Hey guys, this right here is going to be PALS,
the Pediatric Advanced Life Support. And the
way it's going to go is I'm going to try to keep
it in this order. The systematic approach to
the pediatric patients, pediatric shock recognition,
pediatric management of shock, recognizing respiratory
distress, managing respiratory distress. recognizing
cardiac arrest, management of cardiac arrest,
arrhythmias, recognition of those arrhythmias,
and then management of those arrhythmias. I don't
remember PALS being this deep, but again, it's
been almost two years since I've taken PALS,
but it seems like it's a lot more in depth than
just your normal ACLS. So this material is coming
straight from the book. For the course just make
sure that you guys are reading that material
Because I did not add some stuff in there like
team dynamics or resources for respiratory care
or Management of the post cardiac arrest, you
know stuff like that. I didn't include that into
this stuff So if you guys need that or want that,
then by all means, read the book or, you know,
Google it or whatever. But this right here is
going to be the intro for the pals stuff. So
I hope you guys enjoy the pediatric advanced
life support material for the course. This is
all going to happen super fast. Welcome to the
emergency room. Welcome back to The Deep Dive.
Today we are putting away the flashcards and
really getting into the most critical zone of
pediatric emergency care. If you're an ER nurse
and you're gearing up for your PASS certification
or maybe you just want to feel more confident
when that pediatric respiratory call comes in,
well, this Deep Dive is for you. That's absolutely
right. And our focus today, it's not about just
memorizing algorithms, not about where the arrows
point on some flow chart. Our mission is to get
into the path of physiology, the why behind the
path of those guidelines. And we're going to
be focusing specifically on that foundational
pillar, which is recognizing and managing. pediatric
respiratory distress and failure. We want to
translate that textbook knowledge into what you
actually do at the bedside. Exactly. And we're
starting here for a reason, and it's, well, it's
a bit grim, but it's absolutely essential. The
pathos source material says this over and over
again. Respiratory failure is the number one,
the major cause of cardiac arrest in kids. It's
the big one. It's not like adults, you know,
where it's often a primary cardiac event. For
kids, the arrest is usually the final step after
they've been hypoxic for a while. And that means
we have this tiny, tiny window to intervene,
to do something before they code. Because once
a child arrests, the outcomes, they're just dramatically
worse. So the whole goal of PALLAS, especially
for you, the ER nurse, is prevention. It's all
about prevention. So if we can master spotting
and aggressively managing that respiratory failure,
we're actually changing the outcome. We're improving
survival. We're improving survival and neurological
outcomes. The difference between a good palace
provider and a great one. It's often just speed
and a systematic approach to breathing problems.
OK, so let's unpack that, this clinical reality.
You know, we're so often trained to think cardiac
first with adults, but with a kid who's struggling
to breathe, you're saying we have to flip that
entire paradigm. What are the key physiological
differences that make Pella so focused on respiratory
first? Well, the differences are both anatomical
and physiological. First off, just the anatomy.
Kids, especially infants, they have much smaller
airways. I mean, their trachea is shorter. It's
narrower. So a little bit of swelling that an
adult could handle is a huge deal. A huge deal.
Think about croup. That little bit of swelling,
which an adult might barely notice, becomes a
life -threatening critical obstruction for a
two -year -old. And second, they rely way more
heavily on their diaphragm for breathing. Ah,
which is why you see those retractions so clearly.
Exactly. That's why seeing accessory muscle use,
you know, the super sternal or subcostal retractions,
that's an early and really significant sign of
distress. And then there are the metabolic differences.
I think this is where it gets really interesting.
They have a higher metabolic rate. They just
burn through oxygen faster. Precisely. So if
they become hypoxemic, their oxygen reserves
are depleted so, so rapidly. This is why that
decline can be so fast. The kid looks distressed,
then they get quiet, and then they crash. And
that quiet phase is so dangerous. It's often
mistaken for improvement, right? It's a classic,
terrifying sign of fatigue and impending arrest.
That shift from agitation to lethargy is a massive
red flag. Recognizing that is absolutely fundamental.
So we see the signs, we know we have to act fast.
First step is always stabilization. Let's walk
through that initial ABC framework. We stabilize
oxygenation and ventilation, and only then do
we hunt for the cause. Starting with A for airway
interventions. What are the absolute non -negotiables
to get that airway patent? Airway patency is
everything. And, you know, the first, the simplest,
and often the safest move is just allowing the
child to find a position of comfort. So if they're
sitting up, leaning forward in that tripod position,
you just let them be. You let them be. Don't
fight them. Anything you do that increases their
agitation is going to increase their oxygen demand
and can actually make the obstruction worse.
