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Shock

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0% found this document useful (0 votes)
30 views39 pages

Shock

Uploaded by

temoorahmed15
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
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Download as PDF, TXT or read online on Scribd
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SHOCK

SHOCK
Dr Iram Khurshid
MBBS, FCPS
(Histopathology)
Assistant professor, CKMC
1
SHOCK

SHOCK
OUTLINE

DEFINITION
TYPES OF SHOCK
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS
4
SHOCK

DEFINITION
Shock is a state in
which diminished
cardiac output or
reduced effective
circulating blood
volume impairs tissue
perfusion and leads to
cellular hypoxia. 5
SHOCK

Shock: Aetiology
❖ Reduction in
blood volume

❖ Reduction in
cardiac output

❖ Redistribution of
blood
SHOCK

TYPES OF SHOCK
1) Cardiogenic
2) Hypovolemic
3) Septic
4) Anaphylactic
5) Miscellaneous
• Neurogenic

5
SHOCK

7
SHOCK

CLINICAL FEATURES OF SHOCK

In acute circulatory failure the


patient typically
Restless, confused
shows the following: Pale cold sweaty
Peripheral cyanosis
Rapid weak pulse
Low blood pressure
Drowsiness, coma

9
SHOCK
1. HYPOVOLEMIC SHOCK
• CAUSES:
• Blood loss 120

100

• hemorrhage 80

60


40

Body water loss. 20

• Burns (>10% surface area Normal 10% 25%


BLOOD LOSS
50%

• Vomiting/ Diarrhea/ Dehydration.


• EFFECTS:
• Loss 10%: No effect
• Loss 25%: Hypovolemic symptoms 36 hrs
• Loss 50%: Coma → death.
10
SHOCK

Hypovolemic Shock:
Mechanism
Haemorrhage or fluid loss Inadequate blood volume

Decreased cardiac output Hypotension Impaired

tissue perfusion Cellular hypoxia Shock


SHOCK

LOSS OF BLOOD VOLUME


EARLY COMPENSATORY CHANGES 120

When blood is lost the body reacts 100

80

specifically to preserve blood supply to 60

40

the brain and heart. 20

0
Normal 10% 25% 50%

The adrenal gland secretes BLOOD LOSS

catecholamines which increase peripheral


resistance (raising the blood pressure).
The kidneys secrete renin which retains
sodium and thus water by the renin-
angiotensin system
13
SHOCK

LOSS OF BLOOD VOLUME:


MANAGEMENT 120

100
These early compensatory 80

changes suffice if <25% 60

40
blood volume lost. 20
If >25% blood volume lost then 0

transfusion is required as there Normal 10% 25%


BLOOD LOSS
50%

is a risk of shock, dependent


upon the age and health of the
patient.
Transfusion is ideally done with cross-matched
whole blood.
14
SHOCK
HYPOVOLEMIC SHOCK LATE
EFFECTS
If blood volume is not restored, the 120

100
following events take place, resulting 80

in a critically ill patient: 60

40

20

Widespread ischaemic damage occurs 0


Normal 10% 25% 50%
BLOOD LOSS

Brain: Neuronal necrosis


Kidney: Acute tubular necrosis
Heart: Infarction/ coagulative
necrosis

15
SHOCK
2. Septic Shock
• 25-50% mortality
• Common cause of death in ICU
• Caused by bacterial endotoxins or exotoxins in the
blood.
• The toxins can be released, from bacteria in a focus
of sepsis (abscess), septicaemia ( meningococcal)
Infected burns.
• Instrumentation e.g. Urogenital
• Immunosuppression
SHOCK
SEPTIC SHOCK:
ENDOTOXIC and EXOTOXIC
The diagram shows production of
exotoxins by bacteria which
remain intact (left).
This contrasts with endotoxic
shock where the whole bacteria
break up and cell wall
lipopolysaccarides activate the
complement and coagulation cascades.
.
17
 In practice, endotoxic and septic
shock are often used
synonymously
SHOCK

