters.
It's a group of ten firefighters who really want to do what's right for the patient and
(11:11):
it's funny because they tell me you know Joe we've never learned this but when I present
this to them they are just so excited because they're like well this makes sense and you
know Dan my saying is that all makes sense.
If you can understand a little bit of pathophysiology, a little bit of anatomy, a little bit of physiology
it all makes sense and you're right.
(11:33):
And so here's these ten EMRs that are looking at this going well this is going to change
completely how I look at patients and that's the whole purpose of this because again you
know when you start saying so the thing is when you get on the scene and you have a patient
who's sitting there and you begin your primary assessment and you start noticing hey this
(11:56):
patient's a little bit tachycardic, their skin's a little bit pale, cool, clammy you
know they may have some tremors you know while there's an increase in respiratory you know
rate and they're breathing a little bit deeper.
One thing that has to pop into your head is hypoxia.
Hypoxia.
Now again through your differentials you may roll it out and we know that we're huge advocates
(12:19):
of possibilities to probabilities but one of the possibilities has to be is this patient
hypoxic and it's these subtle signs and symptoms that actually could give you those clues you
know.
So another is you know you know so the respiratory center in the medulla then starts sending impulses
(12:44):
to the DRG and the VRG, the dorsal respiratory group and the ventral respiratory group and
so what's happening here is these two centers is primarily the VRG they're receiving these
impulses and so what do they do?
They increase the number of impulses to the respiratory muscles, the diaphragm and the
external inner costals to increase the rate at which they're contracting so therefore
(13:09):
what do you get?
Not only the rate but also the force so you get an increase in respiratory rate and increase
in respiratory depth and these are very subtle signs and symptoms but also one has to realize
that initially this is all just a neural it's a direct nerve stimulation these are actually
electrical impulses that are being sent to the heart to the respiratory muscles and the
(13:33):
vessels and this is a very short-lived thing this can only be sustained for a minute or
two it's not long at most a couple minutes and so one of the impulses that's being sent
out is going to the adrenal medulla gland the adrenal glands that sits on top of the
kidney and when that adrenal medulla gets stimulated well we know it gets released is epinephrine
(13:57):
and norepinephrine so suddenly now you get this epinephrine and norepinephrine dump which
has alpha 1, alpha 2, beta 1, beta 2 which now is providing the long-term sustained effects
okay one thing I want to mention too is the alpha is causing the constant visual constriction
(14:18):
the beta 1 is continuing the increase in heart rate, force of contraction, speed of
conduction, beta 1 or the beta 1 is the cardiac, beta 2 one thing I want to point out is beta
2 is the smooth muscle dilator the bronchial dilator but one other effect is when skeletal
(14:38):
muscle receives beta 2 stimulation it causes tremors and this is where you might see the
patient starting to tremor a little bit and that's from beta 2 stimulation it's like if
you give a beta 2 agonist like a butyrol whether it be by meter dose inhaler or nebulizer and
you start noticing your patient having some tremors afterwards that's a common side effect
(15:01):
and it's because of beta 2 stimulating the skeletal smooth muscle and the other thing
is when epinephrine and norepinephrine are secreted they have a lot of alpha 1 and alpha
1 is what stimulates the sweat glands and causes you to begin to sweat you're getting
clammy now the key to all this is if the patient's hypoxia is worsening the medulla is saying
(15:23):
send more blood more blood more blood by raise the pressure raise the pressure raise the
pressure so what happens heart rate gets higher the respiratory rate gets higher the
tidal volume gets deeper the skin gets more pale because there's greater vasoconstriction
and more clammy because there's more alpha 1 out there and that's a long term effect now we know
(15:45):
we have pulse oximetry we all know that the pulse oximetry is a great tool to determine hypoxemia
but this is very specific to determine hypoxia of the brain and so these are those subtle things
and again it's not just in the primary assessment it's also in your continued assessment so if your
(16:06):
treatment is effective and you're reducing the hypoxia to the brain you should start seeing a
decrease in tachycardia the skin becoming a little bit less pale cool and clammy going back to more
normal respiratory rates going down tidal volumes going down and you know you see this in front of
(16:26):
your eyes but again these are the subtle signs and symptoms that you have to be looking for and
it you know it's so funny because a lot of EMT the EMT's the antics patient you know this you
know you ask them to say well you know what's a what's the sign of hypoxia and most of them their
number one answer is sinosis you know in order for the patient to become cyanotic again you're so
(16:47):
far behind the game because they are so severely hypoxia at that point so my response that is
is what's what's a great sign of hypoxia pale cool clammy skin increase respiratory rate increase
in tidal volume tachycardia and tremors now again we also know for this for the brain start
(17:12):
becoming altered also tastes a significant hypoxia these are early we're talking about slight decreases
in their hypoxemia or in their oxygen status slight hypoxemia that's going to trigger these signs
and symptoms so for again you say well how's pathophysiology related to how's it related clinically
and that's a question people always ask because they don't want to learn the pathophysis this is
(17:36):
exactly right because it makes you so much better of a clinician and the ability to assess your
patients and treat them what what I'm what I'm thinking here and you know we've been presenting
presenting together for a long time and you're mr pathophysiology and I'm the wow let's see how this
relates to the street and what I'm thinking is one is that this will go into our second thing here
(18:02):
but also we are so hung up on 94 percent and we're so we're so mixed up in our heads about when to
give oxygen and when not to give oxygen I think what you've really done in this first section is
been able to tell people that if you see certain things I would even venture to say regardless
(18:26):
of what the pulse ox says you should be looking at this and saying this can be hypoxia the body's
responding in a way to show that there's crisis you've described a fight or flight response
and that is trying to feed the brain so we should assist in feeding the brain by giving some oxygen
(18:47):
and we don't always have to go with the big guns with a non-rebreeder I think we've forgotten how
much a nasal cannula can really do and how much comfort it is for the patient but I think you've
really helped define for our listeners that there's a lot more than pulse ox in the oxygen
decision if your patient has that I'll just call it the shocky look that that's an indication for
(19:12):
oxygen exactly and that is 100 the key to this and Dan you remember when the pulse ox simulators just
came out and if you recall we we used to teach students well don't rely on the pulse ox similar
rely on your clinical findings because that's really going to tell you whether your patient's
(19:33):
hypoxia or not well they've refined pulse oxymetry and pulse like simulators are pretty accurate but
like you said you know take a patient in a cold environment that pulse oxymeter it could be inaccurate
you know or a state of poor perfusion but the key that you said is yeah yeah and again you
walk into a scene and you see tachycardia pale cool clammy skin increased respiratory rate increased
(19:55):
tidal volume you start thinking two things one is hypoxia and poor perfusion the key is not to go
okay hey market in the PCR the key is to say what's going on with my patient what is it and again
those possibilities the probabilities and through hopefully a good assessment you know one's going
(20:16):
to come down to a probability of why this is happening but I couldn't agree with you more it's
like and and the statement you said is so true regardless of what the pulse ox is telling you
if your intuition is saying something's not right here and I think they might be hypoxic
absolutely agree with you put them on nasolcania two liters and you can't believe what that might
(20:39):
actually do and if you put them on a nasolcaniola two liters and these things start improving
then you know that you caught something but but again if you don't understand this most people
are just like well you know yeah they're tachycardic and whoa look they're more tachycardic now but
they don't put it together this whole thing is put it all together because it makes sense and
(21:01):
it's telling that story about your patient and the other thing is the trending look at the trends
is it worsening is it improving is it staying the same well let's roll into number two I think it's
it's peripherally related and I think we're going to get a little bit deeper into the concepts here
