SHOCK

Suryadi Susanto
Pediatric Departement
Krida Wacana Christian University
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
Introduction
Shock

 acute process
 inability of deliver adequate oxygen to meet the metabolic
demands of vital organs and tissues
 shifting to anaerobic metabolism
 irreversible tissue and organ injury if left untreated or death

LACTIC ACIDOSIS
- Progression of shock  uncompensatory oxygen extraction 
progressive clinical deterioration and LACTIC ACIDOSIS
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
Epidemiology
Shock
 occurs in approximately 2% of all hospitalized
patients in developed countries
 Death is usually a result of associated complications
and multiple organ dysfunction
MODS
 alteration in organ function that requires medical
support for maintenance
 the presence in patients with shock increases
the probability of death
 Criteria for Organ Dysfunction
ORGAN SYSTEM CRITERIA FOR DYSFUNCTION
Cardiovascular • Despite administration of isotonic intravenous fluid bolus ≥60 mL/kg in 1 hr:
decrease in BP (hypotension) systolic BP <90 mm Hg, mean arterial pressure
<70 mm Hg, <5th percentile for age, or systolic BP <2 SD below normal for age
or
• Need for vasoactive drug to maintain BP in normal range (dopamine >5 μg/kg/mi
n or dobutamine, epinephrine, or norepinephrine at any dose)
or
• Two of the following:
• Unexplained metabolic acidosis: base deficit >5.0 mEq/L
• Increased arterial lactate: >1 mmol/Liter or >2× upper limit of normal
• Oliguria: urine output <0.5 mL/kg/hr
• Prolonged capillary refill: >5 sec
• Core to peripheral temperature gap >3°C (5.4°F)
Criteria for Organ Dysfunction
ORGAN SYSTEM CRITERIA FOR DYSFUNCTION

Respiratory  PaO2/FIO2 ratio <300 in absence of cyanotic heart disease or preexisting

lung disease
or
 PaCO2 >65 torr or 20 mm Hg over baseline PaCO2
or
 Need for >50% FIO2 to maintain saturation ≥92%
or
 Need for nonelective invasive or noninvasive mechanical ventilation

Neurologic GCS score ≤11

or
Acute change in mental status with a decrease in GCS score ≥3 points from abnorm
al
baseline
Criteria for Organ Dysfunction
ORGAN SYSTEM CRITERIA FOR DYSFUNCTION
Hematologic Platelet count <100,000/mm3 or a decline of 50% in the platelet count
from the highest value recorded over the last 3 days (for patients with chron
ic hematologic or oncologic disorders)
or
INR >1.5
or
Activated prothrombin time >60 sec
Renal Serum creatinine >0.5 mg/dL, ≥2× upper limit of normal for age, or 2-fol
d increase in baseline creatinine value
Hepatic Total bilirubin ≥4 mg/dL (not applicable for newborn)
Alanine transaminase level 2× upper limit of normal for age
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
DEFINITION

 Inadequate oxygen and nutrient delivery to the tissues

to meet metabolic demands

shock does not begin when blood

pressure drops but it merely worsens and
becomes more difficult to treat once
blood pressure is abnormal
5 Major Types of Shock
Hypovolemic shock
the most common cause of shock in children
worldwide

Cardiogenic shock
seen in patients with either congenital heart disease
or with congenital or acquired cardiomyopathies

Obstructive shock
stems from any lesion that creates a mechanical
barrier that impedes adequate cardiac output
Distributive shock
caused by inadequate vasomotor tone 
capillary leak and maldistribution of fluid into
the interstitium

Septic shock
usually involves a more complex interaction of
distributive, hypovolemic, and cardiogenic
shock
 Types of Shock
HYPOVOLEMIC CARDIOGENIC DISTRIBUTIVE SEPTIC OBSTRUCTIVE
Decreased preload Cardiac pump failure Abnormalities of Encompasses multiple Decreased cardiac outp
secondary to internal or secondary to poor vasomotor tone from forms of shock ut secondary to direct
external losses myocardial function loss of venous and Hypovolemic: third impediment to right- or
arterial capacitance spacing of fluids into the left-heart outflow or
extracellular, interstitial restriction of all cardiac
space chambers
Distributive: early shock
with decreased afterload
Cardiogenic: depression
of myocardial function by
endotoxins

