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Transcript
SHOCK
SHOCK
TERMINOLOGY
DEFINITION
TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
Brian Angus Pathology Department
MISCELLANEOUS
University of Newcastle upon Tyne
1
Return to Cardiovascular Pathology Index Page
SHOCK
TERMINOLOGY
• Emotional/psychological
• Electrical
• Cardiovascular
This presentation concerns
acute circulatory failure:
cardiovascular shock.
2
SHOCK
SHOCK
TERMINOLOGY
DEFINITION
TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS
3
SHOCK
DEFINITION
the clinical syndrome
resulting from
ACUTE
CIRCULATORY
FAILURE
4
SHOCK
SHOCK
TERMINOLOGY
DEFINITION
TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS
5
SHOCK
TYPES OF SHOCK
•
•
•
•
•
Cardiogenic
Hypovolaemic
Septic
Anaphylactic
Miscellaneous
pancreatitis
neurogenic
blood transfusion
6
SHOCK
SHOCK
TERMINOLOGY
DEFINITION
TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS
7
SHOCK
CLINICAL FEATURES OF
SHOCK
In acute circulatory failure the
patient typically shows the
following:
Restless, confused
Pale cold sweaty
Peripheral cyanosis
Rapid weak pulse
Low blood pressure
Drowsiness, coma
8
SHOCK
SHOCK
a) TERMINOLOGY
b) DEFINITION
c) TYPES OF SHOCK LISTED
120
100
80
60
40
d) CLINICAL FEATURES OF SHOCK
20
0
e) HYPOVOLAEMIC SHOCK
Normal
10%
25%
50%
BLOOD LOSS
f) CARDIOGENIC SHOCK
g) SEPTIC SHOCK
h) ANAPHYLACTIC SHOCK
i) MISCELLANEOUS
9
SHOCK
HYPOVOLAEMIC SHOCK
AETIOLOGY
120
100
• Haemorrhage
• Burns (>10% surface)
• Vomiting/diarrhoea
80
60
40
20
0
Normal
10%
25%
50%
BLOOD LOSS
10
SHOCK
HAEMORRHAGE:
VOLUME EFFECTS
120
100
80
Loss 10%: no effect
60
40
Loss 25%: hypovolaemic symptoms 36hrs
20
0
Normal
10%
25%
50%
BLOOD LOSS
Loss 50%:
coma. death.
11
SHOCK
LOSS OF BLOOD VOLUME
EARLY COMPENSATORY CHANGES
120
When blood is lost the body reacts
specifically to preserve blood supply to
the brain and heart.
100
80
60
40
The adrenal gland secretes
catecholamines which increase
peripheral resistance (raising the blood
pressure).
The kidneys secrete renin which retains
sodium and thus water by the renin
angiotensin system
20
0
Normal
10%
25%
50%
BLOOD LOSS
12
SHOCK
LOSS OF BLOOD VOLUME:
MANAGEMENT 1
120
100
These early compensatory changes
suffice if <25% blood volume lost.
80
60
40
20
If>25% blood volume lost then
transfusion is required as there is a risk
of shock, dependent upon the age and
health of the patient.
0
Normal
10%
25%
50%
BLOOD LOSS
13
SHOCK
LOSS OF BLOOD VOLUME:
MANAGEMENT 2
120
100
Transfusion is ideally done with
crossmatched whole blood.
80
60
40
20
Macromolecular solutions and saline
can also be used.
0
Normal
10%
25%
50%
BLOOD LOSS
14
SHOCK
LOSS OF BLOOD VOLUME
MANAGEMENT 3
120
In assessing response to
transfusion, measurement of
central venous pressure (CVP)
using a catheter inserted into the
right side of the heart gives a
better idea of the true circulatory
status than simply measuring the
blood pressure, which can be
maintained by the compensatory
mechanisms described until a
critical situation is imminent.
100
80
60
40
20
0
Normal
10%
25%
50%
BLOOD LOSS
15
SHOCK
HYPOVOLAEMIC SHOCK
LATE EFFECTS 1
If blood volume is not restored, the
following events take place, resulting in a
critically ill patient:
Circulation becomes sluggish because:
120
100
80
60
40
20
a) artetioles relax and the vascular beds
fill with subsequent departure of fluid
into the extravascular compartment;
this results in haemoconcentration.
b) blood viscosity is raised because red
cells form rouleaux, and the blood
fibrinogen is raised.
0
Normal
10%
25%
50%
BLOOD LOSS
16
SHOCK
HYPOVOLAEMIC SHOCK
LATE EFFECTS 2
If blood volume is not restored, the
following events take place, resulting in a
critically ill patient:
120
100
80
60
Damaged endothelium releases
thromboplastins which trigger the
coagulation cascade: this results in
disseminated intravascular
coagulation (DIC). Blood clotting
factors are consumed and the patient
therefore has a bleeding tendency.
40
20
0
Normal
10%
25%
50%
BLOOD LOSS
17
SHOCK
HYPOVOLAEMIC SHOCK
LATE EFFECTS 3
If blood volume is not restored, the
following events take place, resulting in a
critically ill patient:
120
100
80
60
Lack of oxygen in the tissues results
in metabolic acidosis: this depresses
myocardial action.
