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 to the deep dive. If
you're joining us, you are probably bracing for
the PLS certification exam. or maybe walking
into a trauma bay right now. Exactly. And you
need that lightning fast, high stakes clinical
decision tree for pediatric arrhythmias. This
isn't just about theory. No, not at all. This
is about saving myocardium. And I mean, at the
end of the day, saving a child's life. So this
deep dive is really for that seasoned critical
care or ER nurse. Right. We're not here to just,
you know, recite algorithms from a card. We are
here to unlock the clinical reasoning, the why
behind every single critical step. Especially
when that heart rate is threatening their stability.
Yes. Our mission is singular, mastering the management
of pediatric arrhythmias. We need to know how
to quickly, and I mean quickly, determine instability
and treat symptomatic bradycardia and tachycardia
before they spiral. Before they go into irreversible
shock or cardiac arrest. Presesimente. And we
have to begin with the non -negotiable foundation
of all pediatric critical care. Before we even
glance at the monitor, before we think about
a drug or a shock, what is the absolute priority?
It's always the ABCs. Airway, breathing, and
circulation. And at the same time, seeking and
treating that underlying cause. That's the step
that really separates the pros, isn't it? It
is. It separates a true critical care provider
from someone who just reads the card. You support
oxygenation. You support ventilation. And then
and only then do you look at the rhythm and decide
if it's the main problem or just a symptom. OK,
so let's really impact this. We're talking about
an abnormal heart rate or rhythm. And pediatric
hearts run faster than adult hearts to begin
with. So what's the critical threshold? What's
that specific line we cross where we go from,
say, monitoring and diagnosing to emergency life
-saving intervention? That line is hemodynamic
instability, an abnormal rate or rhythm because
a true emergency when it's causing significant
cardiopulmonary compromise. And you have to figure
that out in seconds. In seconds. You have to
determine if the arrhythmia is the cause of the
problem or just the result of it. The PLNS guidelines
give us five, you know, need -to -know indicators
that define instability. And these require immediate
treatment. No waiting for labs, no... No waiting
for an expert consult to call you back. You act.
Okay, so let's detail those five signs, but with
a focus on clinical insight. What do they actually
look like at the bedside? Because sometimes these
signs can be pretty subtle, especially in early
shock. Absolutely. So number one is respiratory
distress or failure. If that rapid heart rate
is taxing the body so much that the child just
can't keep up with their own oxygenation or ventilation,
that's an emergency. Makes sense. The second
is shock with poor end -organ perfusion. Now,
this is often associated with hypotension, but
here is the critical clinical parole for you.
Okay. Shock can happen without hypotension. especially
in kids. They compensate like crazy. They clamp
down those vessels to maintain blood pressure
right until the very end. So you can't wait for
the cuff reading? You cannot wait for the cuff.
You look for delayed capillary refill. You look
for cool extremities, thready pulses. You look
for those things before the blood pressure finally
drops. That distinction is huge. I feel like
there's always a tendency to wait for that number
on the monitor, but the kid is often circling
the drain long before that cuff reads low. They
are. So what about the neurological indicators?
The third is irritability, or decreased level
of consciousness, you know, altered mental status.
This is arguably the most powerful early indicator
of poor cerebral perfusion. So a kid who's normally
alert, but is now, what, lethargic? Agitated?
Exactly. A child who suddenly becomes lethargic
or agitated is basically screaming that their
brain is not getting enough oxygenated blood.
Fourth, we look for chest pain or a vague feeling
of discomfort. More common in older kids, I imagine.
Much more common in older kids who can actually
tell you. It signifies myocardial ischemia because
the heart is beating so fast it can't perfuse
itself. And then finally, number five is sudden
collapse. OK. If any of those five are present,
the clock is running and you move straight to
intervention. That makes the nursing priority.
Crystal clear then. If we see symptomatic bradycardia
or tachycardia, box one in the algorithm kicks
in. Walk us through those mandatory initial steps
at the bedside. So these steps have to happen
simultaneously, right, as you're doing your assessment.
First, maintain a patent airway and assist breathing.
That might just be a manual airway maneuver.
