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.
If you are an ER nurse, an ICU tech, or really
anyone preparing to work the sharp end of pediatric
critical care, this deep dive is absolutely custom
built for you. We're cracking open the pay less
algorithms today, not just to help you pass a
test, but to really embed the clinical reasoning,
the why behind every single action you take in
the trauma bay. Yeah, this is so much more than
just certification prep. In a high -stakes pediatric
code, there is just no time to look at a handbook
or trace lines on a little card. None. That knowledge,
it has to be completely internalized. Our mission
today is to translate those protocols into immediate,
decisive action. And we do that by prioritizing
the physiological understanding. We want you
to move past memorization and into real clinical
mastery. Absolutely. Our focus is on that comprehensive
knowledge drawing entirely from the latest advanced
life support guidelines. We're going to break
down. the two vastly different pathways to pediatric
arrest. We'll analyze the specific choreography
of medications and explore how tools like capnography
become like your third eye during CPR. We're
going for rapid, thorough, and just completely
applicable knowledge. Let's do it. Okay, let's
unpack this and jump right into the critical
foundation. The pediatric difference. So when
a siren pulls up to the ED, the default expectation
for an adult patient who's arrested is almost
always a primary cardiac event. Always. We're
talking coronary artery disease, V -fib, a certain
electrical catastrophe. But when we shift our
focus to pediatrics, that fundamental assumption,
it changes completely. And if you forget that
distinction, you really compromise the resuscitation
from the very start. That contrast is, I think,
the single most important concept in all of PALS.
Cardiac arrest in children is overwhelmingly
not a primary heart issue. Right. The key driver
is the body's reaction to progressive systemic
failure. So this means we are usually, almost
always, dealing with the hypoxicus fixiola rest
pathway. This is the end result of profound prolonged
respiratory failure or shock that leads to severe
hypoxemia and acidosis. And only then, after
all that, does the heart finally stop. So, if
the pediatric heart is typically healthy, why
does it ultimately fail in a code? Is it just
exhaustion from running on zero oxygen? Precisely.
That's a great way to put it. Unlike the adult
heart, which fails because of a lack of blood
flow to the muscle itself, you know, a blockage.
A plumbing problem. A plumbing problem. The pediatric
heart stops because the systemic oxygen delivery
has completely collapsed and the metabolic demands
of the body just can't be met. The heart muscle
becomes acidotic, its start of oxygen, it loses
its contractility, and it slows down until it
becomes bradycardic and then eventually a systole
or PEA. So the heart is the victim here, not
the primary culprit. The heart is the victim,
100%. Can you walk us through that fork in the
road then? The guidelines distinguish two pretty
clear pathways leading to arrest. Absolutely.
So the main road, the one taken by about 80 %
to 90 % of pediatric arrests, is that hypoxic
-asphyxial pathway. OK. This is a slow, observable
decline. You can see it happening. Respiratory
distress leads to respiratory failure, or compensated
shock leads to decompensated shock. And eventually,
both of those paths, they merge into cardiopulmonary
failure and arrest. And that's usually a systole
or PEA. Usually a systole or PCA. The child is
just... They're running out of their physiological
reserve and the less common row the one that's
more like the adult version that sudden electrical
path That's the sudden cardiac arrest or the
arrhythmia pathway. This one is rare. We're talking
only five to fifteen percent of cases these are
typically the result of an underlying structural
heart disease something like hypertrophic cardiomyopathy
or An anomalous coronary artery or it could be
genetic electrical problems, the so -called channelopathies,
like Long QT syndrome. So in that case, the heart
does suddenly go into V -fib. It does. In that
case, it suddenly enters ventricular fibrillation
or pulsus ventricular tachycardia. Wow. This
distinction has, I mean, massive clinical implications.
If the common pathway is this slow hypoxic collapse,
then our entire strategy has to pivot to prevention.