But what if that's not enough? We have to intervene
with maneuvers. The default is the head tilt
chin lift, correct? Yes, that's the default.
Unless, and this is a big dig, unless you have
any suspicion of trauma or a C -spine injury.
If that mechanism exists, you immediately switch
to the jaw thrust maneuver without tilting the
head. The goal is the same. Lift the tongue off
the back of the pharynx. Beyond maneuvers, we
have adjuncts. Let's get into the oropharyngeal
airway, the OPA, and the nasopharyngeal, the
NPA. They're crucial tools, but they come with
risks, especially in kids. Absolutely. The OPA
should only be used in a child who is deeply
unconscious. I mean, truly flaccid, no gag reflex.
And why is that so critical? Because if you stimulate
that gag reflex, you're going to make them vomit.
and that could lead to a lethal aspiration. And
you have to size it right, from the corner of
the mouth to the angle of the jaw. No guessing.
And what about the MPA? It's usually better tolerated,
right, even in a conscious child. But what are
the big red flags that contraindications we have
to look for? The MPA is great because it can
bypass the tongue obstruction without causing
that gagging. However, you have to use extreme
caution if there's any known bleeding disorder,
any significant facial trauma, or, critically,
a suspected basal or skull fracture. Because
you could actually insert it into the cranium.
You could. It's a never event, but it's a known
risk. And again, sizing is key. Tip of the nose
to the tragus of the ear. Okay, that's A. Moving
to B for breathing. We've got the pulse oxon,
but we need to be thinking beyond that immediately.
Immediately. You go straight to high -concentration
oxygen with a non -rebreathing mask and NRB.
We're aiming for 95 % saturation or higher. But
you also need to be preparing for advanced respiratory
monitoring. That means getting the end -title
CO2 or ETQ -EROS monitor ready to go. because
that tells you about ventilation and circulation.
It gives you crucial data. And if it's indicated,
say, a kid with a known history of asthma, you're
giving inhaled meds right away. But the number
one nursing priority here is preparation. You're
always, always preparing for an advanced airway
and the need for bag valve mask or BVM ventilation.
Okay, I want to challenge that point a little
because the second you bring out the BVM, you
risk agitating the child. And you mentioned the
risk of air trapping in some diseases. What's
the clinical trigger? When do you make that leap
from a non -rebreather to actually assisting
their breaths with a BVM? That is a great question
because you're right. The BVM is a high risk,
high reward tool. The trigger is failing respiratory
effort or a deteriorating mental status, even
with high flow oxygen. If you see the child's
respiratory rate plummeting. If they're becoming
bradycardic, or if they just physically cannot
maintain an adequate minute volume anymore, that's
when you have to step in. So distress is one
thing, but failure is the trigger. Distress is
acceptable. Failure is not. That's the line.
And C for circulation. Before we're even thinking
about code meds, what's the ER nurse's first
priority? You're monitoring the heart rate, the
rhythm, the blood pressure, of course, but the
absolute number one priority. is establishing
vascular access, an IV or an intraosteus, an
IO line immediately. Why so urgently? Because
respiratory distress can progress to shock so
fast. And if you wait until that child is hypotensive
and crashing, their veins are going to collapse.
Peripheral access becomes nearly impossible.
You need that line ready for fluids and meds
the second you need them, not a minute later.
Let's isolate respiratory arrest for a moment.
This is that critical point where The nurse is
the only thing standing between the patient and
a full cardiac arrest. How do we define it again,
and what are the exact guidelines for rescue
breathing? So respiratory arrest means the child
is apneic, they're not breathing, but they still
have a detectable pulse. There's still cardiac
activity. Our job here is to profuse the brain
and heart with oxygen before they also feel from
the hypoxia. And the rhythm of those breaths.
What's the specific rate? For infants and for
children, you slow it way down compared to what
you do in a full code. You're giving 12 to 20
breaths per minute. That works out to one breath
every three to five seconds. Okay, one breath
every three to five seconds. Yep. And each breath
should just take about one second to deliver,
and you're just looking for visible chest rise.
And of course, use oxygen as soon as you have
it. So why is that three to five second interval
so important? What's the physiology behind that
specific timing? It's all about managing a delicate
balance. You're trying to provide enough oxygen
and allow for CO2 removal, but you're doing it
without causing excessive gastric inflation.