and I think that's good I'll also say to our listeners you're going to hear some pretty important
(21:23):
terms some big terms things you probably should have had in your class and didn't I'm going to
ask you to lean into this this understanding is going to change the way you practice and it's
important that we do this the second one the relationship between hemoglobin anemia and cyanosis
may surprise you that the way that we transport oxygen and some of the relations to what we just
(21:49):
talked about is important as well and we've already said cyanosis is a late sign it's not the
not the thing that should be you should be making your decision on yeah it's interesting I suppose
this question all the time not only thinking my empty classes but also to my paramedic classes
and and it was interesting to find out that they a lot of times couldn't couldn't grasp the relationship
(22:14):
until it was explained especially with the anemic patient so the key here is you know understanding
the hemoglobin okay is on the surface of the red blood cell and hemoglobin has four iron sites
and those four iron sites are binding sites with oxygen and so one thing we know about hemoglobin
and this is basically how the pulse oximeter works the pulse oximeter reads it has a red light and
(22:39):
an infrared light and it basically is shining that light through the skin and is able to determine
through the infrared light and the red light how much hemoglobin is actually saturated with oxygen
and that's how we get a pulse oximeter reading and so it's hemoglobin that is the key and again
is found on the surface of the red blood cells so if you're losing red blood cells you're obviously
(23:01):
losing hemoglobin and if you're losing hemoglobin you're losing the ability to transport oxygen
so this is a this is an interesting question well before we go there I'll say so if you have all the
hemoglobin in your body and we we already said pulse oximetry is reading the amount of hemoglobin
(23:22):
saturated with oxygen versus hemoglobin not saturated and one thing that you know EMTs and
advanced EMTs and EMRs and paramedics know is if we have hemoglobin that's not saturated with oxygen
if we have hemoglobin coming through a vessel and it has it's desaturated it's very low in oxygen
it has carbon dioxide attached to it um what do we see it and most often people say well it's
(23:49):
going to look blue because hemoglobin that doesn't have oxygen attached has this bluish color to it
and that's true deoxygenated hemoglobin appears as blue that's why your veins in your body look
blue or greenish blue instead of red you know arteries if you see your arteries would look
(24:10):
red because that's saturated hemoglobin so we established that hemoglobin with oxygen attached
to it um looks red hemoglobin that doesn't have oxygen attached to it is deoxygenated
it's deoxygenated desaturated looks blue or cyanotic you say well so the the point to remember
(24:31):
there is hemoglobin then is what's responsible for changing the color of the skin you have to
have hemoglobin to change the color of the skin and so if you have a lot of hemoglobin that's not
attached to oxygen hypoxemia the skin starts looking in a later stage the skin starts looking
(24:53):
cyanotic because that hemoglobin is now taking on the appearance of being blue
if we are having a big whoa this does make sense moment here and it and it's important but again
it's important clinically to apply it clinically too and if you have hemoglobin attached to oxygen
your skin's going to take on this relatively normal color now again through vasoconstriction
(25:19):
we're going to start shunting that to the body but you know well you know as well as i do dan
teaching students it's like you just don't look at the skin you look at the oral mucosa you look at
the conjunctiva you look at other core areas to the body the skin may be pale but those areas still
look pretty red meaning that we still have that hemoglobin so here's the thing so the bottom
(25:41):
line to this is in order to change the color of the skin based on a hypoxemic state or or whatever
state it would be you have to have hemoglobin so it has my students so an anemic patient
and there's a lot of different types of anemia but the bottom line is this they have an inability
(26:02):
to either have an appropriate monohemoglobin they don't have the iron sites regardless of what the
cause is they're not carrying as much oxygen as you and I because they have some chronic condition
or short-term condition of anemia so I'd ask my students so is an anemic patient who becomes
(26:24):
hypoxemic are they going to become cyanotic quicker or is it going to take longer and students would
you know ponder that question and a majority of them would say well they're going to become
cyanotic quicker you know and they'd say well again it takes hemoglobin to change the color of the skin
(26:47):
what's the color you know it's funny because we could go to the mall be walking around and look
at a person and go damn they're anemic you know just because they look what pale because they
don't have the hemoglobin to make their skin look normal so therefore they're pale because
they don't have the hemoglobin so you look at this you say well in order to make a patient look
(27:11):
hypoxic you have to have hemoglobin that's not attached to oxygen and because you don't have
the large amounts of hemoglobin you can't turn the skin cyanotic because you don't have the
hemoglobin to do so so an anemic patient could be severely hypoxemic it's still not presenting
(27:31):
with cyanosis they're going to look pale but they're not going to be cyanotic but they're going to be
tachycardic they're going to have the vasoconstriction the clammy skin the increase
respiratory rate and so forth everything we talked about previously so you say one of the things
I've heard you say oh I'm sorry one of the things I've always heard you say when you speak
(27:52):
at presentations on the road is that cyanosis is a very late sign how late well again
so so and again there's why pulse axiometry is important and people have to realize that pulse
axiometry has to catch up to hypoxemia too pulse axiometry is not giving you instantaneous readings
(28:16):
it it it takes some time before it starts to identify hypoxemia that's why again looking at
those subtle signs and symptoms and you said earlier Dan that look if you're seeing this stuff
and your intuition is saying I think they're hypoxic when my pulse ox is still at 94 start
on monsimho too nobody's going to ever criticize anyone for doing that because your intuition
(28:39):
and your assessment findings are saying this so cyanosis Dan it takes a significant amount of
desaturation of hemoglobin to cause a person to become cyanotic so again as far as time it's a
longer period of time because they have to desaturate but it also depends on the severity of
the condition how severely you know is there oxygenation you know transmission in the alveoli
(29:06):
you know if you got a patient like let's say a drowning patient where their lungs are filled
with fluid and they're really not getting any O2 across well you know that person who becomes
cyanotic pretty damn quick but if you got an asthmatic who's still moving air and is still
saturating hemoglobin just not as much as they need to it's going to take a much longer period
(29:27):
of time for them to look cyanotic so so go ahead I was just going to say before we move into
hypoglycemia I've had the good fortune to like I said to present with you on the road narrow to say
the thing that I have we haven't talked about a lot we've talked about many of the physiological
(29:47):
signs of hypoxia hypoxemia what about mental status the change in mental status with this
yes and that's in that you know and that's there again you know the other one that I always you
know uh hit hard on is aerobic and anaerobic metabolism and again a lot of people said well
(30:08):
I learned that in ninth grade biology I did in ninth grade biology learning about aerobic
and anaerobic metabolism thinking when the heck am I ever going to need this in my life
you know believe it or not I use that every day to explain things and you know and that all goes
back Dan to the aerobic versus the anaerobic and we know the aerobic metabolism put a glucose
(30:31):
molecule into a cell and metabolizes it and if oxygen's available it produces large amounts of
ATP 36 38 molecules of ATP but if we don't have the oxygen available this is what's
happening in the brain cell without the oxygen available glucose we know is the major energy
source for the brain cell glucose gets in the brain cell it produces two molecules of ATP because
(30:55):
the initial part of the metabolism is anaerobic whether it's aerobic or anaerobic state that
first part glycolysis produces two molecules of ATP so you got a little bit of energy but then when
it gets in the mitochondria without the oxygen what is the brain cell making it's making no ATP
and lots of acid because it doesn't have oxygen if we don't have the ATP we don't have the energy
(31:21):
to make that brain cell work and if the brain cell doesn't work what do we see
alter mental status I mean if the brain cell the group of brain cells that allows you to tell
the EMT or the paramedic your name is not producing enough ATP they're not going to tell you their
name and that and and this is how this is so clinically related but before we move on here's
(31:47):