It must. The critical concept here is that if
your intervention happens early when the child
is still just in respiratory distress or compensated
shock, you know, before they progress to cardiopulmonary
failure, the outcome is usually reversible and
favorable and highly favorable. Once they progress
to a systole or PEA, the chance of survival just
plummets. It falls off a cliff because the entire
system is profoundly acidotic and damaged. So
we're intervening not just to restart the heart,
but to restore effective breathing and perfusion
that brings us right to the heart. data. The
survival numbers are, they're stark, and they
really show why prevention is so much more effective
than resuscitation in pediatrics. What are the
key metrics we need to internalize about these
survival rates? Yeah, the statistics are sobering,
especially when you compare the location and
the rhythm. The overall outcome for children
who experience an out -of -hospital cardiac arrest,
or OHCA, is tragically poor. It's hovering around
8 % survival to hospital discharge. 8%, that's
terrible. It's terrible. The community resources,
you know, they often arrive too late, and the
period of hypoxia has just been too long. But
the moment that child hits the hospital door,
especially if they arrest in -house, those numbers
change dramatically. They do. Survival for an
in -hospital cardiac arrest, IHCA, is significantly
better. We're looking at something approaching
43%. Wow. And this improvement, it really reflects
early recognition by trained staff, immediate
initiation of high -quality CPR, and just rapid
access to advanced interventions. Okay, now let's
look at the rhythm because there's a huge split
in prognosis here and it really confirms the
importance of that two pathway model you talked
about. Absolutely. The survival rate is highest.
It ranges from about 38 to 43 percent when the
presenting rhythm is shockable. VF or PVT. VFPVT,
this is the electrical problem, right? And it's
often more responsive to intervention. Now, you
compare that to the non -shockable rhythms, a
systole or PEA, which are the end stage of that
hypoxic collapse. Survival rates there drop significantly,
typically only 11 to 27%. It's so counterintuitive
to think that the rare electrical arrest gives
the patient a better chance, but the data is
just crystal clear. Why is that initial rhythm
so prognostic? Because a shockable rhythm implies
a relatively healthy, or at least a metabolically
compensated system that experienced a sudden
electrical fault. If you correct that fault quickly
with defibrillation, the heart is often ready
to disresume function. Non -shockable rhythms,
PEA and a systole, they mean the entire system
is failing. Profound hypoxia, severe acidosis,
electrolyte derangement. You have to fix the
root cause, the H's and T's, while you're attempting
CPR, which is just far more complex and time
-consuming than delivering a single electrical
jolt. That survival disparity is the ultimate
driver for why Pali's focus is so relentlessly
on early intervention before you get to that
point of no return. Exactly. So every algorithm,
every medication, every single intervention rests
on one core task, high quality CPR. You can't
run a successful code without it. We adhere to
the CAB sequence compressions, airway breathing,
and the guidelines give us these incredibly specific
metrics. What are the non -negotiables an ER
nurse must nail for pediatric CPR? The foundational
metrics are everything. Let's start with the
easiest one, the rate. It's standardized across
all ages from an infant to an adult. 100 to 120
compressions per minute. You can use the beat
of staying alive if you need a mental anchor,
but do not go over 120. Why not? Because overly
rapid compressions can actually compromise the
recoil. You don't give the chest enough time
to expand. Ah, OK. Now for the tricky part, depth.
This changes based on the size of the child.
And maintaining that depth manually is, I mean,
it's way harder than it sounds. It is. The target
is always at least one third of the anterior,
posterior, or AP chest diameter. To make it practical,
for infants under one year, the depth is about
one and a half inches, or four centimeters. And
you're using two fingers for that. You're often
using two fingers, or even better, two thumbs
encircling the chest. For children, the depth
increases to about two inches or five centimeters.
This often requires one or two hands, depending
on the child's size. And then for larger adolescents,
you just move to the full adult standard, which
is at least two inches. But and this is crucial,
not more than two point four inches. OK, the
next crucial point and one that often gets missed,
especially when fatigue sets in, is recoil. Why
is full chest recoil so vital? If you lean on
the chest, you prevent the heart from fully expanding.
Full chest recoil allows the ventricles to passively
refill with blood during that relaxation phase.
This refill is what creates the coronary perfusion
pressure, the pressure gradient you need to push
blood into the heart muscle itself. No recoil
means no blood gets to the heart, and so your
CPR is just ineffective. The compressor must
lift their weight completely off the chest between
every single compression. And the ratio, this
determines the flow of the entire BLS effort,
especially before you get an advanced airway.
The compression ventilation ratio, it differs
based on the team size. For a single rescuer,
it doesn't matter what the child's age is. It's
30 compressions to two ventilations. 30 .2. 30
.2. But for two or more rescuers, which is standard
in hospital, it's 15 compressions to two ventilations.
15 .2. Yep, 15 .2. And that ratio maximizes compressions
while still prioritizing the ventilation needs
of the typically hypoxic pediatric patient. Finally,
the metric that separates an organized team from
just chaos. Minimizing interruptions. Yes. Interruptions
must be kept to less than 10 seconds. This applies
to your rhythm checks, shock delivery, or even
placing an advanced airway. If you stop compressions
for longer than 10 seconds, the drop in coronary
perfusion pressure is immediate, and it is severe.
