1. PEDIATRIC SHOCK
Ayse Akcan Arikan
Texas Children’s Hospital
Pediatric Critical Care Section
Fellows Bootcamp 2013

2. Objectives
• By the end of this workshop, the learner will be
able to:
• Differentiate between septic and cardiogenic
shock states according to clinical assessment
and evaluation
• Generate a therapeutic/diagnostic plan
according to institutional and SCCM guidelines
where applicable

3. What is shock?
a. BP less than 5th percentile of age normal
b. Uncontrolled fluid loss/blood loss
c. Tachycardia and hypotension
d. Acidosis and increased lactate
e. Signs of organ dysfunction with decreased
UOP, altered mental status, etc.

4. Pediatric Shock
• Definition – what it is and what it is not
• Pathophysiology
• Recognition – early is key!
• Management- guidelines
• Case scenarios
• Ask for references, and you shall receive

5. Pump
Fluid
Pipes
Site of exchange

6. Pediatric shock
• Cellular pathology
• Has nothing to do with blood pressure (until very late),
cardiac output, heart rate
• Inability to meet the metabolic demands (=oxygen) of the
tissue – or inability of the cell to use oxygen
• Supply-demand imbalance

7. What is shock?
• A hemodynamic abnormality that leads to inability to meet
tissue metabolic demands.
• Dynamic, progressive.
• A systemic reduction in tissue perfusion  decreased
tissue O2 delivery.
• A shift to anaerobic metabolism
• Less efficient – 20-fold less ATP generated
• Leads to lactic acidosis
• Over time, progresses to,
• Cell membrane ion pump dysfunction
• Cellular edema, leakage of cells’ contents
• Inadequate regulation of intracellular pH
• Cell death, organ failure, cardiac arrest, and death.

8. Pediatric shock
• Dynamic process
• Progressive
• Changing physiology*
• Requires bedside management
• Oxygen debt
• Energy uncoupling

9. Vocabulary
• CO –cardiac output
• CI cardiac index – CO indexed to BSA
• SVR, SVRI - systemic vascular resistance
• PVR,PVRI – pulmonary vascular resistance
• MAP – mean arterial pressure
• CVP – central venous pressure
• SV – stroke volume
• PAP – pulmonary artery pressure
• DO2 – oxygen delivery
• VO2 – oxygen consumption

10. Vocabulary - II
• CO – cardiac output: volume of blood ejected by the heart
in one minute 4-8 L/min
• Heart rate
• Stroke volume
• Contractility
• Afterload
• Preload
• SVR = MAP – CVP / CO

11. Oxygen Delivery – DO2
• Oxygen delivery= CO X CaO2 (Arterial oxygen content)
• CO=Heart rate X Stroke volume
• Stroke volume depends on preload, afterload and
contractility
•Arterial Oxygen content (CaO2) =
Hb x Sa02 x 1.34 +(0.003 x Pa02)

12. Oxygen Consumption – VO2
• VO2 = CO x (CaO2 – CvO2)
• Under normal conditions DO2 >> VO2 (physiological
reserve) – this is why you can exercise and don’t die 

13. Oxygen delivery – consumption
imbalance in shock

14. Shock pathophysiology
• Oxygen delivery DO2 < oxygen demand VO2

15. OXYGEN DELIVERY
CARDIAC OUTPUT X ARTERIAL OXYGEN CONTENT
Cardiac
Output
Arterial oxygen content
Heart rate
Stroke Volume
Preload
Afterload
Contractility
Hemoglobin
Oxygen Saturation
Partial pressure of oxygen dissolved in plasma

16. Oxygen extraction ratio= (SaO2-SmvO2)/Sa
SmvO2 = mixed venous oxygen saturations
ScvO2 = upper extremity line

18. Shock – signs and symptoms
• Evidence of end organ hypoperfusion
• Decreased urine output
• Altered mental status
• Poor peripheral perfusion
• Metabolic dysfunction
• Lactic acidosis
• Altered metabolic demands