another question I posed to my students with that anemia is this one of your one more things
one more thing one more thing but it makes sense if you have a trauma patient you know
and you go to a scene and you have a trauma patient let's say you have a patient driving
a car down the road is 65 miles an hour whatever happens and they they hit a concrete you know
(32:12):
barrier at 65 miles an hour unrestrained patient and you're looking at your patient when you get
on the scene and you go into assess your patient and you got this trauma patient looks like they
have some chest trauma just by the the mechanism that they were unrestrained they probably went
forward it was a frontal collision hit the steering wheel and they're severely cyanotic
(32:35):
you're already seeing cyanosis where do you see cyanosis first circle morally you know around the
mouth you know you'll see in the conjunct of other or omucosa the fingertips but you're already
starting to see cyanosis in this patient you just got on the scene you go into the driver's side
door and you're looking at the patient you're going oh crap this guy's cyanotic now you got to
(32:55):
ask yourself right there clinically me personally i'm going to say this guy's got a bad chest injury
a chest injury that's interfering with his ability to either ventilate or oxygenate
and somebody else is going to say oh no he's in shock he say well why don't i think he is
(33:17):
losing a lot of blood now he could be losing blood but why is it that i'm not thinking that this
condition right away why am i thinking immediately we got a severe respiratory ventilation issue
because of the severe because of the hypoxia or the cyanosis
say well why not why am i not thinking that he's bleeding out maybe he lacerated a pulmonary vessel
(33:42):
because in order to change the skin color you have to have hemoglobin if the guy's bleeding out into
his chest or bleeding out into his belly or bleeding out on the ground he's losing whole blood
whole blood has red blood cells red blood cells he even govind he looks what pale he doesn't look
(34:04):
cyanotic although he might be hypoxic he's like now the anemic patient he doesn't have the hemoglobin
to make him look cyanotic but the patient with the severe chest injury who now can't ventilate
appropriately maybe he's got a big flail chest or something or has some major pulmonary contusion
(34:26):
he's got blood volume he just can't get the oxygen into the blood because of a ventilation
or oxygen disturbance he's looking cyanotic so clinically a lot of people a lot of people just
said wow and we all know those patients when we say oh crap or worse yeah right that's a that's a
(34:47):
clinical response to this is bad but now you know why and and you said in this these are those little
things you know we wrote the amls book you know the you know the original amls book and our whole
intention was how do we bring those years of clinical experience to new providers and this
(35:07):
is one of those things when you walk up to a patient involved in a trauma or you walk up to
any patient and you see severe cyanosis either they've been hypoxic for a long period of time
or they have a severe ventilation or oxygen diffusion problem but if you walk up to a trauma
patient shot in the chest and they're looking so cyanotic already when you get on the scene
(35:31):
I'm not I'm not too worried right now about severe blood loss I'm worried about severe
hypoxia hypoxemia or ventilation disturbance those are those little clinical signs and symptoms
and clues and this is where pathophys make sense all right you're taking a breath so I'm going to
move to number three we have about 15 minutes for this one we know we're going to have a two-part
(35:54):
episode there's so much to cover here number three hypoglycemia is easier to understand than you might
think right I mean today we pulled out the blood glucose monitor you know we didn't have that I don't
sound like the old guys but we didn't have that but now everybody just pulls out the blood glucose
monitor and gets an answer but you probably could tell a lot even before you use that blood glucose
(36:20):
monitor and quite frankly we should use that and it might even tell us better when to use the blood
glucose monitor absolutely yeah Dan you remember the days where we used the chem strips where you
took the drop of blood you put it on the chem strip then you had to wait 90 seconds then you had to
have a water source you remember being out on the street you're like where's my water source
(36:43):
we get a bottle of sterile water and pour it over the chem strip and compare the color to the side
of the bottle that's where we came from and those were very inaccurate so we absolutely had to know
clinical signs and symptoms of hypoglycemia so here's another thing you know teaching students
teaching EMTs teaching paramedics two weeks after their exam on endocrinology I would ask
(37:05):
students so what are the signs of hypoglycemia versus diabetic ketoacidosis um well what's
the skin like in hypoglycemia versus decay uh well one's warm and one's which one and you know
we know this that you take an exam two weeks later I was terrible at this this is why I had to
(37:26):
understand because I was terrible at memorizing two weeks later I'd be like I don't remember which
group goes with what what's what and so forth and so to understand and I started looking at
hypoglycemia like hypoglycemia is so simple to understand the clinical presentation again this
relates back to clinical presentation and patient assessment findings and here's the thing Dan you
(37:50):
hit it we got a blood glucose monitor but these clinical signs the symptoms are going to tell
you something about severity too and trending it's trending what are these doing are they
improving are they staying the same are they getting worse because that's going to tell you
something too we know blood glucose monitors a lot of times are not calibrated especially being on
(38:11):
the ambulance sometimes the strips are out of date or they're affected by light heat cold and they're
not providing the most accurate you know reading so we got to keep that in mind so again knowing
clinically what's happening in this patient is so important so I say understanding hypoglycemia
is simple because you only need to know two things one the question you posed earlier was well what
(38:40):
about altered mental status you know well how does this patient who's hypoxic start developing an
altered mental stat not you didn't ask how but just pointing out that altered mental status is a huge
key well that's a huge key in the hypoglycemic patient because what do we know about brain cells
brain cells can pretty much only use glucose as an energy source brain cells can't store it
(39:06):
they can't make it they can't suck it up and concentrate it from the blood they just get
whatever is being sent to them through perfusion and so if we have a patient whose blood glucose
level goes down now we have a diabetic patient who their insulin pump you know goes haywire and is
injecting way too much insulin or they're injecting themselves with insulin and they take way too much
(39:30):
and there's also now some of the hypoglycemic anti-hypo glycemic um i'm sorry the hypoglycemic
agents i'm not saying that right the drugs that people are taking that are type 2 diabetics
they they also could produce hypoglycemia it's a rarer event but it can't occur and it's like
(39:53):
some of these drugs because some of these drugs what they do is they stimulate the pancreas to make
more insulin and if they forgot that they took their you know their oral you know hypoglycemic
agent they take it again and then they've forgotten then they take it again for lunch and
and all of a sudden they're overdosing themselves and their pancreas is just screaming out insulin
(40:13):
it's no different than somebody taking a syringe of insulin and then injecting it three times so
they could become hypoglycemic too keep that in mind because a lot of times we've beaten people's heads
while they got to be a type 1 diabetic that's injecting insulin or somebody who's type 2 that's
injecting insulin or has insulin some pump that's not necessarily true but what do we know we know
we go back to our aerobic metabolism and we say well if the brain can pretty much only use glucose
(40:38):
to make energy and now we don't have enough glucose available well we don't have enough
glucose available to make energy so that means we don't have enough energy for the brain cells to work
and what do we see clinically?
Alternative status everything from from confusion to complete coma seizures are actually a relatively
(41:03):
rare event in hypoglycemia I think we pushed that for a long time like oh my god people are going to
seize what they they are they are more predisposed to seizures than when they're not hypoglycemic
but it's not as common I don't have red one statistic it was less than 30 percent I think
it was actually down to 13 percent of patients in hypoglycemia actually have seizures and they
(41:27):
got to be really severely hypoglycemic too and so you say so what's one group of signs and symptoms
that we will see they're called neuroglucopenic or neuroglycopenic and what that means is
neuro all you got to think is neurogluconuroglyco and that's and the peanut part is being caused by
(41:48):
and you say there's a lack of glucose in the brain cell and the brain cell can't make energy
so it doesn't work what do we see clinically?