And it takes multiple compressions after that
to build that pressure back up. So this is a
huge team coordination goal. A critical one.
Be prepared, move fast, and get back on the chest.
Okay, so with that foundation of high quality
CPR established, let's move into the PLS algorithm
itself. It's conceptually split into two sides,
right? The shockable rhythms, the electrical
emergencies, and the non -shockable rhythms,
the systemic failures. Let's start with the higher
survival path on the left. V -fib and pulseless
V -tatch. These are those relatively rare electrical
faults. They represent, you know, maybe five
to fifteen percent of pediatric arrests, but
they demand immediate action because early defibrillation
is highly effective. As the nurse, how do I visually
distinguish these on the monitor, and why do
they lack a pulse? OK, so ventricular fibrillation,
or VF, is easy to spot. It's just chaotic, irregular
electrical activity. The heart is just quivering.
It's not pumping. It's generating no mechanical
force. And because there's no coordinated contraction,
there's no cardiac output, and so there's no
pulse. Pulseless ventricular tachycardia, PVT,
is a bit more organized, but just as deadly.
You'll see these wide, often rapid QRS complexes
that look rhythmic. But the electrical signal
is so disorganized in the ventricles that the
mechanical pump function fails to generate any
palpable cardiac output. You have to feel for
a pulse. If it looks like V -tach, but there's
no pulse, you treat it as PVT. And we also briefly
mentioned Torasad's the point, the twisting of
the points. How do we spot that specific? often
drug -induced variants. The torsides is a distinct
polymorphic V -tach, and it's characterized by
the cyclical change in the amplitude of the QRS
complexes. It literally appears to twist around
the baseline. It's often linked to a prolonged
QT interval, and it requires a very specific
antiarrhythmic intervention. Got it. Okay, let's
follow the VFPVT algorithm steps. We start CPR.
Immediately check for a rhythm, and if it's shockable,
step two is the shock. What's the rationale for
the energy dose and why do we go immediately
back to CPR? So the initial shock dose is two
joules per kilogram, two J's per kilogram. The
rationale is to deliver just enough energy to
depolarize a critical mass of the ventricular
myocardium. We are essentially giving the heart
a reboot command. A hard reset. A hard reset,
hoping the SA node, the natural pacemaker, can
regain control. And immediately after delivery,
you resume CPR. Do not check for a pulse. Do
not look at the rhythm. You resume compressions
immediately for two full minutes to ensure blood
flow while the heart, you know, hopefully recovers.
After those two minutes of CPR and establishing
IV or IO access, we check the rhythm again. That's
step five. If it's still shockable, we deliver
shock two. Do we escalate the dose here? No,
not yet. The initial increase in dose happens
later. Shock two is also delivered at two joules
per kilogram initially. But if it persists, then
we move to step six epinephrine. And this timing
is a critical nursing pearl. In the VFPVT arm,
epinephrine 0 .01 milligrams per kilo IVIO is
administered after the second shock is found
to be unsuccessful. The priority is electricity
first, then chemical support. And we repeat EPI
every three to five minutes after that. That
timing distinction is so crucial. When do we
finally escalate the shock energy? In step seven.
If the rhythm persists after shock two and after
epinephrine has been given, you then escalate
the energy dose for shock three to four joules
per kilogram. Double it. You double it. And you
can continue escalating up to 10 joules per kilo
or the adult max dose for subsequent shocks.
And again, two minutes of high quality CPR follows
immediately. OK, so if we reach step eight, we
are now dealing with shock refractory VFPVT,
and that requires antiarrhythmics. We've got
amiodrone. Right. This is where we try to stabilize
that irritable myocardium chemically. We use
either amiodarone, which is five milligrams per
kilo, ivyobolus, or lidocaine at one milligram
per kilo, ivyobolus. Is one preferred? Clinically,
amiodarone is often preferred. It has a more
complex mechanism. It affects multiple channels,
which gives it, you know, broader antiarrhythmic
effectiveness. But remember, if you identified
torsades earlier, you have to stop the sequence
and immediately give magnesium sulfate. Right.
That's 25 to 50 milligrams per kilo, ivyobolus.
OK, let's pivot to the right side of the algorithm.
Asystole and PEA. This is the more common, yet
much tougher, road for pediatric resuscitation
because it represents that systemic collapse.
Let's start with identifying them on the monitor.
A cystally is. It's straightforward. It's a flat
electrical line. No electrical activity, no pulses,
no life. And the protocol. Nursing protocol here.
