This document defines shock and describes the different types of shock. It discusses: 1) Shock is characterized by inadequate tissue perfusion to meet metabolic demand and oxygenation. The main types are hypovolemic, distributive, cardiogenic, and obstructive shock. 2) Distributive shock includes septic, anaphylactic, and neurogenic shock. Signs depend on whether vasodilation or vasoconstriction dominates. Early signs of warm shock are bounding pulses and warm skin while later signs are weak pulses and cool skin. 3) Management focuses on optimizing oxygen delivery, improving cardiac output and volume distribution, reducing oxygen demand, and correcting metabolic abnormalities. Positioning

1. Presenter : Dr. Hemang
Moderator : Dr. Rashmi Kapoor

2. DEFINITION OF SHOCK
• It is a pathological state characterized by
inadequate tissue perfusion to meet
metabolic demand and tissue oxygenation.

3. Perfusion
Stroke volume Systemic vascular resistance
Preload
(ventricular filling)
Myocardial
contractility
Resiatance of
vascular tree –
after load
Venous return Atrial compliance
Blood volume Vascular tone
Impendence to
left ventricular
ejection
Tone of peripheral
vasculature

4. TYPES OF SHOCK

5. • Depending upon pathophysiology shock divided
into 4 types.
HYPOVOLEMIC SHOCK: due to inadequate blood
volume or oxygen carrying capacity.
DISTRIBUTIVE SHOCK: Due to inappropriate
distribution of blood volume or flow.
CARDIOGENIC SHOCK: due to impaired cardiac
contractility.
OBSTRUCTIVE SHOCK: due obstructed blood flow.

6. TYPES OF SHOCK BY SEVERITY
COMPENSATED SHOCK:
If systolic blood pressure within normal limits
but there are signs of inadequate tissue
perfusion , child is in compensated shock.

7. • Tachycardia (HR)
• Selective increase in SVR to non vital
organs(skin, intestine, kidney, skeletal
muscles) and shunting of blood to vital organs
(brain, heart )
• Increase in strength of cardiac contractility
with more complete emptying of ventricles.
• Increase in smooth muscle venous tone
improving venous return to heart (preload).
Compensatory mechanisms

8. Signs of compensated shock
• Tachycardia
• Cool, pale, mottled, diaphoretic skin
• Delayed capillary refill
• Weak peripheral pulses, narrow pulse pressure
• Oliguria
• Vomiting, ileus
• Altered mental status ; irritability, anxiety/
restlessness, altered consciousness

9.  HYPOTENSIVE SHOCK:
when physiological mechanism to maintain
systolic blood pressure are not effective
hypotension develops.
A key clinical sign of deterioration change in
level of consciousness as brain perfusion
decline.

10. 5th centile of blood pressure according
to age:
• <Term neonate : <60mm of Hg
• 1month -1yr : <70 mm of Hg
• 1yr-10yr : 70+2(age in years)
• >10 yr : <90 mm of Hg.

11. • Hypotension developes early in septic shock
because mediators of septic shock produce
vasodilatation and reduce SVR.
• So initially patient having warm extremities
brisk capillary refill, full peripheral pulses
despite hypotension.

12. COMPENSATED SHOCK
Possibly hours
HYPOTENSIVE SHOCK
Potentially minutes
CARDIAC ARREST

13. EARLY RECOGNIZATION
OF EACH TYPE OF SHOCK

14. HYPOVOLEMIC SHOCK:
• Most common type of shock in children.
• Etiology:
 Diarrhoea (most common cause)
 Vomiting
 Internal and external haemorrhage
 Inadequate fluid intake
 Third space loss(dengue)
 Burns
 Osmotic Diuresis (DKA)

15. • Hypovolemic shock result from deficiency of
both intravascular and extravascular volume
• It is characterized by decrease preload leading
to reduce stroke volume and reduce cardiac
output.
• Tachypnoea , a respiratory component to
maintain acid base balance is often present
with hypovolemic shock.

