1. SHOCK TERMINOLOGY DEFINITION TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS
Brian Angus Pathology Department
University of Newcastle upon Tyne
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2. TERMINOLOGY Emotional/psychological Electrical Cardiovascular
This presentation concerns acute circulatory failure: cardiovascular shock.

3. SHOCK TERMINOLOGY DEFINITION TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS

4. DEFINITION ACUTE CIRCULATORY FAILURE
the clinical syndrome resulting from
ACUTE CIRCULATORY FAILURE

5. SHOCK
TERMINOLOGY
DEFINITION
TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS

6. TYPES OF SHOCK Cardiogenic Hypovolaemic Septic Anaphylactic
Miscellaneous pancreatitis
neurogenic
blood transfusion

7. SHOCK
TERMINOLOGY
DEFINITION
TYPES OF SHOCK LISTED
CLINICAL FEATURES OF SHOCK
HYPOVOLAEMIC SHOCK
CARDIOGENIC SHOCK
SEPTIC SHOCK
ANAPHYLACTIC SHOCK
MISCELLANEOUS

8. 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

9. 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

10. HYPOVOLAEMIC SHOCK AETIOLOGY
Haemorrhage
Burns (>10% surface)
Vomiting/diarrhoea

11. HAEMORRHAGE: VOLUME EFFECTS
Loss 10%: no effect
Loss 25%: hypovolaemic symptoms 36hrs
Loss 50%: coma. death.

12. LOSS OF BLOOD VOLUME EARLY COMPENSATORY CHANGES
When blood is lost the body reacts specifically to preserve blood supply to the brain and heart.
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

13. LOSS OF BLOOD VOLUME: MANAGEMENT 1
These early compensatory changes suffice if <25% blood volume lost.
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.

14. LOSS OF BLOOD VOLUME: MANAGEMENT 2
Transfusion is ideally done with crossmatched whole blood.
Macromolecular solutions and saline can also be used.

15. LOSS OF BLOOD VOLUME MANAGEMENT 3
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.

16. 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:
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.

17. HYPOVOLAEMIC SHOCK LATE EFFECTS 2
If blood volume is not restored, the following events take place, resulting in a critically ill patient:
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.

18. HYPOVOLAEMIC SHOCK LATE EFFECTS 3
If blood volume is not restored, the following events take place, resulting in a critically ill patient:
Lack of oxygen in the tissues results in metabolic acidosis: this depresses myocardial action.
Damaged cells release potassium resulting in hyperkalaemia.
Corticosteroid action (from the adrenals) results in hyperglycaemia.

19. HYPOVOLAEMIC SHOCK LATE EFFECTS 4
If blood volume is not restored, the following events take place, resulting in a critically ill patient:
Widespread ischaemic damage occurs
Brain: Neuronal necrosis
Kidney: Acute tubular necrosis
Heart: Subendocardial infarction

20. 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

21. 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.

22. 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

23. 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)

24. EXOTOXIC AND ENDOTOXIC SHOCK

25. 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.

26. SEPTIC SHOCK ENDOTOXIC: AETIOLOGY
GRAM NEGATIVE ENDOTOXINS
CELL WALL LIPOPOLYSACCARIDES
E coli
Proteus
Klebsiella
Bacteroides
Pseudomonas (burns)
Meningococci

27. 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

28. SEPTIC SHOCK AETIOLOGY: SOURCES
Infected burns
Septicaemia
Localised infections
Instrumentation e.g. Urogenital
Immunosuppression

29. 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.

30. SEPTIC SHOCK EXAMPLE
This is the haemorrhagic rash of meningococcal septicaemia.
Prompt treatment can prevent the condition on the next slide:

31. SEPTIC SHOCK: EXAMPLE
The brain is covered in purulent exudate: this is meningococcal meningitis
University of Newcastle upon Tyne

32. 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

33. ANAPHYLACTIC SHOCK: AETIOLOGY
Histamine release from blood basophils
Drugs e.g. penicillin
Stings
Foods e.g. Shellfish, Peanuts
Vasodilatation - blood pressure drops

34. 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.

35. ANAPHYLACTIC SHOCK: MECHANISM

36. 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.

37. 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

38. MISCELLANEOUS CAUSES OF SHOCK
Neurogenic : e.g. severe head injury
Pancreatitis: enzymes damage endothelium
Blood transfusion: incompatible

39. END OF PRESENTATION
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40. SHOCK END OF PRESENTATION
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