Always confirm this on multiple leads. Don't
waste critical time on a disconnected or a faulty
lead reading. And PEA, Pulseless Electrical Activity.
This is the ultimate deceiver because the monitor
looks like it's organized, but the patient is
dead. Exactly. PEA means the heart's electrical
system is still working. You see P waves, you
see QRS complexes, maybe even a rhythm. But the
mechanical pumping action has failed to generate
a palpable pulse or sufficient blood pressure.
This is the end stage of that hypoxic decline.
It is. It's fundamentally a mechanical or a metabolic
problem, not a primary electrical one. And because
it's not an electrical problem, we do not shock.
So what's the immediate priority in stack nine?
Continuous, uninterrupted, high -quality CPR
in immediate establishment of IVRIO access. We
are trying to mechanically perfuse the coronaries
in the brain, just buying time to figure out
and reverse the root cause. And unlike the shockable
arm, epinephrine is introduced immediately in
step 10. Why the urgency here? Because the heart
muscle is profoundly weak and vasodilated. Ebenephrine
at 0 .01 milligram per kilo G IVIO is given immediately
and repeated every three to five minutes. Its
primary goal through alpha edrenergic stimulation
is powerful vasoconstriction. This raises the
aortic diastolic pressure, which is absolutely
critical for increasing that coronary perfusion
pressure in a flaccid, non -pumping heart. In
PEA and a systole, chemical support is the first
line of advanced intervention right after...
CPR starts. So step 11 is this never -ending
cycle of CPR, EPI, and the crucial step, treating
reversible causes. Correct. If the rhythm stays
non -shockable after two minutes, you resume
CPR and immediately, simultaneously, you begin
that deep diagnostic workup known as the H's
and T's. The prognosis for PEA and a systole
rests entirely on how quickly and effectively
you can address that underlying physiological
insult. And what if that rhythm suddenly shifts?
What if a systole suddenly becomes V fib? You
have to recognize that switch immediately. If
the rhythm becomes shockable, the non -shockable
algorithm is abandoned, and you jump directly
to the shockable arm, typically starting at step
seven, to deliver that four joule per kilo shock
without any delay. This is where the ER nurse's
ability to multitask and think critically is
tested the most. When you're running a PEA code,
you're not just following a timeline, you're
an investigator. Let's spend some time on the
H's and T's, not just listing them, but talking
about how a nurse identifies them rapidly in
a chaotic code. Exactly. The differential diagnosis
has to happen concurrently with compressions.
If you don't treat the cause, the heart is never
going to stay restarted. Let's focus on the H's
first, the metabolic and volume issues. Hypovolemia
is high on the list, especially in a traumatic
or septic child. Right. Signs of severe hypovolemia
are often evident from, you know, pre -arrival
data or your initial assessment. Flat neck veins,
a history of vomiting or diarrhea or known hemorrhage.
And the diagnostic tool. The rapid diagnostic
tool here is the fluid challenge. If you think
the patient is hypovolemic, you give rapid boluses
of isotonic crystalloid 20 ml per kilo. If the
vital signs transiently improve, you've pretty
much confirmed the cause. If the patient has
known trauma, you move immediately to blood products.
Next is hypoxia, which, as we know, is the most
common killer. Hypoxia demands the absolute highest
priority in every pediatric code. You have to
ensure optimal ventilation and oxygenation. If
the oxygen saturation isn't 100 % and the ETC
show is low, you are not adequately delivering
oxygen. So what do you check? This means checking
the advanced airway, ensuring a proper bag valve
mask seal, and confirming ET tube placement with
everything you've got. Then we have the electrolyte
and acid base issues. Hydrogen ion, so acidosis,
hyperkalemia, and hypothermia. Acidosis is almost
always present in cardiac arrest, but unless
it's severe or the arrest is prolonged, bicarb
isn't routine. Hyperkalemia or severe acidosis,
that usually requires an emergent point -of -care
blood -gas analysis. And if you suspect high
potassium? If hyperkalemia is suspected, maybe
in a child with renal failure, you have to prepare
calcium chloride or sodium bicarbonate immediately
to stabilize the myocardium and shift that potassium.
For hypothermia, if the core temperature is below
30 degrees Celsius, the heart is often refractory
to all drugs and electricity. You must initiate
active rewarming efforts concurrently. OK, now
for the T's, the structural and mechanical issues.
Tension pneumothorax and tamponade. These are
obstructive causes of shock. A tension pneumothorax
is suspected if there's a history of trauma,
marked asymmetry of breath sounds, and it's really
difficult to ventilate. This needs rapid intervention.