If you go too fast, you're just pumping air into
the stomach. That can cause vomiting, aspiration,
and it pushes up the diaphragm, which makes breathing
even harder. It's a deliberate measured rate
to maximize oxygen delivery and minimize those
secondary problems. And how often do you check
to see if things are changing? You have to check
the pulse every two minutes. No longer. And if,
during that check, the pulse is gone, or if the
heart rate drops below 60 and you see signs of
poor perfusion, you don't wait, you immediately
transition, you shout for help, you start chest
compressions, and you are now in the full CPR
sequence, that rapid shift is essential because
the clock on hypoxia is ticking down fast. OK,
so once we've stabilized the ABCs, the Pale S
framework tells us to get more specific with
our management. We have to figure out which of
the four big buckets this kid falls into. upper
airway obstruction, lower airway obstruction,
lung tissue disease, or disordered control of
breathing. Let's start at the top. upper airway
obstruction. Right. This involved the large airways,
so the nose, the pharynx, the larynx. These are
the patients we see all the time in the ER. And
you have to remember, infants are so prone to
this because their airways are just tiny and
their tongue tends to fall back and obstruct
when their muscle tone decreases. So the general
management principles are all about keeping that
airway open and, just as importantly, keeping
the child calm. Beyond just positioning, what's
the crisis pathway look like? Well, if those
conservative measures aren't working and you
see signs of pending respiratory failure, the
conversation changes very quickly. You're moving
towards advanced airway management, which means
preparing for the possibility of a surgical airway
like a tracheostomy or a crick. But thankfully,
most cases will respond to the right medication
for the specific cause. OK, let's drill into
the classic example then, croup or laryngotracheal
bronchitis. This viral infection causes swelling
right below the vocal cords in the subglottic
area, and that's what gives you that signature
barking cough and stridor. How do you quickly
assess how bad it is to guide your treatment?
Severity assessment is everything because it
can change so fast. You hear the barking cough,
sure, but what you're really listening for is
the stridor. Is it only there when the child
is agitated or crying? Or is it present even
when they're at rest? Stridor at rest is a big
warning sign. A huge warning sign. Then you look
at the retractions. Are they mild or are they
deep and significant? And finally, what do you
hear when you listen? How is their air entry?
And the PAL -L -S guidelines give us a really
clear tiered approach based on that assessment.
Let's focus on that moderate to severe crude
patient. You can hear the stridor at rest. You
see significant retractions. What's the immediate
game plan? The immediate game plan starts with
humidified oxygen and you make them NPO, nothing
by mouth. This minimizes aspiration risk and
just reduces the work of breathing that comes
with swallowing. The main medication, the one
you go to right away, is nebulized epinephrine.
Okay, so why nebulized epi and why is the follow
-up period after you give it so incredibly important?
Epinephrine is a powerful alpha adrenergic agonist.
So when it's inhaled, it causes this rapid localized
vasoconstriction in that swollen tissue in the
subglottic area. It shrinks the swelling almost
instantly. But, and this is a huge but, That
effect is often temporary. It wears off. It wears
off. And once that visa constriction is gone,
usually within about two hours, the stridor can
come right back. And sometimes it's even worse
than before. And that is the essential clinical
pearl for the ER nurse, isn't it? You cannot
discharge or transfer that patient until they've
been watched for at least two hours after that
nebulized epi. Correct. That two hour observation
period is completely non -negotiable. While the
epi is giving you that rapid relief, you're simultaneously
giving a systemic corticosteroid like dexamethasone,
either PO, IV, or IM, to tackle the underlying
inflammation with a longer -acting drug. Okay,
now for the worst -case scenario. Impending respiratory
failure and croup. The child is lethargic, pale,
Maybe cyanotic. What now? Now is a full -blown
emergency. You're continuing the high concentration
oxygen, but you're probably providing assisted
ventilation with a BVM to support that failing
effort. You're given the dexamethasone, FETC,
or IM for sure, and you are preparing for an
advanced stairway for ET intubation. And is there
a specific procedural trick for intubating a
croup patient? There is. Because that swelling
is subglottic, the airway below the vocal cords
is much narrower than you'd expect. So you have
to anticipate this and choose an endotracheal,
or ET, tube that is often a half size to a full
size, smaller than what the age -based formula
would predict. Because if you try to force the
predicted size, you could cause more trauma and
completely obstruct the airway. You could make
the situation a hundred times worse. Yeah. Let's
shift gears to anaphylaxis. This also creates
upper airway obstruction but through a totally
different mechanism, a severe systemic allergic
reaction. So we're dealing with both swelling
or edema and bronchospasm, and it's often complicated
by hypotension. Anaphylaxis is a multi -system,
incredibly fast -moving emergency. For any moderate
to severe reaction, the absolute undisputed first
priority is epinephrine. And what are the details
of that epi -administration? How is it given?
