1. Shock is defined as a state of poor tissue perfusion and cellular metabolism due to circulatory failure and hypoxia. 2. The main causes of shock include hypovolemic, cardiogenic, septic, anaphylactic, neurogenic, and respiratory shock. 3. Septic shock occurs due to bacterial toxins and involves an initial hyperdynamic stage with fever and tachycardia followed by a hypodynamic stage with hypotension, organ dysfunction, and poor tissue perfusion.

1. SHOCK
BY:- DR K TARUN RAO
PG IN DEPT OF ORTHOPEDICS,
CAIMS

2. DEFINITION
• Shock is a state of poor perfusion with
impaired cellular metabolism manifesting with
severe pathophysiological abnormalities.
• It is due to circulatory collapse and tissue
hypoxia.
• Normal aerobic metabolism is not maintained
due to hypoperfusion.

4. STARLINGS FORCES

5. Causes of shock
1. Hypovolaemic shock:- due to reduction in
total blood volume.
It may be due to:
a. Haemorrhage:-
– External from wounds, open fractures
– Internal from injury to spleen, liver, mesentery
or pelvis

6. b. Severe burns, which results in loss of plasma
c. Peritonitis, intestinal obstruction
d. Vomiting and diarrhoea of any cause

7. 2. Cardiac causes:-
a. Acute myocardial infarction, acute carditis,
b. Acute pulmonary embolism
c. Drug induced
d. Toxaemia of any causes
e. Cardiac surgical conditions like valvular diseases,
congenital heart diseases

8. f. Cardiac compression causes:-
i. Cardiac tamponade due to collection of
blood, pus, fluid in the pericardial space
which prevents the heart to expand leading
to shock.
ii. Trauma to heart

9. 3. Septic shock:— is due to bacterial infections
which release toxins leading to shock
4. Neurogenic shock:— due to sudden anxious or
painful stimuli causing severe splanchnic vessel
vasodilatation. Here, patient either goes for cardiac
arrest and dies or recovers fully spontaneously—
spinal cord injury/anaesthesia can cause neurogenic
shock

10. 5. Anaphylactic shock:—is due to Type 1
hypersensitivity reaction

11. 6. Respiratory causes:-
a. Atelectasis (collapse) of lung
b. Thoracic injuries
c. Tension pneumothorax
d. Anaesthetic complications

12. 7. Other causes:-
a. Acute adrenal insufficiency (Addison‘s
disease)
b. Myxoedema

13. Pathophysiology of Shock
Any cause of shock
↓
Low cardiac output
↓
Vasoconstriction occurs as a compensation to
perfuse vital organs like brain, heart, muscle,
kidneys, liver
↓
Because of vasoconstriction and tachycardia
↓

14. Dynamic circulation increases
↓
Tachypnoea occurs to increase the oxygen
saturation
↓
Peripheral veins (capacitance vessels constrict
diverting blood from splanchnic system
towards essential vital organs

15. Decreased renal blood flow reduces the GFR and
thereby the urine output
↓
Renin angiotensin mechanism gets activated
causing further vasoconstriction and
aldosterone release
↓
Causes salt and water retention
↓
ADH is released
↓
Further concentration of urine occurs

16. When shock
persists cardiac
output falls
further
Hypotension and
tachycardia occurs
leading to poor
perfusion of
coronaries

17. Hypoxia—metabolic acidosis
Release of cardiac depressants
Cardiac (pump) failure

18. Hypoxia
Anaerobic metabolism
Lactic acidosis
Cell wall damage
Sodium and calcium enter
the cell
Potassium leaks out of the cell
Causes hyperkalaemia, hyponatremia and
hypocalcaemia

19. Intracellular lysosomes break down releasing
powerful enzymes which destroy own cell
SICK CELL SYNDROME
Platelets are activated forming small clots in
many places
Disseminated intravascular
coagulation(DIC)(ConsumptionCoagulopathy)
Further bleeding.

