Shock presentation

1. SHOCK
PRESENTER – VIJAY N
MODERATOR – DR R K CHOUDHARI
1

2. • Shock is defined as the inadequate perfusion
of tissues
• Shock is a systemic state of low tissue
perfusion which is in adequate for normal
cellular respiration
2

3. • Earliest authenticated resuscitation is
miraculous deliverance of ANNE GREEN
executed by hanging on december 14 , 1650.
3

4. • Blood is a highly complex and carries
countless nutrients , buffers , cells antibodies ,
electrolytes , hormones etc.
• Nutrients for cell is required, but which
nutrient are not well defined
• Most critical nutrient is oxygen, but only
concentrating on this in shock is very
elemental
4

5. • Delivery side is affected by the blood volume ,
anaemia and cardiac output
5

6. • Shock appears to first employed in 1743 in a
translation of the French treatise HENRI
FRANCOIS LE DRAN regarding BATTLE FIELD
WOUND
• He used the term to designate the act of
impulsion or collision
6

7. • GUTHRIE 1815 in his book gun shot wounds of
the extremities describe the physiologic
instability for shock
• In 1830 , HERMAN provided the first clear
description of IV fluids therapy in CHOLERA
epidemic
7

8. • In 1831 o’shaughnessy also treated cholera
patients by administration of large volume of
salt solutions
• In 1872 GROSS , defined shock as a
manifestation of the rude unhingling of the
machinery of life
8

9. • Late 1880 , most surgeons accepted that
shock resulted from a malfunctioning of some
part of the nervous system
• Most surgeons relied on RR , PULSE and
DECREASED MENTAL STATUS to evaluate the
condition of patient
9

10. • In 1899 with sphygmomanometer , CRILE
propose that a profound decline in BP could
account for the all the symptoms of shock
• He concluded that shock was not a process of
dying but rather a marshaling of the bodies
defence in patients struggling to live
10

11. • He told that decreased volume of blood rather
than decreased BP was the most critical factor
in shock
• In 1913 crile proposed kinetic theory , that
epinephrine was a key component of the
response to shock
11

12. • Henderson recognized the importance of
decreased venous return and its effect on
cardiac output and arterial pressure
• During WW1 canon theorize that toxin and
acidosis contributed to the lowering of
vascular tone
12

13. • In 1930 BLALOCK told that all acute injuries
are associated with changes in fluid and
electrolyte metabolism
• He told the concept of third space
• Carl john wiggers told the concept of
irreversible shock
13

14. TYPES OF SHOCK
HYPOVOLAEMIC
DISTRIBUTIVE
CARDIOGENIC
ANAPHYLACTIC
ENDOCRINE
OBSTRUCTIVE
14

15. HYPOVOLEMIC SHOCK
• Its due to the reduction in the total blood
volume
• It may due to the
1. Haemorrhage
2. Severe burns
3. Intestinal obstruction , peritonitis
4. Vomiting and diarrhoea
15

17. HAEMORRHAGIC SHOCK
• It may be due to the injury to the liver ,
spleen, haemothorax, vascular injury , severe
bleed on table during major surgeries of
thyroid , liver

19. 19

20. • The problems with the signs and symptoms
clasically shown in the ATLS classes is that in
reality the manifestation of shock can be
confusing and difficulty to asses
• Patients in shock do not always have the
physiologic changes as taught in ATLS
• THE CLASSES OF SHOCK AS IN ATLS NOT
RIGOUROUSLY TESTED AND PROVEN
20

21. • ATLS – designed for physicians who are not
surgeons
21

22. Physiologic response to bleeding
1. ARTERIAL BLEEDING
transected artery lacerated artery
spasm spasm
stop bleed enlarged defect
more bleeding
22

23. 2. VENOUS BLEEDING
• Slower and compensate
• Provides time for the recruitment of water
from intracellular and interstitial spaces
• Large volume of blood can be lost before
hypotension
23

24. HEMATOCRIT
• Its level is not reliable in predicting blood loss
mainly in the high hematocrit or hemoglobin
level
• In patients resuscitated with fluids a rapid
drop in the hematocrit and hemoglobin can
occur immediately
24

25. HYPOTENSION
• It has been traditionally set at 90 mm of hg
and below
• Eastridge and co workers have suggested that
hypotension be redefined as below 110 m hg
25

26. LACTATE AND BASE DEFICIT
• Lactate has been an associated marker of
injury and possible ischemia
• Lactate has been thought to be a byproduct of
anaerobic metabolism and routinely percieved
to be an end waste product
26