Alternative status that's one huge group there's only two groups one huge group so what do we see
in a hypoglycemic patient? Alternative status and that onset is what fast because as soon as you're
(42:10):
not getting the glucose into the cell it can't make energy when it can't make energy what do we see
alterations in mental status okay one thing that all you need to know is we have glucose or we have
counter regulatory hormones when we have disturbances with glucose and the main ones are glucagon
(42:33):
okay then we have insulin we have glucagon and we know that when the blood glucose level is going
down glucagon is being secreted from the pancreas okay from the alpha cells in the pancreas and
they're secreting the glucagon and the glucagon's job is to do what take glycogen that's stored in
the liver convert it back to glucose and put it back into the blood and take non-carbohydrates
(42:55):
and start converting them and trying to make glucose out of them and that's a long process
that doesn't occur real quick but we know there's another hormone that's a counter regulatory hormone
that's epinephrine so not only is epinephrine the fight or flight hormone you know increasing the
heart rate and increasing the system and vascular and so forth epinephrine is a counter regulatory
(43:20):
hormone epinephrine also has the ability to stimulate glycogenolysis which is taking glycogen
in the liver and converting it back to glucose trying to raise the blood glucose level and taking
non-carbohydrates gluconeogenesis and trying to convert them and make glucose so epinephrine has
(43:41):
very similar properties as glucagon so it's considered also a counter regulatory hormone
so when your blood glucose level is falling when the blood glucose level hits 70 milligrams per
deciliter is when you start now dumping glucagon okay you shut off insulin and you start putting
(44:01):
glucagon out there as a blood glucose level continues to fall epinephrine starts getting
secreted too because epinephrine along with glucagon is trying to assist the glucagon
in raising the blood glucose level by converting the glycogen and making non-carbohydrates in the
glucose but what do we know are the what are the side effects when glucagon circulating in the
(44:25):
bar i'm sorry when epinephrine is circulating in the body what are the side effects increase
heart rate it's gonna look yeah it's gonna look like shock and then when you went through your
EMT class what did they call hypoglycemia remember insulin shock insulin shock and that is exactly
why they called it insulin shock because now the hypoglycemic patient presents as a patient that looks
(44:50):
like they're in shock i always said i i used to tell my students i could send you out the room
bring you back in lay down two people and i could ask you here one's hypoglycemic and one is in a
poor perfusion state because they're losing blood in their belly and just by looking at them you tell
me which is which and they wouldn't be able to tell because both of them are doing what dumping out
(45:11):
tons of epinephrine for totally different reasons so in the hypoglycemic patient you don't need to
memorize anything all you need to memorize is if i don't put glucose into the brain cell the brain
cell doesn't work right what do i see altramental status and when the blood glucose level is going
down not only is glucagon getting secreted and being pumped out throughout the body but so is
(45:34):
epinephrine and what am i seeing what's another thing that hypoglycemic patients have attended
seated to do have tremors why are they having tremors because epinephrine has beta 2 and beta 2
is stimulating the skeletal smooth muscle so so this this all makes sense and i always laugh i say
you remember those days working 24 hour shifts you know you get in at seven in the morning you check
(45:59):
your amps and boom you get banged out on your first call and it's nine o'clock at night and
you're finally getting to eat or you know anybody if you got this day and you're not eating you're
not eating you go all day you go all day and all of a sudden you're starving and now what do you
notice my heart rate is elevated i'm shaky my skin is cool and clammy can't concentrate and focus
(46:25):
yeah can't concentrate and focus you have your irritable hangry right irritability what's that
coming from that's coming from that epinephrine dump that's that epinephrine dump because all
of a sudden your glucagon is saying man i need some help so epinephrine gets secreted that's
you don't make sense it all makes sense and i think that we look at this we're talking about
(46:50):
hypoglycemia but we're seeing some of the contrast here we don't have the time to get into a full
hyperglycemia thing but because of dehydration they're gonna have dry skin they're gonna have a
more gradual onset they're gonna have a much different approach but if you found a patient
without trauma that looks like they're in shock you can now say all right the body's releasing
(47:15):
epinephrine they're in some kind of crisis and it makes your list of differentials change dramatically
and the other thing with the 2DN is again in trending and this is why this is so important
with trending is if the heart rate continues to go up the skin is becoming more pale cooler
and this you know the diaphoresis is worsening you know and the respiratory rates going up and so
(47:40):
forth well that we're not treating the glucose level effectively because if the glucose level
was going up heart rate should be coming down skin should be start going back to normal you know
here's another thing i always ask my students too why is it that your patient who's in hypervolamic
shock their skin's only clammy but your your patient who's hyperglycemic these patients
(48:08):
you've seen them they're soaking wet i mean they look like they got out of a swimming pool they
are not clammy they are severely diaphoretic you say well why the sweat glands are both
being stimulated by the same thing alpha one by the circulating epinephrine but what's the difference
(48:29):
the hypervolamic patient doesn't have the volume to sweat they're losing it in their belly or on
the ground the diabetic patient has all their volume so they're sweating off all that plasma
volume tons of it and so that's why they present is severely diaphoretic these people are soaking
wet because they have the volume to sweat i hope that there's people listening that just get these
(48:53):
wow moments even if it's something that you've learned i just think joe's presentations are
are just really amazing now we're gonna call this episode right now we knew it was going to take two
to be able to get all the information out here and and that's okay if we do star seven things
over two episodes i consider this a gift to be able to get explanations like this so i'm going
(49:18):
to invite you back for the second episode the second half of this seven things ems and this is
pathophysiology and assessment our goal in doing this is to have you look at your patients and
understand like never before so thank you joe for this first episode and we'll come back and
we'll do episode number two my pleasure thank you for listening to another limer education
(49:45):
continuing education podcast for more podcasts that are relevant to your practice of ems limer
education dot 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.
(00:33):
And welcome to another Seven Things EMS, I'm your host Dan Limmer from Limmer Education.
I am thrilled today for two reasons.
The first is that we're going to talk about pathophysiology, an important foundation for
everything we need to learn in EMS.
But the second part is that I get to do it with my longtime friend Joe Mistovich and
(00:54):
I will note longtime friend and competing EMT author Joe Mistovich.
Joe is a longtime professor at Youngstown State University.
He's published a bunch of books out there in EMS.
He's a prince among men.
And we don't spend a lot of time in the beginning of this audio series because we like to get
right down to business, right down to those seven things.
(01:17):
So I'll say welcome Joe and we'll get started.
Thanks Dan.
All right, number one.
Hypoxia affects the brain.
But the way it affects the brain provides clues that are important in the primary assessment.
Let's get right into it.
Okay.
And you know through our discussions and you know in our presentations together and
(01:42):
so forth.
And I'm a firm believer like you that pathophysiology is important to understand because it provides
so many clues to the EMS practitioner.
Whether you're an EMR, an EMT, advanced EMT or paramedic, it provides a lot of clues.
And a lot of times these are subtle clues that really will enhance your ability to assess
the patient and also trending of the patient's you know condition.
(02:07):
Whether they're improving, deteriorating or not.
A lot of these little signs and symptoms are things that you have to pay attention to.
I say a lot of times you know people will say like well I found the skins palcone clamia
and they document it and it's like oh I gotta remember to put that in my pre-hospital care
report but they really don't pay much attention to what it actually means about the patient.
And so as I said you know understanding these little you know little pearls of pathophysiology
(02:33):
are really important.
And so you know right hypoxia affects the brain, we know that the brain tissue is the
most sensitive to any insults of hypoxia.
And the hypoxia is coming from hypoxemia which obviously hypoxemia is an inadequate amount
of oxygen found in the blood because the blood we know is the number one carrier of the oxygen
(02:57):
to the brain.
So it's interesting you know in times people say like well you know they weren't cyanotic
and I say well you know when the patient becomes cyanotic you're so far behind the
ball at that point that it's going to be real tough to recover.
And so therefore you have to start looking for these very subtle signs and symptoms of
hypoxia or hypoxemia.
(03:19):
So we already know the brain is the most sensitive organ to hypoxia.
And because of that it is going to respond relatively quickly.
It's kind of like the heart when the heart gets irritable you start having you know
dysrhythmia as well.
When the brain gets irritable because it's hypoxic it starts sending out impulses.
Okay.
And what happens is so the brain gets hypoxic and one of the centers in the brain that's
(03:44):
extremely sensitive to this hypoxia is the medulla.
And we know that medulla houses the respiratory center, the cardiac center, and the vasomotor
center.
And the cardiac center has both the cardio inhibitory and the cardio acceleratory center.
So when the brain starts getting hypoxic what it does instantaneously and this is within
(04:06):
seconds it's sensing this hypoxia it triggers the medulla to start sending out impulses.
It's almost like a distress signal that the brain needs more oxygen.
And so its response by the medulla is to send out impulses from the cardio acceleratory
center, the vasomotor center, and the respiratory center.
(04:28):
And so you start looking at this so okay so that's great.
So clinically though when you apply it what you start to look at is what are the responses
from the medulla.
Well if the cardio acceleratory center is stimulated what you're going to see clinically
is the patient starts to exhibit some tachycardia.
(04:48):
Now initially the patient's resting heart rate might be 70 and you say well you know
what's normally heart rate well a lot of patients don't know that but if they do or if you've
had this patient before you might say or even just judging.
So you have a 32 year old patient and you say well I would speculate that the heart
rate probably resting heart rate would be in the 70s and now they're at 92.
(05:10):
And so although 92 is not considered tachycardia for that patient it is obviously a physiologic
response and the heart rate is higher.
And so suddenly you start looking at these things you start looking at this.
So the cardio acceleratory center triggers the heart it actually sends impulses to the
SA node to increase the speed of the heart rate.
(05:34):
And then also what it does is it sends impulses to increase the force of conduction okay in
which again we know that is inotropy we know that the increasing this speed at which the
heart is beating is the chronotropy.
