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 taking on one of the most high stakes
information dense and frankly clinically relevant
topics for anyone working in or preparing for
critical care. We're talking about shock management.
If you're studying for your mid -surg cert, getting
ready for the NCLEX, or you just want to feel
confident when that emergency call comes in,
this deep dive is absolutely your shortcut. This
is truly where the rubber meets the road. I mean,
in clinical practice, the immediate informed
action you take when shock is identified It directly
dictates the patient's outcome. There's no room
for hesitation. None. We know that early intervention,
it significantly reduces both morbidity and mortality.
And when you're prepping for an exam, you have
to know the why behind the what. Right. Because
the questions aren't just about defining shock.
They're about prioritizing immediate nursing
interventions based on the specific cause. Absolutely.
And the sources we've aggregated for this are
comprehensive clinical guides. They really provide
the absolute blueprint for rapid assessment and
management. tailored to each type of shock. So
our mission today is a precise extraction. We're
applying what we call the Pareto Principle. We're
distilling that 20 % of clinical data that's
going to yield 80 % of your mastery. And we're
focusing relentlessly on nursing assessment,
those critical facts, and the rapid -fire collaboration
that has to happen in those first few minutes.
We're basically converting those dense algorithms
into clear, actionable steps. We will separate
the fluid -hungry shocks from the ones where
you need to be cautious with fluids. And the
pump failures from the vascular disaster. Exactly.
OK, let's unpack this, starting with the fundamental
goals. Why do we intervene the way we do? You
know, if you really understand the core problem
in shock, the goals of management just become
intuitive. At its heart, shock is just inadequate
tissue perfusion and oxygen delivery. So every
single thing we do is aimed at reversing that
systemic failure. And what are those specific
targets we're aiming for? Well, goal number one,
the primary goal, is to directly improve oxygen
delivery. That means optimizing the blood's oxygen
content and then improving its flow. Second,
we have to balance tissue perfusion with metabolic
demand. Think about it, if the body is burning
through resources faster than we can deliver
them, like with a high fever or extreme pain,
we're losing the battle. So we're not just flooding
the system with oxygen and fluids, we're also
trying to reduce the body's need for them. Precisely.
Third, We need to actively reverse perfusion
abnormalities. That might mean getting blood
out of the capillary beds where it's pooling,
like in distributive shock or overcoming a physical
obstruction. And the ultimate goal. The overarching
life saving goal is supporting vital organ function
and critically preventing the progression to
cardiac arrest. Because once that happens. Once
cardiac arrest occurs secondary to shock, the
prognosis is universally poor. I mean, our window
for effective intervention just closes so rapidly.
This might be the single most crucial area for
nursing mastery then, spotting compensated shock.
That's where the body is hiding the problem,
fighting hard, and is buying us time. So what
happens when those compensatory mechanisms start
to fail? What are the priority cues that tell
us the patient is deteriorating fast? You absolutely
have to recognize that hypotension, a drop in
blood pressure, is a late finding. It's a very
late finding. So if you're waiting for that,
you're already behind. You're way behind. If
the blood pressure is low, The body has already
exhausted its vasoconstrictive reserves, and
perfusion to vital organs is severely compromised.
Waiting for hypotension is waiting too long.
So what should we be laser focused on before
that BP alarm even thinks about sounding? The
signs of failing compensation. The progression
toward hypotensive shock. These are your priority
manifestations. The first sign is often an escalating
and persistent tachycardia. A heart rate that's
just climbing and climbing. Exactly. If the heart
rate is high for their age and it's just getting
higher, it means the cardiac output is failing
and the body's trying to compensate by just increasing
the rate. And as the body clamps down on the
periphery to protect the core, What does that
do to the pulses? You'll see a dramatic contrast.
You'll get diminishing or even absent peripheral
pulses and at the same time weakening central
pulses. This is a major sign that the systemic
vascular resistance, the SVR, is trying to climb,
but the pump volume just isn't there. And you
also mentioned pulse pressure. Yes. You have
to monitor for a narrowing pulse pressure. That's
the gap between your systolic and diastolic.
A narrow pulse pressure, say less than 20 mmHg,
indicates intense peripheral vasoconstriction.
That physical assessment is just non -negotiable.
