Ischaemia Flashcards
1
Q
What is the overall explanation for ischaemia?
A
Imbalance of oxygen supply versus oxygen demand
2
Q
What determines oxygen supply to the heart? (2)
A
- Coronary blood flow
- Oxygen saturation and extraction
3
Q
What determines oxygen demand of the heart? (2)
A
- Cardiac contractility force/rate
- Ventricular wall tension (systolic/diastolic)
4
Q
What is ischaemic heart disease?
A
Clinical manifestation of coronary arterial narrowing due to atherosclerosis
5
Q
What is ischaemic heart disease also known as? (2)
A
- Coronary heart disease (CHD)
- Cocronary artery disease (CAD)
6
Q
What are the two major types of ischaemic heart disease? (2)
A
- Stable angina
- Acute coronary syndrome (ACS)
7
Q
What are the types of acute coronary syndromes in order of how critical they are? (3)
A
- Unstable angina
- Acute non-STEMI MI
- Acute STEMI MI
8
Q
What is ischaemia?
A
Reduction in blood supply to tissues causing dysfunction
9
Q
Why does ischaemia lead to tissue damage?
A
- Reduced oxygen (hypoxia)
- Reduced nutrients
- Metabolic waste impaired washout
10
Q
What are the hypoxic causes of ischaemia? (4)
A
- Isolated hypoxemia
- Severe anaemia
- Pulmonary disease
- Cyanotic heart disease (shunt right to lefft)
11
Q
What percentage of obstruction leads to stable angina?
A
60 or less
12
Q
What percentage of obstruction leads to unstable angina?
A
60-70
13
Q
Explain the typical progression of ischaemic damage in the heart wall (3)
A
- Proximal occlusion at the level of coronary artery
- Necrosis distribution from endocardium
- Progresses towards the epicardium transmurally
14
Q
Describe the typical ischaemic necrosis pattern (2)
A
- Largest at endocardium,
- Wedge-shaped extension up to the epicardial surface
15
Q
Why does most ischaemia affect the left ventricle more/earlier? (3)
A
- Thicker
- Needs more blood
- Working against higher pressure
16
Q
What are the 7 stages of gross feature progression from an MI?
A
- 4-12 hrs: Occasional dark mottling
- 12-24 hrs: Dark mottling
- 1-3 days: Mottling with yellow tan infarct centre
- 3-7 days: Hyperaemic (more blood) border with central yellow tan softening
- 7-10 days: maximally yellow tan and soft, depressed red-tan margins
- 2-3 weeks: grey white scar progressive from border towards infarct zone
- Less than 2 months: scarring complete
17
Q
What are the risk factors for complications following an MI? (4)
A
- Female
- 60+ yrs
- Pre-existing hypertension
- No L ventricular hypertrophy
18
Q
How do MIs lead to arrythmias leading to further MI/stroke? (6)
A
- Infarction at level of AV sinus
- Necrotic = not good at transmitting electric stimulus
- Fibrilliation
- Increases chance of intercardial thrombosis
- Can embolise, flow in circulation
- Increases risk of stroke and more MIs
19
Q
What are the complications of an MI? (9)
A
- Contractile dysfunction = pump failure = cardiogenic shock
- Arrythmias/conduction defects=sudden death
- Infarction extension
- Congestive heart failure/pulmonary oedema
- Pericarditus
- Ventricular aneurysm formation
- Myocardial wall rupture = possiblle tamponade
- Papillary muscle rupture = valvular insufficiency
- Ventricular septum rupture = L to R shunt
20
Q
How does an MI lead to cardiac tamponade? (5)
A
- Tissue necrosis transmurally from endocardium to pericardium
- Myocardium rupture
- Massive flow of blood in pericardial cavity = tamponade
- L ventricle higher pressure = shunts to R ventricle lower pressure
- Dysfunction
21
Q
What does papillarly muscle rupture following an MI lead to?
A
Not functioning valves
22
Q
How can an MI lead to pump failure and contractile dysfunction? (3)
A
- Myocardium wall thinning
- Endocardium irregularlity
- Fibrous tissue doesn’t stretch, less able to contract
23
Q
How can an MI lead to ventricular anerysm? (4)
A
- Surviving myocardium layer = severely weakened, - Blood flows into surrounding dead muscle
- Thin weakened layer inflates
- Can block blood flow/rupture
24
Q
Why is there increased chance of a thrombus forming post MI?
A
More inflammatory cells in area with debris
25
How can pericarditus be caused by an MI? And when does this occur? (2)
Early onset = few days
| - Inflamed pericardium overlying infarcted area
26
What is Dressler's syndrome?
Late onset (2-12 weeks) autoimmune abnormal inflammatory response to infarct
27
How long after an MI does it take for Dressler's syndrome to occur?
2-12 weeks
28
How long does it take for gross features and light microscopy of an MI to show up?