Intramuscular. I am epinephrine right away, either
with an auto injector or a standard syringe.
And you can repeat it every 10 to 15 minutes
as you need to. The mechanism is what makes it
so perfect. It causes rapid vasoconstriction
to reverse the hypotension and shrink that laryngeal
edema. And it's also a bronchodilator to treat
the wheezing. It is the single most important
drug you will give. OK, so after the epine, we
add the secondary meds to control that inflammatory
response. Why this cocktail of steroids and two
different kinds of antihistamines? We use IV
corticosteroids like methylprednisolone. to prevent
what's called a biphasic reaction, where the
symptoms come back hours later, and to treat
that underlying inflammation. And we aggressively
treat the bronchospasm with continuous nebulized
albuterol. And the antihistamines. We give diffenhydramine,
which is an H1 blocker, but the guidelines also
say to add an H2 blocker, like ranitidine. What's
the rationale for the H2 blocker? Well, the defenhydramine,
the H1 blocker, it targets the immediate symptoms
like hives and itching. The H2 blockers help
prevent the further release of histamine from
mast cells, and they address the vasodilation
and leaky capillaries that are contributing to
the shock. The evidence for H2 blockers alone
is a bit debated, but in PALS, the goal is comprehensive
histamine blockade. What if the patient is already
crashing into hypotensive shock? Fluid's the
next step. What's the initial bolus? Immediate
resuscitation. You lay the child flat, supine,
and you give a 20 inoleller per kilogram bolus
of an isotonic crystalloid. So normal saline
or lactated ringers. And you have to be ready
to repeat that bolus, sometimes two, three, even
four times. Anaphylaxis causes a massive capillary
leak, and these kids become profoundly volume
depleted very, very quickly. And if the hypotension
is just not responding to fluids and the IM epinephrine,
what's the next escalation? You have to start
a titratable IV epinephrine infusion, a continuous
drip. You titrate it to achieve an adequate mean
arterial pressure and good perfusion. And this
just highlights why it's so critical to have
that early IV or IO axis we talked about. Finally
in this category, foreign body airway obstruction
or FBAO. This might be the highest stress scenario
because the fix is purely mechanical. We have
to reinforce that key distinction. Responsive
versus unresponsive. The PLS source material
is crystal clear on this. If the child is responsive,
they can make sounds or they're coughing forcefully.
You do not intervene physically. You let them
cough. Encourage them to keep coughing. Their
own cough is almost always more effective than
anything we can do manually. We only step in
when that cough becomes silent or ineffective.
They can't speak or you see poor air exchange.
And the maneuvers themselves differ by age? They
do. For an infant so younger than one year, you
do a sequence of five rapid back slaps between
the shoulder blades, followed by up to five chest
thrusts, which are basically compressions. You
repeat that cycle until the object is out or
the infant becomes unresponsive. For a child,
one year and older, you move to abdominal thrusts,
the Heimlich maneuver. Again, you repeat until
the object is expelled or they become unresponsive.
And if they do become unresponsive, we immediately
switch to our code protocol. What's that pathway?
You activate EMS or your code team and you start
CPR immediately. And this is important. You don't
waste time with an initial pulse check if they're
unresponsive and not breathing or only gasping.
You just start compressions. Then every time
you open the airway to give your two breaths,
you look in the mouth for the object. And what's
the clinical pearl about actually removing the
object? You only attempt to remove it if you
can clearly see it. The absolute rule is do not
perform a blind finger sweep. You risk pushing
that object deeper, turning a partial obstruction
into a complete one, or causing serious trauma.
If you see it, carefully remove it. If you don't,
you just keep going with compressions and ventilation.
Okay, let's move down the respiratory tract into
lower airway obstruction, things like bronchiolitis
and asthma. Now the problem is in those tiny
distal airways, the bronchioles, deep inside
the chest, this has to change our whole approach
to ventilation, right? It changes everything.