16. Findings of Hypotensive Shock
Primary
Assessment
Findings
A Typically patent, unless altered consciousness
B Quiet tachypnea
C • Tachycardia
• Adequate Systolic Blood Pressure, Narrow pulse pressure,
or systolic hypotension with a narrow pulse pressure
• Weak or absent peripheral pulse
• Normal or weak central pulse
• Delayed capillary refill
• Cool, pale, mottled, diaphoretic skin
• Pale distal extremities
• Changes in level of consciousness
• oliguria
D Decrease level of consciousness as shock progresses
E Extremities often cooler than trunk

17. DISTRIBUTIVE SHOCK
• Septic shock
• Anaphylactic shock
• Neurogenic shock
• ↓/↑ SVR; vasodilatation and
venodilatation  pooling of
blood
• Increased capillary
permeability  3rd space loss
 reduction of preload
• Depressed myocardial
contractility
• Pulmonary vasoconstriction,
veno arteriolar dilatation,
and increased Cap. Per.
Loss of sympathetic tone  vasodilatation and lack of compensatory
tachycardia and peripheral vasoconstriction

18. • Early in distributive shock, due to
vasodilatation reduce SVR increased blood
flow to skin warm extremities and
bounding pulses. And there is early
hypotension with wide pulse pressure
• As shock progresses myocardial dysfunction
and hypovolemia reduce cardiac output
reduce SVR inadequate blood flow to skin
produces cool extremities and weak pulses.

19. Findings of Distributive Shock
Primary
Assessment
Findings
A Typically patent, unless altered consciousness
B Quiet tachypnea unless pneumonia or ARDS, Cardiogenic Pulmonary
edema
C • Tachycardia or less commonly bradycardia
• WARM SHOCK:
bounding peripheral pulses
brisk capillary refill
warm flushed periphery
hypotension with wide pulse pressure
• COLD SHOCK:
cool, pale, mottled skin
Delayed capillary refill
hypotension with narrow pulse pressure
• oliguria
D Decrease level of consciousness as shock progresses
E Fever / hypothermia ; Patechial or purpuric rash

20. SEPTIC SHOCK
Interaction with infecting organisms
Activates the immune system, neutrophil, monocyte,
macrophages
Infectious organism or their byproducts

21. Cytokines also activate coagulation cascade may result in DIC,
Can impair myocardial contractility and cause myocardial
dysfunction.
Vasodilatation and damage to lining of blood vessel causing
increase capillary permiability
Release or activation of inflammatory mediators(cytokines)

22. ANAPHYLACTIC SHOCK
• Its an acute multysystem allergic response to a
drug, toxin, plant, venom, or other antigens.
• It occurs within seconds or minutes after
exposure to an offending agent
• Characterized by venodilatation,arterial
vasodilatation, increase capillary permiability
pulmonary vasoconstriction.

23. Signs of anaphylactic shock
Anxiety and agitation
Nausea and vomiting
Urticaria
Angioedema
Respiratory distress with stridor or wheezing
Hypotension
tachycardia

24. NEUROGENIC SHOCK/SPINAL SHOCK
• Caused by cervical or upper thoracic(above T6)
spine injury disrupts sympathetic innervation
of blood vessels and heart. so compensatory
mechanism doesn’t occur like hypovolemic shock
• SIGNS:
 Hypotension with wide pulse pressure
 Normal HR or bradycardia
 Increased respiratory rate with diaphragmatic
breathing
 motor and sensory deficits.

25. CARDIOGENIC SHOCK
• Etiology:
congenital heart disease
Myocarditis
Cardiomyopathy
Arrythmias
Myocardial injury
Poisoning or drug toxicity
Sepsis

26. • Marked Tachycardia and left ventricular afterload.
• Decrease stroke volume due to decrease myocardial
contractility and increase afterload
• Increase end diastolic volume in both right and left ventricles
resulting in pulmonary and systemic venous
congestion.  pulmonary edema and res. distress
• Diminished renal blood flow resulting in fluid
retention.
• Intravascular volume is normal or increased unless
associated with vomiting or fever.
Characteristics:

27. Signs of cardiogenic shock
• Tachypnea with increase respiratory effort
(retractions, nasal flaring, grunting) due to
pulmonary edema.
• Tachycardia
• Normal or low BP with narrow pulse pressure.
• Weak or absent peripheral pulses
• Delayed CRT
• Cool, pale, mottled skin

28. • Signs of congestive cardiac failure:
– pulmonary edema
– hepatomegaly
– raised JVP
• Cyanosis: due to cyanotic congenital heart
disease or pulmonary edema.
• Change in level of consciousness
• Oliguria.

