PEDIATRIC SHOCK

Dr. A. William, Sp. A, M.Kes

DEFINITION OF SHOCK
A syndrome which occurs because of
cardiovascular dysfunction and the inability of the
circulatory system to provide adequate oxygen
and nutrients to meet the metabolic demands of
vital organs.

SHOCK CAN & DOES EXIST WITHOUT

HYPOTENSION!!
PHYSIOLOGY OF CIRCULATION

Cardiac Output = Heart Rate x Stroke

Volume
Stroke Volume depends on pre-load, cardiac
contractility, and after-load

Blood Pressure = Cardiac Output x

Peripheral Resistance (SVR)
Figure 1. FACTORS AFFECTING OXYGEN DELIVERY

Hgb

CaO2
A-a gradient
DPG
Acid-Base Balance
Influenced By Blockers
Oxygenation Competitors
Temperature

DO2
Drugs
Influenced By Conduction System
HR

CVP
CO
EDV Venous Volume
Venous Tone
Metabolic Milieu
SV Ventricular Ions
Compliance Acid Base
Temperature
Influenced By
Drugs
ESV Contractility Toxins

Afterload Blockers
Influenced By Temperature Competitors
Drugs Autonomic Tone
CLINICAL MANIFESTATIONS
Early (compensated) Shock

tachycardia may be the earliest sign eventually delayed

(compensates for a decreased stroke
volume) - good perfusion early
(secondary to cutaneous
vasodilatation when cardiac output is
increased)
capillary refill secondary
to peripheral
vasoconstriction and
decreased cardiac output

mild irritability and

decreased urine other signs: dry
output indicating mucuos membranes,
mild tachypnea sunken fontanel,
decreased end-organ
perfusion decreased skin turgor
CLINICAL MANIFESTATIONS
Late (uncompensated) Shock

increased capillary refill

tachycardia markedly
and tachypnea delayed

agitation
oliguria progresses to
coma

hypotension
TYPES OF SHOCK
decreased circulating volume, most common cause of
shock in children
water loss from vomiting / diarrhea most common
Hypovolemic others: blood loss (trauma, GI bleed), plasma loss
(burns, peritonitis), and water losses (glycosuric
diuresis)

pooling of blood in the peripheral vasculature

Distributive most commonly secondary to sepsis
others: anaphylaxis, spinal injuries, drug ingestions

Pump failure
decreased CO as a result of decreased contractility
Cardiogenic clinically: rales, hepatomegaly, JVD, gallop rhythm
causes: late shock, myocarditis, dysrhythmias, drug
ingestions, congenital heart disease

Outflow from left or right side of the heart physically

obstructed
Obstructive mechanical obstruction of ventricular outflow tract with
pericardial tamponade or tension pneumothorax
EVALUATION
Regardless of the cause: ABCs
First assess airway patency, ventilation, then
circulatory system
Respiratory Performance
Respiratory rate and pattern, work of breathing,
oxygenation (color), level of alertness
Circulation
Heart rate, BP, perfusion, and pulses, liver size
CVP monitoring may be helpful
EVALUATION
Early Signs of Late Signs of Shock
Shock
bradycardia
altered mental status
sinus tachycardia (lethargy, coma)
hypotonia, decreased
DTRs
delayed capillary Cheyne-Stokes breathing
refill hypotension is a very
late sign

fussy, irritable Lower limit of SBP = 70

+ (2 x age in year)
CARDIOVASCULAR ASSESSMENT
Skin Perfusion
Heart Rate Capillary refill time
Too high: 180 bpm for Temperature
infants, 160 bpm for Color
children >1year old Mottling
Blood Pressure CNS Perfusion
Lower limit of SBP = 70 + Recognition of parents
(2 x age in years)
Reaction to pain
Peripheral Pulses Muscle tone
Present/Absent Pupil size
Strength (diminished,
normal, bounding) Renal Perfusion
UOP >1cc/kg/hr
TREATMENT
Airway management
Always provide supplemental oxygen
Endotracheal intubation and controlled
ventilation is suggested if respiratory failure
or airway compromise is likely
elective is safer and less difficult
decrease negative intrathoracic pressure
improved oxygenation and O2 delivery and decreased O2
consumption
can hyperventilate if necessary
TREATMENT
Circulation
Based on presumed etiology
Rapid restoration of intravascular volume
PIV-if unstable you have 60-90 seconds
I.O. if less than 4-6 years old
Central venous catheter
Use isotonic fluid: NS, LR, or 5% albumin
PRBCs to replace blood loss or if still unstable after
60cc/kg of crystalloid
anemia is poorly tolerated in the
stressed, hypoxic, hemodynamically
unstable patient
VASOACTIVE/CARDIOTONIC AGENTS
Dopamine
1-5 mcg/kg/min: dopaminergic
5-15 mcg/kg/min: more beta-1
10-20 mcg/kg/min: more alpha-1
may be useful in distributive shock