Cold, clammy skin. That's the classic sign, right?
Yes. Cold, distal extremities with a prolonged
capillary refill. Anything greater than two seconds
is a giant red flag. If it takes three, four,
five seconds for color to return, perfusion is
failing. And what about neurologically? And this
is perhaps the most concerning for the brain,
a decreasing level of consciousness. confusion,
lethargy, decreased responsiveness. That means
cerebral perfusion is dropping. These are the
trends that demand immediate intervention no
matter what that blood pressure reading says.
Okay, so with those warning signs in mind, our
treatment strategies are all about restoring
that blood flow and oxygenation. Exactly. Four
core strategies. Let's start with oxygen content.
We need to maximize the vehicle carrying the
oxygen right, the hemoglobin. Strategy one, optimizing
O2 content. This means immediate administration
of a high concentration of O2, usually 100 %
via a non -rebreathing mask. And if that's not
enough? If the patient has a low hemoglobin,
maybe from a hemorrhage, we have to quickly administer
packed red blood cells, PRBCs, because hemoglobin
determines your oxygen carrying capacity. And
if ventilation itself is the issue, we move quickly
to mechanical ventilation. Strategy two involves
flow and volume. Improving volume and distribution
of cardiac output. This is where your fluid bolus
is going. We're either addressing a true volume
deficit, like in hypovolemia, or a relative one,
like in distributive shock. And if fluids don't
work? Then we move to vasoactive agents to fine
-tune contractility, those are inodropes, or
the vessel tone itself with vasopressors. Okay,
strategy three is minimizing demand. This is
a crucial point. Reducing O2 demand shock states
increase your metabolic needs because of increased
work of breathing, anxiety, pain, fever. So it's
a vicious cycle. It is. So a core intervention
is controlling those factors. We use analgesia,
anxiolytics, antipyretics. Sometimes just putting
a patient on a ventilator drastically reduces
their metabolic burden from breathing. And finally,
strategy four, correcting the chemistry. Correcting
metabolic derangements. As the body shifts to
anaerobic metabolism, acid builds up, glucose
gets depleted, electrolytes shift all over the
place. These chemical imbalances, which we'll
get into, they have to be corrected because they
directly impair cardiac contractility and how
well our life -saving drugs work. All right,
let's move into the hands -on section. When you
walk into the room of a patient in shock, what
are the first steps, the ones that happen almost
at the same time? Right. We assess, monitor,
and intervene, often concurrently. First, let's
talk positioning. If the patient is stable and
comfortable, we can just leave them be. But if
they're unstable or hypotensive, they need to
be placed supine, flat on their back unless this
really compromises their ability to breathe.
Why supine specifically? It just promotes venous
return to the heart. It maximizes the efficiency
of whatever blood volume we do have. And here's
a key detail for your exam. In specific cases,
like neurogenic shock, positioning the patient
flat or even slightly head down can significantly
help improve that lost venous return. Good to
know. OK, next up. airway and oxygenation. We
jump immediately to supplemental O2, high concentration,
aim for 100%. If their work of breathing is increasing,
if they look like they're tiring out, or if they
have that altered mental status, we need to take
over. We have to move fast. The shift to mechanical
ventilation, either non -invasive like CPAP or
invasive intubation, must be rapid. Fatigue and
shock is lethal. And then vascular access. This
is always a point of stress in the ER or ICU.
How long do we spend trying to get a peripheral
IV? Before we move on. You do not waste time.
For compensated shock, sure, a peripheral IV
is fine. But for any patient in hypotensive shock,
or if you can't get peripheral access within,
say, 90 seconds or two attempts. What's the move?
Immediate intraosseous access. An IO is mandatory.
Drill into the bone. Yes. Perfusion is poor.
The veins are collapsed. I .O. access into the
tibia or femur is rapid, it's reliable, and it's
just as effective as a central line for rapid
fluid and drug delivery. This single step can
separate a good outcome from a poor one. With
access secured, we move to fluid. Yes. Isotonic
crystalloids, either normal saline S or lactated
ringers LR. These are the workhorses. The high
yield number we all need to have memorized is
the standard bolus rate. 20 millilaterums over
five to 20 minutes. But the clock is crucial
here for severe hypovolemic or septic shock.