29. OBSTRUCTIVE SHOCK
• Etiology :
 Cardiac temponade
 Tension pneumothorax
 Ductual dependent CHD
 massive pulmonary embolism

30. Cardiac temponade
• Causes are:
penetrating trauma
cardiac surgery
inflammatory disorder
infection of pericardium
tumour

31. • Accumulation of fluid blood or air in pericardial space
• Increase intrapericardial pressure and compression of heart
• Impedes systemic and pulmonary venous return
• Reduces ventricular filling and stroke volume and cardiac
output
• If untreated results in cardiac arrest and PEA

32. • Major signs are:
muffled or diminished heart sound
distended neck veins
pulsus paradoxus

33. TENSION PNEUMOTHORAX
• Caused by entry of air in pleural space and
accumulation under pressure.
• This air enters from lung injured by tear or by
penetrating chest trauma.
• As this pressure increases compression on
underlying lung and pushes mediastinum to
opposite side of chest respiratory failure
• High intrathoracic pressure and direct pressure
on mediastinal structure impedes venous return,
decline in cardiac output.

34. • Major signs are:
 Tracheal deviation toward opposite side
 Hyperresonance and hyperinflation on affected side
Diminished breath sound on affected side.
Distended neck vein
Pulsus peradoxus
Rapid deterioration in perfusion tachycardia to
bradycardia and hypotension
• Suspect tension pneumothorax in a victim of
chest trauma or any intubated patients who
deteriorates rapidly while receiving positive
pressure ventilation.

35. DUCTAL DEPENDENT LEISON
• Cyanotic CHD: ductal dependent pulmonary
blood flow present with cyanosis than signs of
shock
• ductal dependent systemic blood flow (Left
ventricular outflow obstruction )
– coarctation of aorta
– interrupted aortic arch,
– hypoplastic left heart,
– critical AS
• present with signs of shock.

36. • higher preductal vs postductal BP
• higher preductal vs postductal arterial O2
saturation (3-4%)
• AIM : Restoring and maintaining patency of
ductus arteriosus

37. Massive pulmonary embolism
• Rare In children
• Predisposing condition are:
Central venous catheter
Sickle cell disease
Malignancy
Connective tissue disorder
Inherited disorders of coagulation.

38. • systemic venous congestion and right heart
failure.
• chest pain ( hypoxemia of lung tissue )
• tachycardia
• cyanosis
• hypotension
Distinguishing features:

39. MANAGEMENT OF
SHOCK

40. Fundamentals of management
• Optimizing O2 content of the blood
• Improving volume and distribution of cardiac
output
• Reduce O2 Demand
• Correct metabolic derangement

41. Components of management
Positioning
Support Airway and breathing
Vascular access
Fluid resuscitation
Monitoring
Frequent assessment
Laboratory studies
Vasoactive therapy

42. POSITION THE CHILD
• Stable- allow to remain in comfortable
position
• Unstable- if hypotension but breathing is not
compromised, place in supine.

43. AIRWAY AND BREATHING
• Administer O2 via NRBM.
• Ventilatory support (noninvasive positive
pressure ventilation, mechanical ventilation)
• if
increased work of breathing
ineffective respiration
impaired mental status

44. VASCULAR ACCESS:
• Peripheral IV line,
• Consider early Intraosseus access

45. Fluid resuscitation
• Aim : restore intravascular volume and tissue
perfusion
• Rapid fluid resuscitation in case of
hypovolemic distributive and septic shock
• Cardiogenic, obstructive shock, severe
poisoning or fluid loss in DKA need gradual
correction

46. FLUID RESUSCITATION:
• Give isotonic crystalloid bolus of 20 ml/kg over
5-20 min, repeat if needed ( septic shock may
require up to 60 ml/kg during 1st hour)
1
• Assess physiological response to therapy after each bolus
2
• Determine need of bolus
3
• Assess sign of detrimental effect

47. Type of shock Volume of fluid App. Rate of delivery
Hypovolumic shock ( non DKA)
Distributive shock
20ml/kg bolus
Repeat PRN
Over 5 to 10 minutes
Cardiogenic shock (non
poisoning)
5-10ml/kg bolus
Repeat PRN
Over 10-20 minutes
Poisoning ( eg. CCB or Beta
blocker )
5-10ml/kg bolus
Repeat PRN
Over 10-20 minutes
DKA with compensated shock 10-20 ml/kg Over 1 hour