And then also the dromotropy if you want to increase how fast the heart beats you have
to increase the speed at which the impulse gets through the conduction system.
(05:57):
So we have an increase in inotropy which is contractility and increase in chronotropy
which is an increase in heart rate and increase in dromotropy which is the speed through the
conduction system.
Now this makes sense you know in a second here is why the brain is doing this there's
a reason for it.
And the other thing that gets stimulated is the vasomotor center and the vasomotor center
(06:20):
controls the vessel size and it changes the resistance in the vessels primarily in the
arterioles you know in the distal end of the artery right before it enters into the capillary
and in the small arteries it's not the large arteries but it's the arterioles and also
the smaller arteries.
And so what happens there is well the vasomotor center actually increases the systemic vascular
(06:46):
resistance through vasoconstriction.
And so clinically say so what are we seeing there?
Well when you start vasoconstricting the first organ obviously that's going to be affected
is going to be the skin.
So when you start squeezing that nice warm red blood out of the skin that skin starts
becoming pale because the red blood is not out there.
(07:06):
It starts becoming cool because the nice warm red blood is not out there.
And also you start to feel this you know diaphoresis this claminess and that actually is from stimulation
of the sweat glands by the nervous system.
(07:27):
And you know one has to wonder so why is the brain, why is the medulla increasing the heart
rate and trying to increase systemic vascular resistance when it's hypoxic?
Well the bottom line is this the brain thinks if I can get more blood because blood carries
oxygen I'm going to get more oxygen.
And so its intent is to increase the blood flow to the brain.
(07:52):
And the only way to increase blood flow to the brain is to increase blood pressure.
And so if we go back and we say well so what's the equation for blood pressure?
Well blood pressure equals cardiac output times systemic vascular resistance.
And we know that if we can increase cardiac output we could increase blood pressure.
If we increase blood pressure we increase oxygenation of the brain in theory.
(08:14):
That's what the body is hoping.
And at the same time we say well systemic vascular resistance is part of that equation
too.
If we increase systemic vascular resistance through a phase of constriction we can increase
blood pressure.
We increase blood pressure, we increase oxygenation of the brain.
And this is the brain's theory.
And so what does the body do?
What does the medulla intend to do?
(08:36):
And it tends to increase cardiac output.
Well how do you increase cardiac output?
Well we know cardiac output is determined by heart rate and stroke volume.
So if I can increase heart rate I can increase cardiac output.
If I increase cardiac output I increase blood pressure and hopefully get more oxygen to
the brain.
Therefore that's why the heart rate's increasing.
(08:56):
The body's trying to increase the heart rate in an attempt to give more blood flow to the
brain.
To the stroke volume now the only way to increase stroke volume is you've got to put more volume
which in this patient they don't have the ability to increase their volume.
They have their normal volumic.
They have a normal blood volume.
Unless it's a hypolumic patient but that's a whole different case.
(09:18):
But one other way to increase stroke volume is to increase the force of contraction.
So therefore that's your inotropy by increasing the force of contraction you might be able
to increase stroke volume.
If you increase stroke volume you increase cardiac output, you increase cardiac output,
you increase blood pressure and hopefully get more blood to the brain.
So clinically you-
Alright I'm going to stop you for one second.
(09:40):
I think that we've just had about seven or eight minutes of what some people are probably
thinking is some heavy duty pathophysiology.
But the truth is this is stuff that should be taught in every EMT class but it's not.
This concept of understanding is something we've lost with the EMTB curriculum and we're
(10:03):
trying to bring back and that this stuff is so important.
The concept of not memorizing signs and symptoms versus understanding what goes on is what
we're getting here.
So I just wanted just to stop and say as you started this section with is that you need
to understand and that this is the stuff that many people probably should have been taught
(10:28):
in class.
I would even venture to say there's some medics out there that never got this.
So this is just really important stuff and when we look at skin changes in color, temperature
and condition we say oh it's shock but now we're saying even hypoxia can do that.
(10:50):
Right.
You know it's so true Dan and then I'll tell you this you know just this little story and
you're so right is I'm teaching an EMR refresher an emergency medical responder refresher right
now and I'm presenting this stuff to these firefighters.
It's a group of ten firefighters who really want to do what's right for the patient and
(11:11):
it's funny because they tell me you know Joe we've never learned this but when I present
this to them they are just so excited because they're like well this makes sense and you
know Dan my saying is that all makes sense.
If you can understand a little bit of pathophysiology, a little bit of anatomy, a little bit of physiology
it all makes sense and you're right.
(11:33):
And so here's these ten EMRs that are looking at this going well this is going to change
completely how I look at patients and that's the whole purpose of this because again you
know when you start saying so the thing is when you get on the scene and you have a patient
who's sitting there and you begin your primary assessment and you start noticing hey this
(11:56):
patient's a little bit tachycardic, their skin's a little bit pale, cool, clammy you
know they may have some tremors you know while there's an increase in respiratory you know
rate and they're breathing a little bit deeper.
One thing that has to pop into your head is hypoxia.
Hypoxia.
Now again through your differentials you may roll it out and we know that we're huge advocates
(12:19):
of possibilities to probabilities but one of the possibilities has to be is this patient
hypoxic and it's these subtle signs and symptoms that actually could give you those clues you
know.
So another is you know you know so the respiratory center in the medulla then starts sending impulses
(12:44):
to the DRG and the VRG, the dorsal respiratory group and the ventral respiratory group and
so what's happening here is these two centers is primarily the VRG they're receiving these
impulses and so what do they do?
They increase the number of impulses to the respiratory muscles, the diaphragm and the
external inner costals to increase the rate at which they're contracting so therefore
(13:09):
what do you get?
Not only the rate but also the force so you get an increase in respiratory rate and increase
in respiratory depth and these are very subtle signs and symptoms but also one has to realize
that initially this is all just a neural it's a direct nerve stimulation these are actually
electrical impulses that are being sent to the heart to the respiratory muscles and the
(13:33):
vessels and this is a very short-lived thing this can only be sustained for a minute or
two it's not long at most a couple minutes and so one of the impulses that's being sent
out is going to the adrenal medulla gland the adrenal glands that sits on top of the
kidney and when that adrenal medulla gets stimulated well we know it gets released is epinephrine
(13:57):
and norepinephrine so suddenly now you get this epinephrine and norepinephrine dump which
has alpha 1, alpha 2, beta 1, beta 2 which now is providing the long-term sustained effects
okay one thing I want to mention too is the alpha is causing the constant visual constriction
(14:18):
the beta 1 is continuing the increase in heart rate, force of contraction, speed of
conduction, beta 1 or the beta 1 is the cardiac, beta 2 one thing I want to point out is beta
2 is the smooth muscle dilator the bronchial dilator but one other effect is when skeletal
(14:38):
muscle receives beta 2 stimulation it causes tremors and this is where you might see the
patient starting to tremor a little bit and that's from beta 2 stimulation it's like if
you give a beta 2 agonist like a butyrol whether it be by meter dose inhaler or nebulizer and
you start noticing your patient having some tremors afterwards that's a common side effect
(15:01):
and it's because of beta 2 stimulating the skeletal smooth muscle and the other thing
is when epinephrine and norepinephrine are secreted they have a lot of alpha 1 and alpha
1 is what stimulates the sweat glands and causes you to begin to sweat you're getting
clammy now the key to all this is if the patient's hypoxia is worsening the medulla is saying
(15:23):
send more blood more blood more blood by raise the pressure raise the pressure raise the
pressure so what happens heart rate gets higher the respiratory rate gets higher the
tidal volume gets deeper the skin gets more pale because there's greater vasoconstriction
and more clammy because there's more alpha 1 out there and that's a long term effect now we know
(15:45):
we have pulse oximetry we all know that the pulse oximetry is a great tool to determine hypoxemia
but this is very specific to determine hypoxia of the brain and so these are those subtle things
and again it's not just in the primary assessment it's also in your continued assessment so if your
(16:06):
treatment is effective and you're reducing the hypoxia to the brain you should start seeing a
decrease in tachycardia the skin becoming a little bit less pale cool and clammy going back to more
normal respiratory rates going down tidal volumes going down and you know you see this in front of
(16:26):
your eyes but again these are the subtle signs and symptoms that you have to be looking for and
it you know it's so funny because a lot of EMT the EMT's the antics patient you know this you
know you ask them to say well you know what's a what's the sign of hypoxia and most of them their
number one answer is sinosis you know in order for the patient to become cyanotic again you're so
(16:47):
far behind the game because they are so severely hypoxia at that point so my response that is
is what's what's a great sign of hypoxia pale cool clammy skin increase respiratory rate increase
in tidal volume tachycardia and tremors now again we also know for this for the brain start
(17:12):
becoming altered also tastes a significant hypoxia these are early we're talking about slight decreases
in their hypoxemia or in their oxygen status slight hypoxemia that's going to trigger these signs