27. • BASE DEFICIT – a measure of the number of
milli moles of base required to correct ph of a
ltr of whole blood to 7.4 seems to correlate
well with lactate level at least in the first 24hrs
after injury
• When base deficit remained elevated , most
clinicians believe that its an indication of
ongoing shock
27

28. COMPENSATORY MECHANISM
• When needed blood flow to less critical tissue
is diverted to more critical tissue
• The earliest compensatory mechanism in
response to a decrease in intravascular
volume is an increased in sympathetic activity
28

29. • Blood is shunted from
LESS CRITICAL ORGAN MORE CRITICAL ORGAN
1.SKIN 1.BRAIN
2.SKELATAL MUSCLE 2.LIVER
3.SPLANCHNIC CIRCULATION 3.KIDNEY
29

30. LETHAL TRIAD
• ACIDOSIS
• HYPOTHERMIA
• COAGULOPATHY
30

31. ACIDOSIS
• Inadequate tissue perfusion lead to the
formation of the lactate
• It result in the formation of the acidosis
• Body tolerates acidosis nature than the
alkalosis because O2 is more easily off loaded
31

32. • The coagulation cascade is work better in the
optimal ph
• Acidosis interfere in the coagulation cascade
32

33. HYPOTHERMIA
• It can be both beneficial and detrimental
• The beneficial aspects of the hypothermia are
mainly a result of decreased metabolism
• This concept of cooling to slow metabolism is
used to decrease during cardiac transplant ,
pediatric and neuro surgery
33

34. • Amputated extremitie sare iced before
reimplantation
34

35. • In trauma patients , hypothermia is due to the
shock and is thought to perpetuate
uncontrolled bleeding because of the
associated coagulopathy
• ATP production is below its lowest threshold ,
the body try to lower the core temperature
35

36. 36

37. • Hypothermia mainly causes the coagulopathy
• Cold affects coagulopathy by the
1. Decreasing the enzyme activity
2. Enhancing fibrinolytic activity
3. Platelets dysfunction
37

38. COAGULOPATHY
• The main usual cause is decreased clotting factors
• This is caused by the
1. consumption – from the innate attempt to stop
bleeding
2. Dilution – from infused fluids devoid of clotting
factors
3. Genetic
38

39. The most commonly used tests are
• Prothrombin time
• Partial thromboplastin time
• International normalized ratio
39

40. • These tests have been shown to be in accurate
in coagulopathy in surgical patients
• These tests are performed at the normal Ph
and normal temperature , so they cannot take
into accounts of effect of hypothermia and
acidosis on coagulation
• These are performed on serum
40

41. • Most recently thromboelastography and
rotational thromboelastometry
41

42. • THROMBOELASTOGRAPHY
42

43. • R-reaction time
• Alpha angle – rate of fibrin formation
• MA – maximum amplitude – measure of clot
strength
• LY30/LY60- measure of the fibrinolysis rate by
calculating the decrease in clot strength at 30
and 60 min respectively
43

44. • ROTATIONAL THROMBOELASTOMETRY

45. SHOCK INDEX
• Its defined as a heart rate divided by the
systolic blood pressure
• It has been shown to be an better marker for
assessing the severity of shock than heart rate
and BP alone
• Its known as a hemodynamic stability
indicator
45

46. • Its utility in
1. Trauma
2. Sepsis
3. Myocardial infarction
4. Stroke
5. Acute critical illness
46

47. • It has been correlated with need for
intervention
• MSI – defined as a heart rate divided by mean
arterial pressure
1. High MSI – hypodynamic circulation
2. low MSI – hyperdynamic state
47

48. Stages of Shock
Initial Stage
• Usually not clinically apparent
• Metabolism changes from aerobic to
anaerobic
– Lactic acid accumulates and must be removed by
blood and broken down by liver
– Process requires unavailable O2
48

49. Compensatory Stage
• Clinically apparent
– Neural
– Hormonal
– Biochemical compensatory mechanisms
• Attempts are aimed at overcoming
consequences of anaerobic metabolism and
maintaining homeostasis
49

50. 50

51. • Baroreceptors in carotid and aortic bodies
activate SNS in response to ↓ BP
– Vasoconstriction while blood to vital organs
maintained
• ↓ Blood to kidneys activates renin–
angiotensin system
– ↑ Venous return to heart, CO, BP
51