23. Cerebral blood flow = cerebral perfusion pressure / cerebral
vascular resistance
CPP is the difference between mean arterial pressure and intra
cranial pressure.

24. EFFECTS OF SHOCK
Heart: Low perfusion → low venous return →
decreased cardiac output → hypotension →
tachycardia. Persistent shock causes hypoxia and
release of myocardial depressants leading to
further cardiac damage.

25. • Lung: Interstitial oedema → decreased
gaseous exchange →pulmonary arteriovenous
shunting → tachypnoea → Adult/Acute
respiratory distress syndrome (ARDS) and
pulmonary oedema.

26. Metabolic: Shock leads to hypoxia, which
activates anaerobic metabolism leading to lactic
acidosis.

27. • Antidiuretic hormone (ADH) is released which
increases the reabsorption of water from renal
tubules. Other hormones released are ACTH,
prostaglandins, histamine, bradykinin, and
serotonin to compensate the effects of shock
to increase the perfusion of vital organs like
heart, brain and lungs.

28. Cellular changes:- occur in persistent shock due
to release of lysosomal enzymes, which alters
the cell membrane permeability causing cell
death—sick cell syndrome.

29. Sympathetic:-overactivity alters the
microcirculation leading to capillary
dysfunction.
Brain:- perfusion, when decreases the patient
becomes drowsy. Brain is the last organ to get
underperfused in shock.

30. Kidneys: GFR decreases and tubular reabsorption of
salt and water increases for compensatory
response. But in severe cases tubular necrosis sets
in leading into irreversible damage.

31. • Blood: Alteration in cellular components
including platelets leads to Disseminated
intravascular coagulation (DIC). It causes
bleeding from all organs.

32. • Gastrointestinal tract: Mucosal ischaemia
develops causing bleeding from GIT with
haematemesis and malaena. It is aggravated
by DIC. Hepatic ischaemia leads into increased
enzyme levels.

33. Types of Shock
1. Vasovagal Shock and neurogenic
shock:-
It is sudden dilatation of peripheral and
splanchnic vessels causing reduced cardiac
output and shock. Often it may be life-
threatening due to hypoxia.

34. • Episodes of vasovagal syncope are typically
recurrent and usually occur when the
predisposed person is exposed to a specific
trigger

35. Prior to losing consciousness, the individual
frequently experiences early signs or
symptoms such as lightheadedness, nausea,
the feeling of being extremely hot or cold
(accompanied by sweating),

36. • ringing in the ears (tinnitus), an
uncomfortable feeling in the heart, fuzzy
thoughts, confusion, a slight inability to speak
or form words (sometimes combined with
mild stuttering),

37. • weakness and visual disturbances such as
lights seeming too bright, fuzzy or tunnel
vision, black cloud-like spots in vision, and a
feeling of nervousness can occur as well.

38. • The symptoms last for a few seconds before
the loss of consciousness (if it is lost), which
typically happens when the person is sitting
up or standing.

39. • When sufferers pass out, they fall down (unless
prevented from doing so) and, when in this
position, effective blood flow to the brain is
immediately restored, allowing the person to
regain consciousness.

40. • . If the person does not fall into a fully flat,
supine position, and the head remains
elevated above the trunk, a state similar to
a seizure may result from the blood's inability
to return quickly to the brain, and the neurons
in the body will fire off and generally cause
muscles to twitch very slightly but mostly
remain very tense. Fainting occurs with a loss
of oxygen to the brain.

41. CAUSE
Typical triggers for vasovagal episodes
include:
• Prolonged standing or upright sitting
• After or during urination (micturition syncope)
• Straining, such as to have a bowel movement or
during vomiting
• Standing up very quickly (orthostatic hypotension)

42. • During or post-biopsy procedures
• Stress directly related to trauma[8]
• Stress
• Postural orthostatic tachycardia
syndrome (POTS). Multiple chronic episodes
are experienced daily by many patients
diagnosed with this syndrome. Episodes are
most commonly manifested upon standing up.