Needle decompression. Immediate needle decompression,
second intercostal space, mid -clavicular line,
followed by a tube thoracostomy. Cardiac tamponade
is suspected with a rapid drop in blood pressure
and jugular venous distension. A rapid bedside
ultrasound is the fastest way to confirm this,
and that requires an urgent pericardiacentesis.
And finally, toxins and thrombosis. Toxins can
often be identified from the patient history
or toxicology screens. For example, a tricyclic
antidepressant overdose requires bicarb. Thrombosis
pulmonary or coronary is really difficult to
diagnose rapidly but it's a consideration in
children with underlying risk factors like congenital
heart disease or central lines. So the takeaway
is? The key message is during a non -shockable
arrest the nurse must constantly prompt the team
leader what H or T are we treating next and be
ready to prepare that necessary intervention.
Okay so medications are only as effective as
their delivery system. As the nurse, you are
the gatekeeper of vascular access. Let's review
the hierarchy and the non -negotiable step for
drug delivery in a code. The hierarchy is simple.
Intravenous IV is primary. If you can't get a
good peripheral IV quickly, you transition immediately
to the secondary route. Intraosseous access.
I .O. The I .O. route provides drug and fluid
delivery that's comparable to central venous
access, and you can establish it in any age group,
often in under 60 seconds. This is vastly preferred
over the third and final choice, the endotracheal
or ET route. Why is the ET route so universally
disfavored now, especially for epinephrine? It's
problematic because drug absorption is just highly
unreliable and unpredictable. It results in significantly
lower and often subtherapeutic blood concentrations.
Furthermore, some studies suggest that the lower
concentration of epi delivered this way can cause
a transient beta adrenergic effect without the
desired alpha constriction. And that can lead
to detrimental hypotension rather than the beneficial
coronary perfusion you're looking for. It should
only be used as a last resort until you get IV
or IO access. This brings us to probably the
most important nursing parole regarding drug
administration via peripheral IV or IO, the saline
flush. What is the clinical consequence of skipping
that flush? If you skip the saline flush, the
medication, epinephrine, amutorone, whatever
it is, it just sits there. It's static in the
peripheral vein or the IO space. It's just hanging
out? It's just hanging out. If you're giving,
say, half an ml of epi into a peripheral IV without
a flush, it might take several circulation times
to even reach the central circulation where the
heart is. By using a five to 10 ml normal saline
flush, you create a bolus effect. You force the
drug immediately into the central circulation
during those ongoing chest compressions, guaranteeing
rapid delivery and maximizing the drug's impact
within that critical three to five minute dosing
window. So skipping the flush is like? Skipping
the flush is equivalent to delaying the dose
by 30 to 60 seconds. It's a critical error. And
just for reference, if we are absolutely forced
to use the ET route for epinephrine, the dose
adjustment is massive. It is. The recommended
ET dose of epi is 10 times the IVIO dose, recognizing
that 90 % of that drug may be lost to absorption
variability. Okay, let's detail the pharmacology
of the key PALS agents, starting with the alpha
-edrenergic powerhouse. Epinephrine. It's a vasopressor
used in all arrest rhythms. Its mechanism is
multifaceted, but it's really centered on that
alpha -edrenergic stimulation causing powerful
vasoconstriction to increase aortic diastolic
pressure and consequently coronary perfusion
pressure. And the beta effects. Its beta adrenergic
effects are secondary. They promote contractility
and heart rate, but it's the alpha effect we're
after in a code. The indication is cardiac arrest,
a systole, PEA, and VFTVT after the second shock.
Dose is 0 .01 milligram per kilo G IVIO bolus,
repeated every three to five minutes. And a nursing
note here. Be meticulous about using the correct
concentration. It's 1 to 10 ,000 for IVI use,
which often requires careful dilution if your
code card only stocks 1 to 1 ,000. For the shock
refractory rhythms, we rely on the antiarrhythmics.
Let's compare amiodurone and lidocaine. Amiodurone
is a potent antiarrhythmic. It affects sodium,
potassium, and calcium channels, prolonging the
action potential duration and the refractory
period. Indication. shock refractory VF or PVT.
The dose is five milligram per kilo G IVIO bolus.
What's the risk with amyloid run? It must be
administered slowly or diluted if you're giving
it as an infusion post ROSC because rapid boluses
can cause significant hypotension. And the alternative?