52. • Impaired GI motility
– Risk for paralytic ileus
• Cool, clammy skin from blood
– Except septic patient who is warm and flushed
52

53. • Shunting blood from lungs increases
physiologic dead space
• ↓ Arterial O2 levels
• Increase in rate/depth of respirations
• V/Q mismatch
• SNS stimulation increases myocardium O2
demands
53

54. • If perfusion deficit corrected, patient recovers
with no residual sequelae
• If deficit not corrected, patient enters
progressive stage
54

55. Progressive Stage
• Begins when compensatory mechanisms
fail
• Aggressive interventions to prevent
multiple organ dysfunction syndrome
(MODS)
55

56. 56

57. • Hallmarks of ↓ cellular perfusion and altered
capillary permeability:
• Leakage of protein into interstitial space
• ↑ Systemic interstitial edema
57

58. • Anasarca
• Fluid leakage affects solid organs and
peripheral tissues
• ↓ Blood flow to pulmonary capillaries
58

59. • Movement of fluid from pulmonary
vasculature to interstitium
• Pulmonary edema
• Bronchoconstriction
• ↓ Residual capacity
59

60. • Fluid moves into alveoli
• Edema
• Decreased surfactant
• Worsening V/Q mismatch
• Tachypnea
• Crackles
• Increased work of breathing
60

61. • CO begins to fall
• Decreased peripheral perfusion
• Hypotension
• Weak peripheral pulses
• Ischemia of distal extremities
61

62. • Myocardial dysfunction results in
• Dysrhythmias
• Ischemia
• Myocardial infarction
• End result: Complete deterioration of
cardiovascular system
62

63. • Mucosal barrier of GI system becomes
ischemic
• Ulcers
• Bleeding
• Risk of translocation of bacteria
• Decreased ability to absorb nutrients
63

64. • Liver fails to metabolize drugs and wastes
• Jaundice
• Elevated enzymes
• Loss of immune function
• Risk for DIC and significant bleeding
64

65. • Acute tubular necrosis/acute renal failure
65

66. Refractory Stage
• Profound hypotension and hypoxemia
• Tachycardia worsens
• Decreased coronary blood flow
• Cerebral ischemia
66

67. 67

68. • Failure of one organ system affects others
• Recovery unlikely
68

69. IV FLUIDS
• FLUID OF CHOICE IS RINGER LACTATE in
hemorrhagic shock
• THEY are poorly retained in the vascular space
• Fluid replacement is calculated using a 3:1
rule (3 ml of isotonic crystalloid for every 1 ml
of estimated blood loss)
69

70. ACIDOSIS
• SODIUM BICARBONATE
• THAM
70

71. HYPOTHERMIA
Warming the patients
1. Passive warming
2. Active warming
• External
• Internal
71

72. Drugs to stop bleeding and to correct
coagulopathy
1. RECOMBINANT FACTOR 7a
2. Factor 9 or prothrombin complex concentrate
3. Tranexamic acid
72

73. • Pressure packing
• Topical application for local ooze – guaze
soaked with adrenaline ,bone wax , gelatin
sponge , collagen sponge
• Wound exploration and proceeding that is
ligation of small vessel , suturing the wound
pard , excision of tissue

74. • Venous hemorrhage – elevation , ligation of
vein , suturing of venous wall , pressure
bandage
• ICT for haemothorax
• Laparotomy for liver , spleen , bowel injury /
spleenectomy

75. BURNS
It may be
• Thermal
• Electrical
• Chemical burns
• Sun burns

77. Sepsis
• Foci of infection – burn site , catheter site ,
cannula site
• Low immunity , loss of protein and
immunoglobulin
• Immunosuppresion
• Systemic infection

78. Clinical feature
• Fever
• Lethargy
• Leukocytosis
• Thrombocytopenia

79. FLUID RESUSCITATION
• The principle of fluid resucitation is that the
intravascular volume must be maintained in
order to provide sufficient circulation
• Its appropriate if any child with burn > 10%
TBSA / adult > 15% TBSA
• If orally given water should be given not salt
free

80. • PARKLAND FORMULA
4ml × % of burn × body wight
Half should be given in first 8 hrs
Remaining in next 16 hrs
• MODIFIED BROOKE FORMULA
1st 24 hrs – RL – 4ml/kg/% burn in 24 hrs
2nd 24hrs – crystalloid to maintain urine output
Colloid- 0.3 to 0.5 ml /kg/burn in 24hrs