43. • Any painful or unpleasant stimuli, such as:
– Trauma (such as hitting one's funny bone)
– Watching or experiencing medical procedures (such
as venipuncture or injection)
– High pressure on or around the chest area after
heavy exercise
• Severe menstrual cramps
• Sensitivity to pain
• Arousal or stimulants (e.g. sex, tickling,
or adrenaline)

44. • Sudden onset of extreme emotions
• Lack of sleep
• Hunger
• Coughing
• Being exposed to high temperatures
• Random onsets due to nerve malfunctions

45. TREATMENT
1)Avoidance of trigger
2) Exposure-based exercises with therapists if the
trigger is mental or emotional, e.g. sight of
blood. However, if the trigger is a specific drug,
then avoidance is the only treatment.
3) drinks with electrolytes

46. 4) if they experience prodromal warning signs:
they should lie down and raise their legs, or at
least lower their head to increase blood flow
to the brain. If the individual has lost
consciousness, he or she should be laid down
with his or her head turned to the side. Tight
clothing should be loosened.
5) Wearing graded compression stockings may
be helpful.

47. 2. Neurogenic Shock:-
It is usually due to spinal cord injury, which
cause dilatation of splanchnic vessels.
This type can safely be treated with
vasoconstrictor drugs to bring up the blood
pressure. There will be bradycardia, hypotension,
arrhythmias, and decreased cardiac output.

48. • 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

50. • Blood pressure control, oxygen delivery,
maintenance of haemodynamics, airway, fluid
therapy, intravenous methylprednisolone
therapy should be done. Dopamine and /or
phenylephrine (α agonist) can be used.

51. 3. Hypovolaemic Shock— Most Common Type
Haemorrhage, may be due to injury to the liver,
spleen,bone fractures, haemothorax, vascular
injury, severe bleeding on table during surgeries
of thyroid, liver, portalvein or major vessels.
Vomiting, diarrhoea due to any cause, Burns.

53. 4. Cardiogenic Shock:-
Cardiogenic shock is defined as circulatory
failure causing diminished forward flow
leading into tissue hypoxia in the setting of
adequate intravascular volume with systolic
blood pressure < 90 mmHg for 30 minutes;
cardiac index < 2.2 L/minute / sq meter; raised
PCWP (pulmonary capillary wedge pressure) >
15 mmHg. It is commonly seen in acute MI
with. a mortality > 50

54. Cardiogenic shock develops within 24 hours of MI.
it occurs when 50% of left ventricular wall is
damaged by infarction. It leads to pulmonary
oedema and severe hypoxia. Ischemic necrosis
of left ventricular wall causes failure of pump
thereby decreasing stroke volume

55. Diagnosis:- is established by ECG,
echocardiography, arterial blood gas analysis,
cardiac enzymes, PCWP and electrolyte
estimation (hypokalaemia and
hypomagnesaemia are common) are the
essential investigations.

56. • Management:- Proper oxygenation with
intubation, ventilator support, cardioversion,
pacing, antiarrhythmic drugs, correction of
electrolytes, avoiding fluid overload,
prevention of pulmonary oedema as
immediate measures.

57. • Dobutamine (β1 receptor agonist) is used to
raise cardiac output provided there is
adequate preload and intravascular volume (it
is peripheral vasodilator and reduces BP).

58. Dopamine is preferred in patients with
hypotension. But It may increase peripheral
resistance and heart rate worsening cardiac
ischaemia. Often both dopamine and dobutamine
combination may be required.

59. • Careful judicial use of epinephrine,
norepinephrine, phosphodiesterase
inhibitors (amrinone, milrinone) are often
needed. Anticoagulants and aspirin are given.
Thrombolytics can be used. b blockers,
nitrates (nitroglycerine causes coronary
arterial dilatation), ACE inhibitors are also
used.

60. Intra-aortic balloon pump (IABP) may
need to be introduced transfemorally as a
mechanical circulatory support to raise cardiac
output and coronary blood flow.