Lidocaine. It's a simpler sodium channel blocker
that suppresses ventricular arrhythmias and decreases
automaticity. Indication. Alternative to amiodarone
for shock refractory VF -PVT, the dose is one
milligram per kilo G IVIO bolus. And the risk
there? You need to monitor for signs of leadocaine
toxicity post -ROSC, which can include seizures,
altered mental status, and even cardiovascular
collapse. Okay, let's move outside the core arrest
sequence to drugs for specific indications. First,
for symptomatic bradycardia. Atropine. It's an
anticholinergic that increases heart rate by
blocking the effects of the vagus nerve on the
heart. It's indicated for bradycardia caused
by excessive vagal tone or a primary AV block.
But not for everything. Not for routine use in
cardiac arrest, no. Especially if the bradycardia
is due to hypoxia. Treating the hypoxia is the
primary goal there. If you do use it, the dose
is 0 .02 milligram per kilo G IVIO. and the crucial
agent for torsades de pointes. Magnesium sulfate.
This is for arrhythmias associated with hypomagnesemia.
Indication is torsades de points. Dose is 25
to 50 milligrams per kilo G IVI bolus. You'll
want to monitor deep tendon reflexes and for
signs of hypermagnesemia, especially if renal
function is impaired. Finally, the drug that
is now highly restricted, sodium bicarbonate.
Yeah. Sodium bicarb is used to increase serum
pH, which can help treat severe acidosis or decrease
potassium concentrations. Its indications are
very limited now. Severe hyperkalemia, prolonged
cardiac arrest that's refractory to other treatments,
or specific poisonings like a triceclic antidepressant
overdose. And if it is indicated. The dose is
one milli -equivalent per kilogram IVIO, and
the nursing note is critical. Bicarbonate is
an alkaline solution and should never ever be
administered in the same line as calcium because
it will precipitate. It turns to chalk. Pediatric
arrest is primarily a hypoxic event, yet we have
these firm guidelines telling us to avoid excessive
ventilation. That sounds like a contradiction.
Why must we be so restrictive with our breaths?
It's a very delicate balance. The contradiction
exists because hyperventilation is actively harmful.
How so? Excessive ventilation, whether it's too
fast or too forceful, significantly increases
your intra -thoracic pressure. When that pressure
rises, it pinches the vena cava, which impedes
venous return to the heart. Less blood returns,
less blood is pushed out during compressions,
and your coronary perfusion pressure drops dramatically.
You're fighting your own compressions. So we
need to provide just enough oxygen but not so
much pressure that we compromise cardiac output.
What are the specific ventilation rates once
an advanced airway is in place? With an advanced
airway like an ET tube or a supraglottic airway
secured, compressions become continuous at 100
to 120 per minute and ventilation shifts to asynchronous.
The rate is strictly one breath every six seconds.
Which is 10 breaths a minute. 10 breaths per
minute, and use only the volume necessary to
cause visible chest rise, avoiding gastric distension.
And a quick note on cricoid pressure, which often
seems to slow down intubation attempts. The guidelines
are pretty clear. Routine use of cricord pressure
is discouraged. It has not been shown to prevent
aspiration, and it often interferes with successful
placement of the ET tube or even effective bag
mask ventilation. We often think of n -tidal
carbon dioxide, or ETKO, primarily as a tool
for confirming correct ET tube placement. But
in a cardiac arrest setting, its significance
just explodes. It becomes your most reliable
real -time monitor of resuscitation quality.
The so what of ETCO is that it directly correlates
to pulmonary blood flow. OK, break that down.
Since the lungs are being ventilated constantly,
the only way ETCO gets exhaled is if blood flow.
Your cardiac output carries it from the tissues
to the lungs. Therefore, ETCO provides an immediate,
indirect measure of cardiac output and lung perfusion
during CPR. So how does the nurse use this number
to guide compression quality? During high quality
CPR, your initial ET caro target should be between
10 and 15 millimeters of mercury. If your values
are consistently dropping below 10, that is an
immediate red flag. What does it tell you? It
tells the team that their compressions are ineffective,
blood flow is critically poor, or the patient
has some severe metabolic derangements. You have
to immediately adjust compression depth technique
or positioning until that number improves. And
what about the clearest, most undeniable sign
of success, which often precedes the physical
return of a pulse? That is the abrupt and sustained
jump in ETKO. A reading that abruptly rises and
stays elevated, often to a value over 40 millimeters
of mercury, is the most reliable earliest indicator
of return of spontaneous circulation, ROSC. Wow.
That spike signifies a sudden rush of blood flow
carrying all that metabolic Keo that had been
backing up in the system. When you see that spike,
you stop compressions and check for a pulse immediately.