and symptoms so for again you say well how's pathophysiology related to how's it related clinically
and that's a question people always ask because they don't want to learn the pathophysis this is
(17:36):
exactly right because it makes you so much better of a clinician and the ability to assess your
patients and treat them what what I'm what I'm thinking here and you know we've been presenting
presenting together for a long time and you're mr pathophysiology and I'm the wow let's see how this
relates to the street and what I'm thinking is one is that this will go into our second thing here
(18:02):
but also we are so hung up on 94 percent and we're so we're so mixed up in our heads about when to
give oxygen and when not to give oxygen I think what you've really done in this first section is
been able to tell people that if you see certain things I would even venture to say regardless
(18:26):
of what the pulse ox says you should be looking at this and saying this can be hypoxia the body's
responding in a way to show that there's crisis you've described a fight or flight response
and that is trying to feed the brain so we should assist in feeding the brain by giving some oxygen
(18:47):
and we don't always have to go with the big guns with a non-rebreeder I think we've forgotten how
much a nasal cannula can really do and how much comfort it is for the patient but I think you've
really helped define for our listeners that there's a lot more than pulse ox in the oxygen
decision if your patient has that I'll just call it the shocky look that that's an indication for
(19:12):
oxygen exactly and that is 100 the key to this and Dan you remember when the pulse ox simulators just
came out and if you recall we we used to teach students well don't rely on the pulse ox similar
rely on your clinical findings because that's really going to tell you whether your patient's
(19:33):
hypoxia or not well they've refined pulse oxymetry and pulse like simulators are pretty accurate but
like you said you know take a patient in a cold environment that pulse oxymeter it could be inaccurate
you know or a state of poor perfusion but the key that you said is yeah yeah and again you
walk into a scene and you see tachycardia pale cool clammy skin increased respiratory rate increased
(19:55):
tidal volume you start thinking two things one is hypoxia and poor perfusion the key is not to go
okay hey market in the PCR the key is to say what's going on with my patient what is it and again
those possibilities the probabilities and through hopefully a good assessment you know one's going
(20:16):
to come down to a probability of why this is happening but I couldn't agree with you more it's
like and and the statement you said is so true regardless of what the pulse ox is telling you
if your intuition is saying something's not right here and I think they might be hypoxic
absolutely agree with you put them on nasolcania two liters and you can't believe what that might
(20:39):
actually do and if you put them on a nasolcaniola two liters and these things start improving
then you know that you caught something but but again if you don't understand this most people
are just like well you know yeah they're tachycardic and whoa look they're more tachycardic now but
they don't put it together this whole thing is put it all together because it makes sense and
(21:01):
it's telling that story about your patient and the other thing is the trending look at the trends
is it worsening is it improving is it staying the same well let's roll into number two I think it's
it's peripherally related and I think we're going to get a little bit deeper into the concepts here
and I think that's good I'll also say to our listeners you're going to hear some pretty important
(21:23):
terms some big terms things you probably should have had in your class and didn't I'm going to
ask you to lean into this this understanding is going to change the way you practice and it's
important that we do this the second one the relationship between hemoglobin anemia and cyanosis
may surprise you that the way that we transport oxygen and some of the relations to what we just
(21:49):
talked about is important as well and we've already said cyanosis is a late sign it's not the
not the thing that should be you should be making your decision on yeah it's interesting I suppose
this question all the time not only thinking my empty classes but also to my paramedic classes
and and it was interesting to find out that they a lot of times couldn't couldn't grasp the relationship
(22:14):
until it was explained especially with the anemic patient so the key here is you know understanding
the hemoglobin okay is on the surface of the red blood cell and hemoglobin has four iron sites
and those four iron sites are binding sites with oxygen and so one thing we know about hemoglobin
and this is basically how the pulse oximeter works the pulse oximeter reads it has a red light and
(22:39):
an infrared light and it basically is shining that light through the skin and is able to determine
through the infrared light and the red light how much hemoglobin is actually saturated with oxygen
and that's how we get a pulse oximeter reading and so it's hemoglobin that is the key and again
is found on the surface of the red blood cells so if you're losing red blood cells you're obviously
(23:01):
losing hemoglobin and if you're losing hemoglobin you're losing the ability to transport oxygen
so this is a this is an interesting question well before we go there I'll say so if you have all the
hemoglobin in your body and we we already said pulse oximetry is reading the amount of hemoglobin
(23:22):
saturated with oxygen versus hemoglobin not saturated and one thing that you know EMTs and
advanced EMTs and EMRs and paramedics know is if we have hemoglobin that's not saturated with oxygen
if we have hemoglobin coming through a vessel and it has it's desaturated it's very low in oxygen
it has carbon dioxide attached to it um what do we see it and most often people say well it's
(23:49):
going to look blue because hemoglobin that doesn't have oxygen attached has this bluish color to it
and that's true deoxygenated hemoglobin appears as blue that's why your veins in your body look
blue or greenish blue instead of red you know arteries if you see your arteries would look
(24:10):
red because that's saturated hemoglobin so we established that hemoglobin with oxygen attached
to it um looks red hemoglobin that doesn't have oxygen attached to it is deoxygenated
it's deoxygenated desaturated looks blue or cyanotic you say well so the the point to remember
(24:31):
there is hemoglobin then is what's responsible for changing the color of the skin you have to
have hemoglobin to change the color of the skin and so if you have a lot of hemoglobin that's not
attached to oxygen hypoxemia the skin starts looking in a later stage the skin starts looking
(24:53):
cyanotic because that hemoglobin is now taking on the appearance of being blue
if we are having a big whoa this does make sense moment here and it and it's important but again
it's important clinically to apply it clinically too and if you have hemoglobin attached to oxygen
your skin's going to take on this relatively normal color now again through vasoconstriction
(25:19):
we're going to start shunting that to the body but you know well you know as well as i do dan
teaching students it's like you just don't look at the skin you look at the oral mucosa you look at
the conjunctiva you look at other core areas to the body the skin may be pale but those areas still
look pretty red meaning that we still have that hemoglobin so here's the thing so the bottom
(25:41):
line to this is in order to change the color of the skin based on a hypoxemic state or or whatever
state it would be you have to have hemoglobin so it has my students so an anemic patient
and there's a lot of different types of anemia but the bottom line is this they have an inability
(26:02):
to either have an appropriate monohemoglobin they don't have the iron sites regardless of what the
cause is they're not carrying as much oxygen as you and I because they have some chronic condition
or short-term condition of anemia so I'd ask my students so is an anemic patient who becomes
(26:24):
hypoxemic are they going to become cyanotic quicker or is it going to take longer and students would
you know ponder that question and a majority of them would say well they're going to become
cyanotic quicker you know and they'd say well again it takes hemoglobin to change the color of the skin
(26:47):
what's the color you know it's funny because we could go to the mall be walking around and look
at a person and go damn they're anemic you know just because they look what pale because they
don't have the hemoglobin to make their skin look normal so therefore they're pale because
they don't have the hemoglobin so you look at this you say well in order to make a patient look
(27:11):
hypoxic you have to have hemoglobin that's not attached to oxygen and because you don't have
the large amounts of hemoglobin you can't turn the skin cyanotic because you don't have the
hemoglobin to do so so an anemic patient could be severely hypoxemic it's still not presenting
(27:31):
with cyanosis they're going to look pale but they're not going to be cyanotic but they're going to be
tachycardic they're going to have the vasoconstriction the clammy skin the increase
respiratory rate and so forth everything we talked about previously so you say one of the things
I've heard you say oh I'm sorry one of the things I've always heard you say when you speak
(27:52):
at presentations on the road is that cyanosis is a very late sign how late well again
so so and again there's why pulse axiometry is important and people have to realize that pulse
axiometry has to catch up to hypoxemia too pulse axiometry is not giving you instantaneous readings
(28:16):
it it it takes some time before it starts to identify hypoxemia that's why again looking at
those subtle signs and symptoms and you said earlier Dan that look if you're seeing this stuff
and your intuition is saying I think they're hypoxic when my pulse ox is still at 94 start
on monsimho too nobody's going to ever criticize anyone for doing that because your intuition
(28:39):
and your assessment findings are saying this so cyanosis Dan it takes a significant amount of
desaturation of hemoglobin to cause a person to become cyanotic so again as far as time it's a
longer period of time because they have to desaturate but it also depends on the severity of
the condition how severely you know is there oxygenation you know transmission in the alveoli
(29:06):
you know if you got a patient like let's say a drowning patient where their lungs are filled
with fluid and they're really not getting any O2 across well you know that person who becomes