61. • Percutaneous transluminal coronary
angioplasty (PTCA) and coronary artery
bypass graft (CABG) are the final choices.
Relief of pain, preserving of remaining
myocardium and its function, maintaining
adequate preload, oxygenation,
minimizing sympathetic stimulation,
correction of electrolytes should be the
priorities.

62. 5. Cardiac Compression Shock
• It is probably due to pericardial tamponade of any
cause or kinking of great vessels, massive
pulmonary embolism, tension pneumothorax, air
embolism causes obstructive shock with reduced
preload to heart.

63. Acute massive pulmonary embolism from a
thrombus or an air embolism (50 ml of air),
obstructing more than 50% of pulmonary
vasculature leads to severe shock and sudden
death.
Tachycardia, hypotension, pulmonary
oedema, raised JVP, gallop rhythm are the
features.

64. 6. Septic Shock
Septic shock may be due to gram-positive organisms,
gramnegative organisms, fungi, viruses or protozoal
origin.
Gram-negative septicaemia/gram-negative septic
shock is called as endotoxic shock.

65. Gram positive septic
shock
• Due to exotoxin by gram
+ve bacteraemia like
Clostridium tetani/welchii,
staphylococci, streptococci
pneumococci
• Fluid loss, hypotension
is common; with normal
cardiac output
Gram negative septic
shock
• Gram negative bacteria
cause
• endotoxaemia and its
effects.
• Urinary/gastrointestinal/
• biliary and respiratory foci
are
• common

66. Pathophysiology of septic shock
Toxins/endotoxins from organisms like E. Coli,
Klebsiella, Pseudomonas, and Proteus
Inflammation, cellular activation of macrophages,
neutrophils, monocytes
Release of cytokines, free radicals

67. Chemotaxis of cells, endothelial injury, altered
coagulation cascade—SIRS
Reversible hyperdynamic warm stage of septic shock
with fever, tachycardia, tachypnoea
Severe circulatory failure with MODS (failure of lungs,
kidneys, liver, heart) with DIC
Hypodynamic, irreversible cold stage of septic shock.

68. Septic shock is typically a vasodilatory shock
wherein there is peripheral vasodilatation causing
hypotension which is resistant to vasopressors.
This is due to toxin induced release of isoform of
nitric oxide synthetase from the vessel wall which
causes sustained prolonged release of high levels
of nitric oxide

69. Magnitude of infection is quantified as
(1) Sepsis which shows fever, tachycardia,
leukocytosis
(2) Severe sepsis which shows low tissue perfusion
with organ dysfunction (lactic acidosis,
dysfunction of liver, kidney, lungs).
.

70. • (3) Septic shock with systemic hypotension (BP
< 90 mm Hg in spite adequate fluid therapy),
severe organ dysfunction (acute lung, kidney,
liver injury), maldistribution of blood flow,
shunting in microcirculation

71. Stages of septic shock
a. Hyperdynamic (warm) shock: This stage is
reversible stage. Patient is still having
inflammatory response and so presents with
fever, tachycardia, and tachypnoea

72. • . Pyrogenic response is still intact. Patient
should be treated properly at this stage. Based
on blood culture, urine culture (depending on
the focus of infection), higher antibiotics like
third generation cephalosporins,
aminoglycosides, metronidazole are started.

73. • The underlying cause is treated like draining
the pus, laparotomy for peritonitis, etc.
Ventilatory support with ICU monitoring may
prevent the patient going for the next cold
stage of sepsis.

74. b. Hypodynamic hypovolaemic septic shock
(cold septic shock): Here pyrogenic response is
lost. Patient is in decompensated shock. It is an
irreversible stage along with MODS (Multi-organ
dysfunction syndrome) with anuria, respiratory
failure (cyanosis), jaundice (liver failure), cardiac
depression, pulmonary oedema, hypoxia,
drowsiness, eventually coma and death occurs
(Irreversible stage).