Dobutamine
2.5-15 mcg/kg/min: mostly beta-1, some beta-2
may be useful in cardiogenic shock

Epinephrine
0.05-0.1 mcg/kg/min: mostly beta-1, some beta-2
> 0.1 to 0.2 mcg/kg/min: alpha-1
VASOACTIVE/CARDIOTONIC AGENTS
Norepinephrine
0.05-0.2mcg/kg/min: only alpha and beta-1
Use up to 1mcg/kg/min

Milrinone
50mcg/kg load then 0.375-0.75mcg/kg/min:
phosphodiesterase inhibitor; results in increased
inotropy and peripheral vasodilation (greater effect
on pulmonary vasculature)

Phenylephrine
0.1-0.5mcg/kg/min: pure alpha
HYPOVOLEMIC
# 1 cause of death in children worldwide
Causes
Water Loss (diarrhea, vomiting with poor PO intake,
diabetes, major burns)
Blood Loss (obvious trauma; occult bleeding from pelvic
fractures, blunt abdominal trauma, shaken baby)

Low preload leads to decreased SV and

decreased CO.
Compensation occurs with increased HR and
SVR
 Hypovolemic Shock

Clinically, history of vomiting/diarrhea or

trauma/blood loss
Signs of dehydration: dry mucous membranes,
absent tears, decreased skin turgor
Hypotension, tachycardia without signs of
congestive heart failure
 Hemorrhagic Shock
Most common cause of shock in the United
States (due to trauma)
Patients present with an obvious history (but
in child abuse history may be misleading)
Site of blood loss obvious or concealed
(liver, spleen, intracranial, GI, long bone
fracture)
Hypotension, tachycardia and pallor
Hypovolemic/Hemorrhagic Shock: Therapy
Always begin with ABCs
Replace circulating blood volume rapidly:
start with crystalloid
Blood products as soon as available for
hemorrhagic shock (Type and Cross with first
blood draw)
Replace ongoing fluid/blood losses & treat
the underlying cause
HYPOVOLEMIC SHOCK
Mainstay of therapy is fluid
Goals
Restore intravascular volume
Correct metabolic acidosis
Treat the cause

Degree of dehydration often underestimated

Reassess perfusion, urine output, vital signs...

Isotonic crystalloid is always a good choice

20 to 50 cc/kg rapidly if cardiac function is normal
NS can cause a hyperchloremic acidosis
TREATMENT
Solution Na+ Cl- K+ Ca++ Mg++ Buffer
NS 154 154 0 0 0 None
LR 130 109 4 3 0 Lactate
Plasmalyte 140 98 5 0 3 Acetate
& Gluconate