A jaw thrust? Simple jaw thrust. Then immediately
provide high concentration oxygen. usually a
non -rebreather, critically establish vascular
access IV or IO immediately. You can't give life
-saving drugs without it. You can't. And if you
even suspect instability, you call for the IO
supplies right away. Don't wait for three failed
peripheral IV attempts. Right. And while the
team is working on ABCs and getting access, we're
getting the monitors ready? Precisely. Attach
the cardiac monitor, the defibrillator, the pulse
oximeter, get them on right away. And here's
where we hit that diagnostic caveat. The 12 lead
ECG. Right. Obtain a 12 lead ECG if available.
But the pay the last guideline is rigid on this.
Do not delay therapy waiting for it. If the patient
is unstable, treatment comes first. Treatment
always supersedes a precise diagnosis in that
moment. You can get your blood pressure, your
blood gas, glucose, tox screens, but urgent intervention
is the priority. The information you get from
a 12 lead does not outweigh the risk of delaying
cardioversion in an unstable kid. That's such
a critical point for the ER nurse. You might
feel this pressure to get the perfect strip for
the cardiologist, but if the patient is seizing
from poor perfusion, the strip is irrelevant
until you fix the rhythm. Exactly. Stabilize
the patient first. Don't worry about perfecting
the paperwork. OK, let's move on. Here's where
we make a really fundamental physiological distinction.
Radycardia in an adult, that's often a primary
electrical failure, right? Like sick sinus syndrome
or a block. Right. But in kids, it's a totally
different ballgame. It is fundamentally different.
Pediatric bradycardia is usually secondary to
a respiratory or metabolic issue. It's that late
bad sign that profound hypoxia has set in. That
is the core clinical truth, isn't it? It is.
You have to remember, pediatric cardiac output
is highly rate dependent. They rely on a high
heart rate to move volume around. They can't
increase their stroke volume like adults can.
Exactly. So when that rate slows down, it means
the heart muscle is exhausted or it's ischemic
or it's been poisoned. The pediatric bradycardia
algorithm is specifically structured to treat
that secondary cause first. So when you hit the
algorithm, you immediately reassess for compromised
hypertension, altered mental status, signs of
shock. And if it's there, you move fast. You
go very fast. Let's talk about the ultimate red
flag in this algorithm, the CPR trick. That's
box three. If everything we've done to improve
oxygenation and ventilation has failed, when
do we actually start chest compressions on a
child who still technically has a pulse? This
is a decision point that gives a lot of providers
pause, but Paul is very clear on it. If bradycardia
persists, and we define that as a heart rate
less than 60 beats per minute. A hard line at
60. A hard line at 60. If it's under 60 despite
adequate oxygenation and ventilation, You start
high quality CPR immediately. Because a persistent
rate below 60 in a symptomatic child means the
heart is failing to generate enough cardiac output
to sustain life. External circulation is now
required. The lack of oxygen has depressed the
myocardium so severely that the body just can't
compensate anymore. two minutes and we're sure
their respiratory effort is supported, we compress.
You compress. Let's quickly review the metrics
for high quality CPR because execution here matters
so much more than intention. These are foundational
facts you have to know cold. Push fast. 100 to
120 compressions per minute. Push hard. Yeah.
At least one third the depth of the chest. Which
is about 1 .5 inches in an infant or two inches
in a child. Right. And you have to ensure complete
chest recoil. Minimizing interruptions is vital.
Aim for a compression fraction of at least 60%.
And the ventilation ratio. If you're manually
ventilating, it's 15 .2 for two providers, or
30 .2 if you're a lone rescuer, that is, until
they're intubated. After that, compressions are
continuous and you give breath every two to three
seconds. Okay, so once we're doing high quality
CPR because of persistent bradycardia, we move
immediately to the drugs. And the primary drug,
the heavy hitter, is epinephrine. Epinephrine
is the central nervous system drug in cardiac
arrest and severe bradycardia. Its mechanism
is beautifully dual. And if you understand this,
you understand why it's the first choice. OK.
Think of the alpha effect as tightening the pipes.
Vasoconstriction. Exactly. Vasoconstriction.
