Lecture was prepared by Dr.

Pham
So what does the term ‘shock’ mean to you? It is a broad term describing a
very complex syndrome that affects nearly every organ system of the body.
We often describe patients as shocky, septic, ill-appearing, or the ocassional
‘that kid’s sick.’
So what are we really saying when describe a child with these terms? It all
comes down failure of the cardiovascular system to deliver oxygen and
necessary substrates to end-organs, tissues, and cells. It also includes failure
to remove metabolic end-products to some extent.
Shock ensues when metabolic demands exceed the supply.
This condition is reversible up to a point, after which there is irreversible cell
and organ damage and potentially death. This is why early recognition is so
important, so that we don’t get to this point.
You guys are the ones who are going to see these kids when they present in
clinic or acute care settings, so you have to be the ones who recognize early
signs of shock and begin appropriate therapy.
As pediatricians we all know that children are not little adults. Nowhere is this
more evident than in cardiovascular responses in shock.
Children have higher body water and can preserve their blood pressure
longer, but they also have higher resting metabolic demands, increased
insensible losses, and less effective renal concentrating ability.
Also, early signs and symptoms of shock are more subtle in children, such as
poor feeding, lethargy.
Considering all these factors, children are more susceptible to organ
hypoperfusion.
Let understand some of the basic definition of shock and the
components contribute/affect shock stage