48. CRYSTALLIOD VS COLLOID
ISOTONIC CRYSTALLOID
• Distributed throughout
extra vascular space
• Amount needed 1 and1/2
times more than collolid for
equal effect
• Easily available
• Don’t cause sensitivity
reaction.
• E.g RL,NS
COLLOID
• Contain large molecules so
remain intravascular
• Only 20-40 ml/kg can be
given
• Less easily available
• Blood derived causes
sensitivity and synthetic
colloid causes coagulopathy.
• E.g 5% albumin,dextran, FFP

49. Indication of blood transfusion
For replacement of traumatic blood loss if perfusion is inadequate
despite 2-3 bolus of 20ml/kg
• 10ml/kg Packed RBC
– Cross matched
– Type specific
– Type o – ve for female and o [+] or o [-] for male
• Watch for
Hypothermia / myocardial dysfunction/ ionized hypocalcemia

50.  SPO2 : > 94% on room air
Heart rate, respiratory rate
Peripheral pulse
CRT
Skin color and temperature
Blood pressure and pulse pressure
Level of consciousness
Urine output
Ongoing losses
Monitoring

51. FREQUENT ASSESMENT:
• frequently reassess child’s respiratory, CVS and
neurological status to
– evaluate trends in child’s condition.
– determine response to therapy.
– plan next intervention.
• Shock is dynamic clinical condition ;
deteriorate at any moment, need life saving
interventions so ….necessity of reassessment

52. Lab support
• Aim :
– Identify etiology and severity
– Evaluation of organ dysfunction
– Identify metabolic derangements
– Evaluate response to therapy

53. Laboratory
study
Finding Possible etiology
CBC Decreased HB/HCT Hemorrhage, fluid resussication
(dilution), hemolysis
WBC count increase or decrease sepsis
Platelet decreased DIC or decreased platelet production
Glucose Increased or decreased - Stress ( usually increased but may be
decreased in infants)
- Sepsis
- Decreased production (eg. Liver failure)
- Adrenal insufficiency
Potasium Increased or decreased -Renal disorder, adrenal insufficiency
- Acidosis ( K+)
- diuresis (  K+)
calcium Decreased ionized calcium
concentration
-Sepsis
-transfusion of blood products, soda bicarb
Lactate Increased as product of anarobic
metabolism from tissue
hypoperfusion
-Tissue hypoxia,
- increased glucose production
( gluconeogenesis)
-Decreased metabolism ( liver failure)
Lab study to evaluate shock and guide therapy

54. Laboratory study Finding Possible etiology
ABG PH decreased in acidosis
and increased in alkalosis
-Lactic acid accumulation by tissue hypo
perfusion
-IEM
-DKA
-Poisoning or overdose
-Diarrhea or iliostomy loss
- hyper/hypoventilation ( sepsis or poisoning)
-vomiting
ScvO2
Central venous
O2 saturation
variable Low : inadequate O2 delivery or increased
consumption
High : misdistributions of blood flow or
decreased O2 utilization

55. To improve or redistribute cardiac output.
VASOACTIVE DRUGS:

57. MANAGEMENT
ACCORDING TO TYPE OF
SHOCK

58. HYPOVOLEMIC SHOCK:
Components are:
 indentify type of volume loss
non hemorrhagic hemorrhagic
Replace volume deficit
Prevent and replace ongoing losses
Restore acid base balance
Correct metabolic derangement.

59. • Dehydration : loss of water with varying loss of
electrolytes and or protein.
• Resuscitation determined by
– Extent of volume depletion
– Type of volume loss
• General appearance
• Tears/ mucus membrane
• Skin elasticity
• HR, RR, CRT, BP, CRT, UOP and mental status
Diarrhoea, vomiting, osmotic
diuresis
Loss associated with burn
or peritonitis
hemorrhage

60. Stage and sign of dehydration
Severity Estimated wt
loss Infant
Estimated wt loss
In adolescent
Clinical sign
Mild 5% (50 ml/kg) 3% (30) Dry mucus membrane and
oliguria
Moderate 10% (100ml/kg) 5 to 6% (50-60) Poor skin turger
Sunken fontanel
Marked oliguria
Tachycardia
Quiet tachypnoea
Severe 15% (150 ml/kg) 7 to 9 % (70-90) Marked tachycardia
Weak to abscent distal pulse
Narrow pulse pressure
Increase RR
Anuria
Hypotension
altered mental status.

