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Year 2 EMS MoD > Infarction, Shock > Flashcards

Infarction, Shock Flashcards

1
Q

What is meant by hypoxia, and what are the 2 types?

A

Any state of reduced oxygen availability
Generalised - whole body eg. altitude or anaemia
Localised - specific tissue affected

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2
Q

What is meant by ischaemia?

A

Pathological reduction in blood flow to tissues, ischaemia results in tissue hypoxia

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3
Q

What is the most common cause of ischaemia?

A

Usually as a result of obstruction to arterial flow commonly as a result of thrombosis/embolism

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4
Q

What are the consequences of limited compared to prolonged ischaemia?

A

Limited - cell injury is reversible
Prolonged - irreversible cell damage
-Cell death occurs by necrosis

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5
Q

When would therapeutic tissue reperfusion be used?

A

Only if the ischaemia is reversible

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6
Q

Why is therapeutic reperfusion not used in infarcted tissues?

A

Reperfusion of infarcted tissues will have no effect

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7
Q

Why could reperfusion of ischaemic non infarcted tissues be harmful?

A

Whilst the tissue is hypoxic inflammatory cells produce reactive oxygen species
When the tissue is reperfused these reactive oxygen species can travel around the body and cause damage

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8
Q

What is meant by infarction?

A

Ischaemic necrosis caused by occlusion of the arterial supply or venous drainage

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9
Q

What is infarct?

A

An area of infarction in tissues

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10
Q

Other than thrombosis and embolism, name 7 other causes of infarction?

A

1) Vasospasm
2) Atheroma expansion
3) Extrinsic compression eg. tumour
4) Twisting of vessel roots eg. volvulus
5) Rupture of vascular supply eg. AAA
6) Vasculitis
7) Hyperviscosity

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11
Q

How can infarction be classified by colour?

A

White infarction (anaemic)
Single blood supply hence totally cut off
Red infarction
Dual blood supply/venous infarction
Loss of one blood supply, tissue starts to undergo necrosis, damages blood vessels of other supply and blood leaks into tissues

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12
Q

What shape are most infarcts and why?

A

Wedge-shaped

Obstruction usually occurs at an upstream point, the entire down-stream area will therefore be affected

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13
Q

Infarction is normally what type of necrosis?

A

Normally coagulative necrosis - maintains tissue structure

Colliquative necrosis occurs in the brain

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14
Q

If a person died suddenly of an MI what would be seen in the tissues?

A

Nothing as there is no time to develop haemorrhage or inflammatory response

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15
Q

What 4 factors influence the degree of ischaemic damage?

A

1) Nature of blood supply
2) Rate of occlusion
3) Tissue vulnerability to hypoxia
4) Blood oxygen content

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16
Q

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

A
  • An alternative blood supply will mean less damage hence severe ischeamia is required for infarction
  • Tissues with a single blood supply are more vulnerable to infarction
    eg. kidneys, spleen, testis
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17
Q

Name 3 tissues with dual blood supply (and those supplies) which are thus less vulnerable to infarction?

A

1) Lungs (pulmonary and bronchial arteries)
2) Liver (hepatic artery and portal vein)
3) Hand (radial and ulnar artery)`

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18
Q

Why are slow developing occlusions less likely to lead to infarction?

A

Allows time for the development of alternative collateral perfusion pathways

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19
Q

How does rate of occlusion affect coronary arteries?

A
  • Small anastamoses connect major branches and have minimal flow
  • If a coronary arterial branch is slowly occluded flow can be directed through these channels
  • Infarction can therefore be avoided even if the main arterial branch is totally occluded
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20
Q

Why is the brain typically very vulnerable to hypoxia?

A

If a neurone is deprived of O2 irreversible cell damage occurs in 3-4 mins
Brain is 1-2% of total body weight but requires 15% of cardiac output
Therefore very vulnerable to injury

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21
Q

Why is the heart less vulnerable to hypoxia than the brain?

A

The heart is more resistant with cardiac myocyte death taking 20-30 minutes

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22
Q

How does blood oxygen content affect infarction?

