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EMS - MoD > 14. Ischaemia, infarction and shock > Flashcards

14. Ischaemia, infarction and shock Flashcards

1
Q

Is repercussion of non-infarcted but ischaemic tissues always good?

A

Generation of reactive oxygen species by inflammatory cells causes further cell damage (reperfusion injury)

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2
Q

What causes the majority of infarctions?

A
  • thrombosis and embolism

- most common within arteries

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3
Q

Thrombosis and embolism causes the majority of infarctions but what else can cause it?

A
  • vasospasm
  • atheroma expansion
  • extrinsic compression eg. tumour
  • twisting of vessel roots eg. volvulus
  • rupture of vascular supply eg. AAA
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4
Q

How can infarction by morphologically classified?

A

By colour

  • red infarction
  • white infarction
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5
Q

What is red infarction?

A

Haemorrhagic

Dual blood supply/venous infarction

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6
Q

What is white infarction?

A

Anaemic

Single blood supply hence totally cut-off

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7
Q

What shape do infarctions tend to be?

A

Wedge-shaped

Obstruction usually occurs at an upstream point, the entire downstream area will therefore be infarcted

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8
Q

What are the histological characteristics of infarction?

A
  • coagulative necrosis (usually)

- colliquative necrosis (in the brain)

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9
Q

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

A

Nothing!

No time to develop haemorrhagic/inflammatory response

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10
Q

What do you see histologically on a myocardial infarct?

A

Neutrophils entering the early lesion which progresses to fibrosis over time

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11
Q

What are the 4 factors which influence the degree of ischaemic damage?

A
  • nature of the blood supply
  • rate of occlusion
  • tissue vulnerability to hypoxia
  • blood oxygen content
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12
Q

How does nature of blood supply affect degree of ischaemic damage?

A

An alternative blood supply means less damage and so severe ischaemia is needed for infarction

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13
Q

Give examples of organs which a dual blood supply and are therefore less vulnerable to infarction?

A
  • lungs (pulmonary and bronchial arteries)
  • liver (hepatic artery and portal vein)
  • hand (radial and ulnar artery)
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14
Q

Give examples of organs which have a single blood supply and are therefore more vulnerable to infarction?

A
  • kidneys
  • spleen
  • testis
    etc
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15
Q

How does rate of occlusion affect degree of ischaemic damage?

A

slowly developing occlusions are less likely to infarct tissues

allows time for the development of alternative (collateral) perfusion pathways

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16
Q

How are coronary anastomoses beneficial?

A

There are small anastomoses that connect major branches and have minimal flow. If a coronary arterial branch is slowly occluded, flow can be directed through these channels. Infarction can be avoided even if the main arterial branch is totally occluded

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17
Q

How vulnerable is the brain to tissue hypoxia?

A

Very vulnerable

If a neurone is deprived of oxygen, irreversible cell damage occurs in 3-4 mins

Brain is 1-2% of body weight but requires 15% of cardiac output and 20% of body oxygen consumption

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18
Q

How vulnerable is the heart to tissue hypoxia?

A

Slightly more resistant than the brain

Cardiac myocyte death takes 20-30 mins

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19
Q

What percentage of body oxygen does the brain consume?

A

20%

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20
Q

Which type of cell takes 20-30 minutes to die following oxygen deprivation?

A

Cardiac myocytes in the heart

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21
Q

How does blood oxygen content affect degree of ischaemic damage?

A

Reduced oxygen content (in anaemia etc) increased the chance of infarction

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22
Q

How does congestive cardiac failure increase chance of infarction?

A

In congestive cardiac failure there is poor cardiac output and impaired pulmonary ventilation

May develop an infarct with a normally inconsequential narrowing of the vessels

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23
Q

What is a watershed area?

A

Regions of the body that receive dual blood supply from the most distal branches of two large arteries, such as the splenic flexure of the large intestine and the brain

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24
Q

What are the ischaemic diseases of the heart?

A
  • IHD (angina/MI)
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25
Q

What are the ischaemic diseases of the brain?

A
  • cerebrovascular disease (TIA/CVA)
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26
Q

What are the ischaemic diseases of the intestines?

A
  • ischaemic bowel
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27
Q

What are the ischaemic diseases of the extremities?

A
  • peripheral vascular disease/gangrene
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28
Q

What is the leading cause of death in men and women in the West?

A

Ischaemic heart disease

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29
Q

What is characteristic of 90% of cases of ischaemic heart disease?

A

Impaired coronary arterial flow following complications of atherosclerotic disease

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30
Q

Are occluded coronary arteries clear to see?

A

Yes, there are visible both grossly with the naked eye and also histologically

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31
Q

What is the third leading cause of death in the West?

A

Cerebrovascular disease

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32
Q

What does cerebrovascular disease refer to?

A

Any abnormality of the brain caused by a pathological process involving the blood vessels

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33
Q

What are 2 types of cerebrovascular disease?

A
  • ischaemic (thombosis and embolism)

- bleeding (haemorrhagic)

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34
Q

What are the causes of an ischaemic stroke?

A
  • thrombosis secondary to atherosclerosis

- embolism eg. mural thrombus

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35
Q

What is a mural thrombus?