This increases systemic vascular resistance,
which raises aortic diastolic pressure. That
is crucial for perfusing the coronary arteries
in the brain. Then you have the beta effect.
The beta effect is speeding up the pump. Speeding
up the pump. It increases heart rate and cardiac
contractility. So this simultaneous action supports
both oxygenation and perfusion when that myocardium
is just completely compromised. So we're not
just trying to make the heart beat faster. We're
trying to literally squeeze the arteries to drive
blood back into the heart muscle itself. You
have to get that coronary perfusion pressure
up. The indication is clear. Symptomatic bradycardia
that persists despite effective oxygenation,
ventilation, and CPR. And the dose. The standard
IV or IO dose is 0 .01 millochi kilogram. That's
0 .1 millochi IG of the standard 1 .00 concentration.
And you repeat that dose every three to five
minutes. And you have to be strict with that
timing. You have to be. Stick to that three to
five minute interval. What about the less reliable
route, endotracheal? The ET route. Absorption
is unreliable. It's inconsistent. and it needs
a much higher dose. If you have absolutely no
IV or IO access, the ET dose is 10 times higher,
0 .1 milliliter kilogram. But that's a last resort.
It has to be a rescue ride only. Your priority
is to get IO access immediately. Okay, next up
is atropine, the parasympathetic. Its role is
very specific in PAELs. Very specific. Atropine
sulfate is an anti -colonergic drug. Its mechanism
is to accelerate the sinus or atrial pacemakers
and enhance AV conduction by blocking vagal tone.
So it's the drug of choice for bradycardia that's
specifically caused by increased vagal tone.
Right, like from intubation attempts or surgical
stimulus or poisoning by colonergic agents or
for a primary AV block. You mentioned before
why epinephrine is generally preferred over atropine
in the sort of general symptomatic bradycardia
algorithm. Can you just reiterate that for us?
Yeah. I mean, if the child is profoundly hypoxic
or ischemic, atropine won't fix the underlying
problem. The muscle is just too sick. Epinephrine's
broader ALSA and beta effects are just superior
for that generally compromised myocardium. So
if the child doesn't respond to atropine? You
pivot. You pivot immediately to epinephrine and
compression. Atropine is a targeted drug for
a very targeted cause. What's the dose for atropine?
It's 0 .02mg in kilogram IV or IO. You must respect
the minimum dose of 0 .1mg. If you give less,
you can get a paradoxical slowing of the heart
rate. Oh, wow. Yeah. And the maximum single dose
is 0 .5mg. You can repeat it once. And the clinical
pearl about its use in heart blocks? Atropine
may be useful for a symptomatic second degree
AV block. Either Mobitz is the first, and third
degree AV block. But, and this is a big but,
if the block is low down in the bundle of his
or the Purkinje Fibers Atropine is unlikely to
work. And then you're looking at pacing. Then
you need to prepare for transcutaneous pacing,
which is... Honestly, very challenging in pediatric
patients and usually a bridge to getting transvenous
pacing after they're stabilized. Okay, now we
get to what I think is the core of critical nursing
in PALS. If we give epinephrine without fixing
the root problem, the code is going to fail.
We have to master the H's and T's. This is everything.
What are the two most common potentially reversible
causes of pediatric bradycardia that we see in
the trauma bay? Hypoxia and hydrogen ion, which
is acidosis. If a child's rate drops below 80
or certainly below 60, your first thought has
to be their airway and their breathing. Those
two have to be addressed aggressively. Immediately
and aggressively. So let's run through the full
table of reversible causes. Give us the why and
the specific treatment for the ER nurse on the
front line. Okay, for hypoxia, the treatment
is foundational. Give high concentration supplementary
oxygen with assisted ventilation. You must ensure
the chest rises symmetrically and that the pulse
ox improves. And if it doesn't? If it doesn't,
you check for a misplaced tube or a foreign body
obstruction. You troubleshoot that airway. Okay,
next. Hydrogen ion. Acidosis. Right. Remember,
acidosis depresses myocardial function. It makes
the heart muscle weak. So you treat the respiratory
component first. You provide ventilation to blow
off CO2 and correct that respiratory acidosis.
