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year 2 EMS MOD > Ischaemia, Infarction & Shock > Flashcards

Ischaemia, 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

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26
Q

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

A

atherosclerosis

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27
Q

what is the difference between ischaemia and hypoxia?

A

ischaemia is the disturbance of blood flow to cells and tissues whereas hypoxia is when the oxygen saturation of tissue falls. ischaemia always leads to hypoxia whereas hypoxia can occur without ischaemia

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28
Q

which is more harmful hypoxia or ischaemia and why?

A

ischaemia injures tissues faster and more severely than hypoxia and therefore Ischaemia is more harmful.

29
Q

which is the most important factor in determining if vascular occlusion will cause damage

A

alternative blood supply

30
Q

what type of infarction are testis and ovaries vulnerable to and why?

A

venous infarction because they have only a single venous outflow

31
Q

what are watershed regions?

A

these are point of anatomises between 2 vascular supplies

32
Q

give examples of watershed regions

A

splenic flexure colon (SMA, IMA)
myocardium (ventricles and coronary artery)
regions in the brain

33
Q

what are the gross features of a myocardial infarction between 4-12 hours?

A

occasional dark mottling

34
Q

what are the microscopic changes of a myocardial infarction at 2- 8 weeks?

A

increased collagen leading to scar formation

35
Q

what are the gross features of a myocardial infarction at 3- 7 days after occurrence?

A

yellow centre becomes soft

36
Q

what are the microscopic changes to the heart after 4-12 hours after myocardial infarction?

A

oedema, haemorrhage and the start of coagulative necrosis

37
Q

what are the microscopic change to the heart after 1-3 days after a myocardial infarction?

A

oedema with early neutrophil infiltration

38
Q

what are the gross features that occur 1-3days after a myocardial infarction?

A

yellow with haemorrhagic edge

39
Q

what are the microscopic changes to the heart 1-2 week after a myocardial infarction?

A

granulation tissue formation

40
Q

what are the gross features that occur 1-2 weeks to the heart after a myocardial infarction?

A

red- grey colour occurs

41
Q

what are the microscopic features to the heart 12-24hours after a myocardial infarction?

A

ongoing coagulative necrosis

42
Q

what are the microscopic feature to the heart 3-7 days after a myocardial infarction

A

dying neutrophils with macrophage infiltration

43
Q

what are the gross features that occur to the heart 2-8 weeks after a myocardial infarction

A

fibrous scar

44
Q

what are the gross features that occur to the heart 12-24hours after a myocardial infarction?

A

dark mottling

45
Q

what is shock?

A

a pathophysiological state of reduced systemic tissue perfusion resulting in decreased oxygen delivery to the tissues

46
Q

what does impaired tissue perfusion and prolonged oxygen deprivation lead to

A

cellular hypoxia and derangement of cellular biochemistry and eventually end organ dysfunction

47
Q

is shock reversible?

A

yes and no, initially it is reversible but rapidly becomes irreversible

48
Q

what are the sequence events after shock

A
  1. cell death due to hypoxia
  2. end organ damage
  3. multi-organ failure
  4. death
49
Q

what factors contribute to mean arterial pressure

A

Cardiac output (co) x Systemic vascular resistance (svr) SVR and total peripheral resistances are the same thing

50
Q

what factors contribute to cardiac output?

A

Heart Rate (HR) x stroke volume (SV)

51
Q

what factors contribute to heart rate

A

parasympathetic and sympathetic

52
Q

what factors contribute to stroke volume

A

venous return

53
Q

what factors contribute to venous return

A

blood volume
respiratory pump
skeletal pump

54
Q

what factors contribute to SVR

A

arteriolar radius

55
Q

what factors contribute to arteriolar radius

A

metabolic control

sympathetic nonepinephrine and epinephrine

56
Q

what can cause shock?

A

anything that cause and decrease in cardiac output or/and decrease in systemic vascular resistance

57
Q

what are the type of shock/

A
  • hypovolaemic
  • cardiogenic
  • distributive
  • anaphylatic
  • septic
  • toxic shock syndrome
  • neurogenic
58
Q

how does hypovolaemic shock occur?

A

there is intra-vascular fluid los (blood, plasma)
this causes a decrease in venous return the heart (preload)
which causes a decreas in stroke volume and therefore a decrease in cardiac output.

a decreased cardiac output leads to a decreased mean arterial pressure resulting in shock

59
Q

how does the body compensate for the decreased cardiac output during hypovolaemic shock

A

by inccreasing the systemic vascular resistance it does this by vasoconstricting the vessels. this causes the body to feel cool and clammy and an increase in HR. an increased HR will cause an increase in the CO.

60
Q

what are the causes of hypovolaemic shock

A

haemorrhage

  • trauma, GI bleeding, ruptured haematoma
  • Haemorrhagic pancreatitis, fractures
  • ruptured aortic, abdominal or left ventricular free wall aneurysm.

Non-haemorrhagic fluid loss

  • Diarrhoea, vomitting, heat stroke, burns
  • third spacing
    • acute loss of fluid into internal body cavities
    • common postoperatively and in intestinal obstruction, pancreatitis or cirrhosis
61
Q

why does cardiogenic shock occur

A

cardiac pump failure which leads to a decreased cardiac output that leads to a decreased mean arterial pressure and this then leads to shock

62
Q

how does the body compensate to a decreased cardiac output during cardiogenic shock?

A

with an increased Systemic Vascular resistance. As the blood pressure drops the body limits the blood flow t the extremities. Vasoconstriction also occurs

63
Q

what are the categories of cardiogenic shock

A

four categories

  1. myopathic (heart muscle failure)
  2. arrythmia-related (abnormal electrical activity)
  3. mechanical (acquired or developmental defects)
  4. Extra-cardiac (obstruction to blood outflow)
64
Q

what are the main causes of myopathic cardiogenic shock?

A

myocardial infarction
cardiomyopathies
atunned myocardium that usuall occurs following a cariopulmonary bypass

65
Q

what are the main causes of arrhythmia related cardiogenic shock?

A
  • when the heart muscle is okay but not beating as it should
  • atrial and ventricular arrhythmias
  • impaired ventricular contraction or filling - this leads to decreased cardiac output
66
Q

what are the main causes of mechanical cardiogenic shock

A
  • defects relating to blood flow through the heart
  • valvular defects (prolapse), ventricual septal defects
  • atrial myxomas, ruptured ventricular free wall aneurysm
67
Q

what are the causes of extra-cardiac cardiogenic shock?

A
  • anything outside the heart that impairs cardiac filling or ejection of blood from the hearr
  • massive pulmonary embolism, tension pneumothorax
  • severe constrictive pericarditis, pericardial tamponade
68
Q

why does distributive shock occur?

A

there is a decreased systemic vascular resistance due to severe vasodilation

69
Q

how does distributive shock present?

A

it presents with an increased Cardiac output and would hear a flusherd bounding heart.
chest would be warm esp. with septic shock

year 2 EMS MOD (17 decks)

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