19. Shock: Feel the feet, look at the neck
• Tachycardia? - Non-specific, but early
• Skin changes? - Prolonged cap refill (vasoconstriction) with
compensated shock. Flash refill with early distributive shock and with
irreversible shock.
• Pallor? – If Hb is fine, is your patient acidotic
• Impaired mental status? – Fussy, irritable? Sleepy?
• Oliguria? – When was the last diaper?
• Hypotension? – You have missed the ball 
• Widened pulse pressure (>40 mmHg)? - distributive shock, aortic
insufficiency, AVMs?

20. 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
• Renin Angiotensin Aldosterone - Decreased renal
perfusion leads to angiotensin causing vasoconstriction
and aldosterone causing salt and water retentions
• Humoral Responses-Catecholamines
• Autotransfusion-Reorientation of extravascular fluid

22. Stages of Shock
• Compensated Shock:
• Cardiac output (HR x SV) and systemic vascular resistance (peripheral
vasoconstriction) work to keep BP within normal limits.
• Tachycardia; decreased pulses & cool extremities in cold shock; flushing
and bounding pulses in warm shock; oliguria; may have mild lactic acidosis
• Uncompensated Shock:
• Compensatory mechanisms are overwhelmed.
• Hypotension, altered mental status; increased lactic acidosis
• Generally quick progression to cardiac arrest.
• Irreversible Shock:
• Irreversible organ damage, cardiac arrest, death.

23. • Compensated
• Uncompensated
• Irreversible
Act quickly
Think slowly
DEATH

25. Types of shock
•Hypovolemic
•Hemorrhagic
•Cardiogenic
•Distributive
•Septic*
•Obstructive

26. Classifications of Shock
• Hypovolemic Shock
• Decreased preload due to
internal or external losses.
• Distributive Shock
• Decrease in SVR, with
abnormal distribution of
blood flow  functional
hypovolemia, decreased
preload.
• Typically, NL or  CO.
• Cardiogenic Shock
• “Pump failure.”  CO,
systolic function.
• Obstructive Shock
• Outflow from left or
right side of heart
physically obstructed.

29. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Published by Lippincott Williams
& Wilkins, Inc.
2
Table 2.
Clinical practice parameters for hemodynamic support
of pediatric and neonatal septic shock: 2007 update
from the American College of Critical Care Medicine *.
Brierley, Joe; Carcillo, Joseph; Choong, Karen;
Cornell, Tim; DeCaen, Allan; Deymann, Andreas;
Doctor, Allan; Davis, Alan; Duff, John; Dugas, Marc-
Andre; Duncan, Alan; Evans, Barry; Feldman, Jonathan;
Felmet, Kathryn; Fisher, Gene; Frankel, Lorry;
Jeffries, Howard; Greenwald, Bruce; Gutierrez, Juan;
Hall, Mark; Han, Yong; Hanson, James; Hazelzet, Jan;
Hernan, Lynn; Kiff, Jane; Kissoon, Niranjan;
Kon, Alexander; Irazusta, Jose; Lin, John; Lorts, Angie;
Mariscalco, Michelle; Mehta, Renuka; Nadel, Simon;
Nguyen, Trung; Nicholson, Carol; Peters, Mark;
Okhuysen-Cawley, Regina; Poulton, Tom; Relves, Monica;
Rodriguez, Agustin; Rozenfeld, Ranna;
Schnitzler, Eduardo; Shanley, Tom; Skache, Sara;
Skippen, Peter; Torres, Adalberto; von Dessauer, Bettina;
Weingarten, Jacki; Yeh, Timothy; Zaritsky, Arno;
Stojadinovic, Bonnie; Zimmerman, Jerry;
Zuckerberg, Aaron
Critical Care Medicine. 37(2):666-688, February 2009.
DOI: 10.1097/CCM.0b013e31819323c6
Table 2. American College of Critical Care Medicine
hemodynamic definitions of shock

30. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Hypovolemic Volume depletion
absolute or relative,
CO ↓, SVR ↑
Tachycardia,
diminished pulses,
sunken eyes and
fontanels, oliguria,
prolonged cap refill
time
Crystalloid bolus 20
ml/kg until
hemodynamics
improve, reassess
after each bolus,
blood products in
hemorrhagic shock
Cardiogenic CO ↓, SVR ↑ Tachycardia,
diminished pulses,
hepatomegaly, JVD
Inotropic agents
dopamine,
dobutamine,
epinephrine,
milrinone
Small volume
boluses 5-10 ml/kg
might be
administered
carefully while
monitoring response
Get echo early
Consider PGE

31. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Distributive
Anaphylactic
Neurogenic
CO ↑, then ↓, SVR
↓↓
Angioedema,
respiratory distress,
stridor, wheezing,
early hypotension
Start adrenergic
support while giving
fluids, obtain
vascular access
early,
supratherapeutic
doses of inotropes
might be required
CO normal, SVR ↓ Hypotension in the
absence of
tachycardia
Support SVR with
vasopressors,
phenylephrine might
be required, give
fluids as necessary
Obstructive Preload ↓, CO ↓,
SVR normal to ↑
Tachycardia,
hypotension, JVD,
tracheal deviation if
pneumothorax,
equalization of
pressures with
elevated CVP if
invasive monitoring
in place
Rapidly fatal if
underlying process
not recognized and
reversed, fluid
boluses should be
given while
preparation is made
for emergent
drainage

32. Type of shock Mechanism of circulatory
failure
Signs and symptoms Interventions
Septic “Warm shock”
CO ↑, SVR↓
Tachycardia, bounding
pulses, warm extremities with
hypotension, hyperpnoea,
altered mentation
Crystalloid boluses of 20
ml/kg repeat until
hemodynamics stable, first
choice agents vasopressors
(dopamine or norepinephrine)
“Cold shock”
CO ↓, SVR ↑
(60% of pediatric cases)
Tachycardia, poor peripheral
perfusion, diminished pulses,
hyperpnoea, altered
mentation
Crystalloid boluses of 20
ml/kg, repeat until
hemodynamics stable, early
inotropic support with
dopamine or epinephrine
might be required,
echocardiography might be
useful to guide therapy
CO ↓, SVR ↓ Tachycardia, diminished
pulses, with hypotension,
hyperpnoea, altered
mentation
Crystalloid boluses of 20
ml/kg repeat until
hemodynamics stable, early
inotropic support with
dopamine or epinephrine
might be required,
echocardiography might be
useful to guide therapy

33. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Published by Lippincott Williams
& Wilkins, Inc.
2
Table 3.
Clinical practice parameters for hemodynamic support of pediatric and
neonatal septic shock: 2007 update from the American College of Critical Care
Medicine *.
Brierley, Joe; Carcillo, Joseph; Choong, Karen; Cornell, Tim; DeCaen, Allan;
Deymann, Andreas; Doctor, Allan; Davis, Alan; Duff, John; Dugas, Marc-Andre;
Duncan, Alan; Evans, Barry; Feldman, Jonathan; Felmet, Kathryn; Fisher, Gene;
Frankel, Lorry; Jeffries, Howard; Greenwald, Bruce; Gutierrez, Juan; Hall, Mark;
Han, Yong; Hanson, James; Hazelzet, Jan; Hernan, Lynn; Kiff, Jane;
Kissoon, Niranjan; Kon, Alexander; Irazusta, Jose; Lin, John; Lorts, Angie;
Mariscalco, Michelle; Mehta, Renuka; Nadel, Simon; Nguyen, Trung;
Nicholson, Carol; Peters, Mark; Okhuysen-Cawley, Regina; Poulton, Tom;
Relves, Monica; Rodriguez, Agustin; Rozenfeld, Ranna; Schnitzler, Eduardo;
Shanley, Tom; Skache, Sara; Skippen, Peter; Torres, Adalberto; von
Dessauer, Bettina; Weingarten, Jacki; Yeh, Timothy; Zaritsky, Arno;
Stojadinovic, Bonnie; Zimmerman, Jerry; Zuckerberg, Aaron
Critical Care Medicine. 37(2):666-688, February 2009.
DOI: 10.1097/CCM.0b013e31819323c6
Table 3. Threshold heart rates and perfusion pressure
mean arterial pressure-central venous pressure or mean
arterial pressure-intra-abdominal pressure for age

