Shock is defined as a state of reduced effective tissue perfusion leading to cellular injury. The document discusses the classification, pathophysiology, clinical features, and treatment of various types of shock including hypovolaemic, traumatic, cardiogenic, and septic shock. Compensatory mechanisms initially work to maintain blood pressure but progressive shock leads to organ failure and death if not treated promptly with fluid resuscitation, controlling bleeding, and vasoactive drugs.

1. GOOD MORNING
AAFREEN SUMAIYA S
P G STUDENT
DEPT. OF PERIODONTICS
1

2. SHOCK
DEFINITION
CLASSIFICATION AND
PATHOPHYSIOLOGY
2

3. DEFINITION:
Shock is defined as “the state in which profound
and widespread reduction of effective tissue perfusion
leads first to reversible, and then, if prolonged, to
irreversible cellular injury.”
3

4. Classification of Shock
Shock
Hypovolaemic Cardiogenic Distributive
Neurogenic Anaphylactic Septic
4

5. Hypovolaemic shock
This type of shock is due to loss of intravascular volume
It is caused by hemorrhage, burns, vomiting, diarrhoea, dehydration etc.
Pathophysiology:
Hemorrhage mostly occurs from systemic venules and small veins
which usally contains about 50% of total blood volume .
5

6. loss of blood
decrease filling of right heart
decrease filling of pulmonary vasculature
decrease filling of left atrium and ventricle
decrease left ventricular stroke volume
this causes drop in arterial blood pressure
6

7. Blood Cardiac Systemic
Pressure = Output x Vascular
Resistance
BP = CO x SVR
7

8. What happens if you get a drop in BP?
BP = CO x SVR
• We need to maintain homeostasis so need to increase
BP.
• We can increase BP by increasing:
- CO
- SVR
- CO & SVR
to increase BP back up again.
8

9. Compensatory mechanisms:
The compensatory mechanisms which occur after
haemorrhage include,
• Adrenergic discharge
• Hyperventilation
• Release of vaso-active hormones
• Collapse
9

10. • Reabsorption of fluid from the interstitial tissue
• Reabsorption of fluid from the intracellular to the
extracellular space
• Renal conservation of body water and electrolytes
10

11. 1.Adrenergic discharge: starts within 60seconds after blood
loss
It causes -constriction of venules and small veins
-increase in heart rate
-consticts the vascular sphincters in kidney,
splanchnic viscera and in skin
• This selective vasoconstriction improves filling right
heart and increases cardiac output
• Adrenergic discharge takes away a portion of blood flow
from the splanchnic viscera , kidneys, and skin and
diverts it to the heart and brain.
11

12. 2.Hyperventilation :It occurs within 1 minute of blood loss
• This occurs in response to metabolic acidaemia
• Spontaneous deep breathing sucks blood from extra
thoracic sites to the heart and lungs
• This also increases the filling of left ventricle and also its
stroke volume.
12

13. 3.Release of vasoactive hormones:
Release of hormone renin from juxtaglomerular apparatus
Release of vaso-active hormones such as vasopressin and
epinephrine
Release of vaso-active hormones usually takes place after 1
to 2 minutes of haemorrhage
13

14. THIRST
ANGIOTENSIN II
ADRENAL
CORTEX
KIDNEYS increase
Na+ reabsorption
from filtrate
BP
VASOCONSTRICTION
BLOOD
PRESSURE
ALDOSTERONE
BLOOD VOLUME
ANGIOTENSIN
CONVERTING ENZYME
JUXTAGLOMERULAR
cells in the kidney
respond to a
REDUCTION IN BLOOD
VOLUME from EXCESS
VOMITING, SWEATING,
& HAEMORRHAGE etc.
RENIN released
into blood
ANGIOTENSINOGEN ANGIOTENSIN I
14

15. 15

16. 16

17. Baroreceptors detect fall in BP
Sympathetic nervous system activated
1.Cardiac Effects
- increased force of contractions
- increased rate (tachycardia)
- increased cardiac output
17

18. 2.Peripheral Effects
- arteriolar constriction
- increased peripheral resistance
- shunting of blood to main core organs (causing cold
clammy skin)
18

19. 3. Respiratory Effects
Tachypnoea is one of the first signs that reflects reduced
blood flow and oxygen transport.
Cardiovascular and Respiratory systems work together-
• If blood flow around the body is compromised in any way,
oxygen delivery to tissues is reduced.
• To compensate for this, ventilation will increase to attempt to
increase oxygen uptake in the lungs. So how does this happen?
• The Baroreceptors not only stimulate the cardiovascular control
centre but also the respiratory centre in the medulla, increasing
the respiratory rate
19