POTENTIAL ETIOLOGIES
Blood loss: hemorrhage; Congenital heart disease Anaphylaxis Bacterial Tension pneumothorax
Plasma loss: burns, Cardiomyopathies: Neurologic: loss of Viral Pericardial tamponade
nephrotic syndrome; infectious or acquired, sympathetic vascular Fungal (immunocompro- Pulmonary embolism
Water/electrolyte loss: dilated or restrictive tone secondary to spinal mised patients are at Anterior mediastinal
vomiting, diarrhea Ischemia cord or brainstem injury increased risk) masses
Arrhythmias Drugs Critical coarctation of the
aorta
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
 Pathophysiology of Shock
EXTRACORPOREAL FLUID LOSS
Hypovolemic shock may be a result of direct blood loss through hemorrhage or abnormal loss of
body fluids (diarrhea, vomiting, burns, diabetes mellitus or insipidus, nephrosis)
LOWERING PLASMA ONCOTIC FORCES
Hypovolemic shock may also result from hypoproteinemia (liver injury, or as a progressive
complication of increased capillary permeability)
ABNORMAL VASODILATION
Distributive shock (neurogenic, anaphylaxis, or septic shock) occurs when there is loss of vascular
tone—venous, arterial, or both (sympathetic blockade, local substances affecting permeability,
acidosis, drug effects, spinal cord transection)
INCREASED VASCULAR PERMEABILITY
Sepsis may change the capillary permeability in the absence of any change in capillary hydrostati
c pressure (endotoxins from sepsis, excess histamine release in anaphylaxis)
CARDIAC DYSFUNCTION
Peripheral hypoperfusion may result from any condition that affects the heart’s ability to pump
blood efficiently (ischemia, acidosis, drugs, constrictive pericarditis, pancreatitis, sepsis)
 Initial insult Algorithm For Decompensated Shock
Triggers shock
Early phases of shock:: multiple compensatory
physiologic mechanisms act to maintain blood
Decreased perfusion pressure and preserve tissue perfusion and
oxygen delivery

Cardiovascular effects:
heart rate
Body’s compensatory stroke volume
mechanisms vascular smooth muscle tone

Respiratory effects:
CO2 production dt poor tissue
perfusion
CO2 elimination

Compensated shock Decompensated shock

Renal effects:
Renal excretion of H+
Renal retention of HCO3
Tissue damage Na+ regulation through RAAS
and ANF, cortisol and
chatecholamine

Multisystem organ failure

Death
Hypovolemic Shock
 fluid loss and decreased preload
 initial compensatory responses:
tachycardia to maintain cardiac output and
systemic blood pressure
increase in SVR
 Inadequate volume replacement:
HYPOTENSION  TISSUE ISCHEMIA
 Preexisting low plasma oncotic pressure:
endothelial breakdown and worsening capillary leak
 further volume loss and exacerbation of shock
Distributive Shock

 state of abnormal vasodilation and decreased SVR

 sepsis, hypoxia, poisonings, anaphylaxis, spinal cord injury,
or mitochondrial dysfunction
 lowering of SVR
 maldistribution of blood significant decreases
flow away from vital organs in both preload and
 compensatory increase in afterload
cardiac output.

 Therapies address both of these problems simultaneously

Cardiogenic shock
 myocarditis, cardiomyopathy, congenital heart
disease, or arrhythmias, post cardiac
surgery
 myocardial contractility is affected  systolic and/
or diastolic dysfunction  cardiogenic
component to the shock state
Septic shock
 combination of distributive, hypovolemic,
and cardiogenic shock
 Hypovolemia
 from intravascular fluid losses occurs through
capillary leak
 Cardiogenic shock
 results from the myocardial-depressant effects
of sepsis
 Distributive shock
 the result of decreased SVR
 alterations in preload, afterload, and myocardial
contractility.
 Septic Shock
Inciting infection vs Host inflammatory response

Host immunity
cellular
immune
inflammatory system derangement of the
reticular cascade of
endothelial microcirculatory
toxic mediators,
system including hormones, system leads to
cytokines, and subsequent organ
enzymes. and cellular dysfunction.
uncontrolled
humoral
immune
system
Systemic Inflammatory Response
Syndrome (SIRS)

 an inflammatory cascade that is initiated by the host

response to an infectious or noninfectious trigger
 may lead to: hypovolemia, cardiac and vascular failure,
acute respiratory distress syndrome (ARDS), insulin
resistance, decreased cytochrome P450 activity
(decreased steroid synthesis), coagulopathy, and
unresolved or secondary infection
 Superantigens or toxins Hypothetical Pathophysiology Of
Focus of infection
(e.g., endotoxin) The Septic Process

Activated inflammatory cells Activation of host defense

Activation of complement system Activation of coagulation system

Activated endothelium
Increased expression endothelial
derived adhesion molecules

Decreased thrombomodulin
Increased plasminogen activator inhibitor
Thrombosis and antifibrinolysis