Inotropic and vasoactive drugs are not a substitute for

fluid, however...
Can have various combinations of hypovolemic and septic
and cardiogenic shock
May need to treat poor vascular tone and/or poor
cardiac function
HEMORRHAGIC SHOCK
Treatment is PRBCs or whole blood
Treat the cause if able (stop the bleeding)
Transfuse if significant blood loss is known
or if patient unstable after 60cc/kg
crystalloid
In an emergency can give group O PRBCs
before cross matching is complete or type
specific non-cross-matched blood products
CARDIOGENIC
Low CO and high systemic vascular
resistance
Result of primary cardiac dysfunction:
A compensatory increase in SVR occurs to
maintain vital organ function
Subsequent increase in LV afterload, LV work,
and cardiac oxygen consumption
CO decreases and ultimately results in volume
retention, pulmonary edema, and RV failure
CARDIOGENIC SHOCK
ETIOLOGIES
Congenital heart Late septic shock
disease
Infiltrative diseases
Arrhythmias mucopolysaccharidoses
Ischemic heart disease glycogen storage
Myocarditis diseases
Myocardial injury Thyrotoxicosis
Acute and chronic drug Pheochromocytoma
toxicity
 Cardiogenic Shock
Differentiation from other types of shock:
History
Exam:
Enlarged liver
Gallop rhythm
Murmur
Rales
CXR:
Enlarged heart, pulmonary venous congestion
 Cardiogenic Shock
Management:
Improve cardiac output:: Minimize cardiac work:
Correct Maintain normal
dysrhthymias temperature
Optimize preload Sedation
Improve Intubation and
contractility mechanical ventilation
Reduce afterload Correct anemia
CARDIOGENIC SHOCK
Initial clinical presentation can be identical to
hypovolemic shock
Initial therapy is a fluid challenge
If no improvement or if worsens after giving volume,
suspect cardiogenic shock
Usually need invasive monitoring, further evaluation,
pharmacologic therapy
Balancing fluid therapy and inotropic support can be
very difficult.
Call an intensivist and/or a cardiologist
OBSTRUCTIVE SHOCK

Mechanical obstruction to ventricular outflow

Inadequate C.O. in the face of adequate
preload and contractility
Compensatory increased SVR
 Obstructive Shock
Treat underlying cause.
Causes:
Pericardial tamponade
Tension pneumothorax
Congenital heart disease
Massive pulmonary embolism
Cardiac tamponade
Critical coarctation of the aorta
Aortic stenosis
Hypoplastic left heart syndrome
OBSTRUCTIVE SHOCK
Initial clinical presentation can be identical to
hypovolemic shock
Initial therapy is a fluid challenge
Treat the cause
pericardial drain, chest tube, surgical intervention
if the patient is a neonate with a ductal dependent lesion
then give PGE

Further evaluation, invasive monitoring,

pharmacologic therapy, appropriate consults
DISTRIBUTIVE SHOCK
High CO and low SVR (opposite of
hypovolemic, cardiogenic, and obstructive)
Maldistribution of blood flow causing
inadequate tissue perfusion
Due to release of endotoxin, vasoactive
substances, complement cascade activation,
and microcirculation thrombosis
Early septic shock is the most common form
Distributive Shock
Due to an abnormality in vascular tone leading to
peripheral pooling of blood with a relative
hypovolemia.
Etiology
Anaphylaxis
Drug toxicity
Neurologic injury
Early sepsis
Management
Fluid
Treat underlying cause
DISTRIBUTIVE SHOCK
Goal is to maintain intravascular volume
and minimize increases in interstitial fluid
(the primary problem is a decrease in
SVR)
Use crystalloid initially
Additional fluid therapy should be based on lab
studies
Can give up to 40cc/kg without monitoring CVP
Vasoactive/Cardiotonic agents often necessary
Treat the cause (i.e.. antimicrobial therapy)
DISTRIBUTIVE SHOCK
ETIOLOGIES
Anaphylaxis
Anaphylactoid reactions
Spinal cord injury/spinal shock
Head injury
Early sepsis
Drug intoxication
Barbiturates, Phenothiazines, Antihypertensives
 SEPTIC SHOCK
SIRS/Sepsis/Septic shock