A

Thrombi that adhere to the wall of a blood vessel.

  • occur in large vessels such as heart and aorta
  • can restrict blood flow but usually do not block it entirely
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36
Q

What are the causes of a haemorrhagic stroke?

A
  • intracerebral haemorrhage (hypertensive)

- ruptured aneurysm in the circle of Willis (subarachnoid)

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37
Q

What is a CVA?

A

Cerebrovascular accident (stoke)

Can be ischaemic or haemorrhagic

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38
Q

What would a patient with ischaemic bowel disease present with?

A

Abdominal pain

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39
Q

What is ischaemic bowel disease normally caused by?

A

Thrombosis or embolism in the superior or inferior mesenteric arteries

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40
Q

What are 3 different types of gangrene?

A
  • dry gangrene
  • wet gangrene
  • gas gangrene
41
Q

What is gangrene?

A

Infarction of entire portion of limb (or organ)

42
Q

What characterises dry gangrene?

A

Ischaemic coagulative necrosis only

43
Q

What characterises wet gangrene?

A

Superimposed infection

44
Q

What characterises gas gangrene?

A

Superimposed infection with gas-producing organism eg. clostridium perfringens

45
Q

What is shock?

A

A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased oxygen delivery to tissues

46
Q

What is there an imbalance between during shock?

A

oxygen delivery and oxygen consumption

47
Q

What does impaired tissue perfusion and prolonged oxygen deprivation during shock lead to?

A

Cellular hypoxia and derangement of critical biochemical processes at first cellular and eventually systemic levels

48
Q

Shock causes hypoxia at first cellular then systemic levels. What effects does shock have on the cellular level?

A
  • membrane ion pump dysfunction
  • intracellular swelling
  • leakage of intracellular contents into the extracellular space
  • inadequate regulation of intracellular pH
  • anaerobic respiration, creating lactic acid
49
Q

Shock causes hypoxia at first cellular then systemic levels. What effects does shock have on the systemic level?

A
  • alterations in the serum pH (acidaemia)
  • endothelial dysfunction which leads to vascular leakage
  • stimulation of inflammatory and anti-inflammatory cascades
  • end-organ damage (ischaemia)
50
Q

Is shock reversible or irreversible?

A

Shock is initially reversible but rapidly becomes irreversible

51
Q

What are the sequential results of shock?

A
  • cell death
  • end-organ damage
  • mutli-organ damage
  • death
52
Q

Give some different types of shock

A
  • hypovolaemic
  • cardiogenic
  • distributive (has many subtypes)
53
Q

Give some different subtypes of distributive shock

A
  • anaphylactic shock
  • septic shock
  • toxic shock syndrome
  • neurogenic shock
54
Q

Anaphylactic shock is a type of which classification of shock?

A

Distributive shock

55
Q

What characterises hypovolaemic shock?

A

Intra-vascular fluid loss (blood, plasma etc)

56
Q

In hypovolaemic shock, there is intravascular fluid loss. What does this lead to?

A

Decreased venous return to heart (decreased pre-load)

Decreased stroke volume

Decreased cardiac output

57
Q

In hypovolaemic shock, intravascular fluid loss leads to decreased cardiac output. How could this be compensated for?

A

cardiac output x total peripheral resistance = mean arterial pressure

Therefore, we can increase total peripheral resistance/ systemic vascular resistance (SVR)

= vasoconstriction = cool, clammy, “shut down”

58
Q

What are the 2 classifications of causes of hypovolaemic shock?

A
  • haemorrhage

- non-haemorragic fluid loss

59
Q

Hypovolaemic shock can be caused by haemorrhage or non-haemorrhagic fluid loss. In what ways can haemorrhage be caused?

A
  • trauma
  • GI bleeding
  • ruptured haematoma
  • haemorrhagic pancreatitis
  • fractures
  • ruptured aneurysm
60
Q

Hypovolaemic shock can be caused by haemorrhage or non-haemorrhagic fluid loss. In what ways can non-haemorrhagic fluid loss be caused?

A
  • diarrhoea
  • vomiting
  • heat stroke
  • burns
61
Q

What is third spacing? (related to hypovolaemic shock)

A

Acute loss of fluid into internal body cavities

Third-space losses are common postoperatively and in intestinal obstruct, pancreatitis or cirrhosis

62
Q

What characterises cardiogenic shock?

A

Cardiac pump failure

63
Q

Cardiogenic shock is caused by cardiac pump failure. What does this lead to?

A

Decreased cardiac output

64
Q

Cardiogenic shock is caused by cardiac pump failure which causes decreased cardiac output. How could you compensate for this?

A

Cardiac output x total peripheral resistance = mean arterial pressure

so increasing SVR would compensate for decreased CO

65
Q

What are the 4 categories of cardiogenic shock?

A
  • myopathic
  • arrhythmia-related
  • mechanical
  • extra-cardaic
66
Q

What is myopathic cardiogenic shock related to?

A

Heart muscle failure

67
Q

What is arrhythmia-related cardiogenic shock related to?