At the bedside, we can measure some

of these things, directly or indirectly.
Did you notice, however, that blood
pressure is not part of the equation?
Shock is multifactorial, but we need to identify a primary cause to prioritize
interventions.
How they “COHDe”: Cardiogenic, Obstructive, Hypovolemic, and
Distributive.
Let’s review some cardiovascular physiology.
What are the components of cardiac output?
What are the components of stroke volume? PRELOAD - AFTER -
CONTRACTILITY
Shock can develop from failure of any of these components. We are going to
talk about each one more when we talk about shock classification.
Dissolved oxygen is miniscule in normal situation but important in certain
clinical situation
critical Do2=maximum oxygen extvraction ratio { 02ER= vo2/do2 = (sao2-
svo2)/sao2 70%
In children and infants, heart rate is the most important determinant of cardiac
output. Stroke volume is pretty much fixed in kids, as they can’t change their
contractility very much. So in the face of decreased preload, such as in
hypovolemia, or decreased contractility, the main way they can maintain
cardiac output is by increasing their heart rate.
So lets talk a little bit about afterload.
pa02 = .21x760
Some other changes that begin to happen in shock are the effect of
hypoperfusion of vital organs and tissues.
Obviously poor perfusion of a vital organ leads to organ dysfunction
STAGES describe the continuum of disease progression
There are different ways to classify shock, which is confusing in itself, but as
you all know patients don’t always read our textbooks. So keep in mind that
not only can patients have more than one type of shock, but that type can
change during the course of their illness.
So first let’s clear any confusion between types and stages.
Stages refers the where the patient is on the continuum of disease
progression. If you did not intervene at all (or sometimes even if you do
intervene) shock will progress from compensated to hypotensive, to
irreversible.
So, note that hypotension is not a finding until the second stage. Therefore we
need to be recognizing and treating shock BEFORE hypotension becomes
evident.
- CO and BP maintained well up to 25% of the decrease in blood volume 
compensated shock. Compensation by slight increase in vascular resistance
to maintain blood pressure
-CO and BP drop abruptly at 30% of decrease in blood volume 
Uncompensated shock
->50% volume loss  irreversible shock
How they “COHDe”: Cardiogenic, Obstructive, Hypovolemic, and
Distributive.
There are 3 main types of shock, according to the mechanism that leads to
decreased O2 delivery. So remember the 3 components of stroke volume?
Afterload, preload, and contractility.
Each type of shock is a result of failure of one of these mechanisms.
So the problem with septic shock is that it can present in a variety of ways.
Only 20% of pediatric patients present with the classic warm shock picture,
which remember is high CO, low SVR, flash cap refill.
Let me also mention that there is a clinical entity called systemic inflammatory
response syndrome, or SIRS, which as the name implies is a widespread
inflammatory response that can arise as a result of infection, trauma, burns, or
other insult.
It is defined as the presence of 2 of the following.
Septic shock is not an entirely different entity, but is a clinical syndrome that
can include features of both cardiogenic and distributive shock. It is often
described as a continuum of disease
Remember I mentioned SIRS earlier?
Septic Shock
SIRS with suspected or confirmed infection with hypotension despite
adequate fluid resuscitation requiring vasopressor support; septic shock
should still be diagnosed if vasopressor therapy has normalized blood
pressure
This is the PALS Shock algorithm, it is on your PALS cards. We start at the
beginning with our initial assessment. Then in the first 5-15 minutes we should
have an idea of what type of shock we are dealing with.
Establish an IV or IO, and begin the first 20 ml/kg bolus of isotonic crystalloid
(NS or LR). If it looks like anaphylaxis give epi. Get a blood gas, if your IV
draws back use that, if not then do a cap gas. What do you want to look at?
pH, lactate, glucose, ionized calcium.
Then reassess after your first bolus. Any improvement in perfusion? If not and
you are not thinking cardiogenic shock, then continue fluid resuscitation up to
60 ml/kg. Stop and re-evaluation, maybe you have more information now?
If you ARE thinking cardiogenic (pulm edema, liver down, gallop) then you
need a pressor.
Remember the ABC’s are still first. When you find yourself in a situation where
it seems like there are too many things to do at once, come back to your
ABC’s.
Delegate work to people. While someone is getting them on a monitor and
getting a blood pressure, begin your initial rapid assessment
KEY FEATURES OF THE CHILD IN SHOCK
While the primary assessment and resuscitation are being carried out, a
focused history of the child’s health and activity over the previous 24 hours
and any significant previous illness should be gained. Certain key features
which will be identified from this – and the initial blood test results – can point
the clinician to the likeliest working diagnosis for emergency treatment.
Evidence of better outcome with aggressive fluid resuscitation; “golden hours”
in sepsis – the first hour of resuscitation
So the PALS algorithm continues, once you have given up to 60 ml/kg of fluid
boluses. At this point we are now in fluid refractory shock, which means that
we need to add a pressor. So lets talk a little about pressors first and then we
will come back to this.
Alpha – stimulate – vasoconstriction – intestinal relaxation – pupil dilatation
stimulat smooth muscle
A1 smooth muscle vascular,visceral – iris A2 ciliary epithelium platlet cns
neurons
Beta relax- vasodilatation – relax bronchi smooth muscles increase HR
B1 myocardium cns neuron presynabs B2 smooth muscle liver myocardium
skeletal muscls cnas
3 main types
When choosing a vasopressor it is paramount to know what type of shock you
are dealing with, and remember this is based on your clinical assessment at
the time, even though you may not know the whole story at this point.
So we need to think about which adrenergic receptor we need and which
pressor will act on it best.
Let’s start with dopamine. Dopamine is still the recommended first line agent
for patients in fluid-refractory shock. It is readily available, usually pre-mixed
and you can start running it through a PIV or IO if you need to, up to 10
mcg/kg/min.
The result will depend on the dose.
There is no evidence for low dose or renal dose dopamine. It is used to be
thought that running dopamine at 2-5 mcg/kg/min would increase renal
perfusion and prevent acute kidney injury, but this is not the case.
There is also growing evidence that suggests dopamine inhibits secretion of
prolactin, which normally inhibits lymphocyte apoptosis. This alteration of the
immune response could be detrimental in sepsis.
Dopamine is still the suggested starting pressor, especially if you don’t yet
have central access. But if you are approaching 10-12 of dopamine, you need
to be thinking about which pressor you are going to change over to.
Milrinone is not technically a pressor, but it is a vasoactive medication that you
will see us use frequently in the unit.
Poorly study in pediatric population.
Hypotension if discontinue abruptly
So here we are back at our algorithm. We have given 60 ml/kg/min without an
adequate response as determined by our physiologic indicators. We have
fluid-refractory shock.
Now we need to begin dopamine at 5 mcg/kg/min, and start obtaining central
venous access and arterial access if possible for invasive blood pressure
monitoring.
If you are approaching 10-12 mcg/kg/min of dopamine with adequate
response, then you have fluid-refractory dopamine resistant shock and need
to change to a catecholamine.
Reassess your patient. Are they cold and clamped-down with diminished
pulses? Begin epi. Are they warm, with flash cap refill and bounding pulses?
Begin norepi.
If epi and NE are not working, then consider whether the patient is at risk for
From this point we are going to be talking about a lot of interventions we can
make, but we need a way to determine if things are working. One of the hot
terms in shock management is ‘early goal-directed therapy’, which refers
resuscitation that is targeted towards improvement of physiologic indicators of
perfusion and vital organ function within the first 6 hours. Multiple studies have
shown that early targeted therapy by primary care/community physicians
improves outcome in shock.
EGDT protocolfrom the trial: They measured 5 parameters:
1.Central Venous Pressure8-12mmHg
2.Mean Arterial Pressure65-90mmHg
3.Urine output >0.5ml/kg/hr
4.ScvO2 >70% (central venous O2 saturation)
5.Hematocrit> 30%
1- CVP: varied depends on where is the catheter. Can use trends to assess
the resuscitation process.
-Low: intravascular depletion
-High: suggests fluid overload

3- Lactate: same outcome as with venous sat monitoring

-Need a reliable free flowing line
Etomidate can suppress adrenal axis up to 48 hrs.
Dexamethasone (0.1 mg/kg) won’t interfere with stim testa
To prioritize your interventions, remember how patients COHDe: Cardiogenic,
Obstructive, Hypovolemic, and Distributive. Your patient’s shock may be
multifactorial, but mentally prioritize what you think is the MAIN cause of the
shock, and deal with that first
“How FAST you FILL the PUMP and SQUEEZE”
 
Sometimes things are not so cut-and-dried.  We’ll use a practical approach to
diagnose and intervene simultaneously.
Look at 4 key players in shock: heart rate, volume status, contractility, and
systemic vascular resistance.
How FAST you FILL the PUMP and SQUEEZE
First, we look at heart rate — how FAST?
Look at the heart rate – is it sinus?  Could this be a supraventricular
tachycardia that does not allow for enough diastolic filling, leading to poor
cardiac output?  If so, use 1 J/kg to synchronize cardiovert.  Conversely, is the