Mediator release:
exogenous & endogenous

Maldistribution Cardiac Imbalance of oxygen Alterations in

of blood flow dysfunction supply and demand metabolism
SEPTIC SHOCK: WARM SHOCK
Early, compensated, hyperdynamic state
Clinical signs
Warm extremities with bounding pulses, tachycardia,
tachypnea, confusion.
Physiologic parameters
widened pulse pressure, increased cardiac ouptut and
mixed venous saturation, decreased systemic vascular
resistance.
Biochemical evidence:
Hypocarbia, elevated lactate, hyperglycemia
Septic Shock: Cold Shock
Late, uncompensated stage with drop in cardiac
output.
Clinical signs
Cyanosis, cold and clammy skin, rapid thready
pulses, shallow respirations.
Physiologic parameters
Decreased mixed venous saturation, cardiac output
and CVP, increased SVR, thrombocytopenia, oliguria,
myocardial dysfunction, capillary leak
Biochemical abnormalities
Metabolic acidosis, hypoxia, coagulopathy,
hypoglycemia.
 SEPTIC SHOCK
Cold Shock rapidly progresses to multiorgan
system failure or death if untreated
Multi-Organ System Failure: Coma, ARDS, CHF,
Renal Failure, Ileus or GI hemorrhage, DIC
More organ systems involved, worse the prognosis
Therapy: ABCs, fluid
Appropriate antibiotics, treatment of underlying
cause
Dissociative Shock
Inability of Hemoglobin molecule to give up the
oxygen to tissues
Etiology: Carbon Monoxide poisoning,
methemoglobinemia, dyshemoglobinemias
Tissue perfusion is adequate, but oxygen
release to tissue is abnormal
Early recognition and treatment of the cause is
main therapy
INITIAL THERAPY
Breathing Circulation
(supply 100%
Airway FIO2 via bag- must obtain vascular
valve-mask) access and give
fluids immediately
(peripheral vein ,
intraosseous, central
lines)
Antibiotics Reassess ABCs (vital signs 20cc/kg of
for septic shock and physical examination) crystalloid 0.9%
or unclear May give up to 60 - NaCl or Ringers
etiology 80cc/kg of fluids as needed Lactate
Packed RBCs
(10cc/kg) for a low
Hematocrit
Laboratory: Correct acidosis: Watch for DIC -
ABG, CBC, Na Bicarbonate for treat with FFP
Chemistries, LFTs, ph < 7.1 (ventilation (10cc/kg) and
PT/PTT, Dstick, & perfusion must be platelets (0.2
cultures adequate) units/kg) as needed
MONITORING

Continued reassessments
Foley catheter - UOP should be maintained
atleast 1cc/kg/hr
CVP (central venous pressure)
End-tidal CO2 monitor
Echocardiogram
Swanz-Ganz catheter
CONTINUED SUPPORTIVE CARE

Fluid boluses as indicated

Following 60cc/kg of fluids, strongly
consider positive inotropic agents:
Dopamine
2-3 mcg/kg/min >>> dopaminergic effects
(increased renal blood flow)
5-10 mcg/kg/min >>> beta effects (increased
contractility, vasodilatation)
10-20 mcg/kg/min >>> alpha effects (increased
BP from vasoconstriction
CONTINUED SUPPORTIVE CARE
Dobutamine
Beta stimulation leading to
increased cardiac output,
vasodilatation
2.5 - 15 mcg/kg/min
Indicated for cardiogenic
shock
Norepinephrine
alpha and beta 1 stimulation
0.1 - 1.0 mcg/kg/min
consider in conjunction with
low dose dopamine
Epinephrine
beta effects at low dosages
(0.1 - 0.2 mcg/kg/min)
alpha effects (over 0.3
mcg/kg/min) increases BP
Milrinone
decreased afterload and
preload secondary to
vasodilatation
shorter half-life than amrinone
and less risk of
thrombocytopenia
 Algorithm for goal-directed management of hemodynamic support in septic shock.

Phoebe Yager, and Natan Noviski Pediatrics in Review

2010;31:311-319

2010 by American Academy of Pediatrics

FINAL THOUGHTS
Recognize compensated shock quickly- have a high
index of suspicion, remember tachycardia is an early
sign. Hypotension is late and ominous.
Gain access quickly- if necessary use an intraoseous
line.
Fluid, fluid, fluid - Administer adequate amounts of
fluid rapidly. Remember ongoing losses.
Correct electrolytes and glucose problems quickly.
If the patient is not responding the way you think he
should, broaden your differential, think about different
types of shock.
PEDIATRIC SHOCK

2012
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 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
 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)
RJS MANAGEMENT

Increase oxygen delivery, decrease oxygen

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

ABG PT/PTT/Fibrinogen
Blood sugar Type and Cross
Electrolytes Cultures
CBC 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. 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
DIFFERENTIATING CARDIOGENIC SHOCK

History
PE-enlarged liver, gallop, murmur, rales
Chest X ray-Enlarged heart, pulmonary
venous congestion
MYOCARDITIS
MANAGING TN
Increasing Oxygen supply-
Supplemental Oxygen
Improving myocardial output-altering preload, after
load and contractility
Correct Anemia-Blood
Decreasing oxygen demand-
Control temperature
Sedation
Reduce myocardial work and thus oxygen consumption
FLUIDS IN CARDIOGENIC SHOCK

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

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. 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
 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 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 INSUFFICIENCY- Hydrocrtisone 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.