You are pushing that fluid rapidly. You're aiming
for that five to ten minute window. This is where
the nurse's skill in delivery is really tested.
And here comes the critical exception. The smallest
detail that prevents a catastrophe. Cardiogenic
shock. If we even suspect the pump is failing,
giving a huge rapid bolus will drown the lungs
in fluid. So what's the adjustment? The bolus
is smaller and it's slower. 5 to 10 milliliter
alkylidrams over 10 to 20 minutes. The goal is
to gently test the heart's response without causing
pulmonary edema. Let's talk about the physics
of that. As you mentioned, a standard IV pump
is way too slow. If a patient weighs 50 kilograms,
a 20 milliliter alkylidram bolus is a full liter.
How does a nurse get a liter of fluid into a
patient in 10 minutes? This is hands -on nursing.
It's not passive. You have to use a large bore
IV or that IO catheter. You need a pressure bag,
a specialized sleeve that you inflate around
the fluid bag, and it physically compresses it,
forcing the fluid into the patient. And if you
don't have one. If a pressure bag isn't right
there, you use 30 or 60 mL syringes to manually
push the fluid through a stopcock directly into
line. It's labor intensive, it's tiring, but
it's the only way to get true bolus rates of
thousands of mL per hour that you need for resuscitation.
Relying on a standard pump during active shock
is just not enough. The moment that fluid starts
flowing, the continuous assessment begins. We're
looking for trends, not single snapshots, right?
Right. Because no single parameter confirms that
you're resuscitating them adequately. That's
right. And you reassess after every single fluid
bolus. So what are the key positive changes we're
looking for after a bolus? We want to see those
signs of compensation resolving. That means the
heart rate should start declining toward normal
limits. We want peripheral pulses to strengthen
and become less bounding. Capillary refill should
shorten to less than two seconds. The skin should
warm up. And blood pressure. Blood pressure should
increase toward a normal range, but you have
to remember, BP accuracy is really compromised
when perfusion is poor. So don't hang your hat
on that alone. And our key indicator for end
organ perfusion. Yeah. The kiddies. Exactly.
Urine output is a direct measure of renal perfusion
and adequate flow. For infants and young children,
we're aiming for 1 .5 to 2 millipede CHR. For
older kids and adolescents, about 1 LOK CHR.
If urine output is dropping, or zero, a nuria,
hypoperfusion is ongoing. What about the negative
trends? What tells us to stop the fluids? You're
looking for signs of volume overload, especially
in the lungs. The development of crackles or
rails or a sudden, dramatic increase in the work
of breathing suggests pulmonary edema is developing.
And that's the signal to stop. That is the signal
to halt the crystalloids and reconsider the cause.
Maybe we missed a cardiac component. And a foundational
exam fact here. Because assessment relies on
so many parameters, remember that hypotension
is a very late, very grave sign. Relying only
on BP can be really misleading. Let's shift to
the body's chemistry during shock. The failure
to deliver oxygen just turns the internal environment
toxic. What are the four high -yield metabolic
complications we have to anticipate? Hypoglycemia,
hypocalcemia, hyperkalemia, and severe metabolic
acidosis, lactic acidosis. And all four of them
actively make myocardial function worse. Hypoglycemia.
Why is low blood sugar such a danger here? Well,
glucose is the brain's primary fuel, and the
heart muscle relies on it for consistent energy.
In shock, especially septic shock, the body just
burns through its glycogen stores so quickly.
Untreated hypoglycemia can cause irreversible
brain injury and seizures. It has to be ruled
out instantly. Okay, and hypocalcemia. Low calcium,
that seems a little less intuitive than low sugar.
Calcium is absolutely essential for smooth muscle
contraction. That includes the heart and the
blood vessels, what we call vasomotor tone. So
hypocalcemia, low ionized calcium, significantly
reduces your cardiac output, and you frequently
see it after large volume blood transfusions.
Why is that? Because the citrate preservative
they use in packed red blood cells binds to the
patient's calcium, which lowers the free active
calcium levels. It's a key nursing consideration.
when you're transfusing blood rapidly. So this
leads us to mandatory nursing actions. Absolutely.