cyanotic pretty damn quick but if you got an asthmatic who's still moving air and is still
saturating hemoglobin just not as much as they need to it's going to take a much longer period
(29:27):
of time for them to look cyanotic so so go ahead I was just going to say before we move into
hypoglycemia I've had the good fortune to like I said to present with you on the road narrow to say
the thing that I have we haven't talked about a lot we've talked about many of the physiological
(29:47):
signs of hypoxia hypoxemia what about mental status the change in mental status with this
yes and that's in that you know and that's there again you know the other one that I always you
know uh hit hard on is aerobic and anaerobic metabolism and again a lot of people said well
(30:08):
I learned that in ninth grade biology I did in ninth grade biology learning about aerobic
and anaerobic metabolism thinking when the heck am I ever going to need this in my life
you know believe it or not I use that every day to explain things and you know and that all goes
back Dan to the aerobic versus the anaerobic and we know the aerobic metabolism put a glucose
(30:31):
molecule into a cell and metabolizes it and if oxygen's available it produces large amounts of
ATP 36 38 molecules of ATP but if we don't have the oxygen available this is what's
happening in the brain cell without the oxygen available glucose we know is the major energy
source for the brain cell glucose gets in the brain cell it produces two molecules of ATP because
(30:55):
the initial part of the metabolism is anaerobic whether it's aerobic or anaerobic state that
first part glycolysis produces two molecules of ATP so you got a little bit of energy but then when
it gets in the mitochondria without the oxygen what is the brain cell making it's making no ATP
and lots of acid because it doesn't have oxygen if we don't have the ATP we don't have the energy
(31:21):
to make that brain cell work and if the brain cell doesn't work what do we see
alter mental status I mean if the brain cell the group of brain cells that allows you to tell
the EMT or the paramedic your name is not producing enough ATP they're not going to tell you their
name and that and and this is how this is so clinically related but before we move on here's
(31:47):
another question I posed to my students with that anemia is this one of your one more things
one more thing one more thing but it makes sense if you have a trauma patient you know
and you go to a scene and you have a trauma patient let's say you have a patient driving
a car down the road is 65 miles an hour whatever happens and they they hit a concrete you know
(32:12):
barrier at 65 miles an hour unrestrained patient and you're looking at your patient when you get
on the scene and you go into assess your patient and you got this trauma patient looks like they
have some chest trauma just by the the mechanism that they were unrestrained they probably went
forward it was a frontal collision hit the steering wheel and they're severely cyanotic
(32:35):
you're already seeing cyanosis where do you see cyanosis first circle morally you know around the
mouth you know you'll see in the conjunct of other or omucosa the fingertips but you're already
starting to see cyanosis in this patient you just got on the scene you go into the driver's side
door and you're looking at the patient you're going oh crap this guy's cyanotic now you got to
(32:55):
ask yourself right there clinically me personally i'm going to say this guy's got a bad chest injury
a chest injury that's interfering with his ability to either ventilate or oxygenate
and somebody else is going to say oh no he's in shock he say well why don't i think he is
(33:17):
losing a lot of blood now he could be losing blood but why is it that i'm not thinking that this
condition right away why am i thinking immediately we got a severe respiratory ventilation issue
because of the severe because of the hypoxia or the cyanosis
say well why not why am i not thinking that he's bleeding out maybe he lacerated a pulmonary vessel
(33:42):
because in order to change the skin color you have to have hemoglobin if the guy's bleeding out into
his chest or bleeding out into his belly or bleeding out on the ground he's losing whole blood
whole blood has red blood cells red blood cells he even govind he looks what pale he doesn't look
(34:04):
cyanotic although he might be hypoxic he's like now the anemic patient he doesn't have the hemoglobin
to make him look cyanotic but the patient with the severe chest injury who now can't ventilate
appropriately maybe he's got a big flail chest or something or has some major pulmonary contusion
(34:26):
he's got blood volume he just can't get the oxygen into the blood because of a ventilation
or oxygen disturbance he's looking cyanotic so clinically a lot of people a lot of people just
said wow and we all know those patients when we say oh crap or worse yeah right that's a that's a
(34:47):
clinical response to this is bad but now you know why and and you said in this these are those little
things you know we wrote the amls book you know the you know the original amls book and our whole
intention was how do we bring those years of clinical experience to new providers and this
(35:07):
is one of those things when you walk up to a patient involved in a trauma or you walk up to
any patient and you see severe cyanosis either they've been hypoxic for a long period of time
or they have a severe ventilation or oxygen diffusion problem but if you walk up to a trauma
patient shot in the chest and they're looking so cyanotic already when you get on the scene
(35:31):
I'm not I'm not too worried right now about severe blood loss I'm worried about severe
hypoxia hypoxemia or ventilation disturbance those are those little clinical signs and symptoms
and clues and this is where pathophys make sense all right you're taking a breath so I'm going to
move to number three we have about 15 minutes for this one we know we're going to have a two-part
(35:54):
episode there's so much to cover here number three hypoglycemia is easier to understand than you might
think right I mean today we pulled out the blood glucose monitor you know we didn't have that I don't
sound like the old guys but we didn't have that but now everybody just pulls out the blood glucose
monitor and gets an answer but you probably could tell a lot even before you use that blood glucose
(36:20):
monitor and quite frankly we should use that and it might even tell us better when to use the blood
glucose monitor absolutely yeah Dan you remember the days where we used the chem strips where you
took the drop of blood you put it on the chem strip then you had to wait 90 seconds then you had to
have a water source you remember being out on the street you're like where's my water source
(36:43):
we get a bottle of sterile water and pour it over the chem strip and compare the color to the side
of the bottle that's where we came from and those were very inaccurate so we absolutely had to know
clinical signs and symptoms of hypoglycemia so here's another thing you know teaching students
teaching EMTs teaching paramedics two weeks after their exam on endocrinology I would ask
(37:05):
students so what are the signs of hypoglycemia versus diabetic ketoacidosis um well what's
the skin like in hypoglycemia versus decay uh well one's warm and one's which one and you know
we know this that you take an exam two weeks later I was terrible at this this is why I had to
(37:26):
understand because I was terrible at memorizing two weeks later I'd be like I don't remember which
group goes with what what's what and so forth and so to understand and I started looking at
hypoglycemia like hypoglycemia is so simple to understand the clinical presentation again this
relates back to clinical presentation and patient assessment findings and here's the thing Dan you
(37:50):
hit it we got a blood glucose monitor but these clinical signs the symptoms are going to tell
you something about severity too and trending it's trending what are these doing are they
improving are they staying the same are they getting worse because that's going to tell you
something too we know blood glucose monitors a lot of times are not calibrated especially being on
(38:11):
the ambulance sometimes the strips are out of date or they're affected by light heat cold and they're
not providing the most accurate you know reading so we got to keep that in mind so again knowing
clinically what's happening in this patient is so important so I say understanding hypoglycemia
is simple because you only need to know two things one the question you posed earlier was well what
(38:40):
about altered mental status you know well how does this patient who's hypoxic start developing an
altered mental stat not you didn't ask how but just pointing out that altered mental status is a huge
key well that's a huge key in the hypoglycemic patient because what do we know about brain cells
brain cells can pretty much only use glucose as an energy source brain cells can't store it
(39:06):
they can't make it they can't suck it up and concentrate it from the blood they just get
whatever is being sent to them through perfusion and so if we have a patient whose blood glucose
level goes down now we have a diabetic patient who their insulin pump you know goes haywire and is
injecting way too much insulin or they're injecting themselves with insulin and they take way too much
(39:30):
and there's also now some of the hypoglycemic anti-hypo glycemic um i'm sorry the hypoglycemic
agents i'm not saying that right the drugs that people are taking that are type 2 diabetics
they they also could produce hypoglycemia it's a rarer event but it can't occur and it's like
(39:53):
some of these drugs because some of these drugs what they do is they stimulate the pancreas to make
more insulin and if they forgot that they took their you know their oral you know hypoglycemic
agent they take it again and then they've forgotten then they take it again for lunch and
and all of a sudden they're overdosing themselves and their pancreas is just screaming out insulin
(40:13):
it's no different than somebody taking a syringe of insulin and then injecting it three times so
they could become hypoglycemic too keep that in mind because a lot of times we've beaten people's heads
while they got to be a type 1 diabetic that's injecting insulin or somebody who's type 2 that's
injecting insulin or has insulin some pump that's not necessarily true but what do we know we know
we go back to our aerobic metabolism and we say well if the brain can pretty much only use glucose
(40:38):
to make energy and now we don't have enough glucose available well we don't have enough
glucose available to make energy so that means we don't have enough energy for the brain cells to work
and what do we see clinically?