What about sodium bicarbonate? Sodium bicarb
may be considered in a severe documented metabolic
acidosis or for hyperkalemia, but you always
ensure ventilation is maximized first. Bicarb
generates CO2, and if you can't ventilate that
out, you paradoxically make the intracellular
acidosis worse. Good point. Okay, moving to electrolytes
hyperkalemia. We see this in renal failure or
severe crush injuries. Why does it cause such
profound bradycardia? I potassium hyperkalemia.
It destabilizes the cardiac cell membrane. On
the ECG, you'll see those classic tall peak T
waves followed by a widening of the QRS and then
ultimately a sine wave arrest. And the treatment
is multifaceted. Very. You have to stabilize
the myocardium first with calcium chloride or
calcium gluconate that protects the heart from
the potassium. Then you shift the potassium back
into the cells using insulin and dexrose and
potentially sodium bicarb or albuterol. But calcium
is the immediate lifesaver. Calcium is the first
thing you give. It's the immediate lifesaver.
Next, temperature. Hypothermia. I feel like this
is an often ignored cause, especially if the
patient was found down. It is. If the child is
hypothermic, you have to warm them gently but
effectively. Core temperatures below 30 degrees
Celsius make the myocardium highly irritable
and refractory to standard resuscitation drugs.
So you defer shocking and drugs. You defer shocking
and drugs until the core temp is above 30 degrees
Celsius, if possible. And you have to be careful
not to trigger dysrhythmia by moving the patient
roughly during warming. That cold myocardium
can flip into VFib very easily. OK. Then we have
the massive category of toxins, poisons, and
drugs. How do we even begin to narrow the treatment
here? This requires a highly specific antidote
or very targeted supportive care. If it's a calcium
channel blocker or beta blocker overdose, your
first line therapy is often high -dose glucagon,
calcium, or high -dose insulin euglycemic therapy,
not just epi. And opioids. If it's an opioid
overdose, you give Narcan. You have to ask about
recent medications, access to drugs, or suicidal
ideation immediately. Finally, the warning sign
in the neuro or trauma patient, bradycardia associated
with the head injury. This is the classic Cushing's
Reflex Hypertension, bradycardia, and irregular
respirations. It signifies severe increased intracranial
pressure or ICP. So the body is clamping down
the arteries to try and force blood into the
skull. causing the hypertension, and that high
blood pressure triggers a reflex slowing of the
heart rate. So the bradycardia is actually a
protective mechanism, even though it's failing.
What's the nursing intervention? Your first steps
are oxygenation and ventilation. If there are
signs of impending herniation, like pupillary
changes or posturing, a brief period of mild
hyperventilation can be used as a temporary rescue
therapy to acutely decrease that ICP. But ultimately,
this child needs a surgeon. The bradycardia isn't
a heart problem. It's a brain problem. You have
to treat the head. Okay, switching gears completely
to fast rates. With tachycardia, speed matters.
A heart rate that's too fast doesn't allow enough
diastolic filling time, and that leads to shock
really fast. Right. PLS is very clear here. If
the child is unstable, do not delay emergency
treatment while you wait for an expert consult.
The initial management is still your ABCs, monitoring,
and getting vascular access. The problem here
is that the rapid rate reduces stroke volume
so drastically that cardiac output just falls
off a cliff. So unlike bradycardia, where we
focus on the secondary cause, with tachycardia,
we're really focused on the rhythm itself if
it's pathological. Exactly. The critical moment
in the tachycardia algorithm is box two. Evaluate
the QRS duration. This immediately splits our
pathway and dictates our entire therapeutic approach.
It does. The QRS duration tells us where the
electrical impulse is coming from. If it originates
above the ventricles, the path down is normal
and fast, so you get a narrow QRS. And if it
originates in the ventricles? Then the path is
slow and aberrant and you get a wide QRS. So
an narrow complex is defined as less than or
equal to 0 .09 seconds. This suggests probable
sinus tachycardia or supraventricular tachycardia
SVT. And a wide complex is greater than 0 .09
seconds. Which is presumed ventricular tachycardia
VT or maybe SVT with some aberrant conduction.