75. Treatment of septic shock
Correction of fluid and electrolyte by
crystalloids, blood transfusion. Perfusion is
very/most important.
Appropriate antibiotics—third generation
cephalosporins/ aminoglycosides.
Treat the cause or focus—drainage of an
abscess; wound excision

76. Pus/urine/discharge/bile/blood culture and
sensitivity for antibiotics.
Critical care, oxygen, ventilator support,
dobutamine/ dopamine/noradrenaline to
maintain blood pressure and urine output.

77. Monitoring the patient by pulse oximetry,
cardiac status, urine output, arterial blood gas
analysis.
Short-term (one or two doses) high dose steroid
therapy to control and protect cells from effects
of endotoxaemia. It improves cardiac, renal and
lung functions.

78. Single dose of methylprednisolone or
dexamethasone which often may be repeated
again after 4 hours is said to be effective in
endotoxic shock.
Activated C protein(Drotrecogin alfa (Xigris))
prevents the release of inflammatory mediators
and blocks the effects of these mediators on
cellular function.

79. 7. Anaphylactic Shock
Injections—penicillins, anaesthetics,stings,
venom, shellfish may be having antigens which
will combine with IgE of mast cells and basophils,
releasing histamine and large amount of SRS-A
(Slow releasing substance of anaphylaxis).

81. They cause bronchospasm, laryngeal oedema,
respiratory distress, hypotension and shock.
Mortality is 10%.
Rashes all over the body are commonly
observed.

82. TREATMENT
• Sudden onset
• ™. Distributive shock
• ™. Bronchospasm, laryngeal oedema
• ™. Generalised rashes and oedema
• ™. Hypotension, feeble pulse

83. • ™. Mortality 10%
• ™. To start adrenaline 100 ug IV, steroids, IV
fluids, oxygen
• foot end elevation
• ™. Ventilator in severe cases
• ™. Cardiac massage, defibrillation

85. SHOCK(contd)
• DR A PAVAN KUMAR(PROF )
• DR CH RAMU (ASSOCIATE PROF)
• DR VAMSIDHAR REDDY(ASSISTANT PROF)
• DR G VENU(ASSISTANT PROF)
• DR SHASHI (ASSISTANT PROF)
• DR WASIM (ASSISTANT PROF)

86. HAEMORRHAGE
Classification:-
I. Based on the source of bleeding:
a. Arterial is bright red in colour, spurting like jet along
with pulse of the patient.
b. Venous is dark red, steady and continuous flow. Blood
loss may be severe and rapid when bleeding is from
femoral vein, jugular vein, other major veins, varicose
veins, portal vein, oesophageal varices.

87. Pulmonary arterial blood is dark red in colour
and
pulmonary venous blood is bright red in colour.
c. Capillary: Here bleeding is rapid and bright
red. It is often torrential due to continuous
ooze.

88. II. Based on the time of onset of bleeding in
relation to any operative procedure:
1. Primary: Occurs at the time of injury or
operation.
2. Reactionary: It occurs within 24 hours after
surgery or after injury (commonly in 4-6
hours). Anesthetic medics , and slipping of
ligature.
3. Secondary: It usually occurs in 14 days after
surgery. (heavily contaminated wound is
closed primarily)

89. III. Based on the type of haemorrhage:
1) Revealed haemorrhage:- It is visible external
haemorrhage
2) Concealed haemorrhage:- It constituted
internal haemorrhage like liver injury, spleen
injury, # femur, cerebral haemorrhage,
hemothorax etc.
3) Initially concealed but later revealed
haemorrhage:- hematuria, hemetemesis,
melaena.

90. IV. Based on the duration of haemorrhage:
1. Acute haemorrhage: It is sudden, severe
haemorrhage after trauma, surgery.
2. Chronic haemorrhage: It is chronic repeated
bleeding for a long period like in haemorrhoids,
bleeding peptic ulcer, carcinoma caecum, etc
they present with chronic anaemia with
hyperdynamic cardiac failure. (hemophilia)

91. They are in a state of chronic hypoxia. It is
corrected by packed cell transfusion not by
whole blood itself. Cause has to be treated
accordingly.
3. Acute on chronic haemorrage: It is more
dangerous as the bleeding occurs in
individuals who are already hypoxic, which
may get worsened faster.

