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CVS Pathophysiology > Pathophysiology Of Ischaemia And Infarction > Flashcards

Pathophysiology Of Ischaemia And Infarction Flashcards

1
Q

What are the types of hypoxia?

A

Hypoxia hypoxia- low inspired o2 or normal inspired 02 but low pa02
Anemia - normal inspired 02 but abnormal blood
Stagnant - normal inspired 02 but abnormal delivery i.e. local: occlusion of a blood vessel or systemic: shock
Sytotoxic - normal inspired 02 but abnormal at tissue level

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2
Q

What factors affect oxygen supply?

A 
Inspired 02
Pulmonary function
Blood flow
Blood constituents
Integrity of blood vessel I.e. if something is occluding it
Tissue mechanisms
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3
Q

What factors affect oxygen demand?

A

Tissue itself- different tissues have different requirements

Activity of tissue above baseline value

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4
Q

In ischaemic heart disease, what many affect the supply of 02 to the heart?

A

Coronary artery atheroma, pulmonary function due to other disease or pulmonary edema from LVH, anaemia, previous MI

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5
Q

State some of the clinical consequences of ischaemia and infarction

A 
MI
Transient ischameic attack
Cerebral infarction
Abdominal aortic aneurysm 
Peripheral vascular disease
Cardiac failure
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6
Q

What are the clinical effects of ischaemia?

A

Dysfunction
Pain
Physical damage

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7
Q

What is the definition of infraction?

A

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

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8
Q

What factors affect the scale of damage of ischemia/infarction?

A

Time period
Tissue/organ
Pattern of Blood supply (collateral blood supply)
Previous disease

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9
Q

What is the etiology of infarction?

A

Occlusion of blood flow

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10
Q

What are the 2 different forms of necrosis?

A

Coagulative I.e. heart, adrenals, kidney

Colliquitive i.e. brain (digestion of dead cells into a viscous liquid mass)

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11
Q

What is the time limit before myocardial ischaemia progresses to severe ischaemia?

A

20-30 mins at at this stage it is irreversible

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12
Q

How long does it take for myocardial ischemia to cause myocyte necrosis?

A

20-40 mins

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13
Q

From myocardial ischemia, how long does it take to undergo anaerobic metabolism causing depletion of ATP?

A

Seconds

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14
Q

What is the appearance 24-48 after infarction?

A

Pale infarct in kidney, spleen, myocardium
Red infarct in lung, liver, loose tissues
Microscopically loss of specialized cell features & acute inflammation at the edge of infarction

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15
Q

What is the appearance up to 24 hours after infarction?

A

No change in appearance

But in microscopy there may be swollen mitochondria

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16
Q

What is the appearance 72 hours onwards from infarction?

A

Pale infarction - pale / yellow with red periphery
Red infarct - little changes
Microscopically- chronic inflammation, macrophages remove debris, fibrosis, granulation tissue

17
Q

What is the end result of infarction?

A

A scar replaces the area of tissue damage
The shape depends on the territory of the occluded vessel
May result in repercussion injury

18
Q

What is repercussion injury?

A

When blood flow is restored to a previously ischaemic area, this causes tissue damage.
When blood returns you get inflammation and damage from the 02 free radicals

19
Q

What is the reparative process of a myocardial infarction?

A 
Cell death
Acute inflammation
Macrophages phagocytosis of dead cells
Granulation tissue
Collagen deposition, causing fibrosis = fibrous tissue
Scar formation
20
Q

How long does it take for a dense collagenous scar to develop from a myocardial infarction?

A

> 2 months

21
Q

What is the name for ischaemic necrosis which affects the full thickness of the myocardium?

A

Transmural infarction

22
Q

What is a subendocardial infarction?

A

Ischemic necrosis which affects the zone of the myocardium under the endocardial lining of the heart

23
Q

A non-STEMI is usually associated with what type of ischaemic necrosis?

A

Subendocardial infarction

24
Q

Describe the time time frame of the injury caused by ischaemia.

A

Few seconds - anaerobic respiration causing ATP depletion
<2mins -loss of myocardial contractility
Few mins - changes to the ultra structure
20-30 mins - myocyte necrosis
>1 hr - injury to the microvasculature

25
Q

What is a bad end result from infarction?

A

Repercussion injury

26
Q

What follows cell death in the reparative process of infarction?

A

Acute inflammation

27
Q

What follows acute inflammation in the reparative process?

A

Macrophages phagocytosis of dead cells

28
Q

What follows macrophage phagocytosis in the reparative process?

A

Granulation tissue

Collagen deposition

29
Q

How long after an myocardial infarction do you see early neutrophillic infiltrate and then brisk neutrophillic infiltrate?

A

Early infiltrate 12-24 hrs

Brisk infiltrate 1-3 days

30
Q

When does disintegration of dead myofibres occur after an infarction?

A

3-7 days

31
Q

When do you begin to see granulation tissue? And where does this first appear?

A

7-10 days

At the margins

32
Q

What occurs 2-8 weeks after a MI?

A

Increased collagen deposition

Decreased cellularity

33
Q

What are some of the complications of a MI?

A 
Sudden death
Arrhythmia
Angina
Heart failure
Pulmonary embolism secondary to DVT
Ventricular aneurysm
Ventricular wall, septum or papillary muscle rupture
Papillary muscle dysfunction = necrosis/rupture = mitral regurgitation
34
Q

If a MI causes infarction to a papillary muscle what can this result in?

A

Rupture of the papillary muscle = regurgitation

35
Q

What is the time frame when there is irreversible damage to the myocardium?

A

20-30 mins

36
Q

Where would the infarction of an MI occur which would cauze bradyarthymias?

A

Inferior MI

37
Q

What is cardiogenic shock characterised by?

A

Low blood pressure
Low urine output
High mortality

38
Q

What is a late complication of a myocardial infarction?

A

Ventricular aneurysm

CVS Pathophysiology (4 decks)

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