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Cardiovascular block > Pathophysiology of ischaemia and infarction > Flashcards

Pathophysiology of ischaemia and infarction Flashcards

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1
Q

What is ischaemia ?

A

Reduced blood flow to organs/ tissues

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2
Q

What is hypoxia ?

A

Inadequate oxygen supply to meet the needs of tissue/ organs ?

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3
Q

What is hypoxic hypoxia ?

A

Low inspired O2 levels

Normal inspired o2 but low PaCO2

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4
Q

What is anaemic hypoxia ?

A

Normal inspired O2 but blood abnormal;

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5
Q

What is stagnant hypoxia ?

A

Normal inspired O2 but abnormal delivery
Local e.g. occlusion of artery
Systemic e.g. shock

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6
Q

What is cytotoxic hypoxia ?

A

Normal inspired O2 but abnormal at tissue level

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7
Q

What are the factors affecting O2 supply ?

A 
Inspired O2
Pulmonary function
Blood constituents
Blood flow
Integrity of vasculature
Tissue mechanisms
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8
Q

What are the factors affecting O2 demand ?

A

Tissue itself- different tissues have different requirements

Activity of tissue above baseline value

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9
Q

What are the supply issues with iscahmic heart disease ?

A

Coronary artery atheroma
Cardiac failure (flow)
Pulmonary function- other disease or pulmonary oedema (LVF)
Anaemia, previous MI

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10
Q

What are the demand issues with ischaemic heart disease ?

A

Heart has high intrinsic demand

exertion/ stress

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11
Q

What is an atheroma/atherosclerosis ?

A

Localised accumulation of lipid and fibrous tissue in intima of arteries

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12
Q

What is the clinical correlation with established atheroma in coronary artery ?

A

Stable angina

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13
Q

What is the clinical consequence of complicated atheroma in coronary artery ?

A

Unstable angina

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14
Q

What is the clinical correlation of an ulcerated/fissured plaque ?

A

Leads to thrombosis, then leads to ischaemia and infarction

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15
Q

What are the clinical consequences of atheroma ?

A 
MI
TIA
Cerebral infacrtion
Abdominal aortic aneurysm 
Peripheral vascular diease
Cardiac failure 
Coronary artery disease-> MI-> cardiac failure
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16
Q

What are the effects of atheroma on blood flow ?

A

Changes in vessel wall-> thrombosis
Poiseuille’s formula- R= 8ηl/πr2
Blood flow- Q = ∆P/R

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17
Q

What are the functional effects of ischaemia ?

A

Blood/ O2 supply fails to meet demand due to decreased supply; increased demand; or both
Related to rate of onset

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18
Q

What are the general effects of ischaemia ?

A

Acute
Chronic
Acute-on-chronic

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19
Q

What are the biochemical effects of ischaemia ?

A
  • Normal aerobic metabolism
    glucose+36ADP+36Pi+36H++6O2 ®6CO2+36ATP+42H2O
    • Anaerobic metabolism
      glucose+2Pi+2ADP ®2lactate+2ATP+2H2O
    • L-lactate¬®pyruvate
    • Pyruvate+ NAD++CoA®acetylCoA+CO2+NADH
    • O2 ® anaerobic metabolism ® cell death
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20
Q

What are the cellular effects of ischaemia ?

A

Different tissues have variable O2 requirement and are variably susceptible to ischaemia
Cells with high metabolic rate
Cells with low metabolic rate

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21
Q

What are the clinical effects of ischaemia ?

A

Dysfunction
Pain
Physical damage- specialised cells

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22
Q

What is the outcome of the effects of ischaemia ?

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A

No clinical effect
Resolution vs therapeutic intervention
Infacrtion

23
Q

What is infarction ?

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A

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

24
Q

What are the possible aetiologies for infarction ?