Hypovolemia/Cardiac and vascular failure/ Capillary leak/endothelial damage /Acute respirato

ry distress syndrome/ Disseminated intravascular coagulation
Hypovolemia/Cardiac and vascular failure/ Capillary leak/endothelial damage /Acute respirato
ry distress syndrome/ Disseminated intravascular coagulation

Shock

Multiorgan Dysfunction
Syndrome (MODS)

Death
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
CLINICAL MANIFESTATIONS
 depends in part on the underlying etiology
 tachycardia, with or without tachypnea 
UNTREATED:
• decreased urine output,
• poor peripheral perfusion,
• respiratory distress or
failure
• alteration of mental status
• low blood pressure

 hypotension reflects an advanced state of decompensated shock

and is associated with increased morbidity and mortality
 MANIFESTATIONS
Hypovolemic Cardiogenic Obstructive Distributive Sepsis  Shock

• orthostatic hypo- • tachypnea • inadequate • initially peripheral • systemic or

tension associated • cool extremities, cardiac output vasodilation and localized infection
with dry mucous • delayed capillary because of a increased but progresses from
membranes, dry filling time physical restric- inadequate sepsis to severe
axillae, poor skin • poor peripheral a tion of forward cardiac output sepsis  septic
turgor, and decrea nd/or central puls blood flow shock MODS
sed urine output es  death
• normal or slightly • declining mental • alterations in
cool distal extre- status temperature
mities • decreased urine regulation
• pulses may be nor output • initially increase
mal, decreased, or cardiac output 
absent cardiac output
falls
Signs of Decreased Perfusion
ORGAN SYSTEM ↓ PERFUSION ↓↓ PERFUSION ↓↓↓ PERFUSION

Central nervous — Restless, apathetic, anxious Agitated/confused,

system stuporous, coma
Respiration — ↑ Ventilation ↑↑ Ventilation

Metabolism — Compensated metabolic Uncompensated metabolic

acidemia acidemia
Gut — ↓ Motility Ileus

Kidney ↓ Urine volume Oliguria (<0.5 mL/kg/hr) Oliguria/anuria

↑ Urinary specific gravity
Skin Delayed capillary refill Cool extremities Mottled, cyanotic, cold
extremities
Cardiovascular ↑ Heart rate ↑↑ Heart rate ↑↑ Heart rate
system ↓ Peripheral pulses ↓ Blood pressure, central
pulses only
Hemodynamic Variables in Different Shock States
TYPE OF CARDIAC SYSTEMIC MEAN CAPILLARY CENTRAL
SHOCK OUTPUT VASCULAR ARTERIAL WEDGE VENOUS
RESISTANCE PRESSURE PRESSURE PRESSURE
Hypovolemic ↓ ↑ ↔ or ↓ ↓↓↓ ↓↓↓

Cardiogenic
Systolic ↓↓ ↑↑↑ ↔ or ↓ ↑↑ ↑↑
Diastolic ↔
↔ ↑↑ ↑↑ ↑

Obstructive ↓ ↑ ↔ or ↓ ↑↑† ↑↑†

Distributive ↑↑ ↓↓↓ ↔ or ↓ ↔ or ↓ ↔ or ↓

Septic
Early ↑↑↑ ↓↓↓ ↔ or ↓ ↓ ↓
Late ↓↓
↓↓ ↓↓ ↑ ↑ or ↔
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
Diagnosis
 clinical diagnosis based on a thorough history and
physical examination
 suspected septic shock:
• culture of clinically appropriate specimen
• prompt initiation of empiric antimicrobial therapy
based on:
 patient age
 underlying disease
 geographic location
Continuation..

 physical examination findings

 imaging
 presence of white blood cells in normally sterile body fluids
 suggestive rashes such as petechiae and purpura.
International Consensus Definitions for Pediatric Sepsis
Infection Suspected or proven infection or a clinical syndrome associated
with high probability of infection
SIRS Two of 4 criteria, 1 of which must be abnormal temperature or abnormal leukocyte
count:
1. Core temperature >38.5°C (101.3°F) or <36°C (96.8°F) (rectal, bladder, oral, or
central catheter)
2. Tachycardia:
Mean heart rate >2 SD above normal for age in absence of external stimuli,
chronic drugs or painful stimuli
or
Unexplained persistent elevation over 0.5-4 hr
or
In children <1 yr old, persistent bradycardia over 0.5 hr (mean heart rate
<10th percentile for age in absence of vagal stimuli, β-blocker drugs, or
congenital heart disease)
3. Respiratory rate >2 SD above normal for age or acute need for mechanical
ventilation not related to neuromuscular disease or general anesthesia
4. Leukocyte count elevated or depressed for age (not secondary to chemotherapy)
or >10% immature neutrophil
Continuation
Sepsis SIRS plus a suspected or proven infection

