Shock is a life-threatening condition defined by inadequate tissue perfusion and oxygen delivery. It can be caused by hypovolemia, cardiac dysfunction, or vasodilation. The main symptoms include low blood pressure, fast heart rate, fast breathing, and decreased urine output. Untreated shock can lead to organ failure and death. Treatment focuses on restoring circulating volume and oxygen delivery through fluid resuscitation, vasopressors, and treating the underlying cause. Prompt recognition and treatment are essential for recovery.

1. Shock

2. • Worldwide, shock is a leading cause of morbidity
and mortality in the pediatric population.
• Shock is defined as a state of acute energy failure
due to inadequate glucose substrate delivery,
oxygen delivery, or mitochondrial failure at the
cellular level.
• The clinical state of shock is diagnosed on the
basis of vital signs, physical examination, and
laboratory data, although its recognition in the
pediatric patient can be difficult.

3. • Delay in recognizing and quickly treating a state
of shock results in anaerobic metabolism, tissue
acidosis, and a progression from a compensated
reversible state to an irreversible state of cellular
and organ damage.
• Morbidity from shock may be widespread and
can include CNS failure, respiratory failure (ie,
from muscle fatigue or ARDS], renal failure,
hepatic dysfunction, gastrointestinal
ischemia, DIC, metabolic derangements, and
ultimately death.

4. • Shock is the most reversible causes of death in
children.
• An acute , complex state of circulatory
dysfunction that result in failure to deliver
sufficient amount of O2 and nutrient to meet
tissue metabolic demands
• Therefore, basically DO2< VO2
• If prolonged and left untreated- can lead to
multiple organ failure and eventually death.

5. • Oxygen delivery + cardiac output x atrial
oxygen content ( DO2+ COxCaO2)
• Cardiac output + HR x CO

6. • Shock is a physiologic state characterized by
systemic reduction in tissues perfusion,
resulting in decreased tissues oxygen delivery.

7. • It is a condition in which circulation fails to meet
the metabolic need of the tissue and at the same
time fails to remove the metabolic waste
products
• Inadequate tissue perfusion to meet demands
usually result of inadequate blood flow and or
oxygen delivery
• Inadequate peripheral perfusion leading to failure
of tissue oxygenation leads to anaerobic
metabolism

10. Compensatory Mechanism
SNS-adrenal response
- SNS- Neurohormonal response stimulated by
baroreceptors
• Increased heart rate
• Increased contractibility
• Vasoconstriction
• Increased preload

11. • SNS- hormonal: renin angiotensin system
• Decreased renal perfusion
• Release renin Angiotensin I
• Angiotensin II Potent vasoconstriction and
releases aldosterone adrenal cortex
• Water sodium retention( increased
intravascular volume)

12. • SNS-Hormonal :antidiuretic hormone
- Osmoreceptors in hypothalamus stimulated
- ADH released by pituitary
- Vasopressor effects to increase BP
- Acts on renal tubules to retain water

13. • SNS- Hormonal: adrenal cortex
- Anterior pituitary releases ACTH
- Stimulates adrenals to release glucocorticoids
- Blood sugar increases to meet increased
metabolic needs

14. Failure of compensatory responses
• Decreased blood flow to the tissues causes
cellular hypoxia
• Anaerobic metabolism begins
• Cell swelling, mitochondrial disruption, and
eventual cell death
• If low perfusion persist:
Death

15. Stages of shock
• Initial stage – tissues are under perfused,
decreased cardiac output, increased anaerobic
metabolism, lactic acid is building
• Compensatory stage- reversible. SNS activated by
low output, attempting to compensate for the
decrease tissue perfusion
• Progressive stage- falling compensatory
mechanism profound vasoconstriction from SNS
ischemic– lactic acid production is high
metabolic acidosis

16. Clinical presentation( Generalized
shock)
- Vital sign
• hypotension
• Tachycardia
• Tachypnea
- Mental Status
Irritability, restless, LOC, unresponsiveness
- Decreased urine output

17. Compensated
• Confusion
• Tachycardia
• Normal or mild tachypnea
• > CRT
• Urine out adequate
• BP normal

18. Uncompensated
• Drowsiness
• Marked tachycardia
• Tachypnea and acidosis
• Very slow CFT
• Oliguria/Anuria
• Hypotension

