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Year 2 EMS MoD > Ischaemia, Infarction and Shock > Flashcards

Ischaemia, Infarction and Shock Flashcards

1
Q

What are the 2 types of hypoxia?

A

GENERALISED - whole body (e.g. anaemia, altitude)

REGIONAL - specific tissues

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2
Q

What is ischaemia?

A

Pathological reduction in blood flow to tissues.

|&raquo_space; hypoxia

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3
Q

What are the main causes of ishaemia?

A

Thrombosis/embolism.

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4
Q

What are the main types of ischaemia? (2)

A
  • REVERSIBLE CELL INJURY (short duration)

- IRREVERSIBLE CELL INJURY (prolonged duration; cell death by necrosis)

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5
Q

Is therapeutic reperfusion of ischaemic tissue beneficial?

A

Beneficial is ischaemia is reversible.

-no effect on infarcted tissues (permanent cell damage)

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6
Q

How can reperfusion of ischaemic tissue be harmful?

A

Reperfusion of non-infarcted tissue can cause production of reactive oxygen species by inflammatory cells.
» REPERFUSION INJURY

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7
Q

What is infarction?

A

Ischaemic necrosis due to occlusion of arterial supply/venous drainage.

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8
Q

What are the main causes of infarction?

A

Thrombosis and embolism.

-mainly within arteries

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9
Q

What are other causes of infarction? (4)

A
  • Vasospasm
  • Atheroma expansion
  • Extrinsic compression
  • Venous occlusion (rare)
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10
Q

What are the morphological classifications of infarction?

by colour

A
  • RED - haemorrhagic

* WHITE - anaemic

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11
Q

When does red (haemorrhagic) infarction occur?

A

Dual blood supply / venous infarction.

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12
Q

When does white (anaemic) infarction occur?

A

Single blood supply.

-totally cut off

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13
Q

What shape are most infarctions?

A

Wedge-shaped.

-tissue nearest blockage still has some perfusion

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14
Q

What are the histological characteristics of infarction? (2)

A
  • Coagulative necrosis (» pale pink cells)

- Colliquative necrosis (brain; cells break down)

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15
Q

If a person dies suddenly (e.g. massive heart attack) what do you see in the tissues?

A

Nothing.

-no time to develop haemorrhage/inflammatory response

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16
Q

What factors influence the degree of ischaemic damage? (4)

A
  • Nature of blood supply
  • Rate of occlusion
  • Tissue vulnerability to hypoxia
  • Blood oxygen content
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17
Q

How does the nature of the blood supply influence ischaemic damage?

A

Organs with a single supply are more vulnerable to infarction.
-e.g. kidneys, spleen, testis

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18
Q

Give 3 examples of organs with alternative bloody supplies.

A
  • LUNGS (pulmonary/bronchial arteries)
  • LIVER (hepatic artery/portal vein)
  • HAND (radial/ulnar arteries)
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19
Q

How does the rate of occlusion influence ischaemic damage?

A

Slowly developing occlusions are less likely to cause damage.

  • more development of alternative/collateral perfusion pathways
    (e. g. coronary arteries)
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20
Q

How does tissue vulnerability to hypoxia influence ischaemic damage?

A
  • BRAIN; very vulnerable to injury, 3-4 minutes of hypoxia&raquo_space; irreversible damage
  • HEART; more resistant, 20-30 minutes of hypoxia&raquo_space; myocyte death
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21
Q

How much of the body’s cardiac output and O2 consumption is required by the brain?

A

15% cardiac output.

20% oxygen consumption.

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22
Q

How does blood oxygen content influence ischaemic damage?

A

Reduced oxygen increases the chances of infarction.

-e.g. congestive heart failure

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23
Q

What are watershed regions?

A

Areas of the body that receive dual blood supply from the most distal branches of two large arteries.
-e.g. splenic flexure, brain

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24
Q

How does infarction present in the heart?

A

Ischaemic heart disease.

-angina/MI

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25
Q

How does infarction present in the brain?

A

Cerebrovascular disease.

-TIA/CVA

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26
Q

How does infarction present in the intestines?

A

Ischaemic bowel.

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27
Q

How does infarction present in the extremities?

A
  • Peripheral vascular disease

- Gangrene

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28
Q

What is the leading cause of death in the West?

A

Ischaemic heart disease.

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29
Q

What is the 3rd leading cause of death in the West?

A

Cerebrovascular disease.

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30
Q

What is cerebrovascular disease?

A

Any abnormality that affects the circulation of blood to the brain, causing limited or no blood flow to affected areas.

31
Q

Give an example of haemorrhagic cerebrovascular disease.

A

Bleeding.

32
Q

Give an example of ischaemic cerebrovascular disease.

A

Thrombosis/embolism.

33
Q

What causes an ischaemic stroke?

A
  • Thrombosis 2* to atherosclerosis

- Embolism

34
Q

What are the causes of a haemorrhagic stroke?

A
  • Intracerebral haemorrhage

- Ruptured aneurysm in circle of Willis (subarachnoid)

35
Q

What is a mural thrombus?

A

A stationary blood clot along the wall of a blood vessel, frequently causing vascular obstruction.

36
Q

What usually causes ischaemic bowel disease?

A

Thrombosis/embolism in superior/inferior mesenteric arteries.
» abdominal pain

37
Q

What are the different types of limb ischaemia/infarction?