SEPTIC SHOCK ETIOLOGY

ENDOTOXIC
GRAM NEGATIVE ENDOTOXINS
CELL WALL LIPOPOLYSACCARIDES

E. coli, Proteus Klebsiella, Bacteroides,


Pseudomonas (burns),Meningococci Most commonly
EXOTOXIC triggered by gram+ve
GRAM POSITIVE EXOTOXINS bacilli, followed by
Examples: Staph aureus skin
infection,streptococci, pneumococci, gram –ve bacilli and
clostridium
19 etc fungi.
SHOCK

Pathogenesis of Septic shock


Substances from these
microorganisms activate
Macrophages , neutrophils,
endothelial cells,
complements which results
in INFLAMMATORY &
COUNTER INFLAMMATORY
RESPONSE leading to Septic
shock
20
 Inflammatory mediators are
increased, which results in arterial
vasodilation, vascular leakage, and
venous blood pooling thereby
causing Tissue hypoperfusion, cellular
hypoxia, and metabolic derangements
which finally leads to multi organ
failure and death
SHOCK

SEPTIC
SHOCK:
EXAMPLE
The brain is
covered in
purulent
exudate: this
is
meningococc
al meningitis

23
SHOCK
3. CARDIOGENIC SHOCK: CAUSES
Myocardial infarction and its
complications, for example ruptured
papillary muscle, result in
ACUTE PUMP FAILURE
Mortality is high (at least 80%).
The effects are similar to
hypovolaemic shock, but of
course management is different as
there is no urgent requirement for
fluid.
SHOCK

4.ANAPHYLACTIC SHOCK:
ETIOLOGY
❑Drugs
e.g.penicillin
❑Stings
❑Foods e.g. Shellfish,
Peanuts

Histamine release from blood


basophils →
Vasodilatation - blood
pressure drops
SHOCK

ANAPHYLACTIC SHOCK:
MECHANISM
Antigen, for example wasp venom
accesses specific IgE on blood
basophils. IgE dimerises at the
cell surface and the basophil
releases histamine by
degranulation → vasodilatation
causes the blood pressure to
drop.

Clinical features of shock develop


rapidly.
24
SHOCK

ANAPHYLACTIC SHOCK: MECHANISM


SHOCK

ANAPHYLACTIC
SHOCK: TREATMENT
Adrenaline(vasoconstrictor,
bronchodilator) and
hydrocortisone are given in
the acute phase.
The patient may recover
without further specific
treatment.

If not, full support in an intensive


care unit will be required.
29
SHOCK

5. MISCELLANEOUS CAUSES OF
SHOCK

Neurogenic:
e.g. severe head or spinal cord injury.
characterized by organ tissue hypoperfusion due to
disruption of normal sympathetic control over
vascular tone.
This critical condition often arises from spinal cord
injuries and frequently occurs in the cervical and upper
thoracic spinal cord, especially those above the T6 level .
30
SHOCK
SHOCK

Stages of shock
1.Non-progressive stage
2.Progressive stage
3.Irreversible stage
SHOCK

Stages of shock
1.Non-progressive stage:

By the action of
There is baroreceptors,
compensation catecholamines, Tachycardia,
Renin-angiotensin- peripheral
and perfusion vasoconstriction
of vital organs aldosterone system
SHOCK

Stages of shock
2. Progressive stage:
Characterized by tissue hypoperfusion
and onset of worsening circulatory and
metabolic imbalances.
a. Tissue hypoxia
b. Anaerobic glycolysis
c. Lactic acidosis
d. Arteriolar dilatation
SHOCK

Stages of shock
3.3.Irreversible stage: Severe
cellular and tissue injury which is irreversible
a.Tissue injury, necrosis,
infarction
b.Common organs affected:
heart, kidney, brain, lungs, adrenal and
GIT
SHOCK

36
SHOCK

What is the primary cause of


septic shock?
A.Bleeding
B.Medication Allergy
C.Infection
D.Poison

37
SHOCK

A 20-year-old man is brought to the


emergency room after rupturing his spleen
in a motorcycle accident. His blood
pressure on admission is 80/60 mm Hg.This
patient is most likely suffering from which of
the following conditions?
(A)Acute pancreatitis
(B)Cardiogenic shock
(C)Hypersplenism
(D)Hypovolemic shock
38 (E)Septic shock
SHOCK

39

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