34. What is the goal of shock treatment ?
•Optimizing oxygen content of the
blood
•Improving volume and distribution of
cardiac output
•Reducing oxygen demand
•Correcting metabolic derangements

35. Treatment
• Overall goal: Normalization of tissue perfusion and
homeostasis
• A - airway
• Secure, patent
• Oxygen administration – 100% FiO2 (except in some cases of
cardiogenic shock)
• B - breathing
• Decrease WOB, intubation-mechanical ventilation may be
necessary (decrease oxygen consumption)
• C - circulation
• Improve cardiac output
• Ensure adequate preload – FLUIDS!!!

36. Treatment - II
• Have I mentioned fluids?
• Give lots of fluids – fast!
• Then – give some more –up to 200 ml/kg may be required
• REASSESS! (After every step/intervention)
• Pay attention to hepatomegaly, JVD, rales, worsening
respiratory distress – if your patient is not responding to
the fluids, reconsider your diagnosis
• Once you reach 60 ml/kg, consider starting vasoactive
infusions –more on this later

37. Treatment - III
• D – “derangements”
• Correct metabolic abnormalities – hypoglycemia, hypocalcemia, etc
• Etiology specific treatment
•DO NOT DELAY ANTIBIOTICS FOR
ANY REASON IF YOU SUSPECT
SEPTIC SHOCK !
• Source control
• Consider transfusion of PRBCs

38. Assessing efficacy of treatment
• Blood pressure: Normal *
• Quality of central and peripheral pulses: Strong, distal
pulses equal to central pulses.
• Skin perfusion: Warm, with capillary refill 1-2 seconds.
• Mental status: Normal.
 Urine output: >1 mL/kg per hour, once effective
circulating volume is restored.

39. Sepsis
• High mortality despite improvements
• KID database : 4.2% in all-comers, 2.3% in previously
healthy, 7.8% in chronically ill
• Guidelines are not effective unless protocol driven
• Early intervention is critical – no delay is acceptable.
• Every hour spent without reversing shock increases OR of
mortality

41. SIRS SEPSIS SEVERE
SEPSIS
SEPTIC SHOCK
T > 38.5 or < 36
Tachycardia
Tachypnea
 WBC 
SIRS +
Infection
(suspected or
proven)
SEPSIS +
CV dysfunction or
ARDS or
≥ 2 organ failures
SEPSIS +
CV dysfunction
despite >40 ml/kg
in 1 hr
2 of the above 4

