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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
What is the leading cause of deaths in the west?
Ischaemic heart disease
26
What are 90% of cases of cardiac ischaemia due to?
atherosclerosis
27
what is the difference between ischaemia and hypoxia?
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
28
which is more harmful hypoxia or ischaemia and why?
ischaemia injures tissues faster and more severely than hypoxia and therefore Ischaemia is more harmful.
29
which is the most important factor in determining if vascular occlusion will cause damage
alternative blood supply
30
what type of infarction are testis and ovaries vulnerable to and why?
venous infarction because they have only a single venous outflow
31
what are watershed regions?
these are point of anatomises between 2 vascular supplies
32
give examples of watershed regions
splenic flexure colon (SMA, IMA) myocardium (ventricles and coronary artery) regions in the brain
33
what are the gross features of a myocardial infarction between 4-12 hours?
occasional dark mottling
34
what are the microscopic changes of a myocardial infarction at 2- 8 weeks?
increased collagen leading to scar formation
35
what are the gross features of a myocardial infarction at 3- 7 days after occurrence?
yellow centre becomes soft
36
what are the microscopic changes to the heart after 4-12 hours after myocardial infarction?
oedema, haemorrhage and the start of coagulative necrosis
37
what are the microscopic change to the heart after 1-3 days after a myocardial infarction?
oedema with early neutrophil infiltration
38
what are the gross features that occur 1-3days after a myocardial infarction?
yellow with haemorrhagic edge
39
what are the microscopic changes to the heart 1-2 week after a myocardial infarction?
granulation tissue formation
40
what are the gross features that occur 1-2 weeks to the heart after a myocardial infarction?
red- grey colour occurs
41
what are the microscopic features to the heart 12-24hours after a myocardial infarction?
ongoing coagulative necrosis
42
what are the microscopic feature to the heart 3-7 days after a myocardial infarction
dying neutrophils with macrophage infiltration
43
what are the gross features that occur to the heart 2-8 weeks after a myocardial infarction
fibrous scar
44
what are the gross features that occur to the heart 12-24hours after a myocardial infarction?
dark mottling
45
what is shock?
a pathophysiological state of reduced systemic tissue perfusion resulting in decreased oxygen delivery to the tissues
46
what does impaired tissue perfusion and prolonged oxygen deprivation lead to
cellular hypoxia and derangement of cellular biochemistry and eventually end organ dysfunction
47
is shock reversible?
yes and no, initially it is reversible but rapidly becomes irreversible
48
what are the sequence events after shock
1. cell death due to hypoxia 2. end organ damage 3. multi-organ failure 4. death
49
what factors contribute to mean arterial pressure
Cardiac output (co) x Systemic vascular resistance (svr) SVR and total peripheral resistances are the same thing
50
what factors contribute to cardiac output?
Heart Rate (HR) x stroke volume (SV)
51
what factors contribute to heart rate
parasympathetic and sympathetic
52
what factors contribute to stroke volume
venous return
53
what factors contribute to venous return
blood volume respiratory pump skeletal pump
54
what factors contribute to SVR
arteriolar radius
55
what factors contribute to arteriolar radius
metabolic control | sympathetic nonepinephrine and epinephrine
56
what can cause shock?
anything that cause and decrease in cardiac output or/and decrease in systemic vascular resistance
57
what are the type of shock/
- hypovolaemic - cardiogenic - distributive - anaphylatic - septic - toxic shock syndrome - neurogenic
58
how does hypovolaemic shock occur?
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
how does the body compensate for the decreased cardiac output during hypovolaemic shock
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
what are the causes of hypovolaemic shock
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
why does cardiogenic shock occur
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
how does the body compensate to a decreased cardiac output during cardiogenic shock?
with an increased Systemic Vascular resistance. As the blood pressure drops the body limits the blood flow t the extremities. Vasoconstriction also occurs
63
what are the categories of cardiogenic shock
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
what are the main causes of myopathic cardiogenic shock?
myocardial infarction cardiomyopathies atunned myocardium that usuall occurs following a cariopulmonary bypass
65
what are the main causes of arrhythmia related cardiogenic shock?
- 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
what are the main causes of mechanical cardiogenic shock
- defects relating to blood flow through the heart - valvular defects (prolapse), ventricual septal defects - atrial myxomas, ruptured ventricular free wall aneurysm
67
what are the causes of extra-cardiac cardiogenic shock?
- 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
why does distributive shock occur?
there is a decreased systemic vascular resistance due to severe vasodilation
69
how does distributive shock present?
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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