81. • Ryles tube insertion
• Iv rantidine or pantoprazole
• Total parentral nutrition
• Antibiotics
• Tracheostomy / intubation tube may be
required in impending respiratory failure
• Wound care

82. SEPTIC SHOCK
• Infection: microbial phenomenon
characterised by an inflammatory response to
the presence of micro organisms or the
invasion of normally sterile host tissue by
these organisms
• Bacteraemia: the presence of bacteria in the
bloodstream
• Septicaemia: no longer used
82

83. 83

84. • Sepsis: systemic response to infection manifested
by ≥ 2 of:
– Temp > 38oC or < 36oC
– HR > 90 bpm
– RR > 20 bpm or PaCO2 < 32 mmHg
– WBC > 12 x 109/L, < 4 x 109/L or >10% band form
84

85. • Septic shock: sepsis with hypotension despite
adequate fluid resuscitation, with perfusion
abnormalities that could include, but are not
limited to, lactic acidosis, oliguria, and/or
acute mental status.
85

86. • It results from the arterial vasodilation and
venous blood pooling that stems from the
systemic immune response to microbial
infection
86

87. • Mortality rates as high as 50%
• Primary causative organisms
– Gram-negative and gram-positive bacteria
– Endotoxin stimulates inflammatory response
87

88. GRAM POSITIVE
• Due to exotoxin by gram
positive bacteria i.e capsular
polysaccharide like
clostridium tetani ,
staphylococci , streptococci
, pneumococci
• Fluid loss , hypotension
• Normal cardiac output
GRAM NEGATIVE
• Due to the release of the
endotoxin by the lysis of the
organism
• Urinary / GI / Biliary /
Respiratory foci are more
common

89. Molecular architecture of the IR to sepsis
89
Bacterial factors
Cell wall components
Extracellular products
Host factors
Acquired immunity
Innate immunity
Genetic susceptibility
Effector mechanisms
Lymphokine storm
Chemokine activation
Neutrophil migration
Vascular inflammation

90. HOST PARASITE
PAMP
Pathogen associated
Molecular pattern
PRR
Pathogen recognition
receptor
90

92. FACTORS CONTRIBUTING
• Inflammatory mediators
• Endothelial cell activation
• Metabolic abnormality
• Immune suppression
• Organ dysfunction
92

93. 93

94. • Septic shock is typically vasodilator shock ,
where there is peripheral vasodilation causing
hypotension
• This is due to the toxin induced release of
isoform of nitric oxide synthetase from the
vessel wall which cause sustained release of
high level of nitric oxide

95. STAGES OF SEPTIC SHOCK
1.HYPERDYNAMIC (WARM) SHOCK
• Its reversible shock
• Patient is still having inflammatory response
• Pyrogen response is still intact
• Present with fever , tachycardia , tachypnea

96. 2. HYPODYNAMIC HYPOVOLAEMIC SEPTIC
SHOCK
• Here pyrogen response is lost
• Patient is in decompensated shock
• Its irreversible stage

97. • Clinical manifestations
– Tachypnea/hyperventilation
– Temperature dysregulation
– ↓ Urine output
– Altered neurologic status
– GI dysfunction
– Respiratory failure is common
97

98. • Thorough history and physical examination
• No single study to determine shock
– Hemodynamic monitoring
– Blood studies – total count , platelet count ,
– USG
– Blood for culture sensitivity
– Pus for culture sensitivity

99. • Correction of fluid and electrolyte to restore
the perfusion
• Monitoring the patient by pulseoximeter ,
cardiac state , urine output , arterial blood gas
• Treat the cause of foci - drainage of an
abscess , laparotomy for peritonitis, resection
of gangrenous bowel

100. ANTIBIOTICS
• There is no, single, “best” regimen
• Consider the site of the infection
• Consider which organisms most often cause
infection at that site
• Choose antibiotic(s) with the appropriate
spectrum
• After obtaining cultures, give antibiotics quickly
and empirically at appropriate dose

101. • Critical care , oxygen support if required
ventilatory support
• Vasopressor drug therapy; vasopressin for
patients refractory to vasopressor therapy

103. • Activated c protein prevent the release of
inflammatory mediators and block the effect
of these mediators on cellular function
• Drotrecogin alfa

104. • Short term high dose steroid therapy to
control and protects the cell from effect of
endotoxemia
• Did not reverse shock
• Did reduce the time to shock reversal
• No significant problem with super-infection

