PEDIATRIC

SHOCK
2012

SHOCK

Shock is a syndrome that results

from inadequate oxygen delivery to
meet metabolic demands
Sequelae of shock are metabolic
acidosis, organ dysfunction and
death

SHOCK-OXGEN SUPPLY FAILS TO MEET OXYGEN

DEMAND
OXYGEN
SUPPLY

OXYGEN
DEMAND

OYGEN
DELIVERY

CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT

Cardiac
Output

Heart rate

Arterial oxygen content

Stroke Volume

Preload
After load
Contractility

Hemoglobin
Oxygen Saturation
Partial pressure of oxygen dissolve
plasma

Oxygen Delivery

Oxygen delivery=CO X Arterial

oxygen content
CO=Heart rate X Stroke volume
Stroke volume depends on preload,
afterload and contractility
Art Oxygen content= Hb x Sa02 x
1.34 +(0.003 x Pa02)

Factors affecting Oxygen

delivery

Oxygenation-A-a gradient, DPG, acid

base balance, Temp, Blockers
Stroke volume-Ventricular
compliance, CVP, venous tone,
autonomic tone, metabolic milieu,
afterload, conduction system

Types of Shock

Hypovolemic- Hemorrhage, serum or plasma

loss
Distributive-Anaphylactic, Neurogenic, septic
Cardiogenic- Myocardial, dysrrythmia,
CHD(duct dependant)
Obstructive-Pneumo, tamponade, dissection
Dissociative-Heat, CO, cyanide, endocrine

RJ has Hypovolemic shock secondary to

Hemorrhage

Case 1
9 year old girl RJ with a history of variceal bleed
presents with new onset bleed. O/E-responsive,
HR-135, RR-38, BP-88/60, Sats-92%. I stat7.08/24/80/12/-4. Hb-4.2
What type of shock is this?
Hypovolemic Shock
What is the very first thing you would like to do
for this patient?
Oxygen
Is this compensated or uncompensated shockhow does the body compensate?
Compensated

Stages of Shock

Compensated- Vital organ function

maintained, normal BP
Uncompensated-Marginal microvascular
perfusion.Organ and cellular function
deteriorate. Hypotension develops.
Irreversible

RJ has compensated shock because her

blood pressure is normal

Compensatory
Mechanisms

Baroreceptors-In aortic arch and

carotid sinus, low MAP cause
vasoconstriction, increases BP, CO
and HR
Chemoreceptors- Respond to cellular
acidosis, results in vasoconstriction
and respiratory stimulation

Compensatory
Mechanisms

Renin Angiotensin- Decreased renal

perfusion leads to angiotensin
causing vasoconstriction and
aldosterone causing salt and water
retentions
Humoral Responses-Catecholamines
Autotransfusion-Reabsorption of
interstitial fluid

RJs Clinical presentation

Diagnosis is based on exam focused on tissue

perfusion
Neurological-Fluctuating mental status
Skin and extremities-Cool, pallor, mottling,
cyanosis, poor cap refill, weak pulses, weak
muscle tone
Cardio-pulmonary-Hyperpnea, tachycardia
Renal-Scant, concentrated urine
Abject hypotension is a late and premorbid
sign( and is the flag for uncompensated shock)

Hypovolemic shock

Commonest cause worldwide

Decreased blood volume, decreased
preload, decreased stroke volume
Signs of dehydration-tears, mucous
membranes, skin tugor
Site of fluid loss may be obvious or
concealed(liver, spleen, intracranial,
GI)

Oxygen-What a
difference!

Art Oxygen content= Hb x Sa02 x 1.34

+(0.003 x Pa02)
Pa02 on 100% is approx 650
Pa02 on room air is approx 100
If your Hb is 15 this difference in PaO2
does not make much difference- if your
Hb is 5 it makes all the difference!

RJs Management

Increase oxygen delivery, decrease oxygen

demand
Oxygen
Fluid
Blood
Temperature control
Correct metabolic abnormalities
Inotrope if needed

Labs

ABG
Blood sugar
Electrolytes
CBC
PT/PTT/Fibrinogen
Type and Cross
Cultures
Imaging

Volume expansion

Optimize RJs preload with NS or RL

10-20cc/kg q 2-10min. RJ is given 2
boluses.
RJ is given 2 units of blood. Her
heart rate stabilizes at 86. BP112/80.
RJ is deemed stable and gets
sclerotherapy

RJ At Endoscopy

Case 2
TN is a 5 year old girl with a history of URI
symptoms 2 weeks ago presents with
decreased effort tolerance, tachypnea . O/EHR-192, RR-70, BP-45 systolic.
Hepatomegaly, b/l rales, no heart murmur
on exam but a gallop is heard.
What type of shock is this?
Uncompensated cardiogenic shock
What is the diagnosis? How do you manage
this patient?
Myocarditis

Differentiating Cardiogenic
Shock

History
PE-enlarged liver, gallop, murmur,
rales
Chest X ray-Enlarged heart,
pulmonary venous congestion