A
  • Gangrene
  • Dry gangrene
  • Wet gangrene
  • Gas gangrene
38
Q

What is gangrene?

A

Localized death and decomposition of body tissue.

-due to obstructed circulation / bacterial infection.

39
Q

What is dry gangrene?

A

Due to vascular insufficiency.
» ischaemic coagulative necrosis
» black, dry tissue

40
Q

What is wet gangrene?

A

Due to untreated infection&raquo_space; lack of blood supply.

41
Q

What is gas gangrene?

A

Superimposed infection with gas-producing organism.

-e.g. clostridium perfringens

42
Q

What is shock?

A

A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension)&raquo_space; decreased oxygen delivery to the tissues.

43
Q

What critical imbalance does shock lead to?

A

Critical imbalance between oxygen delivery and oxygen consumption.

44
Q

What are the cellular effects of shock? (5)

A
  • Membrane ion pump dysfunction
  • Intracellular swelling
  • Leakage of intracellular contents
  • Poor intracellular pH regulation
  • Anaerobic respiration (» lactic acid)
45
Q

What are the systemic effects of shock? (4)

A
  • Alteration of serum pH (acidaemia)
  • Endothelial dysfunction (vascular leakage)
  • Stimulation of inflammatory cascades
  • Ischaemia
46
Q

Is shock reversible?

A

Initially reversible but rapidly becomes irreversible.

47
Q

What is the sequential result of shock?

A
  • Cell death
  • End-organ damage
  • Multi-organ failure
  • Death
48
Q

What are the main types of shock? (3)

A
  • Hypovolaemic
  • Cardiogenic
  • Distributive
49
Q

What is the mortality rate of septic shock?

A

35-60% die within one month.

50
Q

What is the mortality rate of cardiogenic shock?

A

60-90% mortality.

51
Q

What is hypovolaemic shock?

A

Severe intra-vascular fluid loss (e.g. blood)
» decreased pre-load (venous return to heart)
» decreased stroke volume
» decreased cardiac output
» low mean arterial pressure.

52
Q

How do the body compensate for hypovolaemic shock?

A

Vasoconstriction&raquo_space; increased systemic vascular resistance.

53
Q

What are the causes of hypovolaemic shock? (2)

A
  • Haemorrhage (e.g. trauma, aneurysm)

- Non-haemorrhagic fluid loss (diarrhoea, burns)

54
Q

What is third spacing?

A

Acute loss of fluid from blood vessels to internal body cavities.
» oedema and hypotension

55
Q

What is cardiogenic shock?

A

Cardiac pump failure&raquo_space; decreased cardiac output.

-can no longer meet body’s needs

56
Q

How can you compensate for cardiogenic shock?

A

Increased systemic vascular resistance.

57
Q

What are the 4 categories of cardiogenic shock?

A
  • Myopathic
  • Arrhythmia-related
  • Mechanical
  • Extra-cardiac
58
Q

What is myopathic cardiogenic shock, and what causes it?

A

Heart muscle failure.

-MI, right ventricular infarction, prolonged ischaemia

59
Q

What is arrhythmia-related cardiogenic shock, and what causes it?

A

Abnormal electrical activity.

-arrhythmias, AF, ventricular tachycardia, complete heart block

60
Q

What causes mechanical cardiogenic shock? (3)

A
  • Valvular defects
  • Ventricular septal defects
  • Atrial myxomas
61
Q

What is extra-cardiac cardiogenic shock, and what causes it?

A

Obstruction to blood flow (cardiac filling and ejection).

-pulmonary embolism, tension pneumothorax, pericarditis

62
Q

What is distributive shock?

A

Severe vasodilation causes decreased systemic vascular resistance.
-leads to abnormal distribution to smaller vessels

63
Q

How does the body compensate for distributive shock?

A

Increase cardiac output&raquo_space; flushed/bounding heart.

64
Q

How do patients with distributive shock normally appear?

A

Flushed, warm and tachycardic.

65
Q

What are the sub-types of distributive shock? (4)

A
  • Septic shock
  • Anaphylactic shock
  • Neurogenic shock
  • Toxic shock syndrome
66
Q

What is septic shock?

A

Severe systemic infection (bacteria/fungi)&raquo_space; low BP and abnormal metabolism.

67
Q

What role do cytokines and mediators play in septic shock?

A

Increased cytokines and mediators&raquo_space; vasodilation.

68
Q

What is anaphylactic shock?

A

Severe type 1 hypersensitivity reaction to an antigen.

-e.g. peanut allergy

69
Q

What happens during an anaphylactic shock?

A
  • Allergen&raquo_space; IgE cross-linking
  • Massive mast cell degranulation
  • Vasodilation
70
Q

What is neurogenic shock?

A

Loss of sympathetic vascular tone in spinal cord&raquo_space; vasodilation and low BP.
-e.g. spinal injury

71
Q

What is toxic shock syndrome?

A

S. aureus/S. pyogenes produce exotoxins
» non-specific binding of class II MHC to T cell receptors.
» lots of cytokine release
» decreased systemic vascular resistance

72
Q

Why are the exotoxins produced by S. aureus and S. pyogenes known as ‘superantigens’?

A
  • Don’t require processing by APCs

- Non-specific binding of class II MHC to T cell receptors

73
Q

Can you have a combination of shock sub-types?

A

Yes.

-e.g. septic and cardiogenic (myocardial dysfuntion)

Year 2 EMS MoD (20 decks)

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