A rapid point of K glucose check is non -negotiable
for any critically ill patient who presents with
shock or altered mental status. And if we find
it's low, how do we intervene? We give dextrose.
D25W or D10W depending on the patient's size,
but here's that smallest detail that prevents
a new crisis. Never rapidly infuse large volumes
of concentrated dextrous fluids if it's not clinically
indicated. Why not? What's the risk? If you dump
highly concentrated sugar in rapidly, it creates
hyperosmolarity in the bloodstream. This pulls
fluid out of the cells, causes diuresis, and
can actually lead to dehydration and severe electrolyte
shifts, especially hyponatremia. So we treat
the low glucose carefully, not carelessly. OK,
now metabolic acidosis. The result of that anaerobic
metabolism. Lactic acid buildup is the defining
feature. How does the nurse manage that? The
primary intervention is always, always to restore
tissue perfusion. If we can get oxygen flowing
again, the body will start making lactic acid.
Simple as that. But what if it's really profound?
If the acidosis is so profound, with a very low
pH, that it's impairing vital function so the
heart can't contract effectively or the vasopressors
aren't working, we might use buffer therapy.
That means sodium bicarbonate. Yes, but sodium
bicarb is a temporary measure. It's a bridge.
It buffers the excess hydrogen ions, which buys
us time, but it only works until the primary
issue, which is perfusion, is corrected through
fluids and drugs or until ventilation is optimized
to blow off the CO2 it creates. Let's review
the lab studies that guide our therapy. starting
with the CBC. Complete blood count. Look at the
hemoglobin and hematocrit. If HDB and HDAT are
decreased, it suggests hemorrhage or hemodilution.
The intervention there is obvious. Right. Control
the bleeding, maximize O2, transfuse, PRBCs.
On the other hand, an increased white blood cell
count, WBC, immediately makes you suspicious
of sepsis. That means you need to get cultures
and start antibiotics fast. Next, lactate. This
is the gold standard for tracking hyco perfusion,
isn't it? It is. Elevated lactate is the product
of anaerobic metabolism. The intervention is
to improve tissue perfusion. But the critical
application for the nurse is serial monitoring.
Watching the trend. Exactly. We watch for lactate
clearance. If the lactate level is falling, our
resuscitation is working. If it stays high, we
need to escalate therapy, maybe change our agents,
or reassess the source of the shock. Persistent
hyperlactatemia is a sign of refractory shock,
and it carries a very poor prognosis. We mentioned
acidosis that's tracked on the ABG. Barterial
blood gas. A decreased pH in bicarbonate confirms
acidosis. We also look at the anion gap. If it's
widened, that helps confirm it's from... acid
production, like lactic acid. Intervention is
fluids, ventilation support, and maybe that buffer
therapy we talked about. And finally the more
advanced concept, SCVO2. SCVO2 or central venous
oxygen saturation. This measures how much oxygen
is left in the blood returning to the heart.
A low SCVO2, typically less than 70%, means tissues
are extracting too much oxygen because delivery
is inadequate. So you need to increase delivery.
Increase delivery. Transfuse blood, increase
cardiac output. Interestingly, though, a high
SCVO2 over 70 % can also be a problem. You often
see that in warm septic shock where the tissues
can't effectively use the oxygen being delivered.
It's a maldistribution problem. Okay, let's do
a deep dive into hypovolemic shock, the volume
issue. Hypovolemic shock is the most frequent
type you'll see, and it results from a really
simple, direct problem. not enough intravascular
volume. Because the container is the right size,
but the volume inside is low, it's usually highly
responsive to fluids. And the causes are divided
into nonhemorrhagic and hemorrhagic. Nonhemorrhagic
means you're losing fluid without losing red
blood cells. I think GI losses like vomiting
and diarrhea, big fluid shifts from burns, DKA
with its osmotic diuresis or diabetes insipidus.
And hemorrhagic. Hemorrhagic is just acute blood
loss, usually from trauma. The key difference
in management, though the initial fluids are
the same, is the rapid need for blood products
in the hemorrhagic type. Since non -hemorrhagic
shock is often preceded by dehydration, let's
analyze the progression of those clinical signs.
This is where nursing assessment really guides
what you need to do first. We use the estimated
percentage of weight loss as a marker for severity.
