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02. Cardiovascular System > pathophysiology of ischaemia + infarction > Flashcards

pathophysiology of ischaemia + infarction Flashcards

1
Q

what is ischaemia?

A

relative lack of blood supply to organ/tissue leading to inadequate oxygen supply to meet needs of tissue/organ

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2
Q

what are the 4 ways that hypoxia can occur?

A
  1. low inspired oxygen level or normal inspired oxygen but low PaO22 anaemia-normal inspired oxygen but blood abnormal3. stagnation- normal inspired oxygen but abnormal delivery4. cytotoxic- normal oxygen inspired but abnormal at tissue level
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3
Q

what can cause low in inspired oxygen levels leading to hypoxia?

A

high altitude

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4
Q

what can lead to local stagnation of blood flow leading to hypoxia?

A

occlusion of vessel

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5
Q

what can causes systemic stagnation of blood flow leading to hypoxia?

A

shock

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6
Q

what is cytotoxic hypoxia?

A

organelles cannot function properly even though they have adequate oxygen

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7
Q

what are the factors that affect oxygen supply?

A
  1. Inspired O22. Pulmonary function3. Blood constituents4. Blood flow5. Integrity of vasculature6. Tissue mechanisms
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8
Q

when might blood flow be compromised, decreasing oxygen supply?

A

when there is heart failure

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9
Q

when might the integrity of vasculature be compromised, decreasing oxygen supply?

A

occlusion/compression of vessels

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10
Q

what are the 2 factors that affect the oxygen demand of a tissue?

A

the type of tissueactivity of the tissue above the baseline

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11
Q

what are the supply issues that can cause ischaemic heart disease?

A

coronary artery atheromacardiac failurepulmonary function- pulmonary oedema (from LVF)anaemiaprevious MI

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12
Q

what are demand issues that can cause ischaemic heart disease?

A

heart has high intrinsic demandexertion/stress

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13
Q

how can atherosclerosis cause stable angina?

A

when it is established and doesnt occlude the coronary artery so much as to cause inadequate oxygen supply at rest. however on exertion oxygen supply becomes inadequate

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14
Q

how can atherosclerosis cause unstable angina?

A

when the atheromatous plaque in the coronary artery is complicated and so causes inadequate delivery of oxygen at rest

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15
Q

what do ulcerated and fissure plaques in the coronary artery lead to?

A

thombosis then ischaemia or infarction

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16
Q

how does atheroma cause an aortic aneurysm?

A

dilatation of the aorta due to weakening of the vascular wall from inflammation

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17
Q

what conditions can atheromatous plaques lead to?

A

MITIACerebral infarctionabdominal aortic aneurysmperipheral vascular diseasecardiac failure (could be from MI)

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18
Q

a reduction in radius of an artery from 4 to 2 will cause a decrease of what in blood flow? and how does this explain how plaques cause ischaemia?

A

16 fold decrease. this highlights the large effect of radius of vessels on flow. this explains why plaques significantly reduce flow and cause ischaemia

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19
Q

give an example of where ischaemia can be chronic?

A

sufferers of peripheral vascular disease getting claudication when walking

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20
Q

give an example of when ischaenia can be acute-on-chronic ?

A

claudication in peripheral vascular disease (chronic) but can turn into and acute event

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21
Q

how does ischaemia affect the biochemistry of cells?

A

causes cells to metabolise more by anaerobic respiration. So lactate builds up on cells, causing acid-bace imbalance and leads to cell death

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22
Q

which cells are more affected by ischaemia?

A

those with high metabolic rate, eg. renal tubule, myocyte, neurons

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23
Q

which cells are less affected by ischaemia?

A

those with a slower metabolic rate

24
Q

what are the three general clinical effects of ischaemia?

A

-dysfunction-pain-physical damage

25
Q

what dysfunction can ischaemia cause in the heart?

A

if it is next to the SA node then there is the chance that it may lead to cardiac arrhythmia

26
Q

how does ischaemia cause heart pain/

A

due to pH changes and bracycardia

27
Q

what are the three potential outcomes of ischaemia?