Okay, let's talk about the stable patient. If
the child has good pulses, good perfusion, their
mentation is intact. We have a little bit of
time, precious time to think and differentiate
between sinus tach and SVT. And this distinction
is the single most common diagnostic error I
see in the PEDS ER. I believe it! It is! Because
if you treat ST like it's SVT, you're treating
the compensation, not the problem, and you risk
a really serious error. So we have to distinguish
them. OK, let's nail down those differentiating
factors. Sinus tachycardia, or ST, is compatible
with a known cause. Fever, pain, anxiety, dehydration.
You look for normal P waves. Crucially, the R
to R interval is variable. The heart rate speeds
up and slows down. It does, depending on the
child's activity or hydration. And the rate limits
are usually less than 220 in infants and less
than 180 in children. ST is the heart just doing
its job to compensate. Okay, and SVT is the pathological
one, the sudden rhythm. SVT is sudden onset.
The history is also not compatible with ST. The
heart rate is usually constant and does not vary
with activity. The RR is fixed? It's fixed. P
waves are usually absent, or they're merged with
the QRS, or they look abnormal, and the rates
are extreme. Usually 220 are greater in infants
and 180 are greater in children. If the rate
is that high and it was sudden, it's SVT until
you prove otherwise. So if it's sinus tachycardia,
we have to resist that urge to slow the heart
down with drugs. You absolutely have to. You
treat the cause. You give a fluid bolus if they're
dehydrated or acetaminophen if they're febrile.
You do not give adenosine or other antiarrhythmics.
If you do, you take away the child's essential
compensatory mechanism and you risk sending them
into shock. But if we have stable SVT, we move
to rhythm control, starting with vagal maneuvers.
Always attempt these first. They stimulate the
vagus nerve and slow down that AV conduction.
If they work, they terminate the rhythm instantly.
No drugs needed. But the technique is very age
dependent. So what are the specific nursing coaching
techniques here? For infants, the safest most
effective method is the ice water facial immersion.
You place a bag of ice water over the upper half
of the face for about 15 to 20 seconds. But don't
cover their nose or mouth? Critically, do not
cover their nose or mouth. For older children
who can follow directions, the modern approach
is a modified Valsalva maneuver. How does that
work? You have them blow forcefully into a 10
millil syringe trying to move the plunger, or
through an obstructed straw for 15 seconds while
they're lying flat. And then you immediately
raise their legs up to 45 degrees for another
15 seconds. That combination significantly increases
the success rate. Okay, if vagal maneuvers fail...
We move to the definitive drug for stable SVT,
Adenosine. Adenosine is the drug of choice for
reentrant SVT. Its mechanism is pretty dramatic.
It blocks conduction through the AV node and
temporarily stops the heart. Let's spend some
time on the dosing and maybe more importantly
the nursing technique. This is where clinical
failure so often happens. It really is. Dosing
is 0 .1mgkg IV or IO with a max first dose of
6mg. If it's ineffective, you immediately give
the second dose, 0 .2mgkg with a max second dose
of 12mg. And the technique is everything. It's
paramount. A tenocene has an incredibly short
half -life, less than 10 seconds. You must use
a central or proximal IV line if you can. You
give the doses a rapid IV bolus and you follow
it immediately with a rapid flush of 5 to 10
milliliter of normal saline, elevating the arm
at the same time. This just shoves the drug into
the central circulation so it can get to the
AV node before it gets metabolized. Okay, now
let's shift to the wide QRS, greater than 0 .09
seconds, but in a stable patient. This is presumed
VT until proven otherwise, and the stakes just
immediately go up, even if the patient looks
okay for the moment. A wide QRS strongly suggests
a ventricular origin, which carries a high risk
of degenerating into VFib. If the rhythm has
a uniform QRS morphology and a regular RR interval,
and the patient is stable, we treat it as VT.
This situation, box 12 demands immediate expert
consultation. A cardiologist or an ICU doc? Yes,
but you have to start treatment while you're
waiting for them to arrive. And provided the
patient is truly stable, we consider pharmacologic
conversion here. Yes. The primary drugs are amiodarone
or prokanamide. You consider amiodarone at 5
millijoy kilogram given IV or IO, but slowly,
over 20 to 60 minutes. Or, prokanamide at 15
millijoy kilograms infused over 30 to 60 minutes.