19. Irreversible
• Child is unresponsive
• Bradycardia
• Apnea
• Cold cyanotic skin
• Anuria
• Un-Recordable BP

20. • Hypotension formula
Ages- 1-10 years is defined as
<70 mm of hg +(age in years x2)mm of hg

21. Shock syndrome
• Hypovolemic shock
- Blood volume problem
• Cardiogenic shock
- Blood pump problems
• Distributive shock
- Blood vessels problem

22. Hypovolemic shock
• Loss of circulating volume “empty tank”
decrease tissue perfusio general shock
response
• Etiology
- Internal / external l fluid loss
- Intracellular/ extracellular compartments
• Most common cause
Hemorrhage and dehydration

23. External loss
• Fluid loss: dehydration
Nausea and vomiting, diarrhoea, massive
diuresis, extensive burns
• Blood loss
Trauma visible or invisible bleeding

24. Internal loss
• Loss of intravascular integrity
• Increased capillary membrane permeability
• Decreased colloidal osmotic pressure( third
spacing)

28. Presentation
• Tachycardia and tachypnea
• Weak, thready pulses
• Hypotension
• Skin cool and clammy
• Mental status changes
• Decreased urine output dark and
concentrated

29. Treatment
• Main goal- restore circulating volume and tissue
perfusion, correct the cause
1. Assess airway
2. Administer oxygen
3. Control bleeding and balance
4. Establish IV assess
5. Fluid boluses ( max-3) isotonic fluid
6. In case of shock refractory to fluids, start
inotrope(dopamine)

30. Cardiogenic shock
• The impaired ability of the heart to pump
blood
• Pump failure of the right or left ventricle
• Most common causes of MI

31. • When heart Is unable to contract and pump
blood efficiently due to inadequate supply of
O2 and nutrient to the heart

32. • Older age
• History of heart attack , heart failure
• CHD
• Hypertension
• Diabetic
• obesity

33. Etiological factor
• Acute MI
• Hypertension
• Cardiomyopathy
• Pericardial tamponade
• Acidosis dysrhythmias
• Trauma
• Structural abnormality
- Vulvur anomalies

37. Clinical manifestation
angina pectoris
Dysrhythmias
Diminished heart sound
Hypotension
Decreased cardiac output
SOB
Weak, thready pulse
decreased urine output
Cold clammy skin

38. Complication
• Brain damage
• Kidney damage
• Liver damage
• Multiple organ failure
• Coma
• Death

39. Management
• Correction of the underlying cause is important
to prevent
- Fail of the compensatory mechanism
- Reduces effectiveness of intervention
Correction of
- Dysrhythmias
- Acidosis, electrolyte imbalance:
-

40. • Initiation of 1st line treatment
- oxygenation-(2-6 lit)
- Hemodynamic monitoring
- Fluid balance
- Pain control

41. • Pharmacological management
- Dobutamine
- Dopamine
- Vasoactive medication
Epinephrine
Nor-epinephrine
vasopressin

42. • Surgical management
CBAG( coronary artery bypass graft)
Valve replacement

43. Distributive shock
• Inadequate perfusion of tissues through
misdistribution of blood flow
• Intravascular volume is mal-distributed
because of alterations in blood vessels
• Cardiac pump and blood volume are normal
but blood is not reaching the tissues

44. • Etiologies
- Septic shock (most common)
- Anaphylactic shock
- Neurogenic shock

45. Anaphylactic shock
• A type of distributive shock that result from
wide spread systemic allergic reaction to an
antigen
• The hypersensitive reaction is life threatening

46. • Anaphylaxis: reaction sudden life threatening
because the process immunologic of allergen-
antibody reaction
• Anaphylactic reaction causing physical the
same symptoms but caused no immunological
reaction

47. Stages of anaphylactic shock
• Changes in mast cell towards stimuli
• Activation of cell wall enzyme
• Meditators release
• Functional pathophysiology response
• Inflammation and release of secondary
meditators

48. Etiology
1) Associated with IgE
2) Non IgE
3) Causes of anaphylatoid
- Drugs like NSAID, antibiotics, alkaloids, food
additives

51. Clinical features
• Skin- itching erythema, urticaria
• Respiratory- sneezing runny nose, wheezing,
swollen larynx. Tightness, hoarseness, stridor,
cyanosis
• Digestive- nausea vomiting diarrhoea, abd
pain
• Eye- itching, tears
• Cardiovascular- collapse fainting, hypotension
pale, cold, tachycardia