4 hours
29
What are the light microscopy features 4-12 hours after an MI? (4)
- Early coagulation necrosis
- Oedema
- Haemorrage
- More neutrophils: inflammatory response
30
What are the light microscopy features 1-3 days after an MI? (3)
- Coagulation necrosis
- Nucleui loss and striations
- Brisk interstitial neutrophils infiltrate
31
What are the light microscopy features 3-7 days after an MI? (4)
- Dead myofiber disintegration
- Dying neutrophils
- Dead cell phagocytosis by macrophages at infarct border
32
What are the light microscopy features 7-10 days after an MI? (2)
- Well developed dead cell phagocytosis
| - Fibrovasccular granulation tissue early formation at margins
33
What are the light microscopy features 10-14 days after an MI? (2)
Well established granulation tissue with blood vessels and collagen deposition
34
What are the light microscopy features 2-8 weeks after an MI? (2)
- Increased collagen deposition
| - Decreased cellularity
35
What are the light microscopy features 12-24 hours after an MI? (5)
- Ongoing coagulation necrosis
- Nuclei pyknosis (chromatin condensation)
- Mycocyte hypereoisophilia
- Marginal contraction band necrosis
- Early neutrophilic infiltrate
36
What are the light microscopy features more than 2 months after an MI? (2)
Dense collagenous scar
37
Summarise how heart tissue changes afer an MI microscopically (3)
- 1-2 days: few inflammatory cells
- 3-5 days: more inflammatory cells, tissue necrosis, dark granules of calcium deposits due to damage
- 1-2 weeks: necrotic material and granulation tissue
38
What are the 2 types of treatment for an MI?
- Medical therapy
| - Revascularisation
39
What are the 2 types of revascularisation treatment for an MI?
- Percutaenous coronary intervention (PCI)
| - Coronary artery bypass graft (CABG)
40
When is PCI used as a revascularisation treatment for an MI? (2)
- Localised obstruction
| - Expand blood vessel to repurfuse specific damaged area
41
What happens in PCI? (3)
- Stent inserted into vessel
- Guided into coronary artery with wire
- Progressively expanded to full size with balloon inserted with catheter
42
When is CABG used as a revascularisation treatment for an MI? (2)
Widespread coronary disease - multiple areas of obstruction affecting different coronary arteries
43
What does a CABG involve? (2)
- Bypass area of obstruction by making connection between subclavian artery and aorta
- With stem from saphenous vein/mammary artery/intercostal artery
44
Where is the stem for a CABG taken from? (3)
- Saphenous vein
- Mammary artery
- Intercostal artery
45
What is a common complication of CABG? (2)
- Atherosclerosis building up in bypass graft
| - Vein not adapted to increased pressure in arterial system
46
How can repurfusion cause more damage than the original obstruction? (2)
- Limits necrosis area
| - But causes shock to issue as was limited in perfusion so has accumulated metabolites
47
When must restoration of coronary flow occur to salavage ischaemic myocardium and prevent all necrosis?
15-20 mins
48
What occurs in lethally injured cells on repurfusion?
Contraction bands
49
How can reperfusion lead to a lack of reflow? (7)
- Leukocytes in reperfused blood
- Myocytes apoptosis
- Microvascular injury
- Haemorrhage
- Endothelial swelling
- Occludes capillaries
- Prevents local repurfusion = no flow
50
What used to be as cardiac biomarkers but have found to be non specific? (3)
- Creatinine kinase MB (CK-MB)
- Aspatate transaminase (AST)
- Lactate dehydrogenase (LDH)
51
What biomarkers are most specific to cardiac muscle damage? And which isomer is the most common? (2)
- Troponin T (most common)
| - Troponin I
52
What is CK-MB? How is it different to (2) CK?
- CK = rhambdomyolysis = skeletal muscle damage
| - CK-MB = iso-enzyme specific to cardiac muscle damage
53
What is the advantage to using troponin over CK-MB as a cardiac biomarker?
- Specific to cardiac muscle
- CK-MB tails off quickly after damage, so if late presentation= nothing seen
- Troponin rises higher, quicker and tails off later
54
How is tropononin used as a cardiac biomarker?
Specific to heart, detected in blood after myocardial injury
55
Why is troponin alone not enough to diagnose an MI?
Not specific to ischaemia e.g can be due to blood trauma, physical damage to heart
56
What are the similarities between a STEMI and nSTEMI in terms of diagnosis? (4)
- Rise in cardiac biomarker valves - 1 value above 99th percentile of reference limit
- Ischaemia symptoms
- Imagining evidence of viable myocardium loss
- Angiography intracoronary thrombus
57
What are the differences between a STEMI and nSTEM? (4)
- Sudden total occlusion of major vessel vs incomplete occlusion
- Full thickness myocardium segment ischaemia vs less extensive
- 1mm+ ST elevation in 2 adjacent limb leads vs not
- Other ECG changes: new LBB/pathological Q waves vs not
58
What is the difference between stable angina and ACS? (6)
- Slow/insidious vs sudden
- Trigger vs at rest
- Greater pain
- SA= no heart damage vs ACS = heart damage
- SA=stable coronary artery plaque vs ACS = Rupture/erosion of the fibrous cap of a coronary artery plaque
- SA=relieved within 5 mins of rest/GTN spray vs ACS=not
59
What are the disadvantages of using high sensitivity troponin? (2)
- More sensitive = picks up smaller damages to heart
- But less specific = misdiagnosing small damages as something serious
- More interventions - NHS on budget
60
What is infarction?
Tissue death (necrosis) due to insufficient blood supply (ischaemia)