Myocarditis

OYGEN
DELIVERY

CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT

Cardiac
Output

Heart rate

Arterial oxygen content

Stroke Volume

Preload
After load
Contractility

Hemoglobin
Oxygen Saturation
Partial pressure of oxygen dissolve
plasma

Managing TN
Increasing Oxygen supplySupplemental Oxygen
Improving myocardial output-altering
preload, after load and contractility
Correct Anemia-Blood
Decreasing oxygen demandControl temperature
Sedation
Reduce myocardial work and thus oxygen
consumption

Fluids in Cardiogenic
Shock

Give small volume boluses of 510ml/kg

TN has myocarditis and because of
this she has diastolic dysfunctiongiving her extra fluid may overload
her heart.

Ionotropes/Cardiotonics

Dopamine-Low dose increases renal and

splanchnic blood flow, high dose increases
HR and SVR.

Dobutamine- Increases contractility, may

reduce SVR, PVR.

Milrinone-Inotropy and venodilation.

Improve contractility and decrease after
load

Ionotropes/ Cardiotonics

Epinephrine- Increases HR,SVR and

contractility. End point-adequate BP,
acceptable tachycardia

Norepinephrine-0.05-1.0mcg/kg/min. Increases
SVR.

Be hesitant to use either of these drugs for TN as

they increase myocardial oxygen consumption

TNs Hospital Course

10ml/kg bolus with normal saline

results in minimal elevation of blood
pressure
Started on Dopamine of 5mcg/kg/min
and Milrinone 0.5 mcg/kg/min
Stable for transport to Cardiac ICU
Attempted intubation results in
circulatory collapse-TN goes up on
ECMO

Other causes of
Cardiogenic Shock

Dysrhythmia
Infection
Metabolic
Obstructive
Drugs
Congenital heart disease
Trauma

Case 3
4 year old boy RS presents with 3 day h/o fever,
malaise. He has a past history of nephrotic
syndrome.O/E-Minimally responsive,skin appears
flushed and warm, and he has bounding pulses. HR170 RR-30 BP-40 systolic, sats-88%.
What type of shock does the patient have
Uncompensated distributive shock- Warm septic shock
What medications could be used in the management
of this patient?
Fluid, antibiotics, pressors, steroids

Septic Shock

Mediator release- both exogenous

and endogenous lead to
misdistribution of blood, imbalance
of oxygen supply and demand,
alterations in metabolism and
cardiac dysfunction

Warm Shock

Early compensated hyperdynamic

state of septic shock
Warm extremities, bounding pulses,
tachycardia, wide pulse pressure,
decreased systemic vascular
resistance and increased cardiac
output
Often with hyperglycemia

Cold Shock

Late uncompensated stage of septic

shock with drop in cardiac output
and increased SVR
Cold and clammy skin, rapid thready
pulses, shallow breathing
Associated metabolic acidosis,
hypoxia, coagulopathy,
hypoglycemia, capillary leak

PALS ALGORITHM

1ST hour-20ml/kg/boluses.
Correct hypoglycemia and
hypocalcemia.
Administer 1st dose of antibiotics
Consider vasopressor drip and stress
dose hydrocortisone
DETERMINE WHETHER FLUID
RESPONSIVE

PALS ALGORITHM
IF NOT FLUID RESPONSIVE
Normotensive-Start Dopamine
Hypotensive vasodilated(warm shock)Norepinephrine
Hypotensive vasoconstricted(cold
shock)-Epinephrine
EVALUATE MIXED VENOUS SAT,
GOAL>70%

RS- Hospital Course

100ml/kg of fluid is given, BP improves to

60/30
Started on Norepinephrine drip following
which BP improves to systolic of 80.
Rt IJ placed ScVO2-74%
Hydrocortisone 2mg/kg-1 dose given
Starts Vancomycin and Ceftriaxone

Microbiology calls to tell you there are Gram

Neg rods on blood culture smear

PALS ALGORITHM

ScvO2>70%, Low BP, warm shock-Additional

fluid. Norepinephrine +/- Vasopressin
ScvO2<70%, normal BP, poor perfusionTransfuse to Hb>10g/dl. Consider milrinone/
nitroprusside/dobutamine
ScvO2<70%, low BP, poor perfusionTransfuse to Hb>10g/dl. Consider
epinephrine or dobutamine +norepinephrine
ADRENAL INSUFFICIENCYHydrocrtisone 2mg/kg

How much fluid is to

much?
Fluids in early septic shock- Carcillo,
JAMA 1991
Three treatment groups
1-20cc/kg in first hour
2- Upto 40cc/kg in first hour
3- More than 40cc/kg in first hour
NO DIFFERENCE IN ARDS
BETWEEN GROUPS

Conclusions

Recognise shock quickly-tachycardia

is the first sign, hypotension is late
Gain access quickly-if needed use IO.
PIV better than a central line
If patient is not responding the way
you think broaden your differential,
think about other types of shock.