A

Abnormal electrical activity

68
Q

What is extra-cardiac cardiogenic shock related to?

A

Obstruction to blood outflow

69
Q

What are the possible causes of myopathic cardiogenic shock?

A
  • myocardial infarction (>40% left ventricular myocardium)
  • right ventricular infarction, dilated cardiomyopathies
  • “stunned myocardium” following prolonged ischaemia or cardiopulmonary bypass
70
Q

What are the possible causes of arrhythmia-related cardiogenic shock?

A
  • atrial and ventricular arrhythmias
  • atrial fibrillation/flutters
  • ventricular tachycardia, bradyarrhythmias and complete heart block (decrease CO)
71
Q

How does atrial fibrillation cause arrhythmia-related cardiogenic shock?

A

Decrease in cardiac output due to impairment of co-ordinated atrial filling of the ventricles

72
Q

How does ventricular fibrillation affect cardiac output? (and therefore causes arrhythmia-related cardiogenic shock)

A

Ventricular fibrillation completely abolishes CO (cardiac output)

73
Q

What are the possible causes of mechanical cardiogenic shock?

A
  • valvular defects (eg. prolapse)
  • ventricular septal defects
  • atrial myxomas
  • ruptured ventricular free wall aneurysm
74
Q

What is an atrial myxoma?

A

An atrial myxoma is a benign tumor of the heart, commonly found within the left and right atria on the interatrial septum.

75
Q

What are the possible causes of extra-cardiac cardiogenic shock?

A
  • anything that impairs cardiac filling or ejection of blood from heart
  • massive pulmonary embolism
  • tension pneumothorax
  • severe constrictive pericarditis
  • pericardial tamponade
    etc
76
Q

What characterises distributive shock?

A

Decreased systemic vascular resistance due to severe vasodilation

77
Q

Distributive shock is caused by severe vasodilation which decreases SVR (systemic vascular resistance). How could this be compensated for?

A

Cardiac output x total peripheral resistance = mean arterial pressure

Compensation = increase cardiac output = look flushed, bounding heart

78
Q

Toxic shock syndrome is a subtype of which classification of shock?

A

Distributive shock

79
Q

What causes septic shock? (a type of distributive shock)

A

Severe, overwhelming systemic infections

Gram+ve bacteria, gram-ve bacteria, or fungi

80
Q

Who is more vulnerable to septic shock?

A

Immunocompromised, elderly, very young etc

81
Q

Septic shock is caused by infection. How?

A

Infection leads to an increase in cytokines/mediators, this causes vasodilation

82
Q

What is DIC (disseminated intravascular coagulation)?

A

Part of septic shock

Pro-coagulation

Widespread clotting/thrombi

Used all clotting factors and so also get haemorrhage

83
Q

What type of reaction is anaphylactic shock?

A

Type 1 hypersensitivity reaction

84
Q

Give examples of allergies which may cause anaphylactic shock?

A

Hospital e.g. drugs (penicillin etc)

Community e.g. peanuts, shellfish, or insect toxins

85
Q

What do small doses of allergen cause in sensitised individuals?

A

IgE cross-linking

86
Q

Mast cells contain IgE antibodies. What happens when this comes into contact with the antigen?

A

It causes mast cell degranulation

87
Q

Which type of cell contains IgE antibodies?

A

Mast cells

88
Q

During allergy/anaphylactic shock, mast cells release chemicals including histamine. What does this cause?

A

Vasodilation

Constriction of bronchioles/respiratory distress

Laryngeal oedema

89
Q

What are the 2 ultimate problems in anaphylactic shock?

A
  • low blood pressure

- difficulty breathing

90
Q

What is characteristic of neurogenic shock?

A

Loss of sympathetic vascular tone

91
Q

In neurogenic shock, there is loss of sympathetic vascular tone which causes widespread vasodilation. What is this caused by?

A

Spinal injury or anaesthetic accidents

92
Q

Which bacteria causes toxic shock syndrome?

A

S. aureus

S. pyogenes

93
Q

What do S. aureus and S. progenes produce that causes toxic shock syndrome?

A

exotoxins “superantigens”

94
Q

What is unusual about superantigens?

A

They do not require processing by antigen-presenting cells

There is non-specific binding of class II MHC to T cell receptors

Therefore, up to 20% of T cells can be activated at one time

95
Q

In toxic shock syndrome, superantigens are produced. What do they cause?

A

They activate lots of T cells at one time which causes widespread release of massive amounts of cytokines which decreases SVR (systemic vascular resistance)

96
Q

What are ‘insensible losses’?

A

Fluid losses due to sweating etc.

97
Q

What are the main reasons for shock in hypovolaemic, cardiogenic, and distributive shock?

A

hypovolaemic = intravascular fluid loss (decreased cardiac output)

cardiogenic = cardiac pump failure (decreased cardiac output)

distributive shock = severe vasodilation (decreased systemic vascular resistance)

98
Q

What is the equation for mean arterial pressure?

A

cardiac output x total peripheral resistance = mean arterial pressure

99
Q

What is equation for cardiac output?

A

heart rate x stroke volume = cardiac output

EMS - MoD (17 decks)

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