20. 4.Renal Effects
- decreased renal blood flow
- renin released from kidney
- initiation of RAAS results in peripheral
vasoconstriction, reabsorption of Na+ and H2O
20

21. 5.Hypothalamus Effects
- decreased blood flow to hypothalamus
- release of ADH from post pituitary results in retention
of salt, water and peripheral vasoconstriction
21

22. 6.Hormonal Effects
- Glucagon (contributes to hyperglycaemia)
- ACTH (stimulates cortisol release and glucose
production)
22

23. 4.Collapse:
Recumbent posture due to collapse automatically displaces
blood from the lower part of the body to the heart and
increases cardiac output.
23

24. 5.Reabsorption of fluid from the interstitial tissue:
• Due to adrenergic discharge the arterioles, pre capillary
sphincters the venules and the small veins of the skin and
splanchnic organs and skeletal muscles constricts
• This leads to decrease of the capillary intravascular
hydrostatic pressure.
• This leads to the influx of water, sodium and chloride from
the Interstitial tissue space into the capillaries
24

25. 6.Reabsorption of fluid from the intracellular to the
extracellular space
• Release of epinephrine, cortisol, glucagon and inhibition
of insulin all lead to high extracellular glucose
concentration .
• Products of anaerobic metabolism also accumulate in the
extracellular space .
• Both these causes hyperosmolarity of the extracellular
tissue which draws water out of the cells.
• Interstitial pressure increases ,which forces water, sodium
and chloride across the capillary endothelium into the
vascular space.
25

26. 7.Renal conservation of body water and electrolytes:
• ACTH is released by any stress including shock.
• This hormone and angiotensin II stimulate the synthesis
and release of hormone aldosterone from adrenal cortex.
• Aldosterone is concerned with reabsorption of sodium
from the glomerular ultrafiltrate into the vascular space.
• Reabsorption of sodium and water by the kidneys help to
maintain the vascular volume.
26

27. Compensatory shock
• Presentation:
- Increased respiratory rate, restlessness,
anxiety (earliest signs of shock)
- Tachycardia
- Falling BP = late sign of shock
- Possible delay in capillary refill
- Pale, cool skin (Cardiogenic,
Hypovolaemic shock)
27

28. - Flushed skin (Anaphylactic, Septic,
Neurogenic shock)
- Nausea, vomiting, thirst
- Decreased body temperature
- Feels cold
- Weakness
28

29. Progressive Shock
1.Cardiac Effects
- decreased RBC oxygenation
- decreased coronary blood flow
- myocardial ischaemia
-decreased ventricular filling
- decreased force of contraction
29

30. 2. Peripheral Effects
- peripheral pooling of blood
- plasma leakage into interstitial
spaces
- cold, grey waxy skin
- restlessness, confusion, slow speech
- tachycardia, weak thready pulse
- decreased BP
- decreased body temperature
30

31. 3. Respiratory effects
• If oxygen delivery to tissues continues to be
inadequate, cells must do anaerobic respiration to
continue ATP production.
• Anaerobic respiration produces lactic acid as a waste
product – this must be removed.
• Central chemoreceptors will detect a fall in pH and
stimulate the respiratory centre to increase ventilation.
• This allows the excess acid to be ‘blown off’ in the
form of CO2
.
31

32. Anaerobic
respiration
Lactic
acid
PCO2 and
H+ in blood
expiration of PCO2
H+ in CSF
stimulation of
central
chemoreceptors
frequency of
impulses to
medullary
rhythm
generator
rate and
depth of
ventilation
Response to acidosis
32

33. 33

34. Irreversible Shock
• Loss of peripheral vascular resistance
• Confusion, slurred speech, unconscious
• Slow, irregular, thready pulse
• Falling BP (diastolic is zero)
34

35. • Cold, clammy cyanotic skin
• Slow, shallow, irregular respirations
• Dilated, sluggish pupils
• Severely decreased body temperature
35

36. Irreversible Shock leads to:
• Renal failure
• Hepatic failure
• Multiple organ systems failure
• Acute respiratory distress syndrome
• Death
36

37. Clinical features: Depend on the degree of loss of blood
volume and on the duration of shock.
1. Mild shock:
- loss of less than 20% blood volume is included in this
category- the feet become pale and cool.
-sweat in forehead, hands and feet due to
adrenergic discharge.
-urinary output, pulse rate and blood pressure at
this stage remains normal.
37