92. Clinical Features of Haemorrhage
1)Pallor, thirsty, cyanosis.
2)Tachycardia, tachypnoea.
3)Air hunger.
4)Cold clammy skin due to vasoconstriction.

93. 5)Dry face, dry mouth and goose skin appearance
(due to contraction of arrector pilorum).
6)Rapid thready pulse, hypotension.
7)Oliguria.
8)Features related to specific causes.
9)Shock index (ratio of pulse rate to blood pressure)
> 1 (cardiac index)

94. Measurement of Blood Loss
1) Clot size of a clenched fist is 500 ml.
2) Blood loss in a closed tibial fracture is 500-
1500 ml; in a fracture femur is 500-2000 ml.
3)Weighing the swab before and after use is an
important method of on-table assessment of
blood loss.
4)Roughly 1kg soaked swab= 1000ml

95. Rains Factor
Total amount =
of blood loss
Total difference in swab weight × 1.5
or
Total difference in swab weight × 2
(For larger wounds and larger
operations)

98. Treatment
1)Restoration of blood loss: By blood transfusion, albumin
4.5%, SAG-M blood, saline, Haemaccel (Gelatin), dextran,
plasma infusions.
Note: One unit of blood should raise 1 gm% of
haemoglobin.
2) Catheterisation, foot end elevation, monitoring.

99. 3)Oxygen support/intubation/ventilator and
critical care.
4) Pressure, packing and head down
(Trendelenburg) position to restore BP and
blood supply of brain.
5)Wound exploration and proceeding, i.e.
ligation of the small vessel, suturing the
wound part, vessel suturing (anastomosis),
excision of the tissues.

100. Trendelenberg position
(Head down position)

101. 6)Absolute rest, analgesics, morphine 10-20 mg
IM/IV to relieve pain, sedation.
7)ICT placing for haemothorax.
8) Laparotomy for liver or spleen or mesentery or
bowel injuries, suturing, splenectomy.
Fluid replacement is calculated
using a 3:1 rule (3 ml of isotonic
crystalloid for every 1 ml of
estimated blood loss)

102. 9) Topical applications for local ooze—Oxycel,
gauze soaked with adrenaline, bone wax for
oozing from bone and other local haemostatic
agents (collagen, thrombin).
10) In venous haemorrhage, elevation, ligation
of vein or in case of large vein suturing of
venous wall, pressure bandaging, packing will
be helpful.

103. 11)Tourniquet are often used in operation
theatre for control of haemorrhage in limbs.
But it is not advisable as a first aid measure.
12)TPN, CVP monitoring, electrolyte
management are all equally important.
13) Steroid injection, antibiotics, ventilator
support are often required.

107. Local haemostatic agents™
. Gelatin sponge (Gel foam)
™. Oxidised cellulose (Surgicel)
™. Collagen sponge (Helistat)
™. Microfibrillar collagen powder (Avitene)
™

108. . Topical thrombin
™. Bone wax (derived from bees wax + almond oil)
™. Gelatin matrices (Floseal)
™. Topical EACA, topical cryoprecipitate

112. ARTIFICIAL BLOOD
1. Perfluorocarbon (Fluosoleda)—abiotic
substitute as synthetic oxygen carrier. Its half life
is 7 days. It is RBC substitute.
a)It has got high affinity for O2.
b)It is inert, colourless, odourless, dense, poorly
soluble liquid.

113. c)It is biocompatible.
d)It is emulsified with albumin or lipids before
infusion.
e)Its emulsion alone injection can cause
pulmonary embolism.
f)It can bind and release oxygen. But as it
reduces the PPO2 quickly, it is a disadvantage.
Patient ideally to be kept in hyperbaric place.

114. 2. Stroma free haemoglobin—biomimetic
haemoglobin based substitute.
3. Chelates which reverse bound O2.
Intraoperative— salvage of blood: On table
blood is collected, washed, filtered and
transfused. Used in trauma.