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A

Thrombosis
Embolism
Strangulation e.g. gut
Trauma - cut/ruptured vessel

25
What does the scale of damage of ischamia/infarction depend on ?
Time period Tissue/organ Pattern of blood supply Previous disease
26
What is the mechanism of tissue breakdown caused by infarction ?
Anaerobic metabolism - cell death - liberation of enzymes
27
What are the two types of necrosis ?
Coagulative necrosis e.g. Heart, lung | Colliquative necrosis e.g. Brain
28
What can coronary arterial obstruction lead to ?
Reduced blood flow to region of myocardium, leads to ischaemia, rapid myocardial dysfunction, leads to myocyte death
29
What happens within seconds of myocardial ischaemia ?
Anaerobic metabolism, onset of ATP depletion
30
What happens in under two minutes of myocardial ischaemia ?
Loss of myocardial contractility (heart failure)
31
What happens within a few minutes of myocardial ischaemia ?
Ultrastructural changes (myofibrillar relaxation, glycogen depletion, cell and mitochondrial swelling) ?reversible
32
How long does it take for ischaemia to cause irreversible damage to the heart ?
20-30 minutes Myocyte necrosis (disruption of integrity of sarcolemma membrane leading to the leakage of intracellular macromolecules: blood tests) - Troponin? Injury to the microvasculature - over 1 hour
33
What do areas of infarction look like less than 24 hours after insult ?
No change on visual inspection | A few hours to 12 hours post insult, see swollen mitochondria on Electron Microscopy
34
What do areas of infarction look like within 24-48hrs ?
Pale infarct: e.g. myocardium, spleen, kidney, Solid tissues Red infarct: e.g. in lung, liver, Loose tissues, previously congested tissue; second/continuing blood supply, venous occlusion Microscopically: acute inflammation initially at edge of infarct; loss of specialised cell features
35
What do areas of infarction look like within 72hrs and onwards ?
Macroscopically: - Pale infarct - yellow/white and red periphery Red infarct - little change Microscopically: chronic inflammation; macrophages remove debris; granulation tissue; fibrosis
36
What is the appearance of end result infarcts ?
Scar replaces area of tissue damage Shape depends on territory of occluded vessel Reperfusion injury
37
What is the reparative process of myocardial infarction ?
``` Cell death Acute inflammation Macrophage phagocytosis of dead cells Granulation tissue Collagen deposition (fibrosis) Scar formation ```
38
What happens between 4-12hrs of an MI ?
Early coagulation necrosis, oedema, haemorrhage
39
What happens between 12-24hrs of an MI ?
Ongoing coagulation necrosis, myocyte changes, early neutrophilic infiltrate
40
What happens between 1-3 days of an MI ?
Coagulation necrosis, loss of nuclei and striations, brisk neutrophilic infiltrate
41
What happens between 3-7 days of an MI ?
Disintegration of dead myofibrils, dying neutrophils, early phagocytosis
42
What happens between 7-10 days of an MI ?
Well developed phagocytosis, granulation tissue at margins
43
What happens between 10-14 days of an MI ?
Well established granulation tissue with new blood vessels and collagen deposition
44
What happens between 2-8 weeks of an MI ?
Increased collagen deposition, decreased cellularity
45
What happens over 2 months of an MI ?
Dense collagenous scar
46
What is a transmural infarction ?
Ischaemic necrosis affects full thickness of the myocardium
47
What is a subendocardial infarction ?
ischaemic necrosis mostly limited to a zone of myocardium under the endocardial lining of the heart
48
What are the histological feature of transmural and subendocardial infarcts ?
Histological features are the same (repair time - granulation tissue stage followed by fibrosis - in subendocardial infarct possibly slightly shortened compared to transmural infarct)
49
How are acute infarcts classified ?
According to whether there is elevation of the ST segment on the ECG
50
What are the features of a NSTEMI ?
No ST segment elevation but a significantly elevated serum troponin level
51
What does a NSTEMI correlate with ?
subendocardial infarct
52
What do the effects of infarction depend ?
Site Size of infarct Death and dysfunction (pain) Contribution of previous disease and infarction
53
What are the complications of myocardial infarction ?
Immediate; early; late 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

Cardiovascular block (28 decks)

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