Mild dehydration, maybe 5 % loss, often just
presents with slightly dry mucous membranes,
maybe they're thirsty, slight alguria. Was the
diagnostic pitfall there a common mistake? The
pitfall is assuming one sign is definitive. For
example, a child might have dry mucus membranes
just because they're mouth breathing from a stuffy
nose. You have to combine these cues. And skin
turgor is notoriously unreliable in an obese
patient. Right. Moving to moderate dehydration,
about 10 % loss. Now we're seeing clear physical
signs. Yes. The classic signs start to appear.
poor skin trigger, or skin tinting, a sunken
fontanel in infants, marked ulgeria, and that
increasing tachycardia. You might also see quiet
tachypnea, which is the body trying to blow off
CO2 to compensate for a developing metabolic
acidosis. And then the life -threatening stage,
severe dehydration, 15 % loss or more. This is
compensated shock on the verge of complete failure.
You should expect marked tachycardia, weak or
absent peripheral pulses, anuria, no urine output,
and then those late signs we talked about, a
narrow pulse pressure, and eventually altered
mental status and hypotension. Intervention here
has to be immediate IV or IO access and rapid
fluid bolusing. Focusing now on blood loss. Hemorrhagic
shock. The initial management is still that 20
milli uki NS or LR. bolus repeated. But when
do we stop relying just on crystalloids? You
can give up to about three boluses, so 60 milli
-UQA total, before you have to seriously consider
the patient refractory and move on to blood products.
Let's explain the 3 -MLL to 1 -MLL rule. This
is such a critical concept for trauma and hemorrhagic
shock. Why do we need three times the crystalloid
volume for every unit of blood lost? It's all
about where the fluid goes. Isotonic crystalloids,
like normal saline, they don't stay in the blood
vessels. Right, they leak out. They distribute
rapidly throughout the entire extracellular space,
which includes the interstitial space. Only about
a third of what you give actually stays in the
vessels after 30 minutes. So, to effectively
replace one LML of lost blood volume, you have
to infuse three mmL of crystalloid just to make
sure enough stays inside the vessels to raise
the blood pressure. So when do we make the switch
to blood? If hypotension persists, despite those
initial boluses, we immediately switch to packed
red blood cells, PRBCs. We give a 10 millilangmg
bolus. Blood is critical because it replaces
both the volume and the oxygen carrying capacity.
What about the details on emergency blood administration,
the blood type? If the patient is bleeding out
and unstable, you can't wait for a cross match.
You use universal donor blood. Type O negative
is what we prioritize for females of childbearing
age because of rhesus factor concerns. For everyone
else, O negative or O positive can be used. If
the hypotension is severe and they're still bleeding,
you use unmatched blood immediately. You prioritize
saving their life over the small risk of a reaction.
Okay, let's move on to distributive shock. Yep.
The vessel issue. This is the opposite scenario,
right? Yeah. The volume is okay, but the container's
just too Exactly. Massive vasodilation has expanded
the vascular space, which leads to a relative
hypovolemia. Septic shock is the most common
and dangerous example. So with septic shock,
what's happening pathophysiologically? It's an
overwhelming systemic inflammatory response to
an infection. Inflammatory mediators are released,
leading to massive vasodilation, which gives
you a low SVR capillary leak, so fluid shifts
out of the vessels, and sometimes it directly
depresses the myocardium. Our goals are comprehensive,
restore stability, support the organs, and control
the infection. This sounds like it demands rapid
integrated care. What does that interprofessional
management look like in the first hour? It's
a synchronized dance. The MD or DO is focused
on diagnosis, source control, titrating drugs.
Nursing is the absolute driver, securing access,
delivering rapid fluids, initiating monitoring,
making sure drugs are given on time. And pharmacy.
Pharmacy has to ensure those crucial antibiotics
and vasoactive agents are mixed and immediately
available, and you need early subspecialty consultation
infectious disease critical care to make sure
the treatment plan is comprehensive, especially
if the shock isn't responding. So let's get into
the nursing management. The first hour bundle
is basically the law here. The urgency just cannot
be overstated. So what are the interventions
that have to happen immediately, no matter where
the patient is? You have to recognize the signs
altered mental status, perfusion changes, temperature
dysregulation, which can be either very high
or surprisingly low. Right. Then you secure access.