38. 2. Moderate shock:
- loss of blood volume from 20-40% causes this type of
shock
-oligouria
Pulse rate is increased but usually less than 100 beats per
minute
3. Severe shock:
-loss of blood volume more than 40% usually causes severe
shock . At this stage there is
- pallor
-low urinary output
-rapid pulse
-low blood pressure
38

39. • Clinical monitoring:
• Once shock is diagnosed, constant monitoring of patient
is required to asses the degree of blood loss and
hemodynamic impairment.
Blood pressure: measurement of BP is very essential in
shock.
The diastolic pressure is the main indication of degree of
vasoconstriction .
The systolic pressure indicates vasoconstriction along with
stroke volume and rigidity of main vessels.
39

40. Respiration : hyperventilation i.e. increase in rate and depth
of respiration is an important indicator of shock.
Hyperventilation is a normal response of early shock.
Persistent hyperventilation is important sign and indicates
improper treatment of shock.
Urine: urine output is a good indicator of severity of shock
Urine output is affected quite early even in moderate shock.
It is a good index of adequacy of replacement therapy
40

41. • CVP: Measurement of central venous pressure is
important in assessing shock.
• In hypovolaemic shock the blood volume is decrease,so is
the CVP
41

42. 42

43. ECG: in severe shock electrocardiogram may show signs of
myocardial ischemia with depression of ST-T segments
SWAN-GANZ Catheter: this catheter is used in
sophisticated centers to get valuable information.
• flow in the cardiovascular system
• Samples of blood from the pulmonary artery
• Filling pressure of both right and left side of the heart can
be measured
43

44. 44

45. Treatment:
Resuscitation –it should begin immediately as the patient is
admitted with hypovolaemic shock.
This starts with establishment of clear airway and
maintaining adequate ventilation and oxygenation.
Lowering of head with support of jaw to prevent airway
obstruction and administration of oxygen are usually
needed.
45

46. 46

47. 47

48. 48

49. 49

50. Immediate control of bleeding:
• It is highly important in case of haemorrhagic shock
• This may be achieved by raising the foot end of bed and
by compression bandage to tamponade external
haemorrhage.
• Operation may be required to stop such bleeding .
50

51. Extracellular and fluid replacement:
A non-sugar, non-protein crystalloid solution with a sodium
concentration approximately that of plasma is preferable.
That solution can be Ringer’s lactate, Ringer’s acetate or
normal saline supplemented with 1 or 2 ampules of
sodium bicarbonate.
This solution is run at a rapid speed i.e. 1000-2000ml in
45min intravenously
51

52. Drugs :
A few drugs are sometimes used in different types of shock.
1. Sedatives: these drugs are commonly used to alleviate
pain in patients with shock.
Some amount of sedation is always required in any type of
shock.
Morphine should be given intravenously.
For children Barbiturates are preferred whereas in head
injuries Largactil is a better choice
52

53. 2.Chronotropic agents:
They primarily increase the heart rate hence used in patients
in shock who have slow heart rate
Atropine is the most widely used in this group, followed by
isoproterenol.
3.Inotropic agents:
These drugs improve the strength of cardiac muscle
contraction.
Used in cardiogenic and severe septic shock
The most commonly used drugs in this group are Dopamine
and Dobutamine
53

54. 4.Vasodilators : patients in severe septic, traumatic and in
cardiogenic shock may require these drugs.
Most commonly used drugs in this group are nitroprusside
and nitroglycerine.
5.Vasoconstrictors : these drugs are beneficial in neurogenic
shock.
The main role of this drug is that they increases blood
pressure and increases perfusion pressure for coronary
circulation.
These drugs also increases myocardial contractility.
Most commonly used drugs are Phenylephrine and
Metaraminol. 54

55. 6.Beta-blockers:propranolol is most widely used drug in
this group.
7.Diuretics: These drugs are sometimes used in treating
patients with cardiogenic shock.
Diuretics should not be used in haemorrhagic and traumatic
shock.
55

56. Traumatic shock
• This type of shock is caused by major fractures, crush injuries,
extensive soft tissue injuries and intra abdominal injuries.
• There is hypovolaemia in this type of shock due to bleeding
both externally and internally (intraperitoneal haemorrhage)
from ruptured liver or spleen or from torn vessels of
mesentary.
56

57. • Along with this there are toxic factors resulting from
fragments of tissue entering the blood stream.
• This activates intravascular inflammatory response.
• The vascular permeability also increases resulting in
further hypovolaemia.
57