With lower airway obstruction, the problem isn't
getting air in, it's getting air out. Those small
downstream airways collapse during expiration
and that leads to massive air trapping. So we
have to completely rethink how we assist their
breathing. This is where we need to talk about
the huge life -threatening risks of hyperventilation.
The PLS materials really stress this, but let's
get into the physiological why. Why is the bag
valve mask, if you use it wrong, maybe the most
dangerous tool you have in a severe asthma attack?
Because you're essentially forcing air into a
closed off container. If you give too many breaths
per minute or the breaths are too large, you
just don't give the child enough time for passive
expiration. This leads to a phenomenon called
dynamic hyperinflation, where the lungs just
get more and more full of trapped air with every
breath you give. And what's the physiological
cascade? How does that trapped air lead to a
cardiac arrest? It causes a few catastrophic
things to happen all at once. First, gastric
distension, which increases aspiration risk.
Second, the high pressures increase the risk
of a pneumothorax, a collapsed lung. But the
deadliest result is that the severe air trapping
creates this massive increase in intra -thoracic
pressure. And when that pressure inside the chest
goes up, what does that do to the heart? The
pressure physically squeezes the large veins,
the superior and inferior vena cava that are
returning blood to the right side of the heart.
This crushes venous return, which means less
preload, which instantly means less stroke volume,
and therefore a sudden drop in cardiac output.
It's basically a form of obstructive shock that
we, the providers, are causing. The child can
crash from that sudden drop in cardiac output
and the worsening hypoxemia. So our attempt to
save them with ventilation can actually be the
thing that causes the arrest? It can precipitate
the arrest, yes. That clinical reasoning is so
important. The solution is slow, effective ventilation.
We stick to that slow rate one breath every three
to five seconds to give them as much time as
possible for expiration to minimize that air
trapping. Prioritize exhalation time. That's
the mantra, absolutely. Don't rush the breaths.
Okay, so let's apply that to managing an acute
asthma attack. Assessment comes first. How does
the PLS severity assessment guide our decisions?
We use a set of objective criteria which are
laid out right in the PAL materials. We look
at their ability to speak. Can they speak in
full sentences, phrases, or only single words?
That tells you how much work it's taking them
to breathe. We look at the respiratory rate.
Anything over 30 per minute is severe. We look
for accessory muscle use, but most importantly
we look at the objective measures. What are the
warning signs that just scream impending failure?
An oxygen saturation below 90 % despite being
on supplemental oxygen. That is a massive red
flag. We can also look at peak expiratory flow
or PEF if the child can cooperate. A reading
below 60 % of their predicted value is a sign
of a severe life -threatening attack. Well what's
that critical cardiovascular sign? The one that
means the child is right at the edge. bradycardia.
If you see the heart rates start to drop in a
patient who has been tachypneic and working this
hard, it means they are exhausted. They are profoundly
hypoxic and they are about to have a respiratory
arrest. bradycardia in a pediatric respiratory
patient should trigger an immediate code activation
and prep for advanced interventions. Let's run
through the interventions for a moderate to severe
acute asthma attack. We're fighting two battles
at once, inflammation and bronchoconstriction.
So we give high concentration, humidified oxygen
to keep their SO2 at 95 % or higher. We use inhaled
bronchodilators, albuterol, often mixed with
iprotropium bromide through a nebulizer or an
MDI with a spacer. And we give oral or IV corticosteroids
right away to break that inflammatory cycle.
What about when the asthma is refractory? The
child is failing despite all that standard therapy.
We have to escalate. The first one is magnesium
sulfate. What's its mechanism and what is the
nurse's priority when giving it? Magnesium sulfate
is a potent, smooth muscle relaxant. It acts
as a secondary bronchodilator. It can be a true
lifesaver in status osmaticus. The dose is given
as an IV infusion over 15 to 30 minutes. And
the critical nursing priority is continuous cardiac
monitoring and frequent blood pressure checks.
If you give it too fast, it can cause profound
hypotension and bradycardia. So you have to be
ready to slow the infusion or give fluids. And
if they're still failing, even after the magnesium?
At that point, we might consider subcutaneous.
or IAM epinephrine or turbutaline, but really
the next big step is moving to non -invasive
positive pressure ventilation or NIV like CPAP
to try and stent those airways open, or we prepare
for ET intubation. And intubating a fever asthmatic
has got to be one of the highest risk procedures
in pediatric critical care. What are the key
things to think about? You have to anticipate
extremely high peak inspiratory pressures because
of that severe airway resistance. The team needs
to use paralytics carefully, ensure deep sedation,
and be ready to use very slow ventilation rates
once that tube is in place to allow for exhalation.