When you achieve ROSC, an organized rhythm, palpable
central pulses, measurable blood pressure, The
resuscitation hasn't ended. It's just changed
phase. The goal shifts to optimizing recovery
and preventing that secondary injury. The post
-arrest phase is crucial. It often determines
the neurological outcome. The immediate goals
are stabilization and optimization. Starting
with hemodynamics. Yes. We have to maintain blood
pressure and spontaneous arterial pressure. Hypotension
post -ROSC is incredibly common and it is devastating.
So what's the management? It requires aggressive
management. Initial fluid boluses of isotonic
crystalloid to treat any residual hypovolemia,
followed immediately by initiating pressors like
epinephrine or dopamine if the shock persists,
were aiming for a systolic blood pressure above
the fifth percentile for age. And respiratory
targets. We just spent the whole code worrying
about getting enough oxygen. Right. Post -ROSE,
we actually focus on avoiding hyperoxia and hyperventilation.
We target oxygen saturations between 94 and 99
percent. 100 percent saturation can actually
cause reperfusion injury. And ventilation. For
ventilation, the goal is to maintain normal carbia,
a PCO of about 35 to 45 millimeters of mercury,
which you monitor with ET2 and blood gases. Hyperventilation,
which gives you a low PCOROS, causes cerebral
vasoconstriction, and that reduces blood flow
to the recovering brain. Finally, temperature
management. Targeted temperature management,
or TTM, is a standard component of post -cardiac
arrest care, particularly for comatose children
post -ROSC. While the specific target temperature
might vary by institution, the goal is always
to strictly avoid hyperthermia or fever. Why
is fever so bad here? Because elevated temperature
significantly increases cerebral metabolic demand
and it worsens the neurological outcome. The
nurse must initiate cooling measures or monitor
closely immediately post R .O .S .C. In the chaos
of a code, the difference between a smooth operation
and a disaster is often not pharmacology, but
choreography. Pay Ellis requires a high -functioning
team. As an ER nurse, you might be the documenter,
the medication preparer, or the compressor. What
are the fundamentals of team dynamics that guarantee
adherence to the algorithm? Structure and clarity
are completely non -negotiable. Successful resuscitation
revolves around rigid adherence to the two -minute
CPR cycle. This is the clock that guides all
team tasks. And the most important job to maintain
quality within that two -minute cycle is the
compressor. Exactly. Compressor rotation must
occur every two minutes. or sooner if the compressor
is visibly fatigued. This rotation ensures that
depth and quality do not degrade. The leader
should anticipate the switch and cue the next
compressor right before the rhythm check so that
transition is seamless. From the perspective
of the documenter or the medication nurse, how
does the team leader use closed -loop communication
to maintain safety and flow? Closed -loop communication
prevents critical tasks from being dropped. If
the leader says, nurse, give 0 .01 milligrams
per kilo of epinephrine, the nurse must respond,
I am preparing epinephrine 0 .01 milligrams per
kilo. And then confirm when it's given. When
the drug is administered, the nurse confirms
epinephrine 0 .01 milligrams per kilo given at
1042 AM, followed by a 10 ml flush. This confirmation
ensures the message was received, the action
was performed correctly, and the documentation
is exact. And what role does the nurse play in
minimizing that critical less than 10 -second
interruption? The nurse is the critical link
between the decision and the action. For a rhythm
check, the defibrillator nurse must have the
pads placed and the required energy to joules
per kilo or four joules per kilo calculated and
precharged before compression stop. Be ready
to go. Be ready. For medication delivery, the
drug must be drawn up, labeled, and placed right
next to the line. The only thing that should
happen during that 10 -second pause is rhythm
interpretation, shock delivery, or drug administration
followed by the flush. Any preparation done during
the pause is a failure of team preparation. We've
covered the core mechanics. Now let's wrap up
with the nice -to -know clinical pearls and the
critical adaptations necessary for special circumstances
that commonly walk through the ER door. The algorithms
look so clean on paper, but in the heat of the
moment, these common errors just emerge. Let's
revisit that timing error in the shockable arm.
The major mistake is drug sequence mistakes in
VFPVT. Because epinephrine is so prominent in
a systole and PEA, there's this tendency to give
it too early in the shockable arm. Remember,
shock one CPR, shock two CPR, then EPI. Electricity
first. You have to give the electrical therapy
priority first. Administering EPI too early can
distract the team and it just violates the principle
of rapid defibrillation for an electrical problem.
What about the physical process of drug administration?