The key word here is slow. Why slow? Because
these drugs can induce pretty severe hypotension
and just make the situation worse if you push
them too fast. What about the absolute caution
regarding combining these two powerful drugs?
This is a huge safety concern. Do not routinely
administer amyterone and procainamide together.
Both are strong sodium and potassium channel
blockers, and they both prolong the QT interval.
So you get an additive effect. A very dangerous
additive effect. You significantly increase the
chance of inducing a lethal rhythm, specifically
polymorphic VT or torsades de pointes. If one
fails, you can switch to the other, but you never
combine them. And what about using adenosine
in a wide complex tachycardia? I know a lot of
providers get tripped up there. It's high risk.
I mean, if the wide complex rhythm is truly VT,
adenosine won't terminate it, and it might even
accelerate it, which is dangerous. The only time
you might even consider it is if you have really
strong evidence that the rhythm is actually SVT
with aberrancy. Meaning the patient has a pre
-existing bundle branch block or something? Exactly.
But honestly, if you're not sure, you treat the
wide QRS as VT, you use the designated antiarrhythmics,
or you prepare for cardioversion. And this is
that critical transition. When the stable tachycardia
patient suddenly becomes unstable, poor perfusion,
hypotension, signs of shock, we skip all the
drug trials. We move straight to electricity.
Time is myocardium. That's right. When we hit
cardiopulmonary compromise, we go straight to
synchronized cardioversion. This is the definitive
intervention for hemodynamically unstable SVT,
atrial flutter, or VT with a pulse. It takes
seconds, not minutes, to deliver. Now, cardioversion
is a painful procedure, so how do we balance
the need for sedation and analgesia with the
urgency of delivering that shock? That is the
art of critical care, right there. If the patient
is unstable and has a depressed level of consciousness,
you skip sedation and you shock immediately.
And if they're awake? If the child is unstable
but awake, you should quickly deliver a rapid
sequence, analgesic or sedative, something like
ketamine or midozolam. if it's available, but
the pay -alist instruction is firm. You do not
delay the shock waiting for the sedation to kick
in or for the perfect airway setup if the patient
is crashing. A brief moment of pain is worth
avoiding a full -blown cardiac arrest. Absolutely.
Let's focus on the energy dose. It's lower than
for V -fib defibrillation. Right. Cardiaversion
requires less energy because we're just trying
to reset the electrical rhythm, not completely
depolarize the entire heart. The initial dose
is 0 .5 to 1 joule. per kilogram. And if that
doesn't work? If that shock is ineffective, you
have to increase the dose for the next attempt.
You escalate to the second dose of two joules
per kilogram. Always use the lowest effective
dose. Okay, now for the critical nursing steps
for synchronized cardioversion. What are the
common pitfalls you see that jeopardize the shock?
Pitfall number one. And it's a big one, not selecting
synchronization. You have to turn on the defibrillator,
select your pads, and most importantly, select
the synchronize mode. And you have to see the
sync marks. You must look for the sync marks
to appear above the R waves on the monitor. If
you can't see them, increase the gain or switch
leads until you can. And if you can't see them
and you shock anyway, what's the risk? The machine
will deliver an unsynchronized shock. That means
the energy could land exactly on that vulnerable
period of the T wave. R on T phenomenon. Exactly.
Hitting the T wave can induce ventricular fibrillation,
turning a salvageable rhythm into a full cardiac
arrest. Confirming synchronization is a mandatory
safety check. OK, sync is confirmed. We charge
and deliver. You announce charging defibrillator,
make sure everyone is clear, and crucially, you
have to hold the shock button down until it delivers.
The machine is waiting for the next R wave. If
you press and release too quickly, it won't fire.
And then immediately after. Immediately after,
you check the monitor. If VF develops a total
catastrophe, you must immediately turn off the
synchronization mode and proceed to unsynchronized
defibrillation and CPR. And remember, the defibrillator
defaults back to unsynchronized mode after every
shock. You have to reselect synchronization for
every subsequent cardioversion attempt. Okay,
let's dedicate this section to the high -level
nursing implications of our PANS drug arsenal.