Severe Sepsis plus 1 of the following:

1. Cardiovascular organ dysfunction, defined as:
sepsis
• Despite >40 mL/kg of isotonic intravenous fluid in 1 hr:
• Hypotension <5th percentile for age or systolic blood pressure
<2 SD below normal for age
or
• Need for vasoactive drug to maintain blood pressure
or
• 2 of the following:
• Unexplained metabolic acidosis: base deficit >5 mEq/L
• Increased arterial lactate: >2 times upper limit of normal
• Oliguria: urine output <0.5 mL/kg/hr
• Prolonged capillary refill: >5 sec
• Core to peripheral temperature gap >3°C (5.4°F)
2. ARDS as defined by the presence of a PaO2/FIO2 ratio ≤300 mm Hg, bilateral
infiltrates on chest radiograph, and no evidence of left heart failure
or
Sepsis plus 2 or more organ dysfunctions (respiratory, renal, neurologic,
hematologic, or hepatic)
Continuation
Septic shock Sepsis plus cardiovascular organ dysfunction as defined above

MODS Presence of altered organ function such that homeostasis cannot be maintained without
medical intervention
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
LABORATORY FINDINGS
hematologic abnormalities and electrolyte disturbances
Hematologic Abnormalities
• thrombocytopenia
• prolonged PT and PTT
• reduced serum fibrinogen
• elevations of fibrin split products
• anemia
• elevated neutrophil counts and i
ncreased immature forms
Toxic Döhle bodies
• vacuolation of neutrophils
Granulations
• toxic granulations
• Döhle bodies
• neutropenia or leukopenia
Electrolyte disturbances

• glucose dysregulation
• hyperglycemia or hypo glycemia.
• hypocalcemia
• hypoalbuminemia
• metabolic acidosis

Renal and/or Hepatic

• Patients with ARDS or pneumonia
• impaired oxygenation and ventilation

Hallmark Of Uncompensated Shock:
imbalance between Oxygen Delivery (Do2)
and Oxygen Consumption (Vo2)
Falling SVO2 as measured by
cooximetry =
• increasing oxygen
extraction ratio
• decrease in oxygen
delivery relative to
consumption
manifest as increased lactic
acid production dt anaerobic
metabolism and the compen-
satory increase in tissue
oxygen extraction
Gold Standard:
Pulmonary Arterial Catheter
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII.Treatment
IX. Prognosis
RECOGNITION AND MANAGEMENT
OF SHOCK

Early recognition and prompt intervention

Stabilization of
 Airway
 Breathing
 Circulation
(American Heart Association’s pediatric advanced life support and neonatal ad
vanced life support guidelines)
Initial Management
Hospital Setting
1. obtain central venous and arterial access
 renal and liver function
 acid–base balance (presence of lactic acidosis)
 hypoxemia and/or hypercapnia
 coagulopathy or disseminated intravascular
coagulation
 Other labs:
 chest radiography
 echocardiography
2. Respiratory and cardiovascular support
Focus: Modifiable determinants of oxygen while delivery
reducing the imbalance between oxygen demand
and supply
 A multipronged approach is recommended
 optimizing the oxygen content of the blood
 improving the volume and distribution of
cardiac output
 correcting metabolic derangements
 reducing oxygen demand
.

 transfusion
• presence of hemorrhagic or distributive shock
 high oxygen saturations through oxygen administration to
increase cardiac output
• nasal cannula or face mask
• positive pressure, such as CPAP, BiPAP
• mechanical ventilation
Sepsis and Hypovolemia are the most common causes of
shock in the pediatric population

 IV or intraosseous access
 Rapid IV administration of 20 mL/kg isotonic fluid
(repeated quickly up to 60-80 mL/kg )
 sometimes require as much as 200 mL/kg or greater
 Measures:
 normalize heart rate (according to age-based HR)
 urine output (to 1 mL/kg/hr)
 capillary refill time (to <2 sec)
 mental status
 refractory following 60-80 mL/kg of volume resuscitation
 vasopressor therapy should be instituted while additi
onal fluids are administered
 World Health Organization’s
Hypovolemic/ septic Shock
definition of shock that
requires fluid boluses:
IV or intraosseous access  cold hands
 capillary refill >3 sec
20 mL/kg isotonic  fast and weak pulses
Resolve ?  Measures:
No
 normalize heart rate (according
Yes to age-based HR)
to 60-80 mL/kg  urine output (to 1 mL/kg/hr)
 capillary refill time (to <2 sec)
Resolve ?
No  mental status