Alternative status everything from from confusion to complete coma seizures are actually a relatively
(41:03):
rare event in hypoglycemia I think we pushed that for a long time like oh my god people are going to
seize what they they are they are more predisposed to seizures than when they're not hypoglycemic
but it's not as common I don't have red one statistic it was less than 30 percent I think
it was actually down to 13 percent of patients in hypoglycemia actually have seizures and they
(41:27):
got to be really severely hypoglycemic too and so you say so what's one group of signs and symptoms
that we will see they're called neuroglucopenic or neuroglycopenic and what that means is
neuro all you got to think is neurogluconuroglyco and that's and the peanut part is being caused by
(41:48):
and you say there's a lack of glucose in the brain cell and the brain cell can't make energy
so it doesn't work what do we see clinically?
Alternative status that's one huge group there's only two groups one huge group so what do we see
in a hypoglycemic patient? Alternative status and that onset is what fast because as soon as you're
(42:10):
not getting the glucose into the cell it can't make energy when it can't make energy what do we see
alterations in mental status okay one thing that all you need to know is we have glucose or we have
counter regulatory hormones when we have disturbances with glucose and the main ones are glucagon
(42:33):
okay then we have insulin we have glucagon and we know that when the blood glucose level is going
down glucagon is being secreted from the pancreas okay from the alpha cells in the pancreas and
they're secreting the glucagon and the glucagon's job is to do what take glycogen that's stored in
the liver convert it back to glucose and put it back into the blood and take non-carbohydrates
(42:55):
and start converting them and trying to make glucose out of them and that's a long process
that doesn't occur real quick but we know there's another hormone that's a counter regulatory hormone
that's epinephrine so not only is epinephrine the fight or flight hormone you know increasing the
heart rate and increasing the system and vascular and so forth epinephrine is a counter regulatory
(43:20):
hormone epinephrine also has the ability to stimulate glycogenolysis which is taking glycogen
in the liver and converting it back to glucose trying to raise the blood glucose level and taking
non-carbohydrates gluconeogenesis and trying to convert them and make glucose so epinephrine has
(43:41):
very similar properties as glucagon so it's considered also a counter regulatory hormone
so when your blood glucose level is falling when the blood glucose level hits 70 milligrams per
deciliter is when you start now dumping glucagon okay you shut off insulin and you start putting
(44:01):
glucagon out there as a blood glucose level continues to fall epinephrine starts getting
secreted too because epinephrine along with glucagon is trying to assist the glucagon
in raising the blood glucose level by converting the glycogen and making non-carbohydrates in the
glucose but what do we know are the what are the side effects when glucagon circulating in the
(44:25):
bar i'm sorry when epinephrine is circulating in the body what are the side effects increase
heart rate it's gonna look yeah it's gonna look like shock and then when you went through your
EMT class what did they call hypoglycemia remember insulin shock insulin shock and that is exactly
why they called it insulin shock because now the hypoglycemic patient presents as a patient that looks
(44:50):
like they're in shock i always said i i used to tell my students i could send you out the room
bring you back in lay down two people and i could ask you here one's hypoglycemic and one is in a
poor perfusion state because they're losing blood in their belly and just by looking at them you tell
me which is which and they wouldn't be able to tell because both of them are doing what dumping out
(45:11):
tons of epinephrine for totally different reasons so in the hypoglycemic patient you don't need to
memorize anything all you need to memorize is if i don't put glucose into the brain cell the brain
cell doesn't work right what do i see altramental status and when the blood glucose level is going
down not only is glucagon getting secreted and being pumped out throughout the body but so is
(45:34):
epinephrine and what am i seeing what's another thing that hypoglycemic patients have attended
seated to do have tremors why are they having tremors because epinephrine has beta 2 and beta 2
is stimulating the skeletal smooth muscle so so this this all makes sense and i always laugh i say
you remember those days working 24 hour shifts you know you get in at seven in the morning you check
(45:59):
your amps and boom you get banged out on your first call and it's nine o'clock at night and
you're finally getting to eat or you know anybody if you got this day and you're not eating you're
not eating you go all day you go all day and all of a sudden you're starving and now what do you
notice my heart rate is elevated i'm shaky my skin is cool and clammy can't concentrate and focus
(46:25):
yeah can't concentrate and focus you have your irritable hangry right irritability what's that
coming from that's coming from that epinephrine dump that's that epinephrine dump because all
of a sudden your glucagon is saying man i need some help so epinephrine gets secreted that's
you don't make sense it all makes sense and i think that we look at this we're talking about
(46:50):
hypoglycemia but we're seeing some of the contrast here we don't have the time to get into a full
hyperglycemia thing but because of dehydration they're gonna have dry skin they're gonna have a
more gradual onset they're gonna have a much different approach but if you found a patient
without trauma that looks like they're in shock you can now say all right the body's releasing
(47:15):
epinephrine they're in some kind of crisis and it makes your list of differentials change dramatically
and the other thing with the 2DN is again in trending and this is why this is so important
with trending is if the heart rate continues to go up the skin is becoming more pale cooler
and this you know the diaphoresis is worsening you know and the respiratory rates going up and so
(47:40):
forth well that we're not treating the glucose level effectively because if the glucose level
was going up heart rate should be coming down skin should be start going back to normal you know
here's another thing i always ask my students too why is it that your patient who's in hypervolamic
shock their skin's only clammy but your your patient who's hyperglycemic these patients
(48:08):
you've seen them they're soaking wet i mean they look like they got out of a swimming pool they
are not clammy they are severely diaphoretic you say well why the sweat glands are both
being stimulated by the same thing alpha one by the circulating epinephrine but what's the difference
(48:29):
the hypervolamic patient doesn't have the volume to sweat they're losing it in their belly or on
the ground the diabetic patient has all their volume so they're sweating off all that plasma
volume tons of it and so that's why they present is severely diaphoretic these people are soaking
wet because they have the volume to sweat i hope that there's people listening that just get these
(48:53):
wow moments even if it's something that you've learned i just think joe's presentations are
are just really amazing now we're gonna call this episode right now we knew it was going to take two
to be able to get all the information out here and and that's okay if we do star seven things
over two episodes i consider this a gift to be able to get explanations like this so i'm going
(49:18):
to invite you back for the second episode the second half of this seven things ems and this is
pathophysiology and assessment our goal in doing this is to have you look at your patients and
understand like never before so thank you joe for this first episode and we'll come back and
we'll do episode number two my pleasure thank you for listening to another limer education
(49:45):
continuing education podcast for more podcasts that are relevant to your practice of ems limer
education dot com slash seven things
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