43. Early Goal-directedTherapy

44. Pediatrics 2003; 112:793
Early Resuscitation

45. © 2009 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Published by Lippincott Williams
& Wilkins, Inc.
2
Figure 1.
Clinical practice parameters for hemodynamic support
of pediatric and neonatal septic shock: 2007 update
from the American College of Critical Care Medicine *.
Brierley, Joe; Carcillo, Joseph; Choong, Karen; Cornell,
Tim; DeCaen, Allan; Deymann, Andreas; Doctor, Allan;
Davis, Alan; Duff, John; Dugas, Marc-Andre; Duncan,
Alan; Evans, Barry; Feldman, Jonathan; Felmet, Kathryn;
Fisher, Gene; Frankel, Lorry; Jeffries, Howard; Greenwald,
Bruce; Gutierrez, Juan; Hall, Mark; Han, Yong; Hanson,
James; Hazelzet, Jan; Hernan, Lynn; Kiff, Jane; Kissoon,
Niranjan; Kon, Alexander; Irazusta, Jose; Lin, John; Lorts,
Angie; Mariscalco, Michelle; Mehta, Renuka; Nadel,
Simon; Nguyen, Trung; Nicholson, Carol; Peters, Mark;
Okhuysen-Cawley, Regina; Poulton, Tom; Relves, Monica;
Rodriguez, Agustin; Rozenfeld, Ranna; Schnitzler,
Eduardo; Shanley, Tom; Skache, Sara; Skippen, Peter;
Torres, Adalberto; von Dessauer, Bettina; Weingarten,
Jacki; Yeh, Timothy; Zaritsky, Arno; Stojadinovic, Bonnie;
Zimmerman, Jerry; Zuckerberg, Aaron
Critical Care Medicine. 37(2):666-688, February 2009.
DOI: 10.1097/CCM.0b013e31819323c6
Figure 1. Algorithm for time sensitive, goal-directed
stepwise management of hemodynamic support in
infants and children. Proceed to next step if shock
persists. 1) First hour goals-Restore and maintain heart
rate thresholds, capillary refill MAP]-central venous
pressure [CVP]) for age, central venous O2 saturation
>70%, and CI >3.3, 2 in pediatric intensive care unit
(PICU). Hgb, hemoglobin; PICCO, pulse contour cardiac
output; FATD, femoral arterial thermodilution;
ECMO, extracorporeal membrane oxygenation;
CI, cardiac index; CRRT, continuous renal replacement
therapy; IV, intravenous; IO, interosseous;
IM, intramuscular.

49. TCH Shock Protocol

51. Definitions
• Pressor-increases SVR, and therefore BP
• Inotrope-Increases contractility, SV
• Chronotrope- increases HR
• Lusitrope- improves diastolic relaxation, SV
• Vasodilator- decreases SVR, afterload
• “Inodilator”

55. TCH BOOTCAMP
Shock II – Cardiogenic shock

56. Pump
Fluid
Pipes
Site of exchange

60. • Tachycardia
• Tachypnea
• Hx of sweating/tiring with feeds
• Vomiting, feeding intolerance
• Fussiness
• Gallop
• Hepatomegaly
• Rales
• Decreased UOP
• Cardiomegaly
• Altered mentation
• “Septic” newborn !
• Cyanosis

62. VENTRICULAR FUNCTION CURVES
NORMALAND FAILING LV

64. Cardiogenic shock
• Electrical failure
• Mechanical failure
• Myocarditis
• Cardiomyopathy
• Anatomic
• Obstructive
• Congestive
• Ischemic
• Trauma

65. Cardiogenic shock
• Anatomic
• Left sided obstructive = ductal dependent systemic flow
 IAA, critical AS, HLHS, etc
 HCM*
• Congestive
• large L R shunts
• Acute valvular regurgitation
• Ductal dependent pulmonary blood flow
• Parallel circulation – TGA-IVS
• Obstructed pulmonary flow – TAPVR, obstructed

66. Ischemic Heart Disease in Children
• ALCAPA
• Anomalous Left Coronary Artery arising from the Pulmonary
Artery
• Kawasaki Disease
• Aneurysms
• Other vasculitis

70. Treatment
• Support the failing pump
• Decrease oxygen consumption/metabolic demand
• Intubation*, mechanical ventilation
• Sedation, NMB
• Prevention of fever, stress
• Consider bolus 5-10 ml/kg
• Consider PGE
• Echo early

71. Treatment - II
• Optimize contractility
• Correct metabolic derangements
• Inotropic support
• Afterload reduction
• Decongestion
• Address the underlying cause – surgery?
• Mechanical support
• ECMO
• Implantable devices, VAD, EXCOR, etc