105. • Intensive insulin therapy
– tight glycaemic control

106. CARDIOGENIC SHOCK
• Definition
–Systolic or diastolic dysfunction
–Compromised cardiac output (CO)
106

107. • Precipitating causes
– Myocardial infarction
– Cardiomyopathy
– Blunt cardiac injury
– Severe systemic or pulmonary hypertension
– Cardiac tamponade
– Myocardial depression from metabolic problems
107

108. Pathophysiology of
Cardiogenic Shock
108

109. • Early manifestations
– Tachycardia
– Hypotension
– Narrowed pulse pressure
– ↑ Myocardial O2 consumption
109

110. • Physical examination
– Tachypnea, pulmonary congestion
– Pallor; cool, clammy skin
– Decreased capillary refill time
– Anxiety, confusion, agitation
• ↑ in pulmonary artery wedge pressure
• Decreased renal perfusion and UO
110

111. Cardiogenic Shock
• Restore blood flow to the myocardium by
restoring the balance between O2 supply and
demand
• Thrombolytic therapy
• Angioplasty with stenting
• Emergency revascularization
• Valve replacement
111

112. • Hemodynamic monitoring
• Drug therapy (e.g., diuretics to reduce
preload)
• Circulatory assist devices (e.g., intra-aortic
balloon pump, ventricular assist device)
112

113. NEUROGENIC SHOCK
• Hemodynamic phenomenon that can
occur within 30 minutes of a spinal cord
injury at the fifth thoracic (T5) vertebra or
above and can last up to 6 weeks
• Can be in response to spinal anesthesia
• Results in massive vasodilation leading to
pooling of blood in vessels
113

114. Pathophysiology of
Neurogenic Shock
114

115. Clinical manifestations
• Hypotension
• Bradycardia
• Temperature dysregulation (resulting in heat
loss)
• Dry skin
• Poikilothermia (taking on the temperature of the
environment)
115

116. Neurogenic Shock
• In spinal cord injury: Spinal stability
– Treatment of the hypotension
and bradycardia with
vasopressors and atropine
– Fluids used cautiously as
hypotension is generally not
related to fluid loss
– Monitor for hypothermia
116

117. ANAPHYLACTIC SHOCK
• Acute, life-threatening hypersensitivity
reaction
–Massive vasodilation
–Release of mediators
–↑ Capillary permeability
117

118. • Clinical manifestations
– Anxiety, confusion, dizziness
– Sense of impeding doom
– Chest pain
– Incontinence
118

119. • Clinical manifestations
– Swelling of the lips and tongue, angioedema
– Wheezing, stridor
– Flushing, pruritus, urticaria
– Respiratory distress and circulatory failure
119

120. Anaphylactic Shock
• Epinephrine, diphenhydramine
• Maintaining a patent airway
• Nebulized bronchodilators
• Endotracheal intubation or
cricothyroidotomy may be necessary
120

121. • Aggressive fluid replacement
• Intravenous corticosteroids if significant
hypotension persists after 1 to 2 hours of
aggressive therapy
121

122. OBSTRUCTIVE SHOCK
• There is a reduction in a preload due to
mechanical obstruction of cardiac filling
• Causes –
1.Cardiac tamponade
2.Tension pneumothorax
3.Massive pulmonary embolus

123. • There is reduced filling of the left and right
side of the heart
• It result in decreased preload
• Decreased cardiac output

124. ENDOCRINE SHOCK
• It’s the combination of hypovolaemia ,
cardiogenic, distributive shock
• Cause
1. Hypothyroidism
2. Hyperthyroidism
3. Adrenal insufficiency

125. HYPOTHYROIDISM
• It cause shock similar to the neurogenic shock
due to the disordered vascular and cardiac
responsiveness to circulating catecholamines
• Decreased cardiac output due to decreased
inotrophy and bradycardia
HYPERTHYROIDISM
• High output cardiac failure

126. ADRENAL INSUFFICIENCY
• Lead to the shock due to the hypovolaemia
and a poor response to circulating and
exogenous catecholamines
• It may be due to the
1. addison’s disease
2. Relative insufficiency
3. Systemic sepsis

127. REFERENCES
• SABISTON TEXT BOOK OF SURGERY 20TH
EDITION
• BAILEY AND LOVE 26TH EDITION
• SCHWARTZ TEXT BOOK OF SURGERY
• ROBBIN’S TEXT BOOK OF PATHOLOGY
• G K PAL TEXT BOOK OF PHYSIOLOGY