52. Management
• Primary treatment
-Adrenaline 1:1000 with dose of 0.001ml/kg
maximum 0.3 ml SC
-Can be repeated 3 times
-head extended , ventilated position
-O2 2-3 lit

53. • Place patient in shock position
• Pulmonic resuscitation
• Oro-pharyngeal airway
• E insertion
• Tracheostomy
• Cardiac compression

54. Complementary treatment
• Intended for complication
- seizures- diazepam, phenobarbital, midazolam
- Bronchial spasm- Aminophylline 7mg with 10-
20 ml of 0.9& NaCl followed 9mg/kg/24
hours( divided into 3 dose)
- B-2 agonist: ventolin nebulizer

55. Additional
• Antihistamine
• H-2 receptor antagonist
• Corticosteroids

56. Septic Shock

57. • Septicemia is a condition when there is prolonged
presence of bacteria in the blood accompanied
by systemic reaction
• SIRS,I s a syndrome characterized by presence of
two or more of the following clinical criteria
- Temperature increased or decreased
- Tachycardia
- Respiratory rate >20b/m or PaCO2 <32 mm of hg
- Increased or decreased WBC

58. • Result from moderate to severe sepsis or
tissues damage. It is considered as part of a
spectrum and a progression of SIRS
• Sepsis: SIRS with a clearly established focus of
infection
• Septic Shock: refers to severe sepsis which is
not responsive to intravenous fluid infusion
for resuscitation and requires inotropic or
vasopressor agent to maintain SBP

59. • Multiple organ dysfunction (MODS)- altered
function of more than one organ system in an
actually ill patient requiring medical
intervention homeostasis.

60. • Epidemiology
-4.6cases/1000 in US
200,000 cases annually with 50% mortality
M>F
Leading cause in pediatric ICU

61. • Bacteria: gram negative nearly 2/3rd, gram
positive 1/3rd
• E.coli is commonest
• Gram negative

62. Source
Endogenous-
Skin
Urinary
Respiratory
Bowel
Exogenous-
surgical intervention
Drapes
Imaging machines
staff

63. Risk factors
• Age <10yr,<70yr
• Malnutrition
• Anemia
• Primary disease, malignancies, DM, CLD, CRF
• Necrotic issues
• Hematoma
• Poor surgical technique
• Catherization
• Prolong hospitalization
• Major surgeries

64. Pathogenesis
• Microorganism or product of tissue damage
stimulate production of pro-inflammatory
cytokines, which in turn stimulate production of
secondary mediators of inflammation
• The production of the pro-inflammatory
cytokines is regulated to limit damage
• However poorly control sepsis or extensive tissue
damage, there is excessive inflammatory
response which is poorly regulated

67. • Hypovolemic state, cardiac depression,
interstitial loss, AV shunt all causes cellular
hypoxia and ultimate septic shock

70. Clinical features
• Early stage- (compensated/warm shock) or
condition not associated with hypovolemia
- febrile(38-41)
- Shivering and malaise
- Warm dry flushed skin
- Hyperventilation
- Rapid bounding pulse
- Wide pulse pressure

71. Decompensated/cold shock
• Altered sensorium
• Cold clammy skin
• Feeble pulse
• Hypothermia
• Oliguria
• Jaundice
• UGI
• DIC

72. • Localizing infection
- A good systemic examination is done to detect
any focus of infection.

73. Diagnosis
• Blood/urine/sputum culture
• CBC
• BUN and Creatinine
• PT and PTT
• ECG
• Serum lactate dehydrogenase level
• Urinalysis
• ABG

74. Treatment
• Septic shock is a medical emergency that
requires prompt and sufficient resuscitation
• Treatment should be carried out in ICU setting
Aims
To improve hemodynamic state
Restore tissues perfusion
Eliminate toxin from body

75. 1) volume replacement
- Iv assess with large bore cannula
- Prompt investigation
- Crystalloids start: 1lit in 30 min-45min,
reassess and repeat appropriate
- Catherization
- CVP monitoring

76. • Vasopressor
2) Oxygen
3)Antibiotic
4) Steroid
5)NSAID
6)Free radical scavengers
7) Glycemic control
8) Naloxone
9) Coagulation
10) Surgery