58. Pathophysiology:
1. The peculiarity of this type of shock is that traumatised tissue
activate the coagulation system and release microthrombi into the
circulation.
2. These may occlude or constrict parts of pulmonary micro-
vasculature to increase pulmonary vascular resistance.
3. This increases right ventricular diastolic and right atrial pressures
4. Humoral products of these microthrombi induce a generalised
increase in capillary permeability.
5. This leads to the loss of plasma into the interstitial tissue
throughout the body. This depletes the vascular volume to a great
extent. 58

59. Clinical features:
The two differentiating features are:
• Presence of peripheral and pulmonary oedema
• Infusion of large volumes of fluid which may be adequate for
pure hypovolaemic shock, is usually inadequate for traumatic
shock.
59

60. Treatment :
1.Resuscitation : In this type of shock mechanical ventilatory
support is more needed.
2.Local treatment of trauma and control of bleeding: this is
similar to hypovolaemic shock .
• Surgical debridment of ishchaemic and dead tissues .
• Immobilisation of fractures is required
.
60

61. 3.Fluid replacement: more fluids should be required to
bring back the patient to normalcy than hypovolaemic
shock.
4.Anticoagulation therapy: one intravenous dose of
10,000units of heparin seems to be effective.
61

62. Cardiogenic shock
This type of shock is usually caused by injury to the heart,
myocardial infarction, cardiac arrhythmias or congestive cardiac
failure.
In this condition the heart fails to pump the blood.
62

63. Pathophysiology:
• It is usually due to primary dysfunction of one ventricle or
other.
• In cardiogenic shock caused by dysfunction of right ventricle, the
right heart is unable to pump blood in adequate amount to the
lungs.
• Filling of the left heart decreases .
• So left ventricular output decreases.
• In cardiogenic shock caused by dysfunction of left ventricle, the
left ventricle unable to maintain an adequate stroke volume.
63

64. • Left ventricular output and systemic arterial blood pressure
decrease.
• There is engorgement of the pulmonary vasculature due to
normal right ventricular output, but failure of the left heart.
• Cardiac compressive shock arises when the heart is compressed
enough from outside to decrease cardiac output.
• The important causes are tension pneumothorax, pericardial
tamponade and diaphragmatic rupture with herniation of the
bowel into the chest.
64

65. Clinical features:
In the beginning the skin is pale and cool and the urine output is
low.
Gradually the pulse becomes rapid and the arterial blood
pressure becomes low.
In case of right ventricular dysfunction the neck veins become
distended and the liver may also be enlarged.
In left ventricular dysfunction the patient has broncheal rales and
a third heart sound is heard.
Gradually the heart becomes enlarged and when right ventricle
also fails distended neck veins will be visible.
65

66. Treatment:
• Airway must be clear with adequate oxygenation.
• In case of right sided failure caused by massive pulmonary
embolus should be treated with large doses of heparin
intravenously.
• If pain is complained in case of left sided failure eg: morphine
should be prescribed.
• Fulminant pulmonary edema should be treated with a diuretic.
66

67. Neurogenic shock
•This is caused by paraplegia, quadriplegia, trauma to
the spinal cord or spinal anaesthesia.
•Such shock is primarily due to blockade of
sympathetic nervous system resulting in loss of arterial
and venous tone.
•With pooling of blood in the dilated peripheral venous
system.
67

68. Pathophysiology
• In this type of shock there is dilatation of systemic vasculature which
lowers the systemic arterial pressure.
• Blood pools in the systemic venules and small veins.
• The right heart filling and stroke volume decreases.
• This decreases pulmonary blood volume and left heart filling so that
left ventricular output decreases.
• Discharge of adrenergic nervous system to the innervated parts of
the body and release of angiotensin and vasopressin are the
compensatory mechanisms which of course fails to restore cardiac
output to normal, though systemic arterial pressure response in part.
68

69. Clinical features:
The peculiar features are that the skin remains warm, pink and
well perfused in contradistinction to the hypovolaemic shock.
Urine output may be normal.
But the heart rate is rapid and the blood pressure is low.
69

70. Treatment:
• Elevation of the legs is effective in treating patients with
neurogenic shock .
• Trendelenburg position displaces blood from the systemic
venules and small veins into the right heart and increases
cardiac output .
• Administering fluid is important though not so as in
hypovolaemic shock.
• This increases filling of right heart which in its turn increases
the cardiac output.
• Use of vasoconstrictor drug.
70

71. Septic shock
This type of shock is due to gram negative septicaemia.
Such a type of shock may occur in cases of
severe septicaemia,
cholangitis,
peritonitis ,
meningitis.
71