74. Type of shock Mechanism of
circulatory failure
Signs and
symptoms
Interventions
Hypovolemic Volume depletion
absolute or relative,
CO ↓, SVR ↑
Tachycardia,
diminished pulses,
sunken eyes and
fontanels, oliguria,
prolonged cap refill
time
Crystalloid bolus 20
ml/kg until
hemodynamics
improve, reassess
after each bolus,
blood products in
hemorrhagic shock
Cardiogenic CO ↓, SVR ↑ Tachycardia,
diminished pulses,
hepatomegaly, JVD
Inotropic agents
dopamine,
dobutamine,
epinephrine,
milrinone
Small volume
boluses 5-10 ml/kg
might be
administered
carefully while
monitoring response
Get echo early
Consider PGE

75. Question
• 13 month old patient with DCM, HR 180 (sinus), CVP 25
mm Hg, BP 55/24, lactate 4->8, SvO2 50%, cap refill of 5
seconds, best choice of action is:
a. Epinephrine gtt
b. Milrinone gtt
c. Phenylephrine gtt
d. NS bolus 20 ml/kg
e. Esmolol (B-blocker) for HR control

76. Question
• 12 year old female presents with fever, tachycardia, right
flank pain, WBC count is elevated. Vital signs are HR 155,
RR 35, BP 124/73, T 102. She is somnolent. Working
diagnosis is sepsis secondary to pyelonephritis. What is
the next most appropriate intervention?
A. Renal US
B. Normal saline bolus
C. Antibiotics
D. Vasopressor infusion
E. Urinalysis

77. Question
• 12 year old female presents with fever, tachycardia, right
flank pain, WBC count is elevated. Vital signs are HR 110,
RR 25, BP 124/83, T 102. She is AAO x 3 and is .
Working diagnosis is sepsis secondary to pyelonephritis.
What is the next most appropriate intervention?
A. Renal US
B. Normal saline bolus
C. Antibiotics
D. Vasopressor infusion
E. Urinalysis

78. Case 1
• 15-year-old male is just transferred to 11 WT from PICU, POD #3
from partial small bowel resection after multiple gunshot wounds
to the abdomen. The nurse calls an RRT because his HR has
increased in the last hour from 90 to 130, despite pain score of
1/10 on morphine drip. On exam, he is afebrile, HR is 140, BP
80/50. Cap refill is >3 seconds in his cool extremities and pulses
are 1+.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your initial management?

79. Case 2
• 6-year-old previously healthy girl is transferred from West
Campus ER with fever, bloody diarrhea x 1 day. She’s had no
urine x 24 hrs and is becoming harder to awaken. On exam, her
HR is 152, BP 72/32, temp 103. She’s sleepy but arousable.
She’s flushed with capillary refill <1 second.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your differential for the etiology?
• What is your initial management? If a higher level of care is needed,
how would you obtain it?

80. Case 3
• 4-month-old boy former premie, presents to ED with decreased po
x 2 days with 2 times daily emesis, following what sounds like viral
URI. Urine output has been 3 wet diapers daily. He is afebrile
with HR 180; BP has not been obtained. He has a weak cry, is
mottled with 3-second capillary refill, pulses 1+ in all extremities.
Liver is palpable 4 cm below RCM. S4 is present without murmur.
• What is your assessment?
• What is the stage of shock?
• What is the classification of shock?
• What is your differential for the etiology?
• What is your initial management?

81. What is the end goal for resuscitation ?
• Mixed venous sats
• Lactate clearance
• Traditional clinical variables –
UOP, perfusion, pulses, CVP
• Combination of all three with common sense

82. Minimize variationEarly Resuscitation
Intensive Care Med 2008; 34:1065

83. Intensive Care Med 2008; 34:1065
Minimize variationEarly Resuscitation

85. • crashingpatient.com
• ccmtutorials.com
• cvphysiology.com
• learnhemodynamics.com*
• library.med.utah.edu