The risk of barotrauma and causing a pneumothorax
is incredibly high. It's a rescue procedure you
perform with extreme caution. OK, let's shift
to the next category, lung tissue disease or
parenteral disease. This is when the alveoli
themselves, the gas exchange units, are sick.
So things like pneumonia, cardiogenic pulmonary
edema or ARDS. The common thread here is severe
hypoxemia that doesn't get better with just oxygen.
Exactly. And the management for all of these
fundamentally relies on supporting those failing
alveoli. And that means using positive end -expertory
pressure or PEEP. PEEP is what keeps those tiny
airways and alveoli from collapsing at the end
of expiration, and it maximizes the surface area
you have for gas exchange. Let's compare two
big causes where PEEP is used, but for slightly
different reasons. In fact, just pneumonia and
cardiogenic pulmonary edema. Let's start with
pneumonia. For infectious pneumonia, you need
urgent diagnostics, an ABG, a chest x -ray, blood
cultures, and the nurse has to ensure that antibiotics
are on board within the first hour, especially
if you're worried about sepsis. You can treat
any associated wheezing with albuterol, but the
main supportive strategy is PEEP, delivered either
via NIV or a ventilator, to overcome that alveolar
collapse and fix the hypoxemia. You also have
to aggressively manage any fever to reduce their
metabolic demand. Now, cardiogenic pulmonary
edema. This is fluid in the lungs because the
heart's ventricle isn't working right. How does
PEEP work here physiologically? This is a really
elegant piece of clinical reasoning. In cardiogenic
edema, yes, PEEP helps push fluid out of the
lungs, but it also has a profound hemodynamic
effect. By increasing the pressure inside the
chest, PEEP actually helps reduce venous return.
It decreases the preload to the failing left
atrium. It essentially unloads the failing ventricle,
which lowers the pressure in the capillaries
and slows down the leakage of fluid into the
lungs. So in this case, PEEP is acting a bit
like a diuretic by lowering that hydrostatic
pressure on top of helping with oxygenation.
What other non -ventilatory treatments do we
use? Diuretics are absolutely critical, something
like furosemite, to quickly pull off circulating
volume and lower that left atrial pressure. And
if the ventricular dysfunction is really severe,
we'd also consider inotropic support or actor
load -reducing agents. And finally, ARDS, or
acute respiratory distress syndrome. This is
non -cardiogenic lung injury from something systemic
like sepsis or major trauma. This is diffuse
severe injury to the lungs. How do we define
ARDS in the PLS world? ARDS is defined by its
acute onset, severe hypoxemia, that is refractory
to oxygen, and bilateral infiltrates, or whiteout,
on a chest x -ray. We quantify that hypoxemia
using the PO2 -FIO2 ratio. If that ratio is below
300, it's suggestive of ARDS. The management
strategy here is very specialized. It's called
lung protective ventilation, which brings us
to this complex idea of permissive hypercarbia.
Why on earth would we intentionally let the carbon
dioxide level in the blood get high? We accept
that elevated PACO2, the hypercarbia, to protect
the injured lungs from what's called ventilator
-induced lung injury, or VILI. We do this by
strictly limiting the amount of air we deliver
with each breath, so low tidal volumes around
5 to 8 millimals per kilo, and by keeping the
peak inspiratory pressures low, If we try to
blow off all that CO2 by pushing more air, we
overstretch and damage the already injured alveoli,
making everything worse. So we're trading a mild
respiratory acidosis for mechanical safety. Exactly.
We are prioritizing protecting the lung tissue
over getting perfect lab numbers. We're deliberately
setting the ventilator to be gentle, knowing
that the priority is surviving the injury, not
having a normal blood gas. Correcting the hypoxemia
is still the number one priority, but we permit
the CO2. The final big category of respiratory
failure is disordered control of breathing. This
is when the central or peripheral nervous system
fails to actually run the show. Things like increased
intracranial pressure or ICP and poisoning or
drug overdose. Right. Starting with increased
intracranial pressure. This can be from trauma,
a hemorrhage, a severe infection. And the respiratory
consequence is huge because it directly affects
the central respiratory drive in the brain stem
leading to weird breathing patterns or just stopping
breathing altogether apnea. And the classic sign
is Cushing's triad irregular breathing, hypertension,
and bradycardia. but the Bilalosaurus gives a
really important warning for kids. It does. While
we all learn about bradycardia, children with
a rapidly rising ICP might initially present
with hypertension and tachycardia, or even a
normal heart rate. They don't always show that
profound bradycardia you see in adults. We can't
wait for the heart rate to drop to intervene.
