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Cardio > Pathophysiology of Ischaemia & Infarction > Flashcards

Pathophysiology of Ischaemia & Infarction Flashcards

1
Q

What is ischaemia?

A

a restriction in blood supply to tissues, causing a shortage of oxygen that is needed for cellular metabolism (hypoxia)

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2
Q

What is infarction?

A

obstruction of the blood supply to an organ or region of tissue, typically by a thrombus or embolus, causing local death of the tissue

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3
Q

What are the causes/types of hypoxia?

A

Low inspired O2 level or normal inspiration but low PaO2

Anaemia

Stagnant blood

Cytotoxic

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4
Q

Describe how hypoxia due to stagnant blood may arise

A

Abnormal delivery of blood

Can be local - due to occlusion of a vessel

Can be systemic - due to shock

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5
Q

Describe why cytotoxic hypoxia may arise

A

Normal delivery of oxygen to tissues

However, oxygen uptake/usage is ineffective at a cellular level

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6
Q

What factors affect oxygen supply?

A

Inspired O2
Lung function

Blood constituents

Blood flow
Integrity of vasculature

Tissue mechanisms

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7
Q

What factors affect tissue demand?

A

What type of tissue it is

What it’s doing:
- activity of tissue above baseline value

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8
Q

In terms if supply & demand

What is Ischaemic heart disease?

A

Mismatch between supply & demand of oxygen

Hypoxia of the heart muscles

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9
Q

What can cause a mismatch in supply & demand, for ischaemic heart disease?

A

Supply issues:

  • coronary artery atheroma
  • cardiac failure (flow)
  • pulmonary function – other disease or pulmonary oedema (LVF)
  • anaemia
  • previous MI

Demand issues:

  • heart has high intrinsic demand
  • exertion/stress
  • stenosis of aorta & all them ones
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10
Q

What are the clinical consequences of atheromas in the coronary arteries?

A

Normal atheroma = stable angina

Complicated atheroma = unstable angina

Fissured/ulcerated plaque = thrombosis = ischaemia or infarction (BAD)

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11
Q

What is the main risk associated with an atheroma in the aorta?

A

Aneurism

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12
Q

What are the clinical consequences of Ischaemic heart disease?

A 
MI 
TIA
Cerebral infarction
Abdominal aortic aneurysm
Peripheral vascular disease
Cardiac failure

Coronary artery disease —-> MI —-> cardiac failure

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13
Q

Using physics n shit

What effect does an atheroma have on flow in an artery?

A

Resistance proportional to 1/r^4

So a very small decrease in lumen size due to a plaque causes a HUGE increase in resistance & therefore flow in an artery

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14
Q

What cells are most at risk of damage from ischaemia?

A

Cells with high metabolic rate

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15
Q

What are the general effects of ischaemia?

A

Dysfunction

Pain

Physical damage

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16
Q

“If a significant ischaemic event does not receive medical intervention or therapy, it will either _______ or progress to ________”

A

It will either resolve or progress to infarction

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17
Q

Define infarction

A

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

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18
Q

What are the main causes of infarction?

A

Thrombosis

Embolism

Strangulation - eg of gut

Trauma - cut/ruptured vessel

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19
Q

What determines the scale of damage done by ischaemia/infarction to an organ/tissue?

A

Time period

What organ/tissue it is

Patterns of blood supply

Previous disease

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20
Q

Why is the length of time that a tissue has been ischaemic/infarcted for an important determinant of damage?

A

Necrosis doesn’t happen instantly - cells/tissues can survive for some time without supply of blood

Blood supply lost –> Anaerobic M –> cell death –> Liberation of enzymes –> Breakdown of tissue

^the stage that the tissue is at determines the scale of damage

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21
Q

What are the 2 types of necrosis?

A

Coagulative necrosis:

  • Heart, lungs etc
  • Due to infarction/ischaemia

Colliquitive necrosis:

  • Brain
  • Associated with bacterial or fungal infections
22
Q

Myocardial infarction happens when…

A

Coronary arteries are obstructed ∴ no blood flow to area of myocardium ∴ ischaemia ∴ dysfunction ∴ myocyte death

23
Q

“Within seconds of the coronary arteries being blocked, ischaemia of areas of the myocardium begins and …..”

A

Anaerobic metabolism begins, depleting ATP levels

24
Q

“Within 2 minutes of the onset of myocardial ischaemia, there is a loss of …”

A

There is a loss of Myocardial contractility - heart failure

25
Q

“After a few minutes of myocardial ischaemia, there are permanent changes to the myocardium such as…”

A

Myofibrillar relaxation

Glycogen depletion

Cell & mitochondrial swelling

26
Q

“After 20-30 mins of severe myocardial ischaemia, …”

A

The damage to the myocardium is irreversible, and monocyte necrosis has begun

27
Q

Why can monocyte necrosis be detected in a blood test?