77. WATCH
• Clinical sign
- Sensorium
- Conjunctiva
- Capillary refill
- Warm dry skin
• Urine output
• Vitals
• CVP
• Lungs and JVPABSG

78. Complication
• ARDS
• ARF
• DIC
• Encephalopathy
• Liver failure
• Coma
• Death

79. Prognosis
• Poor prognostic factor
- Advanced age
- Immunosuppression
- Infection
- Need for inotropes for >24hrs
- Availability and mode of treatment

80. Prevention
• Early recognition
• Prompt treatment of infection
• Meticulous surgical treatment
• Pre op antibiotics
• Aseptic technique

81. Treatment
• 1. Recognize signs of poor perfusion (0-5min)
• Decreased mental status
• Cold extremities
• Delayed capillary refill
• Weak pulses, differential central and peripheral
pulses
• Low urine output
• Hypotension or low BP: Minimum systolic BP by
age: < 1mo: 60 mmHg; 1mo to 10y: 70 + (2 × age
in years); ≥10y: 90 mmHg

82. 2. Assess ABCs (0-5 min)
• Provide 100% oxygen at high flow rate (15L)
• Early intubation may be necessary in neonates and infants
• Breathing assistance as necessary, including mechanical
ventilation
3. Establish IV access and place on monitor (0-5min)
• 2 large-bore peripheral IVs (PIVs) preferred: if difficult IV,
place IO access per PALS guidelines; 1 PIV may be sufficient
unless vasoactive drugs needed (see Step No. 6, below)
• Consider labs on IV placement: blood gas, lactate, glucose,
ionized calcium, CBC, cultures (glucose check through
finger stick preferred for rapid result)

83. 4. Fluid and electrolyte resuscitation (5-15min)
• Fluids:
• Push 20 mL/kg fluid (isotonic crystalloid) IV/IO over 5-
20min or faster if needed (reassess for signs of shock;
see Step No. 11, below)
• Repeat 20 mL/kg bolus push of fluid (up to 60 mL/kg)
until clinical symptoms improve or patient develops
respiratory distress/rales/ hepatomegaly
• May continue to require additional fluid above 60
mL/kg (fluid refractory) (see Step No. 6, below)
• Fluid needs may approach 200 mL/kg in warm septic
shock (warm extremities, flash capillary refill)

84. Correct hypoglycemia:
• Glucose levels in hypoglycemia: Neonates < 45 mg/dL;
infants/children < 60 mg/dL
• Glucose dosage: 0.5-1 g/kg IV/IO (max that can be
administered through a peripheral vein is 25% dextrose
in water) (see alternative treatments immediately
below)
• Treatment options to provide 0.5-1 g/kg glucose: For
infant/child: dextrose 25% in water: 2-4 mL/kg IV/IO;
dextrose 10% in water: 5-10 mL/kg IV/IO; for neonate:
dextrose 10% in water: 2-4 mL IV/IO; consider
maintenance fluid containing dextrose

85. Correct hypocalcemia for low ionized calcium:
• Calcium gluconate 100 mg/kg IV/IO (max 2g) PRN
• Calcium chloride 20 mg/kg IV/IO PRN ( Note: central
line administration preferred over 60min in nonarrest
situation)
5. Infection control (5-60min)
• Immediate considerations:
• Administer antibiotics immediately after cultures
obtained (blood, urine, +/- CSF/ sputum)
• Do not delay antibiotics because of delay in obtaining
cultures; initial antibiotics should be given within 1h

86. Neonates >2kg:
• Ampicillin plus gentamicin: Ampicillin for 0-7d:
50 mg/kg IV/IM/IO q8h; ampicillin >7d: 50 mg/kg
IV/IM/IO q6h plus gentamicin (dosing institution
dependent): 4mg/kg IV/IO/IM q24h (alternative
for 0-7d: 2.5 mg/kg IV/IO/IM q12h; alternative for
>7d: 2.5 mg/kg IV/IO/IM q8h) or
• Ampicillin plus cefotaxime: Ampicillin for 0-7d:
50 mg/kg IV/IM/IO q8h; ampicillin >7d: 50 mg/kg
IV/IM/IO q6h plus cefotaxime 50 mg/kg IV/IO q8h