If you see hypertension and a decreasing level
of consciousness, you have to act. And the interventions
are about optimization. Head midline, C -spine
stabilization if needed, maintain an open airway.
But the caution around hyperventilation here
is maybe the most heavily emphasized point in
the entire Pallas manual. It's the ultimate tightrope
walk. You have to maintain the airway and ensure
adequate ventilation, but you must, must avoid
prophylactic severe hyperventilation. You cannot
just start bagging them fast to drive that CO2
down. Why is severe hyperventilation so dangerous
when ICP is high? Because our main goal in ICP
management is to maintain adequate cerebral perfusion
pressure, or CPP, and CPP is your mean arterial
pressure minus your ICP. Hyperventilation blows
off CO2, and that causes rapid cerebral vasoconstriction.
The blood vessels in the brain clamp down. While
this does shrink the volume in the skull and
acutely lowers the ICP, it also drastically reduces
blood flow to the brain. So you're starving the
already injured brain of oxygen and blood. You
lower the pressure, but you reduce the supply.
Precisely. You might get a great ICP number on
the monitor, but you're actually making the underlying
brain injury worse. That's why Pallas is so strict
about avoiding severe hyperventilation after
that initial 48 -hour period. So when is it okay
to use mild hyperventilation? Only as a temporary
last -ditch rescue therapy for acute deterioration.
You see signs of impending brain herniation like
a blown pupil or sudden bradycardia. It's a break.
It buys you minutes while you get osmotic agents
like mannitol or hypertonic saline ready. It
is never a long -term strategy. Okay, let's move
to poisoning or drug overdose. This usually causes
respiratory failure by just depressing the central
respiratory drive. Yeah, and supportive care
is everything here. Airway and ventilation support
are paramount because the patient can become
apneic very, very quickly. You need to contact
poison control immediately and you have to be
ready for aggressive suctioning. Loss of consciousness
means a huge risk of vomiting and aspiration.
And the specific drug we often see used in the
ER. If you suspect an opioid overdose and the
patient is in respiratory arrest but still has
a pulse, you give naloxone. The IM or intranasal
routes are often faster than waiting to get an
IV. But remember, if the patient is pulseless,
you don't mess with naloxone, you go straight
to CPR. And of course, you're sending off a whole
panel of diagnostics, ABG, ECG, drug screens
to guide the rest of the care. We've got a few
crucial procedural airway perils that an ER nurse
prepping for this exam has to have down cold,
especially around and advanced airway management.
First one is about cuffed ET tubes, which are
now standard in pediatrics. The nursing team
has to be meticulous about managing that cuff
pressure. Why is that? What's the target range?
You want to keep that cuff pressure between 20
to 25 centimeters of water. If the pressure is
too low, you get a big air leak around the tube,
which means ineffective ventilation. That's especially
bad in ARDS or asthma, where you need high pressures.
But if the pressure is too high, you risk causing
tracheal ischemia and long damage to the airway.
It needs to be checked regularly with a cuff
manometer. And another big procedural pearl is
about using neuromuscular blocking agents paralytics
for intubation, specifically succinylcholine.
You have to be so cautious with succinylcholine
in kids, especially if you suspect an underlying
neuromuscular disease or in patients with burns,
crush injuries, or prolonged immobility. Succinylcholine
can cause a massive dangerous efflux of potassium
from the cells. It can lead to severe hyperkalemia
and fatal arrhythmias, or it can trigger malignant
hyperthermia. And what's a key drug interaction
pearl that relates to respiratory muscle weakness?
The clinical pearl here is to remember that some
of our most antibiotics, specifically amino glycosides
like gentamicin and also vancomycin, they have
some intrinsic neuromuscular blocking activity.
So if you have a child with a known neuromuscular
issue or even just a very septic kid who is already
weak and struggling to breathe, giving these
antibiotics can actually worsen their respiratory
muscle weakness and make it harder to ventilate
them. Lastly, let's just confirm the absolute
necessity. of end -tidal CO2 monitoring across
all of these different respiratory problems.