You draw blood cultures and labs immediately.
But the most time sensitive, life saving intervention
is administering adequate broad spectrum antibiotics.
within the first hour of recognition. Don't delay
antibiotics waiting for test results. You treat
empirically. And fluid resuscitation remains
aggressive. Yes. We start the 20 -mL -degylde
isotonic crystalloid boluses and we repeat them.
But you must reassess for signs of overload those
crackles between each bolus. It is very common
for children in septic shock to need 40 to 60
-mL -degyldes, sometimes more, in that first
hour. So what defines fluid refractory shock
and sepsis and what's the immediate nursing intervention
then? If the shock persists despite 40 to 60
milliliter illigerics of crystalloids, it is
by definition fluid refractory. The intervention
is immediate initiation of vasoactive drug therapy
vasopressors. And crucially, you have to consider
hydrocortisone administration if you suspect
adrenal insufficiency. Especially in patients
with a history of chronic steroid use. Especially
then, yeah. Okay, the choice of vasoactive agent
is really high yield because it depends on the
clinical presentation. Are they cold or warm?
This is a classic test question. Cold shock means
the patient has poor peripheral perfusion cold
extremities and often low cardiac alcohol. This
usually suggests severely depressed myocardium
or intense vasoconstriction leading to poor systemic
flow. And for that the preferred agent is epinephrine.
Why epinephrine specifically for cold shock?
Epinephrine is a balanced drug. It stimulates
both alpha -edrenergic receptors, which causes
vasoconstriction and raises SVR, and beta -edrenergic
receptors, which gives you positive inotropic
effects, increasing contractility. So it hits
both problems. It addresses both the pump failure
and the loss of tone, making it ideal for that
cold shock state. And then we have warm shock.
Warm shock is often seen in early sepsis. The
extremities are warm. Cap refill might even be
brisk. But the blood pressure is low, and the
SCVO is often high. This points to profound vasodilation
and maldistribution of flow. So the problem is
vascular collapse. It is. So the preferred agent
here is norepinephrine. Which is known as a pure
pressor, right? That's right. Norepinephrine
is a powerful alpha -adrenergic agonist. It primarily
causes vasoconstriction, which dramatically increases
SVR to combat that massive vasodilation without
significantly jacking up myocardial oxygen consumption
like a powerful inotrope might. We use it to
regain vascular tone. And if both of those primary
agents fail, what are the next lines of defense?
If the shock is refractory to both fluid and
norepinephrine, we might add vasopressin. It's
a non -adrenergic presser that works on different
receptors to increase SVR. And if myocardial
dysfunction is clearly evident, the pump is failing,
we might use milrinone. And what's unique about
milrinone? Milrinone is a phosphodiesterase inhibitor.
It enhances contractility, so it's an inotrope,
but it also acts as a powerful vasodilator, which
reduces afterload. This unique profile is excellent
for improving heart function without forcing
it to pump against extreme pressure. Okay, switching
gears to another distributive issue, anaphylactic
shock. This is life -threatening because of that
rapid release of mediators. What is the non -negotiable
immediate first -line intervention? Epinephrine.
It has to be given immediately, usually IM in
the vastus lateralis, to slow mediator release,
reverse bronchospasm, and stabilize the vessels.
For severe sustained hypotension, a low -dose
IV epinephrine fusion is started to maintain
perfusion. And beyond epinephrine, what does
the rest of the medication approach look like?
We aim to control all the subsequent effects.
So, albuterol for bronchospasm. We use antihistamines,
both H1 blockers like diffenhydramine and H2
blockers like ranadetine, because the combination
is highly effective. And corticosteroids. Finally,
corticosteroids, like methylprednisolone, are
given, not for the acute reversal, but to prevent
the dangerous and unpredictable late phase symptoms
that can occur hours after the initial reaction
seems to have resolved. And fluid replacement
is still needed here because of the capillary
leak, correct? Absolutely. The vasodilation and
capillary leak lead to a significant relative
hypovolemia. So those 20 LLKG NSLR boluses are
necessary. And the key education point for the
family and for your exam is that risk of a biphasic
reaction. About 25 % to 30 % of patients experience
these late symptoms, which means they need prolonged
monitoring, even if they look stable initially.