We've covered the doses. Now let's focus on the
how and the what to watch for. The titration,
the side effects, the complex stuff. Great idea.
Let's start with adenosine for SVT. So we know
adenosine blocks conduction through the AV node
and causes that transient assistal. The nursing
management is all centered around its rapid decay.
That half -life is so short, you need to use
a three -way stopcock or a proximal port. Pushing
the drug, spinning the stopcock, flushing immediately.
Rapidly, yes. What should the nurse warn the
patient or the family about, especially if the
child is conscious during this? The child will
likely feel a sensation of profound momentary
chest pressure or dizziness as their heart stops.
You have to warn them about this brief cardiac
standstill which lasts maybe 10 to 15 seconds.
explain that it's necessary to reset the rhythm.
That anxiety management is key. And you're glued
to the ECG monitor. Continuous ECG monitoring
is essential. If the SVT converts, your immediate
priority is monitoring for recurrence. Okay,
Omiodurone for a wide QRS. It's a complex drug.
For the nurse, what are the primary concerns
when you're infusing this for a perfusing VT?
Amidurone affects pretty much everything, sodium,
potassium, calcium channels, and it has anti
-adrenergic properties. So our immediate concerns
are twofold. First, hypotension. Okay. Rapid
administration, even over 20 to 60 minutes, can
cause significant peripheral vasodilation and
decreased contractility. You have to monitor
their blood pressure every five minutes during
that infusion. And the second major concern related
to its mechanism. The second concern is related
to its effect on potassium channels, QT prolongation.
Amiodarone increases the risk of dangerous arrhythmias,
particularly torsades to point. The nurse has
to ensure the patient isn't also hypokalemic
or hypomagnesemic, because those electrolyte
issues just exacerbate the risk of torsades.
Right, and the dose is 5 mg of a kilogram IVIO
infused slowly. Very slowly. The slower the better
if they're perfusing. And remember, the maximum
cumulative dose is 15 mg per day. Okay, prokainamide.
Our other strong option for wide QRS, how does
its mechanism, mainly sodium channel blockade,
translate to different nursing management concerns
compared to amiodarone? Procatamide primarily
blocks a sodium channel, so it slows conduction
velocity and it prolongs the QRS duration. It's
highly effective, but it comes with significant
risks. The main nursing focus is just preventing
toxicity by infusing it slowly. So you're infusing
15 milligrams over 30 to 60 minutes. Right. What
are the key signs of procatamide toxicity that
would make you stop the infusion immediately.
The three big ones are hypotension just like
amiodarone and then excessive QRS or QT interval
prolongation. If the QRS complex widens by 50
% or more from baseline Or if it widens to greater
than 0 .12 seconds, you stop the infusion immediately.
Because that's a sign of dangerous conduction
depression. Exactly. And again, the combination
of amiodarone and brocanamide is strictly avoided
because of that additive QT risk. Okay, let's
touch on magnesium and sodium bicarb. These have
really specific roles, often tied to the H's
and T's. Right. Magnesium sulfate is specifically
indicated for two situations, torsades de pointe,
that polymorphic VT, and severe refractory asthma.
It acts as a physiologic calcium channel blocker,
and it's crucial for stabilizing the membrane
when torsides is present. And sodium bicarb.
Sodium bicarbonate is used to treat severe documented
metabolic acidosis or specific drug overdoses,
like presciclic antidepressants, where it helps
narrow the QRS and counter that tartar toxicity.
But remember, it's not a generalized drug. Maximize
ventilation first. Finally, let's address the
drug that must be avoided in a specific pediatric
population and explain the critical physiological
why. Varepamil. It's a calcium channel blocker,
and it should not be used routinely to treat
SVT in infants. This is a Palau certification
deal -breaker question. And the physiological
reason is profound. It is. Infants, especially
those under one year, are highly rate dependent,
and they rely heavily on adequate cardiac contractility.