A

Reduced oxygen supply in the blood (anaemia etc.) increases the chances of infarction

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23
Q

Why does congestive heart failure make people more vulnerable to infarction?

A
  • Poor cardiac output and impaired pulmonary ventilation

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

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24
Q

Name 4 clinical manifestations of infarction?

A

1) Ischaemic heart disease
2) Cerebrovascular disease
3) Ischaemic bowel
4) Peripheral vascular disease/ gangrene

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25
Q

What is the leading cause of deaths in the west?

A

Ischaemic heart disease

26
Q

What are 90% of cases of cardiac ischaemia due to?

A

Impaired coronary artery flow following complications of atherosclerotic disease

27
Q

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

A

Cerebrovascular disease

28
Q

What does cerebrovascular disease refer to?

A

Any abnormality of the brain caused by a pathological process involving the blood vessels
Includes thrombosis and embolism (ischaemic)
and Bleeding (haemorrhagic)

29
Q

What is a cerebrovascular accident?

A

A stroke

30
Q

Name 2 causes of an ischaemic stroke?

A

Thrombosis secondary to atherosclerosis

Embolism eg. mural thrombus

31
Q

Name 2 causes of a haemorrhagic stroke?

A

1) Intracerebral haemorrhage (hypertensive)

2) Ruptured aneurysm in the circle of Willis (subarachnoid)

32
Q

What is ischaemic bowel disease usually caused by and how does it present?

A
  • Usually caused by a thrombosis or embolism in the superior or inferior mesenteric arteries
  • Presents with abdominal pain
33
Q

What is gangrene and what are the 3 types?

A

1) Gangrene - infarction of entire portion of a limb or organ
2) Dry gangrene - Ischaemic coagulative necrosis only
3) Wet gangrene - superimposed infection
4) Gas gangrene - superimposed infection with gas producing organism eg. clostridium perfringens

34
Q

What is shock?

A

A physiological state characterised by a significant reduction of systemic tissue perfusion (severe hypotension) resulting in decreased O2 delivery to tissues

35
Q

What can shock eventually lead to?

A

The impaired tissue perfusion and ultimately prolonged oxygen deprivation leads to cellular hypoxia and derangement of critical biochemical processes at first cellular and eventually systemic levels

36
Q

What are the 6 cellular effects of shock?

A

1) Membrane ion pump dysfunction
2) Intracellular swelling
3) Leakage of intracellular contents into the extracellular space
4) Inadequate regulation of intracellular pH
5) Anaerobic respiration - lactic acid

37
Q

What are the 4 systemic effects of shock?

A

1) Alterations in serum pH (acidaemia)
2) Endothelial dysfunction - vascular leakage
3) Stimulation of inflammatory and anti-inflammatory cascades
4) End-organ damage (ischaemia)

38
Q

Is shock reversible?

A

Shock is initially reversible but rapidly becomes irreversible

39
Q

What is the sequential result of shock one it becomes irreversible?

A

1) Cell death
2) End-organ damage
3) Mutli-organ failure
4) Death

40
Q

What is hypovolaemic shock?

A

Intra-vascular fluid loss (blood, plasma etc.)

1) Get decreased venous return to the heart thus reduced pre-load
2) Decreased stroke volume thus decreased cardiac output

41
Q

How can the body compensate for hypovolaemic shock?

A

it increases the systemic vascular resistance through vasoconstriction - pt appears cool and clammy - ‘shut down’

42
Q

Give the 2 main causes of hypovolaemic shock (and some example of them)?

A

1) Haemorrhage - trauma, GI bleeding, ruptured haematoma, haemorrhagic pancreatitis, fractures, ruptured AAA, ruptured left ventricular free wall
2) Non-haemorrhagic fluid loss: diarrhoea, vomiting, heat stroke, burns

43
Q

What is meant by ‘third spacing’ when referring to non-haemorrhagic fluid loss causing hypovolaemic shock and when does it commonly occur?

A

Acute loss of fluid into internal body cavities

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

44
Q

What is meant by cardiogenic shock?