Yes 200 mL/kg or greater

Resolve ?
No

Yes vasopressor therapy

fluid therapy
Goal-directed endpoint
Additional Early Considerations
early administration of broad-spectrum
Septic Shock antimicrobial agents is associated with a
reduction in mortality
Neonate:
ampicillin plus cefotaxime and/or gentamicin
acyclovir if herpes simplex virus is suspected

Infants and Children

 Community-acquired Infections with Neisseria meningitides
3rd-generation cephalosporin (ceftriaxone or cefotaxime)
 Haemophilus influenzae 
3rd-generation cephalosporin
 Resistant Streptococcus pneumoniae
requires the addition of vancomycin
 Staphylococcus aureus Methicillin-Resistantinfection
 vancomycin
 Nosocomial sepsis
 3rd- or 4th-generation cephalosporin
or
 penicillin with an extended Gram-negative spectrum
(e.g., piperacillin-tazobactam)
Vancomycin is added to the regimen with the following condition:
 has an indwelling medical device
 Gram-positive cocci are isolated from the blood
 methicillin-resistant S. aureus infection is suspected
 empiric coverage for S. pneumoniae in a patient with meningitis

Empirical coverage for fungal infections should be considered

for selected immunocompromised patients
Distributive shock

 primary abnormality in vascular tone

 may benefit temporarily from volume resuscitation
 early initiation of a vasoconstrictive agent to increase SVR is an important
element of clinical care

 Spinal Cord Injury and Spinal Shock

 phenylephrine or vasopressin to increase SVR

 Anaphylaxis
 epinephrine is the treatment of choice
Cardiogenic Shock

 poor cardiac output secondary to systolic and/or diastolic myocardial

 depression often with a compensatory elevation in SVR
 poor response to fluid resuscitation
 may decompensate quickly with fluid
 Smaller boluses of fluid (5-10 mL/kg)
 to replace deficits and maintain preload.
 Early initiation of myocardial support with epinephrine or dopamine
 May consider inodilator, Milrinone
Cardiovascular Drug Treatment of Shock
DRUG EFFECT(S) DOSING RANGE COMMENT(S)
Dopamine ↑ Cardiac contractility 3-20 μg/kg/min ↑ Risk of arrhythmias at
Significant peripheral high doses
vasoconstriction at
>10 μg/kg/min
Epinephrine ↑ Heart rate and ↑ cardiac 0.05-3.0 μg/kg/min May ↓ renal perfusion at
contractility high doses
Potent vasoconstrictor ↑ Myocardial O2 consumption
Risk of arrhythmia at high
doses
Dobutamine ↑ Cardiac contractility 1-10 μg/kg/min —
Peripheral vasodilator
Norepinephrine Potent vasoconstriction 0.05-1.5 μg/kg/min ↑ Blood pressure secondary to
No significant effect on cardiac ↑ systemic vascular resistance
contractility ↑ Left ventricular afterload
Phenylephrine Potent vasoconstriction 0.5-2.0 μg/kg/min Can cause sudden
hypertension
↑ O2 consumption
Obstructive Shock
 the primary insult must be immediately addressed
 pericardiocentesis for pericardial effusion
 pleurocentesis or chest tube placement for pneumothorax
 thrombectomy/thrombolysis for pulmonary embolism
 initiation of a prostaglandin infusion for ductus-dependent
cardiac lesions

“last-drop” phenomenon associated with some obstructive lesions,

in that small additional amounts of intravascular volume
depletion may lead to a rapid deterioration, including cardiac
arrest, if the obstructive lesion is not corrected
Management of Shock Regardless of Etiology

Monitor and Correct:

 metabolic status
 electrolyte levels
 hypoglycemia
 hypocalcemia
 adrenal dysfunction
 hydrocortisone replacement
 Considerations for Continued Therapy
Shock Remains Refractory Despite Maximal
Therapeutic Interventions
 Extracorporeal Membrane Oxygenation:
 effective for refractory shock regardless of underlying
etiology
 Ventricular Assist Device
 cardiogenic shock in the setting of cardiomyopathy or
recent cardiac surgery
Outline
I. Introduction
II. Epidemiology
III. Definition
IV. Pathophysiology
V. Clinical Manifestations
VI. Diagnosis
VII. Laboratory Findings
VIII. Treatment
IX. Prognosis
Prognosis
Septic Shock

 Mortality Rates
 3% in previously healthy children
 6-9% in children with chronic illness
 Shock and MODS
 one of the leading causes of death in infants and children
 Risk Of Death
 underlying etiology
 presence of chronic illness
 host immune response
 timing of recognition and therapy