This document defines shock in children and discusses its physiology, classification, etiologies, recognition, assessment, and management. Shock is defined as an acute circulatory dysfunction resulting in insufficient oxygen delivery to tissues. The main types of shock discussed are hypovolemic, distributive, cardiogenic, obstructive, and septic shock. Signs of shock progress from early compensated stages to later uncompensated stages with declining perfusion. Management involves identifying and treating the underlying cause while stabilizing circulation through fluid resuscitation, vasopressors, and inotropes. Early goal-directed therapy is important for managing septic shock.

1. SHOCK IN CHILDREN
Sanju Susan Samuel
Fellow-Pediatric Critical Care Medicine

2. OBJECTIVES
 Definition
 Physiology
 Classification of Shock
 Common Etiologies
 Recognition and Assessment
 Management

3. DEFINITION
 An acute, complex state of circulatory
dysfunction that results in failure to deliver
sufficient amount of oxygen and nutrients to
meet tissue metabolic demands.
 Therefore, basically DO2 < VO2.
 If prolonged and left untreated- Can lead to
multiple organ failure and eventually death.

4. igure 1. FACTORS AFFECTING OXYGEN DELIVERY
DO2
CaO2
CO
SV
HR
Oxygenation
Hgb
A-a gradient
DPG
Acid-Base Balance
Blockers
Competitors
Temperature
Drugs
Conduction System
Ventricular
Compliance
EDV
ESV Contractility
CVP
Venous Volume
Venous Tone
Afterload Blockers
Temperature Competitors
Drugs Autonomic Tone
Metabolic Milieu
Ions
Acid Base
Temperature
Drugs
Toxins
Influenced By
Influenced By
Influenced By
Influenced By

5. What is needed to maintain
Perfusion??
 PUMP- Heart
 PIPES- Vessels
 FLUID- Blood
 Pump Failure
 Pipe Failure
 Loss of Volume
How can Perfusion fail??

6. Causes of Inadequate Perfusion
 Inadequate Pump
 Inadequate preload
 Poor contractility
 Excessive Afterload
 Inadequate HR
 Inadequate Fluid Volume
 Hypovolemia
 Inadequate Container
 Excessive Dilatation
 Inadequate systemic vascular resistance

7. So-what happens??
Anaerobic MetabolismAnaerobic MetabolismAnaerobic Metabolism
GLUCOSE METABOLISM
2 LACTIC ACID
2 ATP
HEAT (32 kcal)
Aerobic MetabolismAerobic MetabolismAerobic Metabolism
6 O2
GLUCOSE
METABOLISM
6 CO2
6 H2O
36 ATP
HEAT (417 kcal)

8. PHASES OF SHOCK
 Compensated Shock
- Intrinsic regulatory mechanisms
- Vital organ function is maintained
 Uncompensated Shock
- Compromise of microvascular perfusion
- Deterioration of organ function
- Hypotension develops
 Irreversible Shock
- Damage to key organs
.

9. RECOGNITION & ASSESSMENT
 Respiratory
- Quality of Respirations
- Auscultatory Findings
 Cardiovascular
- Pulse
- Blood Pressure, Pulse pressure
 Skin
-Color
-Capillary Refill
-Temperature
-Moist/ Dry

10. Recognition & Assessment..
 Neurological
-Full/ flat/ sunken fontanelle
-Calm/ anxious/ irritable
-Alert/ lethargic
-Responsive to parents
-level of consciousness
-Muscle tone
-pupillary size
 Renal
- Urinary output

11. SIGNS OF SHOCK
 Early Signs
1. Tachycardia
2. Normal blood pressure
3. Mildly delayed capillary refill
4. Fussy child

12. Signs of Shock..
 Late Signs
1. Persisting tachycardia or bradycardia
2. Hypotension- LATE sign!!
3. Poor capillary refill
4. Altered mental status
5. Irregular breathing pattern
6. Poor muscle tone
7. Lower limit of SBP=70 + (2 x age in years)

14. FUNCTIONAL CLASSIFICATION
OF SHOCK
Hypovolemic Distributive Cardiogenic Obstructive Septic
Whole blood
loss
Plasma loss
Fluid/
electrolyte
losses
Septic
Anaphylaxis
Spinal
anesthesia
Infectious
CMP
Carditis
Metabolic
Arrythmia
Pericardial
tamponade
Tension
Pneumothorax
Pulmonary
HTN

15. HYPOVOLEMIC SHOCK
 MCC of shock in children
 Decrease in the intravascular blood volume to
such an extent that effective tissue perfusion
cannot be maintained.
 Preload decrease
Decreased Stroke Volume
Decreased C.O.