They're anotropy. Calcium channel blockers kill
contractility. So when you combine that severe
decrease in squeeze with a rapid SDT -induced
rate, you cause immediate refractory hypotension
and cardiac collapse. It's just too risky. Far
too risky in that age group. In older children,
if it's used for stable SVT that's resistant
to adenosine, it requires an immediate cardiologist
consult. Okay, this is where we bring the textbook
back to the bedside. We've covered the mechanics,
but algorithms fail when humans make high pressure
errors. Let's talk about the common traps and
pitfalls we see in real -life codes. The algorithms
are clear, but clinical pressure definitely warps
decision -making. Let's start with the bradycardia
trap. The natural instinct is to grab the epinephrine
when you see that heart rate dropping. And that's
the trap. You see a low number on the monitor
and you react to the monitor. But you have to
remember Pediatric bradycardia is almost always
a sign of a ventilation or oxygenation failure
first. So don't jump to epinephrine. Don't jump
to epinephrine if you haven't maximized oxygenation
and ventilation. I remember a case where the
teen treated the low heart rate first, forgetting
the patient was profoundly hypoxemic from an
unsecured airway. The pump was pressed, but the
gas tank was empty. Exactly. Always maximize
your ABCs first, then compress or medicate. Then
there's the more subtle but equally dangerous
tachycardia trap. Mistaking ST for SVT. This
is where treating the patient, not the monitor,
is absolutely paramount. Sinus tachycardia is
a sign of an underlying systemic illness sepsis,
hemorrhage, severe dehydration. And if you mistakenly
treat that with adenosine? You interrupt the
child's attempt to maintain cardiac output via
rate. You've taken away their only coping mechanism.
You have to treat the underlying cause -give
fluids for dehydration, blood products for hemorrhage.
A continuous ECG should show that heart rate
coming down as the underlying issue is resolved.
And the cardinal sin during electrical intervention,
the cardioversion mistake. Forgetting to hit
the sync button. It seems so obvious when we're
sitting here talking about it, but in the chaos
of a code, providers forget. And the result is
a potentially harmful unsynchronized shock. Right.
Risking induced V -fib. Always confirm those
sync marks are visible before you charge and
deliver, and remember to check it again after
the first shock, as the machine always reverts
back to unsynchronized mode. As the ER nurse,
documentation is essential for quality improvement
for legal defense. What are the absolute essentials
that have to be captured during a high stakes,
tacky, or bratty event? We need objective evidence
of the rhythm and the interventions effect. So
that means an ECG strip before and after every
single intervention. Bagel maneuver, every drug,
every shock. Every single one. For adenosine,
you have to record the exact timing and dosage
and the precise size of that flush, like six
milligram adenosine followed immediately by 10
milliliter LNS flush. For electrical therapy,
the exact energy dose for every single attempt
is mandatory. So what's the final thought we
leave the ER nurse with as they're walking into
that critical situation? When you're managing
pediatric arrhythmias, you have to master the
distinction between adequate and poor perfusion.
That single assessment determines your timeline.
Poor perfusion means you have seconds. You have
30 seconds to deliver a life -saving shock or
start compressions. If perfusion is adequate,
you have little time for precise diagnosis, for
an expert consult, for non -electrical interventions.
Use that QRS split wide versus narrow to narrow
your drug choice. And never forget that pediatric
bradycardia is most often airway problem disguised
as a heart problem. We covered a tremendous amount
of ground today. The critical signs of instability,
respiratory failure, shock with or without hypotension,
and altered mental status. We emphasize that
in bradycardia, the ABCs come before drugs, and
that a persistent bradycardia below 60 means
immediate, high -quality CPR. Yes. We broke down
the critical QRS split, the high -stakes technique
of synchronized cardioversion, and detailed the
crucial nursing implications for amiodarone and
procainamide. And if you take one lesson away
from this... Let it be this. Always remember
the reversible causes of bradycardia. Often the
best cardiac care you can provide is swift and
effective pulmonary care. Good ventilation and
oxygenation. Exactly. Never forget that the child's
slow heart rate is usually their body's final
desperate attempt to survive hypoxia. The solution
is often right there in your hands managing the
airway and breathing long before you ever reach
for the epinephrine. An excellent point to end
on. Thank you for going on this deep dive with
us, focusing on the details that truly matter
when facing critical pediatric arrhythmias. Stay
sharp out there.