40
20
0
Normal
10%
25%
50%
BLOOD LOSS
Damaged cells release potassium
resulting in hyperkalaemia.
Corticosteroid action (from the
adrenals) results in hyperglycaemia.
18
SHOCK
HYPOVOLAEMIC SHOCK
LATE EFFECTS 4
If blood volume is not restored, the
following events take place, resulting in a
critically ill patient:
120
100
80
60
Widespread ischaemic damage
occurs
40
20
0
Normal
Brain:
Kidney:
Heart:
Neuronal necrosis
Acute tubular
necrosis
Subendocardial
infarction
10%
25%
50%
BLOOD LOSS
19
SHOCK
SHOCK
a) TERMINOLOGY
b) DEFINITION
c) TYPES OF SHOCK LISTED
d) CLINICAL FEATURES OF SHOCK
e) HYPOVOLAEMIC SHOCK
f) CARDIOGENIC SHOCK
g) SEPTIC SHOCK
h) ANAPHYLACTIC SHOCK
i) MISCELLANEOUS
20
SHOCK
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.
21
SHOCK
SHOCK
a) TERMINOLOGY
b) DEFINITION
c) TYPES OF SHOCK LISTED
d) CLINICAL FEATURES OF SHOCK
e) HYPOVOLAEMIC SHOCK
f) CARDIOGENIC SHOCK
g) SEPTIC SHOCK
h) ANAPHYLACTIC SHOCK
i) MISCELLANEOUS
22
SHOCK
SEPTIC SHOCK: CAUSES
Septic shock is caused by
bacterial endotoxins or exotoxins
in the blood .
The toxins can be released, for
example from bacteria in a focus
of sepsis such as an abcess, or
from bacterial growth in the
flowing blood (septicaemia e.g.
meningococcal)
23
SHOCK
EXOTOXIC AND ENDOTOXIC SHOCK
24
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.
In practice endotoxic and septic
shock are often used
synonymously.
25
SHOCK
SEPTIC SHOCK
ENDOTOXIC:
AETIOLOGY
GRAM NEGATIVE ENDOTOXINS
CELL WALL LIPOPOLYSACCARIDES
E coli
Proteus
Klebsiella
Bacteroides
Pseudomonas (burns)
Meningococci
26
SHOCK
SEPTIC SHOCK
EXOTOXIC:
AETIOLOGY
GRAM POSITIVE EXOTOXINS
Much rarer than endotoxic shock
Example of cause: Staph aureus skin
infection
TOXIC SHOCK SYNDROME
Straph aureus in tampons
27
SHOCK
SEPTIC SHOCK
AETIOLOGY:
SOURCES
Infected burns
Septicaemia
Localised infections
Instrumentation e.g. Urogenital
Immunosuppression
28
SHOCK
SEPTIC SHOCK
MECHANISM
The toxins from bacteria damage
endothelium. Nitric oxide (NO) is
released which causes vasodilatation.
Unlike hypovolaemic shock there is
no vasoconstriction phase.
However, as with late phase
hypovolaemic shock, endothelial
damage results in DIC as previously
explained.
29
SHOCK
SEPTIC SHOCK
EXAMPLE
This is the haemorrhagic
rash of meningococcal
septicaemia.
Prompt treatment can
prevent the condition on
the next slide:
30
SHOCK
SEPTIC
SHOCK:
EXAMPLE
The brain is
covered in
purulent
exudate: this is
meningococcal
meningitis
University of Newcastle upon Tyne
31
SHOCK
SHOCK
a) TERMINOLOGY
b) DEFINITION
c) TYPES OF SHOCK LISTED
d) CLINICAL FEATURES OF SHOCK
e) HYPOVOLAEMIC SHOCK
f) CARDIOGENIC SHOCK
g) SEPTIC SHOCK
h) ANAPHYLACTIC SHOCK
i) MISCELLANEOUS
32
SHOCK
ANAPHYLACTIC SHOCK:
AETIOLOGY
Histamine release from blood
basophils
Drugs e.g. penicillin
Stings
Foods e.g. Shellfish, Peanuts
Vasodilatation - blood
pressure drops
33
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.
34
SHOCK
ANAPHYLACTIC SHOCK: MECHANISM
35
SHOCK
ANAPHYLACTIC SHOCK:
TREATMENT
Adrenaline 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.
36
SHOCK
SHOCK
a) TERMINOLOGY
b) DEFINITION
c) TYPES OF SHOCK LISTED
d) CLINICAL FEATURES OF SHOCK
e) HYPOVOLAEMIC SHOCK
f) CARDIOGENIC SHOCK
g) SEPTIC SHOCK
h) ANAPHYLACTIC SHOCK
i) MISCELLANEOUS
37
SHOCK
MISCELLANEOUS CAUSES OF SHOCK
Neurogenic :
e.g. severe head injury
Pancreatitis:
enzymes damage
endothelium
Blood transfusion:
incompatible
38
SHOCK
END OF
PRESENTATION
Return to Cardiovascular
Pathology Index Page
39
SHOCK
SHOCK
END OF PRESENTATION
Return to Cardiovascular
Pathology Index Page
40