OK. Last one for distributive. Neurogenic shock.
Neurogenic shock, usually from a high spinal
cord injury, is unique because of its effect
on the sympathetic nervous system. You get that
loss of vascular tone, but it's compounded by
the loss of cardiac accelerator function. And
this gives us that classic triad of manifestations.
Hypotension, a wide pulse pressure, and critically,
bradycardia, a slow heart rate. This is a sharp
contrast to the compensatory tachycardia you
see in almost every other type of shock. So interventions
focus on volume first and then replacing that
lost tone. Right. We start with a trial of isotonic
crystalloid fluids to make sure any hypovolemia
is addressed. If it's fluid refractory, we need
potent vasopressors, norepinephrine or epinephrine,
to artificially restore that systemic vascular
tone. And a vital nursing point for these patients
is temperature regulation. They lose the ability
to vasoconstrict or vasodilate to maintain core
temp, so you often need aggressive supplementary
warming or cooling. We shift now to cardiogenic
and obstructive shock. Let's start with cardiogenic.
This is a fundamental failure of the pump. It
is. It's a failure of the myocardial pump to
generate adequate cardiac output, usually from
cardiomyopathy, severe congenital heart disease,
arrhythmias. Something wrong with the heart muscle
itself. And what's happening pathophysiologically?
The output is low, so pressure builds up in the
venous system because the pump can't push it
forward. Clinically, you see signs of systemic
venous congestion. rails and crackles from pulmonary
edema, jugular venous distension or JDD, and
hepatomegaly and enlarged liver from all that
backup. Given that backup, our fluid strategy
has to change completely. No more 20 -millikio
G boluses. Absolutely not. Cautious fluid administration
is mandatory. Bollaces are smaller and slower.
5 to 10 millikyoji administered over 10 to 20
minutes. And the nurse has to be listening for
those signs of pulmonary edema continuously.
If you hear crackles developing, you stop the
fluid immediately. The risk of drowning the lungs
is just too high. So if we can't use aggressive
fluids, we have to rely on medications to fix
the mechanics. We use medications to reduce the
heart's workload and boost its contractility,
diuretics to reduce preload and congestion, vasodilators
to reduce afterload, the pressure the heart pumps
against, and inotropes like dopamine, dobutamine,
milrinone, or epinephrine are used to increase
contractility. And milrinone seems to be a favorite
here, too. It is because it helps the pump and
eases the afterload at the same time. Interprofessional
management here involves immediate consultation,
I assume. Early consultation with pediatric critical
care and cardiology is non -negotiable. If the
patient is refractory to maximum drug therapy,
mechanical support like ECMO, extracorporeal
membrane oxygenation, becomes the definitive
treatment. Okay, now, obstructive shock. Yeah.
A physical blockage. Right. The pump works, the
volume might be fine, but there is a physical
impedance to flow, reducing venous return or
cardiac outflow. Examples being tension pneumothorax,
cardiac tamponade, a massive pulmonary embolism,
and certain ductal -dependent congenital heart
lesions. The management principle is simple.
Identify and remove the obstruction fast. An
initial fluid bolus might be attempted, but it's
secondary to the definitive intervention. So
delaying treatment to push fluids is a mistake.
A huge mistake. Let's focus on those two immediate
life -saving interventions. First, tension pneumothorax.
Air accumulates, it compresses the lung, and
it pushes the entire mediastinum, including the
vena cava, over to the other side. Venous return
just plummets, and shock ensues rapidly. And
the intervention is immediate needle decompression.
Where exactly is the nurse aiming? You use an
18 to 20 gauge catheter and you insert it over
the rib at the top of the child's third rib in
the mid -clavicular line or the second intercostal
space. This is an emergency procedure that releases
that trapped air and immediately restores venous
return. And the most critical point. This intervention
should not wait for a chest x -ray confirmation.
Clinical suspicion based on unilateral breath
sounds and tracheal deviation is enough to act.
This is followed by a formal chest tube, of course.
Second, cardiac tamponade. Fluid around the heart
squeezes the ventricles, preventing them from
filling. The intervention is pericardiocentesis,
draining the fluid from the pericardial sac.