61. Systemic response to blood loss
System Mild loss <30% Moderate 30-45% Severe >45%
Cardiovascular ↑ HR,
weak peripheral pulse,
Normal systolic BP,
normal pulse pressure
↑↑ HR,
weak central pulse,
Low Normal systolic BP,
Low pulse pressure
Tachy f/by brady
BP 80-90 + (2* age in yrs) 70-80 + (2* age in yrs) <70 + (2*age in
yrs)
CNS Anxious, irritable,
confused
Lethargic, dull
response to pain
comatose
Indication of BT :
colloid refractory shock or known significant blood loss
PRBC 10ml/kg or whole blood 20ml/kg as Bolus
Approx 3ml of crystalloid is needed for every 1 ml blood loss.

62. Management of hypovolemic shock
• Initiate fluid resuscitation as quickly as possible
– Isotonic fluid bolus 20ml/kg bolus, repeat as needed
– Crystelloid refrectory hemorrhagic shock : PRBC
– Loss of protein containing fluid consider colloid if crystelloid
refractory
• Correct metabolic derangements
• Identify type of volume loss
• Control external hemorrhage with direct pressure, replace
ongoing loss
• Ix CBC, cross match, ABG, electrolyte, RBS, ionized calcium,
• S. Lactate
• Diagnostic Imaging

65. MANAGEMENT OF SEPTIC SHOCK

68. Therapeutic end points
• ScVO2 > 70%, Cardiac index 3.3-6L/m2
• Normal heart rate
• Adequate BP
• Good distal pulse with CRT < 2 sec
• Improved respiration and consciousness
• Appropriate UOP
• Improvement of metabolic acidosis and lactate
concentration
• Identification of source of infection

69. ANAPHYLACTIC SHOCK
• Place child in supine position, maintain airway, O2
support
• IM epinephrine(1:1000) most important to reverse
hypotension and release of histamine and other
allergic mediators.
• If needed second dose after 10-15 min.
• Fluid bolus to restore circulation
• Nebulized salbutamol for bronchospasm
• Antihistaminics:
H1 blocker(diphenhydramine)
H2 blocker(ranitidine)

70. • Corticosteroids
methylprednisolone or other steroid
• Hypotension refractory to IM epinephrine and
fluid bolus, use vasopressor
• epinephrine infusion, low dose <0.05
microgram/kg/min effective
• Observation for late phase symptoms

71. NEUROGENIC SHOCK
• Position child flat or head down to improve
venous return.
• Trial of fluid therapy and assess response.
• If fluid refractory use vasopressor
(norepinephrine or epinephrine)
• Provide supplementary warming or cooling.

72. CARDIOGENIC SHOCK
• Cardiomegaly on cxr in patient with evidence of
shock suggest cardiogenic shock with adequate
intravascular volume.
• Echo provide data about preload and cardiac
function.
• If history suggest fluid loss(vomiting or inadeqate
intake) fluid boluse of 5-10 ml/kg over 10-20 min
with frequent watch on respiratory function for
development of pulmonary edema

73. • Decrease metabolic demands by appropriate use
of analgesics, sedatives
• O2 support by non invasive or invasive ventilation
reduce WOB thus reducing metabolic demand
• If BP is normal, diuretics and vasodilators/
ionodilators
• If hypotension : drugs which improve
contractility, increase cardiac output, and
decrease SVR are used.
vasodilators, inotropes, inodilators.
milrinone is preffered drug.

74. OBSTRUCTIVE SHOCK
TENSION PNEUMOTHORAX:
• Immediate needle decompression
• Tube thoracostomy
CARDIAC TEMPONADE:
• Fluid bolus to augment cardiac output and
improve perfusion
• percardiocentesis

75. Needle decompression and
Tube thoracostomy
Needle placement for pericardiocentesis. The
needle should be inserted into the skin incision
site at a 45-degree angle to the skin and
directed toward the left nipple or the tip of the
left scapula.

76. DUCT DEPENDENT LEISON:
• Prostaglandin E1 infusion to restore ductal
patency.
• Expert consultation.
MASSIVE PULMONARY EMBOLISM:
• O2, ventilator assistance, Fluid therapy
• 2D ECHO, contrast CT chest and angiography,
• ABG, CBC, D Dimer, CXR, VQ Scan
• Anticoagulants mainstay of therapy in
hemodyanamically stable.
• Fibrinolytics in severe cardio vascular
compromise. Expert consultation.