The pitfall here is inadequate flush volume and
speed. So many providers forget the necessity
of that 5 to 10 ml rapid saline flush after IV
or IO drug administration. Right. If you inject
the drug but don't follow it instantly with a
rapid flush during compressions, you are essentially
delaying the drug's effect. Ensure the flush
is done with the same urgency as the drug administration
itself. And the recurring issue of overventilation.
Excessive ventilation rate or volume. You have
to fight the urge to hyperventilate. The detrimental
impact of increased intra -thoracic pressure
on venous return will undermine every single
high -quality compression you perform. Stick
rigidly to that one breath every six seconds
with an advanced airway. Okay, so the core Pallas
algorithm is built for the average child, but
the ER sees critical exceptions. How do we adapt
the framework for trauma arrests? Trauma requires
immediate recognition of specific reversible
causes. Arrest and trauma is often due to hypovolemia
from hemorrhage or obstructive shock, like attention
pneumothorax or tamponade. So the priority shifts?
The priority shifts immediately. Maintain C -spine
control, secure the airway, and for circulation
you have to move immediately past crystalloids
if massive hemorrhage is suspected. Rapid transfusion
of O -negative or type -specific blood products
is essential. And simultaneously, the team must
address those structural issues like attention
pneumothorax with needle decompression. The clock
is running faster here. How about drowning, which
is often linked to severe hypothermia? Drowning
involves severe primary hypoxia and requires
a full court press on oxygenation and ventilation.
If hypothermia is present, with a core temp below
30 degrees Celsius, you have to initiate active
rewarming measures. Warmed for fluids, forced
air warming. And their prognosis. Critically,
CPR should not be terminated early in the severely
hypothermic patient, as they may have exceptional
neuroprotection. However, the heart is unlikely
to respond to defibrillation or pacing until
that core temperature is raised above 30 degrees
Celsius. And for anaphylaxis, which involves
massive vasodilation and airway collapse. Anaphylaxis
requires immediate attention to the airway, standard
dose epinephrine, and aggressive volume resuscitation.
Because that massive histamine release causes
severe vasodilation, which leads to relative
hypovolemia, you have to give rapid large volume
fluid boluses. Not much. We're talking multiple
20 ml per kiloboluses to restore adequate circulating
volume and reverse that distributive shock. Steroids
and H1H2 blockers follow, but volume and epi
are the immediate lifesavers. Let's end with
how this internal rhythm translates into professional
practice. For the nurse designated as the documenter,
what is the best way to record the code so that
the notes become a tool for the team leader,
not just a historical record? Documentation is
the team's external memory and timekeeper. You
have to use the pay less rhythm, that two minute
cycle, as your guide. Every critical action,
a rhythm check, a shock, a drug administration
should be time stamped precisely. If compression
started at 10 .30 a .m., the first rhythm check
is at 10 .32. If epinephrine is given at 10 .33,
the team leader immediately knows the next epi
is due between 10 .36 and 10 .38, which coincides
with the next rhythm check after that. So the
notes should actually anticipate the next move.
Exactly. Clear timestamp records allow the team
leader to look ahead, to calculate the next shock
dose, pre -draw the next medication, and ensure
the team is ready to minimize interruptions.
Good documentation is predictive, not just reflective.
This level of organization is what separates
an experienced critical care team from one that
struggles. We've taken the PAL -S algorithm and
just dismantled it, focusing on the clinical
reasoning that empowers you as the ER nurse.
We learned that the pediatric heart is usually
a victim of hypoxia, making early intervention
and the treatment of H's and T's paramount. We
detailed the two sides of the algorithm, emphasizing
the critical timing of efferine and the necessary
energy escalation for shockable rhythms. Crucially,
we highlighted the non -negotiable nursing task
of that 5 to 10 mL saline flush and the power
of ETCO as your real -time measure of perfusion.
And here is the final thought for you to carry
forward. While PELUS provides the map, the real
skill in the emergency setting is rapid differential
diagnosis in the face of chaos, particularly
when you're dealing with PEA. Never stop asking
why. Was this arrest due to a known cardiac issue?
Was it trauma? Was it an ingestion? The clock
on the algorithm is running, but the diagnostic
investigation has to be running even faster.
Knowing the nuances of special circumstances,
the need for blood and trauma, the aggressive
rewarming and drowning, the massive fluid boluses
and anaphylaxis, that is what allows you to truly
master the resuscitation beyond just the basic
protocol. directly translates into the confidence
required when a sick child arrives, and that
confidence saves lives. You are now equipped
for clinical mastery.