A

Disruption of the integrity of sarcolemmal membrane causes leakage of intracellular macromolecules into the blood

28
Q

How long does it take, after the onset of myocardial ischaemia, before the body’s microvasculature to be injured?

A

> 1 hour

29
Q

How long does it take before infarction becomes visible?

A

Visual changes of infarcted tissue after 24-48 hours

Microscopic changes occur in under 12 hours, for example, swollen mitochondria, which can be viewed under an electron microscope

30
Q

How does infarction initially change the physical appearance of a tissue?

A

It depends on the tissue:

Pale infarcts - myocardium, spleen, kidney, solid tissues

Red infarcts - lung, liver, loose tissue, previously congested tissue & tissue that has venous occlusion

31
Q

When looking under a microscope, what features would indicate infarction?

A

Swollen mitochondria & cells

Acute inflammation, initially at edge of infarct

Loss of specialised cell features

32
Q

Describe the physical appearance of infarcted tissue after 72 hours

A 
Pale infarct (heart, spleen, kidney etc):
- yellow/white with red periphery 
Red infarct (lung, liver etc)
- little change
33
Q

What is the end fate of an infarcted area?

A

Scar replaces the area of tissue damage

Reperfusion injury

34
Q

What is reperfusion injury?

A

Damage to infarcted tissue when blood flow is restored

“Restoration of circulation results in inflammation and oxidative damage”

35
Q

Summarise the repair process for infarcted tissue

A

Necrosis (cell death) of infarcted area

Acute inflammatory response recruits neutrophils (& macrophages i think)

Phagocytosis all the debris/dead cells

Granulation tissue formed & collagen secreted

Scar formed

36
Q

Describe the state of myocardial tissue, 4-12 hours after infarction

A

Early coagulative necrosis

Oedema

Haemorrhage

(No macroscopic change to appearance)

37
Q

What begins to happen in infarcted myocardium, 12-24 hours after infarction begins?

A

Ongoing coagulative necrosis

Mitochondria have swollen up, and myocytes have begun to change

Inflammatory response begins:
- Early neutrophilic infiltrate

38
Q

What happens to the myocardial tissue, 1-3 days after infarction begins?

A

By this time, coagulative necrosis has caused significant changes to the myocyte’s cell architecture:
- Loss of nuclei and striations

There is also a large amount neutrophilic infiltrate

39
Q

What happens 3-7 days after infarction of myocardial tissue begins?

A

By the end of the first week, myocytes have properly begun to break down:

  • Disintegration of dead myofibrils
  • Neutrophils are dying

Phagocytosis of all the dead stuff has begun^

40
Q

What happens 7-10 days after infarction of myocardial tissue begins?

A

Lots of ongoing phagocytosis of all the dead stuff & debris

This is also when granulation tissue starts being produced, so this would start appearing at the edges of the infarcted area

41
Q

What happens towards the end of the 2nd week of infarction of myocardial tissue?

(10-14 days)

A

Well established area of granulation tissue has formed with newly formed:

  • Blood vessels
  • Collagen
42
Q

After 2 weeks of infarction, well established granulation tissue has formed.

Over the next few weeks, what happens to this granulation tissue?

A

Collagen is continually deposited into the granulation tissue

Loss of cellularity

^is basically turning into a scar

43
Q

How long does it take before infarcted myocardium becomes all scarred n stuff?

A

> 2 months

Dense collagenous scar

44
Q

What is a transmural infarction?

A

a myocardial infarction that involves the full thickness of the myocardium

Thus ischaemic necrosis involves the whole thickness of the myocardium

45
Q

What is a sub-endocardial infarction?

A

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

46
Q

What are the different types of MI’s

A

STEMI

NSTEMI

47
Q

What is the difference between STEMI & NSTEMI?

A

Whether or not the ST segment on an ECG is elevated

If ST elevated = STEMI
If ST is not elevated but serum troponin levels are elevated, then NSTEMI

48
Q

What type of MI is related to subendocardial infarction?

A

NSTEMI related to Subendocardial infarction

49
Q

What are examples of complications of Myocardial infarctions?

(absolute fuck ton)

A 
Sudden death
Arrhythmias
Angina
Cardiac failure
Cardiac rupture - ventricular wall, septum, papillary muscle
Reinfarction 
Pericarditis
Pulmonary embolism secondary to DVT
Papillary muscle dysfunction - necrosis/rupture  
Mitral incompetence
Mural thrombosis
Ventricular aneurysm 
Dressler's syndrome
50
Q

How long after the onset of infarction should you wait before taking bloods?

A

20-40 minutes

Macromolecules such as cTn are only released into the blood after myocyte necrosis (sarcolemmal membrane disruption)

Cardio (41 decks)

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