PEDIATRIC SHOCK
2012
SHOCK
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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 dissolved in plasma
Oxygen Delivery
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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
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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
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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 stat-7.08/24/80/12/-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 shock- how does the
body compensate?
Compensated
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Stages of Shock
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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
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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
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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
RJ’s Clinical presentation
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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
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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!
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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!
RJ’s Management
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Increase oxygen delivery, decrease oxygen demand
Oxygen
Fluid
Blood
Temperature control
Correct metabolic abnormalities
Inotrope if needed
Labs
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ABG
Blood sugar
Electrolytes
CBC
PT/PTT/Fibrinogen
Type and Cross
Cultures
Imaging
Volume expansion
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Optimize RJ’s 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. BP-112/80.
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/E-HR-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
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Differentiating Cardiogenic Shock
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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 dissolved in 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
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Fluids in Cardiogenic Shock
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Give small volume boluses of 5-10ml/kg
TN has myocarditis and because of this she has
diastolic dysfunction- giving her extra fluid may
overload her heart.
Ionotropes/Cardiotonics
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Dopamine-Low dose increases renal and splanchnic
blood flow, high dose increases HR and SVR.
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Dobutamine- Increases contractility, may reduce SVR,
PVR.
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Milrinone-Inotropy and venodilation. Improve
contractility and decrease after load
Ionotropes/ Cardiotonics
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Epinephrine- Increases HR,SVR and contractility. End
point-adequate BP, acceptable tachycardia
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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
TN’s Hospital Course
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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
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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. HR-170 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
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Septic Shock
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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
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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
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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
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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%
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RS- Hospital Course
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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
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ScvO2>70%, Low BP, warm shock-Additional fluid.
Norepinephrine +/- Vasopressin
ScvO2<70%, normal BP, poor perfusion-Transfuse to
Hb>10g/dl. Consider milrinone/
nitroprusside/dobutamine
ScvO2<70%, low BP, poor perfusion-Transfuse 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
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Conclusions
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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.