A

Cardiac pump failure leading to reduced cardiac output

45
Q

How does the body compensate for cardiogenic shock?

A

Increasing systemic vascular resistance

46
Q

What are the 4 categories of causes of cardiogenic shock?

A

1) Myopathic (heart muscle failure)
2) Arrythmia related (abnormal electrical activity)
3) Mechanical
4) Extra-cardiac (obstruction to blood flow)

47
Q

Give 4 causes of myopathic cardiogenic shock?

A

1) MI (>40% left venticular myocardium)
2) Right ventricular infarction
3) Dilated cardiomyopathies
4) “Stunned myocardium” following prolonged ischemia or cardiopulmonary bypass

48
Q

Give 5 causes of arrhythmia-related cardiogenic shock and briefly describe mechanism?

A

1) atrial fibrilation - decreased CO by impairment of coordinated atrial filling of ventricles
2) Ventricular tachychardia - decreased CO
3) Bradyarrhythmias - decreased CO
4) Complete heart block - decreased CO
5) Ventricular fibrilation - abolishes CO

49
Q

Give 4 causes of mechanical cardiogenic shock?

A

1) Valvular defects eg. prolapse
2) Ventricular septal defects
3) Atrial myxomas
4) Ruptured ventricular free wall aneurysm

50
Q

Give 4 causes of extra-cardiac cardiogenic shock?

A

Anything that impairs cardiac filling or ejection of blood from the heart

1) Large PE
2) Tension pneumothorax
3) Severe constrictive pericarditis
4) Pericardial tamponade

51
Q

What is meant by distributive shock?

A

decreased systemic vascular resistance due to severe vasodilation

52
Q

How does the body compensate for distributive shock, thus how does the patient appear?

A

Increased cardiac output

patient appears flushed with a bounding heart

53
Q

What are 4 familiar sub types of distributive shock?

A

1) Septic shock
2) Anaphylactic shock
3) Neurogenic shock
4) Toxic shock syndrome

54
Q

What is meant by septic shock?

A

Severe overwhelming systemic infection with gram +ve, gram -ve or fungi, typically in the immunocompromised, very elderly, very young etc.
Get an increase in cytokines/mediators leading to vasodilation
Also get pro-coagulation DIC leading to ischaemia

55
Q

What is meant by anaphylactic shock?

A

A severe type I hypersensitivity reaction
occurs in sensitized individuals, such as in hospital due to drugs, or in the community due to peanuts, shellfish or insect toxins

56
Q

What is the mechanism of anaphylactic shock?

A

Sensitized indivduals
Small doses of allergen leads to IgE cross-linking leading to massive mast cell degranulation
Leading to vasodilation, contraction of bronchioles/respiratory distress, laryngeal oedema and circulatory collapse which leads to shock and possibly death

57
Q

What is neurogenic shock and what is it typically caused by?

A

Loss of sympathetic vascular tone leading to vasodilation

Typically caused by spinal injury/ anesthetic accidents

58
Q

Is toxic shock syndrome the same as septic shock?

A

No

59
Q

What is the mechanism of toxic shock syndrome?

A

S.aureus/ S.pyogenes produce exotoxins (superantigens) which do not require processing by APCs
There is non-specific binding of Class II MHC to T cell receptors, up to 20% of T cells can be activated at one time
Wide spread release of massive amounts of cytokines leading to decreased systemic vascular resistance

60
Q

Different type of shock can co-exist, give an example of how distributive, hypovolaemic and cardiogenic components can all play a role in a patient with septic shock?

A

Primary distributive shock - inflammatory and anti-inflammatory cascades lead to increased vascular permeability/vasodilation
Hypovolaemic component - decreased oral intake, insensible losses, vomiting, diarrhoea
Cardiogenic component - sepsis-related myocardial dysfunction

61
Q

What percentage of patients die within one month of the onset of septic shock?

A

35-60%

62
Q

What percentage of patients die from cardiogenic shock?

A

60-90%

Year 2 EMS MoD (16 decks)

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