shock 1 terminology definition types of shock listed clinical features of shock hypovolaemic shock...

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SHOCK

SHOCKTERMINOLOGY

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

Return to Cardiovascular Pathology Index Page

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SHOCK

TERMINOLOGY

• Emotional/psychological

• Electrical

• Cardiovascular

This presentation concerns acute circulatory failure: cardiovascular shock.

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SHOCK

SHOCKTERMINOLOGY

DEFINITION

TYPES OF SHOCK LISTED

CLINICAL FEATURES OF SHOCK

HYPOVOLAEMIC SHOCK

CARDIOGENIC SHOCK

SEPTIC SHOCK

ANAPHYLACTIC SHOCK

MISCELLANEOUS

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SHOCK

DEFINITION

the clinical syndrome resulting from

ACUTE CIRCULATORY FAILURE

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SHOCK

SHOCKTERMINOLOGY

DEFINITION

TYPES OF SHOCK LISTED

CLINICAL FEATURES OF SHOCK

HYPOVOLAEMIC SHOCK

CARDIOGENIC SHOCK

SEPTIC SHOCK

ANAPHYLACTIC SHOCK

MISCELLANEOUS

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SHOCK

TYPES OF SHOCK

• Cardiogenic• Hypovolaemic• Septic• Anaphylactic• Miscellaneous pancreatitis

neurogenic

blood transfusion

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SHOCK

SHOCKTERMINOLOGY

DEFINITION

TYPES OF SHOCK LISTED

CLINICAL FEATURES OF SHOCK

HYPOVOLAEMIC SHOCK

CARDIOGENIC SHOCK

SEPTIC SHOCK

ANAPHYLACTIC SHOCK

MISCELLANEOUS

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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

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SHOCK

SHOCKa) 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

0

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Normal 10% 25% 50%

BLOOD LOSS

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SHOCK

HYPOVOLAEMIC SHOCKAETIOLOGY

• Haemorrhage

• Burns (>10% surface)

• Vomiting/diarrhoea0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

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SHOCK

HAEMORRHAGE:VOLUME EFFECTS

0

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40

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80

100

120

Normal 10% 25% 50%

BLOOD LOSS

Loss 10%: no effect

Loss 25%: hypovolaemic symptoms 36hrs

Loss 50%: coma. death.

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SHOCK

LOSS OF BLOOD VOLUMEEARLY COMPENSATORY CHANGES

0

20

40

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80

100

120

Normal 10% 25% 50%

BLOOD LOSS

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

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SHOCK

LOSS OF BLOOD VOLUME:MANAGEMENT 1

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

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.

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SHOCK

LOSS OF BLOOD VOLUME:MANAGEMENT 2

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

Transfusion is ideally done with crossmatched whole blood.

Macromolecular solutions and saline can also be used.

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SHOCK

LOSS OF BLOOD VOLUMEMANAGEMENT 3

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

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.

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SHOCK

HYPOVOLAEMIC SHOCKLATE EFFECTS 1

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

If blood volume is not restored, the following events take place, resulting in a critically ill patient:

Circulation becomes sluggish because:

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.

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SHOCK

HYPOVOLAEMIC SHOCKLATE EFFECTS 2

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

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.

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SHOCK

HYPOVOLAEMIC SHOCKLATE EFFECTS 3

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

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.

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SHOCK

HYPOVOLAEMIC SHOCKLATE EFFECTS 4

0

20

40

60

80

100

120

Normal 10% 25% 50%

BLOOD LOSS

If blood volume is not restored, the following events take place, resulting in a critically ill patient:

Widespread ischaemic damage occurs

Brain: Neuronal necrosisKidney: Acute tubular

necrosisHeart: Subendocardial

infarction

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SHOCK

SHOCKa) 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

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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.

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SHOCK

SHOCKa) 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

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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)

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SHOCK

EXOTOXIC AND ENDOTOXIC SHOCK

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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.

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SHOCK

SEPTIC SHOCKENDOTOXIC: AETIOLOGY

GRAM NEGATIVE ENDOTOXINSCELL WALL LIPOPOLYSACCARIDES

E coliProteusKlebsiellaBacteroidesPseudomonas (burns)Meningococci

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SHOCK

SEPTIC SHOCKEXOTOXIC: AETIOLOGY

GRAM POSITIVE EXOTOXINS

Much rarer than endotoxic shock

Example of cause: Staph aureus skin infection

TOXIC SHOCK SYNDROMEStraph aureus in tampons

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SHOCK

SEPTIC SHOCKAETIOLOGY: SOURCES

Infected burnsSepticaemiaLocalised infectionsInstrumentation e.g. UrogenitalImmunosuppression

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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.

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SHOCK

SEPTIC SHOCK EXAMPLE

This is the haemorrhagic rash of meningococcal septicaemia.

Prompt treatment can prevent the condition on the next slide:

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SHOCK

SEPTIC SHOCK:EXAMPLE

The brain is covered in purulent exudate: this is meningococcal meningitis

University of Newcastle upon Tyne

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SHOCK

SHOCKa) 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

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SHOCK

ANAPHYLACTIC SHOCK: AETIOLOGY

Histamine release from blood basophils

Drugs e.g. penicillinStingsFoods e.g. Shellfish, Peanuts

Vasodilatation - blood pressure drops

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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.

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SHOCK

ANAPHYLACTIC SHOCK: MECHANISM

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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.

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SHOCK

SHOCKa) 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

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SHOCK

MISCELLANEOUS CAUSES OF SHOCK

Neurogenic : e.g. severe head injury

Pancreatitis: enzymes damage endothelium

Blood transfusion: incompatible

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SHOCK

END OF PRESENTATION

Return to Cardiovascular Pathology Index Page

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SHOCK

SHOCK

END OF PRESENTATION

Return to Cardiovascular Pathology Index Page