ET Co -euros monitoring is completely essential
and non -negotiable. It gives you instant continuous
feedback on three critical things. First, ventilation
effectiveness. It tells you if you're actually
clearing CO2. This is so important when you're
trying for permissive hypercarbia in ARDS or
using those slow rates in asthma. Confirmation
of tube placement. After you intubate, ET Co
-euros is the gold standard for confirming that
the tube is in the trachea and not in the esophagus.
And third, it's an indicator of circulation,
which is so important during an arrest. Yes.
During a respiratory arrest or full -blown CPR,
the ETKO level reflects pulmonary blood flow,
which is directly tied to your cardiac output.
A sudden drop in ETKO during CPR means your compressions
are bad or circulation is failing. And on the
flip side, a sudden sustained jump in ETKO is
the earliest sign you'll get a return of spontaneous
circulation. or ROSC. It connects the breath
to the heart. So, to synthesize this whole respiratory
management approach, PALIS success is overwhelmingly
measured in prevention. We win when we recognize
and manage that respiratory distress and impending
failure long before the patient becomes pulseless.
That shift from compensated distress to uncompensated
failure is so fast, and it requires mastery of
these targeted drugs and ventilation strategies.
Okay, let's do a quick final review of the key
pharmacological agents just to reinforce that
structured PALIS thinking. will categorize them
by the condition they treat. Perfect. For upper
airway obstruction like croup, it's that one
-two punch of rapid -acting nebulized epinephrine
and the long -acting corticosteroids like dexamethasone.
For anaphylaxis, immediate IM epinephrine, that's
number one, followed by your bronchodilators,
corticosteroids, and that dual anahistamine blockade.
For lower airway obstruction, specifically that
really bad refractory asthma, the foundation
is still bronchodilators and corticosteroids,
but the big rescue drug is that magnesium sulfate
infuser. And for lung tissue disease, whether
it's pneumonia, cardiogenic edema, or ARDS, the
key mechanical support is PEEP. Then you add
diuretics for the cardiogenic causes and, of
course, antibiotics for infection. And for disordered
control of breathing, the most critical interventions
are defensive. You're avoiding hypoxia. avoiding
severe hypercarbia, and avoiding hyperthermia
in your ICP patients. And you're having the right
antidote, like naloxone for an overdose, ready
to go. And translating all this palace knowledge
into the high -pressure world of the ER, the
ICU, that really requires internalizing a few
essential clinical pearls. Okay, first, let's
hammer home the importance of constant, meticulous
reassessment, especially after you've given certain
drugs. never ever assume stability, especially
with croup and asthma. We talked about that post
-epinephrine observation for croup. They can
rebound hard. And similarly, in severe asthma,
a kid who goes from being anxious and fighting
to being quiet and lethargic, that child is often
entering the failure phase. They're just too
tired to compensate anymore. The quiet child
is the most frightening child. Second, the critical
nursing priority of getting early vascular access
in those moderate to severe cases. If you see
a kid with moderate to severe anaphylaxis or
status asthmaticus, your first thought after
oxygen should be getting that IV or IO access
immediately. You're going to need it for high
volume fluid resuscitation, for continuous infusions
of steroids, magnesium, maybe even IV epinephrine.
If you wait until they're crashing, that peripheral
vasoconstriction will make getting access nearly
impossible and you'll have a critical delay.
And finally, the need for concurrent management.
You're treating the cause while aggressively
providing support care at the same time. So mastering
PALS respiratory management really means training
your eye to see those subtle cues, the change
in how they're speaking, the depth of the retractions,
that slow shift toward bradycardia long before
the patient ever needs chest compressions. That
systemic physiologically based knowledge is your
ultimate power in that critical moment. So as
you take this deep dive and integrate it into
your clinical prep, here's one final provocative
thought for you to think about. This one is specifically
about that high stakes procedure we discussed.
Given the profound risks of hyperkalemia from
using succinylcholine in certain pediatric patients,
especially those with an unknown or underlying
neuromuscular disease, and the absolute need
for rapid paralysis for intubation, how does
that risk assessment change your immediate choice
of paralytic agent, say, rocoronium versus succinylcholine,
during a non -traumatic severe status asthmaticus
presentation in the chaos of the emergency department?
Think about that clinical judgment call, the
trade -off between speed and safety and how you
prepare your drugs ahead of time. We'll catch
you next time for the next Deep Dive.