72. Pathophysiology
•The most frequent causative organisms are gram-positive and
gram-negative bacteria.
•Any agents capable of producing infection (including viruses,
parasites and fungi) may cause septic shock.
•The common organisms which are concerned with septic shock
are –
1.E.Coli
2.Klebsiella aerobacter
3.Proteus
4.Pseudomonas
5.Bacteroids 72

73. Pathogenesis of Shock
Infectious or noninfectious triggers
Cytokine and inflammatory mediator cascade
Cardiac dysfunction and microvascular injury
Hypotension and shock
73

74. EFFECTS OF EXCESS CYTOKINE RELEAS
Primary mediators (IL-1, TNFα)
Endothelial/Leukocyte molecular activation
Secondary mediators (NO,PAF)
Vasodilation, capillary leak, endothelial damage
Shock ,MODS,DEATH 74

75. General signs and symptoms:
– fever, chills
– general malaise, irritability, lethargy
• Tachycardia and hypotension
• Hyperventilation
• Site of infection may or may not be
evident
75

76. Cardiovascular signs:
• Systemic vasodilation and hypotension (Psys <
90mmHg)
• Tachycardia (>100 beats/min)
• Increased cardiac output (hyperdynamic),
although contractility is depressed; hypodynamic
in late shock
• Ventricular dilation; decreased ejection fraction
• Loss of sympathetic responsiveness
76

77. • Hypovolemia due to vascular leakage; central
venous pressure may be decreased or
increased depending upon fluid resuscitation
• Compromised nutrient blood flow to organs;
decreased organ oxygen extraction
77

78. • Hyperventilation with respiratory alkalosis
• Pulmonary hypertension and edema
• Hypoxemia (arterial pO2 < 50 mmHg)
• Reduced pulmonary compliance; increased work
• Respiratory muscle failure
• Renal hypoperfusion; oliguria
• Acute tubular necrosis and renal failure
78

79. Disseminated intravascular coagulation (DIC)
• Blood dyscrasias
– leukopenia
– thrombocytopenia
– polycythemia
• Central and peripheral nervous dysfunction
• Increased lactate occurs early
79

80. Treatment of Septic Shock
• Antibiotics (early administration)
• Hemodynamic support
– (fluid resuscitation)
• Restore tissue perfusion
• Normalize cellular metabolism
– Vasopressor agents
• Dopamine, norepinephrine, dobutamine
80

81. • Source control
– Surgical debridement of infected, devitalized tissue
– Catheter replacement
• Supplemental oxygen (treatment of acute
respiratory distress syndrome,ARDS)
• Nutritional support
81

82. Controversial Current Therapies for Septic Shock
• Anti-inflammatory agents
– Cortocosteroids
– Ibuprofen
– Prostaglandin E1
– Pentoxifylline
• Oxygen Scavengers
– N-acetylcysteine
– selenium
82

83. • Drugs modifying coagulation
– Anti-thrombin III
• Drugs enhancing host defenses
– Intravenous immunoglobulin (IVIG)
– Interferon-gamma
– immuno-nutrition
83

84. Other drugs
– Growth hormone, antibiotics, fresh frozen plasma,
anesthetic sedative and analgesic agents, catecholamines
Hemofiltration, plasma filtration, plasma exchange
84

85. Experimental Therapies of Septic Shock
• Anti-endotoxin therapies
– IVIG
• Anti-TNF-alpha, soluble TNFR
• PLA2 inhibitors, PAF inhibitors
• Anti-coagulants
85

86. Miscellaenous types:
This include , Anaphylactic shock, insulin shock etc.
Anaphylactic shock is commonly seen after administration
of penicillin, serum, dextrose, anaesthetics etc.
Such type of shock is due to increased released of histamine
and slow release substance(SRS) of anaphylaxis by
combination of antigen with IgE on the mast cells and
basophils.
86

87. This histamine and SRS are concerned to cause
bronchospasm, laryngeal edema and respiratory distress
which totally lead to hypoxia.
This is aggravated by massive vasodilatation which causes
hypotension and ultimately shock.
87

88. REFERENCES
• Bailey & Love’s SHORT PRACTICE OF SURGERY , 23rd Edition.
• Critical Care Cardiovascular Disease , Anand Kumar and Joseph E.
Parrillo
• Manipal Manual of Surgery.
• Kumar Cotran Robbins, BASIC PATHOLOGY 6th edition.
• Stanley F Malamed,Medical Emergencies In Dental Office 6th
edition
• Das , Somen A TEXT BOOK OF SURGERY 3RD EDITION
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