87. Infants (>1mo) and children:
• Ceftriaxone 75 mg/kg (max 2g) IV/IO/IM
q24h plus vancomycin 15mg/kg (max 1g) IV/IO
q8h
Immunosuppressed patients:
• Vancomycin 15 mg/kg IV/IO (max 1 g/dose)
q8h plus cefepime 50 mg/kg IV/IO (max
2g/dose) q8h; consider antifungal therapy

88. 6. Fluid-refractory shock (persisting after 60 mL/kg fluid) (15-60 min)
• Continue fluid resuscitation and initiate vasopressor therapy titrated to
correct hypotension/poor perfusion
• Central line placement and arterial monitoring if not already established;
vasopressors should not be delayed for line placements
• Normotensive shock (impaired perfusion but normal blood pressure):
Dopamine 2-20 mcg/kg/min IV/IO, titrate to desired effect; if continued
poor perfusion, consider dobutamine infusion 2-20 mcg/kg/min IV/IO,
titrate to desired effect (may cause hypotension, tachycardia)
• Warm shock (warm extremities, flash capillary refill): Norepinephrine 0.1-
2 mcg/kg/min IV/IO infusion, titrate to desired effect
• Cold shock (cool extremities, delayed capillary refill): Epinephrine 0.1-1
mcg/kg/min IV/IO infusion, titrate to desired effect

89. 7. Shock persists following vasopressor initiation (60 min)
• Continued fluid replacement; obtain CVP measurement to guide
SvO2 < 70% (cold shock): Transfuse Hgb >10 g/dL; optimize arterial
saturation through oxygen therapy, ventilation; epinephrine 0.1-1
mcg/kg/min IV/IO infusion, titrate to desired effect
• SvO2 < 70% (normal BP but impaired perfusion): Transfuse Hgb >10
g/dL; optimize arterial saturation through oxygen therapy,
ventilation; consider addition of milrinone 0.25-0.75 mcg/kg/min
IV/IO (titrate to desired effect) ornitroprusside 0.3-5 mcg/kg/min
IV/IO (titrate to desired effect)
• SvO2 >70% (warm shock): Norepinephrine 0.1-2 mcg/kg/min IV/IO
infusion, titrate to desired effect; consider vasopressin 0.2-2
mU/kg/min infusion, titrate to desired effect

90. 8. Fluid refractory and vasopressor-dependent shock) (60
min)
• Consider adrenal insufficiency
• Hydrocortisone 2 mg/kg (max 100mg) IV/IO bolus; obtain
baseline cortisol level; if unsure, consider ACTH stimulation
test; duration depends on response, laboratory evaluation
9. Continued shock
• Consider cardiac output measurement to direct further
therapy
• Consider extracorporeal membrane oxygenation (ECMO)
10. Supplemental therapies

91. Neurogenic Shock

92. • Neurogenic shock is a medical condition which
occurs as a result of disturbance in the
sympathetic outflow causing loss of vagal tone
• Experiences neurogenic shock after injury to
the spinal cord and when there is disruption in
the blood circulation throughout the body due
to injury/ illness.
•

93. • It is a serious and life-threatening condition, which
requires prompt medical attention without any delay. If
the treatment is delayed, then it causes irreversible
tissue damage and even death.
• Out of the different types of the shocks, neurogenic
shock is the most difficult to manage, mainly because
of the irreversible damage to the tissues.
• Neurogenic shock mainly affects the spinal cord; the
function of which is transmitting neural signals from
the brain to the entire body and back.

96. • Most common causes is spinal injury above T
6.
• Most rare form of shock

97. sign
• Hypothermia, hypotension, decreased CO,
bradycardia, flaccid paralysis

98. Management
• Main aim is to prevent complication and
maintain perfusion

99. • Hypovolemic- with fluid
• Observe for fluid overload
• Vasopressors
• Hypothermia
• Treat hypoxia
• Maintain ventilator support

100. • Observe for bradycardia- major Dysarrthemia
• Observe for DVT- Venous pooling in
extremities make patients high risk
• Use prevention modalities

101. • Alpha agonist to augment tone if perfusion
still in adequate
• Dopamine(>10 mcg/kg per min)
• Ephedrie(12.5-25mg iv every 3-4 hour)
• Treat bradycardia with atropine 0.5-1mg doses
to maximum 3 mg
• May need transcutaneous or transv svenous
pacing temporarily