U

T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

SHOCK IN CHILDREN
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Definition
Circulatory system failure to supply
oxygen and nutrients to meet cellular
metabolic demands
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Other Definitions
Blood Pressure
BP = CO x SVR
Cardiac Output
CO = SV X HR
Vascular Tone (SVR)
Regulated by several mechanisms
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Oxygen Delivery
DO
2
= CO x CaO
2
x 10
Remember: CO depends on HR, preload,
afterload, and contractility
CaO
2
= Hgb x 1.34 x SaO
2
+ (PaO
2
x 0.003)
Remember: hemoglobin carries more than 99%
of oxygen in the blood under standard
conditions
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Hemodynamics
Myocardial
Contractility
Stroke Volume Preload
Cardiac Output Afterload
Blood
Pressure Heart Rate
Systemic Vascular
Resistance
Textbook of Pediatric Advanced Life Support, 1988
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Defending the blood pressure
Neural Sympathetic
Baroreceptors
Carotid Body
Aortic Arch
Volume receptors
Right Atrium
Pulmonary vascular
Chemoreceptors
Aortic and carotid
Medullary
Cerebral ischemic
response
Humoral
Adrenal medulla
Catecholamines
Hypothalamopituitary
response
Adrenocorticotropic
hormone
Vasopressin
Renin-angiotensin-
aldosterone system
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Cardiovascular function
Cardiac Output
Clinical Assessment
peripheral perfusion, temperature, capillary
refill, urine output, mentation, acid-base
status
CO = HR x SV
HR responds the quickest
SV is a function of three variables
preload, afterload, and myocardial
contractility
A noncompliant heart cannot increase SV
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Stroke Volume
Preload (LVEDV)
Reflects patients volume status
CVP or PCWP
Starling curve
Afterload
The resistance to ventricular ejection
Two variables:
vascular tone and transmural pressure
Myocardial Contractility (squeeze)
Many factors including coronary perfusion,
baseline myocardial function, use of cardiotonic
medications
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Classification of Shock
COMPENSATED
blood flow is normal or increased and may be
maldistributed; vital organ function is
maintained

UNCOMPENSATED
microvascular perfusion is compromised;
significant reductions in effective circulating
volume

IRREVERSIBLE
inadequate perfusion of vital organs; irreparable
damage; death cannot be prevented
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Other Classifications
Hypovolemic or Hemorrhagic
Cardiogenic
Obstructive
Distributive
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Cardiovascular Changes in Shock
Type Preload Afterload Contractility
Cardiogenic
Hypovolemic No change
Distributive
Septic
early
late
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Evaluation
Early Signs of Shock
sinus tachycardia
delayed capillary refill
fussy, irritable
Late Signs of Shock
bradycardia
altered mental status (lethargy, coma)
hypotonia, decreased DTRs
Cheyne-Stokes breathing
hypotension is a very late sign
Lower limit of SBP = 70 + (2 x age in years)
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Cardiovascular Assessment
Heart Rate
Too high: 180 bpm for
infants, 160 bpm for
children >1year old
Blood Pressure
Lower limit of SBP =
70 + (2 x age in years)
Peripheral Pulses
Present/Absent
Strength (diminished,
normal, bounding)
Skin Perfusion
Capillary refill time
Temperature
Color
Mottling
CNS Perfusion
Recognition of
parents
Reaction to pain
Muscle tone
Pupil size
Renal Perfusion
UOP >1cc/kg/hr
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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 O
2
delivery and
decreased O
2
consumption
can hyperventilate if necessary
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Cardiogenic Shock
Etiologies
Congenital heart
disease
Arrhythmias
Ischemic heart
disease
Myocarditis
Myocardial injury
Acute and chronic
drug toxicity
Late septic shock
Infiltrative diseases
mucopolysaccharidoses
glycogen storage
diseases
Thyrotoxicosis
Pheochromocytoma
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Obstructive Shock
Low CO secondary to a physical obstruction to flow
Compensatory increased SVR
Causes:
Pericardial tamponade
Tension pneumothorax
Critical coarctation of the aorta
Aortic stenosis
Hypoplastic left heart syndrome
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

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)
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Distributive Shock
Etiologies
Anaphylaxis
Anaphylactoid reactions
Spinal cord injury/spinal shock
Head injury
Early sepsis
Drug intoxication
Barbiturates, Phenothiazines,
Antihypertensives
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Metabolic Issues
Acid-Base
Metabolic acidosis develops secondary to tissue
hypoperfusion
Profound acidosis depresses myocardial
contractility and impairs the effectiveness of
catecholamines
Tx: fluid administration and controlled
ventilation
Buffer administration
Sodium Bicarbonate 1-2meq/kg or can calculate a
1/2 correction = 0.3 x weight (kg) x base deficit
hyperosmolarity, hypocalcemia, hypernatremia,
left-ward shift of the oxyhemoglobin dissociation
curve
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Metabolic Issues
Electrolytes
Electrolytes
Calcium is important for cardiac function and
for the pressor effect of catecholamines
Hypoglycemia can lead to CNS damage and is
needed for proper cardiovascular function
Check the BUN and creatinine to evaluate renal
function
Hyperkalemia can occur from renal dysfunction
and/or acidosis
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Metabolic Issues
Special Topics
Congenital adrenal hyperplasia
Infant presents in shock, usually in the second
week of life, typically a boy, with metabolic
acidosis, hyponatremia, hypoglycemia, and
hyperkalemia

Hyperammonemia
mild elevations are common with shock
levels > 1000 are consistent with inborn errors
of metabolism
consider Reye Syndrome, toxins, hepatic
failure
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Other Studies
Look for etiology of shock
Evaluate hemoglobin, hematocrit, and platelet
count
Should be followed as these values may drop after
fluid resuscitation
Shock from any etiology can lead to DIC and
end organ damage
CBC, PT, INR, PTT, Fibrinogen, Factor V, Factor
VIII, D-dimer, and/or FDPs
Check LFTs, follow CNS and pulmonary status
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Other Studies II
Think about inborn errors of metabolism
Lactate and pyruvate
Ammonium, LFTs
Plasma amino acids, urine organic acids
Urinalysis with reducing substances
Urine tox screen
U
T
H
S
C
S
A

P
e
d
i
a
t
r
i
c

R
e
s
i
d
e
n
t

C
u
r
r
i
c
u
l
u
m

f
o
r

t
h
e

P
I
C
U

Conclusion
Goal of therapy is identification, evaluation, and
treatment of shock in its earliest stage
Initial priorities are for the ABCs
Fluid resuscitation begins with 20cc/kg of
crystalloid or 10cc/kg of colloid
Subsequent treatment depends on the etiology of
shock and the patients hemodynamic condition
Successful resuscitation depends on early and
judicious intervention