16. Management of Hypovolemic
Shock
 Establishment of adequate oxygenation and
ventilation
 O2- ALWAYS the first drug administered.
 Adequate IV or IO
 Early correction of hypovolemia
-Crystalloids: Readily available, safe, least expensive
-First bolus 20cc/kg- ASAP
-Continuous monitoring of vitals
-Monitoring of CVP: Maintain > 10mmHg
-Identify causes of ongoing losses
- Blood available: if hemorrhagic shock.

17. Solution makeup
Osmol Glucose Na+ Cl- K+ Ca+ Lactate
 5% D/W 278 50g/l 0 0 0 0 0
 10%D/W 556 100g/l 0 0 0 0 0
 .45% NS 154 0 77 77 0 0 0
 .9% NS 308 0 154 154 0 0 0
 LR 274 0 130 109 4 1.5 28
Na, Cl, K, Ca, and lactate are measured in mmol/liter.

18. The Stages of Shock
Normal Eucardia, normal BP and CR
Tachycardia alone, normal BP and CR
HR is maintaining CO despite reduced stroke volume (CO =
HR x SV)
Hypotension with normal CR = Warm shock
Vascular tone cannot maintain blood pressure but HR maintains
CO
Prolonged CR with normal BP = Cold shock
HR does not maintain CO but vascular tone maintains BP
Prolonged CR + hypotension = Decompensated Cold Shock
HR does not maintain CO and vascular tone does not maintain
(Carcillo et al., Pediatrics 2009)(Slides are courtesy of Dr. Carcillo)

19. CARDIOGENIC SHOCK
1. a. Toxic substances released during
course of shock.
b. Myocardial Edema
c. Adrenergic receptor dysfunction
d. Impaired sarcolemmic Calcium flux
e. Reduced coronary blood flow
2. Diastolic Dysfunction

20. Pathophysiology
LV able to eject less volume of bld/ beat
Dec. Stroke Volume
Increased Venous Return
Increased EDV
Increased LV diastolic filling pressure
Backflow from LV to lungs
Dec.C.O
Increased O2
extraction by
tissues
Arterial O2
desaturation

21. Etiology of Cardiogenic Shock
 Dysrrhythmias
 Cardiomyopathies
 Congenital Heart Disease
 Trauma
Hypoxic-Ischemic event
Infectious
Metabolic
Connective Tissue Disorder
NM disorders
Toxins
Others

22. Recognizing Cardiogenic Shock
History Physical Examination CXR
 Excessive
Resp
effort
 Prolonged
feeding time
 Poor weight
gain
 Excessive
sweating
 Frequent
resp. tract
infections
 Inc HR, Inc RR
 Gallop
 Cold extremites, weak peripheral
pulses
 Rales
 Dyspnea, cyanosis
 Hepatomegaly
 Neck V dsitension
 Peripheral edema
 Hypotension
Cardiomegaly
Pulm venous
congestion
Hyperinflation

23. Managing Cardiogenic Shock…
Minimize Myocardial
O2 demands
Maximize Myocardial
Performance
Exclude & Explore
Intubation
Maintain normothermia
Provide sedation
Correct anemia
Correct Dysrhythmias
Optimize Preload
Improve Contractility
Reduce Afterload
Exclude traumatic or
CHD
Explore surgical options

24. OBSTRUCTIVE SHOCK
 Normal Preload
 Normal myocardial function
 Inadequate C.O.
 Etiology
 Recognize and treat underlying cause!!
Tension Pneumothorax
Pulmonary/ Systemic HTN
Congenital/ Acquired outflow
obstructions
Ac. Pericardial Tamponade

25. DISTRIBUTIVE SHOCK
 PathoPhysiology:
a. Maldistribution of blood flow to tissue due to abnormal
vasomotor tone.
b. Profound inadequate tissue oxygenation.
c. Normal or High C.O.
 Etiology
 Management: Recognize and treat underlying cause
Anaphylaxis
Spinal or Epidural anesthesia
Disruption of spinal cord
Iatrogenic