A

-no clinical effect-resolution (normally need therapeutic intervention)-infarction

28
Q

what is infarction?

A

Ischaemic necrosis within a tissue/organ in living body produced by occlusion of either the arterial supply or venous drainage

29
Q

what are the 4 possible causes of infarction?

A
  1. thrombosis2. embolism3. strangulation4. trauma-cut/ruptured vessel
30
Q

if an infarction occurs for a short time, how is the long-term damage different from if it was for a long time?

A

it is less

31
Q

what are the factors that determine the scale of damage from ischaemia or infarction?

A

-Time period-Tissue/organ -Pattern of blood supply -Previous disease

32
Q

what is coagulative necrosis?

A

necrosis in which the organ maintains its shape after necrosis

33
Q

what is colliquitive necrosis?

A

necrosis in which the tissue loses its gross structure as there is loss of connective tissue

34
Q

describe the sequence of events in necrosis

A
  1. Anaerobic metabolism 2. cell death3. liberation of enzymes 4. breakdown of tissue
35
Q

give examples of tissue that undergo coagulative necrosis?

A

heart, lung

36
Q

give examples of a tissue that undergo colliquitive necrosis?

A

brain

37
Q

how long is severe ischaemia and is it reversible?

A

20-30 minutesirreversible damage

38
Q

what happens in the first seconds of myocardial ischaemia?

A

anaerobic matabolism causes ATP depletion

39
Q

what happens in the first 2 minutes of myocardial ischaemia?

A

loss of myocardial contractility leading to heart failure

40
Q

what happens after the first 2 minutes of myocardial ischaemia?

A

-ultrastructural changes:-myofibrillar relaxation-glycogen depletion-cell and mitochondial swelling

41
Q

after how long of ischaemia is there injury to the microvasculature of the heart?

A

> 1 hour

42
Q

after 24-48 hours what is the appearance of an infarct in dense tissues such as the myocardium, spleen, kidney solid tissues

A

pale

43
Q

after 24-48 hours what is the appearance of an infarct in loose tissues such as the lung, liver and perviously congested tissues?

A

red

44
Q

under the microscope what can be seen around the edge of infarcts at 24-48 hours?

A

inflammatory cells such as neutrophils

45
Q

under the microscope what can be seen i infarcts at 72 hours after event?

A

chronic inflammation:-macrophages remove debris-granulation tissue-fibrosis

46
Q

what is the end result of infarction?

A

scar replaces area of tissue damagereperfusion injury

47
Q

what is reperfusion injury?

A

after a period of ischaemia blood reperfuses the tissue.this causes inflammation and further damage to the tissue as there inflammation and oxidative injury

48
Q

what are the reparative processes of mysocardial infarction?

A

Cell deathAcute inflammationMacrophage phagocytosis of dead cellsGranulation tissueCollagen deposition (fibrosis)Scar formation

49
Q

what is a transmural myocardial infarction?

A

ischaemic necrosis affects full thickness of the myocardium

50
Q

what is a subendocardial infarction?

A

ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart

51
Q

what sort of MI is a non-STEMI most likely to be?

A

subendocardial infarct

52
Q

what sort of myocardial infarction is likely to have occurred if there is no ST elevation and elevated serum troponin level?

A

non-STEMI

53
Q

what are some of the complication of myocardial infarction?

A

sudden deatharrythmiasanginacardiac failurecardiac rupture-ventricular wall, septum, papillary musclereinfarctionpericarditispulmonary embolism secondary to DVT-papillary muscle dysfunction from necrosis or rupture causing mitral incompetencemural thrombosisventricular aneurysmdressler’s syndrome

54
Q

what is dressler’s syndrome?

A

Dressler syndrome is a secondary form of pericarditis that occurs in the setting of injury to the heart or the pericardium

55
Q

what does papillary muscle dysfunction lead to?

A

usually mitral (but can be tricuspid) incompetence

02. Cardiovascular System (72 decks)

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