Okay, and lastly, the unique one, ductal -dependent
lesions. This is a unique form of obstructive
shock seen in newborns. Their circulation relies
on the patent ductus arteriosus, the PDA. If
it closes, either systemic or pulmonary blood
flow is catastrophically blocked. And this requires
a specific drug to keep that ductus open. An
immediate continuous infusion of prostaglandin
E or PGE. PGE is a potent vasodilator that maintains
the patency of the ductus, and it can often reverse
severe shock symptoms within minutes, buying
time until surgery is possible. A nurse has to
have this ready immediately if this diagnosis
is even suspected. All right. We have covered
a massive amount of material. This final summary
is designed to be a rapid recall tool. We'll
focus on the core defect, the fluid rule, the
vasoactive priority, and the single most critical
nursing action for each type. Let's synthesize
these high -yield facts. Let's start with general
shock. The core defect is inadequate tissue perfusion.
Fluid management is a 20 mL -L -Q -G -N -G -N
-S -L -R bolus. Repeat as needed. Vasoactive
agents are used when it's fluid refractory. And
the nursing priority cue is frequent reassessment
after every bolus. Remember, hypotension is a
late sign. Hypovolemic shock. The defect is volume
loss. Fluid management is a rapid 20 mL -L -Q
-G -G bolus using that 3 to 1 crystalloid to
blood loss rule. Vasopressors are generally not
indicated. And the nursing priority is IO access
if peripheral is delayed and transfuse PRBCs
early if it's hemorrhagic. Septic shock. Distributive.
The defect is massive vasodilation and maldistribution.
Fluid management is aggressive boluses, often
40 -60 millilkeragy, plus antibiotics. Vasoactive
priority is epinephrine for cold shock, norepinephrine
for warm shock. And the nursing priority is antibiotics
within one hour, and consider hydrocortisone.
Cardiogenic shock. Defect is pump failure, myocardial
dysfunction. Fluid management is cautious, slow,
small boluses. 5 -10 millikiruging over 10 -20
minutes. Vasoactive priority is inotropes like
milrinone or dobutamine. And the nursing priority
is to monitor for pulmonary edema, those crackles,
and stop fluids immediately if you hear them.
And finally, obstructive shock. The defect is
a physical blockage. Fluid management is an optional
initial bolus followed by definitive treatment.
Vasoactives are not applicable. And the nursing
priority is immediate needle decompression for
attention pneumothorax, or PGE, for ductal -dependent
lesions. That table is the ultimate clinical
roadmap. It really separates the push fluid hard
scenarios from the hold the fluid scenarios.
Knowing that 5 to 10 milnealkio... exception
for cardiogenic shock is just essential to pass
those scenario -based exam questions. We've navigated
the complexities of shock management, prioritizing
the nursing implications and the precise knowledge
you need to intervene effectively and pass your
critical care exams. Remember the urgency of
early intervention, the power of IO access, and
the absolute necessity of reevaluating that fluid
strategy after every single bolus. You know,
if we connect this to the bigger picture... The
rapid shift from compensated to hypotensive shock
is the single most crucial trend the nurse must
anticipate and intervene on. It means you have
to be ahead of the curve, constantly checking
those perfusion parameters, cap refill, pulses,
mental status, not just the BP. And to wrap up
with that final advanced detail that often separates
the expert from the novice, the hydrocortisone
question in sepsis. That's the key clinical pearl
that often determines the outcome in a fluid
refractory septic patient. If a patient is severely
septic and their blood pressure is failing despite
aggressive fluid resuscitation and they're already
on a vasopressor, you have to consider adrenal
insufficiency. Especially with that history of
steroid use. Exactly. If they have a history
of chronic steroid use or features of an adrenal
crisis, giving them stress dose hydrocortisone
is required. If you fail to address this relative
lack of their own endogenous steroids, the vasopressors
we're relying on will be ineffective and the
patient will continue to decline. So keep hydrocortisone
in your mental checklist for refractory septic
shock. A perfect high stakes final thought. Thank
you for joining us on this deep dive into shock
management. You are now armed with the knowledge
to make those life -saving priority decisions.
Go ace that exam.