26. SIRS/Sepsis/Septic shock
Mediator release:
exogenous & endogenous
Maldistribution
of blood flow
Cardiac
dysfunction
Imbalance of
oxygen
supply and
demand
Alterations in
metabolism
SEPTIC SHOCK

27. ACUTE ORGAN
DYSFUNCTION
(Severe Sepsis)
DEATH
SEPSIS

28. SIRS Sepsis Severe
Sepsis
Septic Shock
Systemic
inflammatory
response to variety
of severe clinical
insults indicated by
2 or more of the
following:
Temp > 38 or < 36
HR > 90bpm
(adults)/ >2SD(ped)
RR > 20/min
(adults)/>2SD(ped)
OR PACO2
<32mmhg
WBC>12000,
<4000 or > 10%
bands
Systemic response
to infection
manifested by 2 or
more of the following
as a result of
infection:
 Temp > 38 or < 36
HR>90
RR>20 or PaCO2 <
32
WBC>12000.
<4000 or >10%
bands
Sepsis associated
with:
Organ dysfunction
Hypoperfusion
(Lactic acidosis,
oliguria, altered
mental status)
Hypotension

29. Warm Shock Cold Shock Fluid-Refractory/
Dopamine resistant
Catecholamine
Resistant
Refractory Shock
Early,
compensated
Clinical Signs
-Inc.HR
-Warm
extremities,
bounding pulses
Physiologic
Parameters
-Wide PP
-Inc. C.O.
-Inc. MvO2
-Dec.SVR
Lab Data
-Hypocardia
-Inc. Lactate
-Inc.Glucose
Late, Uncompensated
Clinical Signs
-Cold, clammy extremities
-Rapid, thready pulses
-Shallow breathing
Physiologic Parameters
-Narrow PP
-Dec.CVP, C.O
-Dec. MvO2 sat
-Inc. SVR
-Oliguria
-Capillary Leak
Lab Data
-Metab. Acidosis
-Hypoxia
-Coagulopathy
-Hypoglycemia
Persistance of shock
despite > 60cc/kg
fluid resuscitation
Persistance of shock
despite Dopamine at
>10mcg/kg/mn
Persistance of shock
despite administration of
direct acting
catecholamines
Epinephrine/
Nor-Epinephrine
Persistance of shock
despite:
-Goal direct inotropic/
pressor therapy
-Use of vasodilators
-Maintenance of
metabolic and
hormonal homeostasis

31. Early Goal directed therapy in treatment of sepsis and septic shock- Rivers et al., NEJM, Nov 2001

32.  Community-Acquired Sepsis
 Pneumonia-Quinolone PLUS B-lactam
 Abdominal-Carbapenem OR Pip-Tazo
 Skin/Soft Tissue-Vanco PLUS Carbapenem or Pip-Tazo
 Urinary Tract-Quinolone PLUS Amp/Vanco
 Unknown-Vanco PLUS B-lactam
 Health-Care Associated Sepsis
 Lung-B-lactam PLUS Vanco
 Bloodstream -B-lactam PLUS Vanco +/- Antifungal
 Surgical Site -B-lactam PLUS Vanco +/- Anaerobic coverage
 Suspected Candida-Caspofungin
 Unknown-B-lactam PLUS Vanco
Antibiotic Guidelines in Sepsis by Suspected SiteAntibiotic Guidelines in Sepsis by Suspected Site

33. HEMODYNAMIC VARIABLES IN
SHOCK STATES
↑ or ↔↑↓↓↑↑↓↓Septic: Late
↓↓↔ Or ↓↓↓↓↑↑↑Septic: Early
↔ Or ↓↔ Or ↓↔ Or ↓↓↓↓↑↑Distributive
↑↑↑↑↔ Or ↓↑↓Obstructive
↑↑↑↑↔ Or ↓↑↑↑↓↓Cardiogenic
↓↓↓↓↓↓↔ Or ↓↑↑Hypovolemic
CVPWedgeMAPSVRCO

34. B.P or Systemic Vascular Resistance
Therapies for Hemodynamic Patterns in Shock
State

35. Therefore, the Basics….
 Stabilize respiration
 Assess perfusion
 Fluid administration
 IV Access
 Vasopressors
 Inotropic therapy
 Red blood cell transfusions if needed

36. References
 Pediatric Critical Care: Fuhrman, Zimmerman
 Surviving Sepsis Guidelines
 E-medicine
 Uptodate online
 SCCM website