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Cardiology > Ischaemia > Flashcards

Ischaemia Flashcards

1
Q

What is the overall explanation for ischaemia?

A

Imbalance of oxygen supply versus oxygen demand

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2
Q

What determines oxygen supply to the heart? (2)

A
  • Coronary blood flow

- Oxygen saturation and extraction

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3
Q

What determines oxygen demand of the heart? (2)

A
  • Cardiac contractility force/rate

- Ventricular wall tension (systolic/diastolic)

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4
Q

What is ischaemic heart disease?

A

Clinical manifestation of coronary arterial narrowing due to atherosclerosis

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5
Q

What is ischaemic heart disease also known as? (2)

A
  • Coronary heart disease (CHD)

- Cocronary artery disease (CAD)

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6
Q

What are the two major types of ischaemic heart disease? (2)

A
  • Stable angina

- Acute coronary syndrome (ACS)

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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
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8
Q

What is ischaemia?

A

Reduction in blood supply to tissues causing dysfunction

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9
Q

Why does ischaemia lead to tissue damage?

A
  • Reduced oxygen (hypoxia)
  • Reduced nutrients
  • Metabolic waste impaired washout
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10
Q

What are the hypoxic causes of ischaemia? (4)

A
  • Isolated hypoxemia
  • Severe anaemia
  • Pulmonary disease
  • Cyanotic heart disease (shunt right to lefft)
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11
Q

What percentage of obstruction leads to stable angina?

A

60 or less

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12
Q

What percentage of obstruction leads to unstable angina?

A

60-70

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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
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14
Q

Describe the typical ischaemic necrosis pattern (2)

A
  • Largest at endocardium,

- Wedge-shaped extension up to the epicardial surface

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15
Q

Why does most ischaemia affect the left ventricle more/earlier? (3)

A
  • Thicker
  • Needs more blood
  • Working against higher pressure
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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
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17
Q

What are the risk factors for complications following an MI? (4)

A
  • Female
  • 60+ yrs
  • Pre-existing hypertension
  • No L ventricular hypertrophy
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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
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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
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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
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21
Q

What does papillarly muscle rupture following an MI lead to?

A

Not functioning valves

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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
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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
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24
Q

Why is there increased chance of a thrombus forming post MI?

A

More inflammatory cells in area with debris

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25
Q

How can pericarditus be caused by an MI? And when does this occur? (2)

A

Early onset = few days

- Inflamed pericardium overlying infarcted area

26
Q

What is Dressler’s syndrome?

A

Late onset (2-12 weeks) autoimmune abnormal inflammatory response to infarct

27
Q

How long after an MI does it take for Dressler’s syndrome to occur?

A

2-12 weeks

28
Q

How long does it take for gross features and light microscopy of an MI to show up?

A

4 hours

29
Q

What are the light microscopy features 4-12 hours after an MI? (4)

A
  • Early coagulation necrosis
  • Oedema
  • Haemorrage
  • More neutrophils: inflammatory response
30
Q

What are the light microscopy features 1-3 days after an MI? (3)

A
  • Coagulation necrosis
  • Nucleui loss and striations
  • Brisk interstitial neutrophils infiltrate
31
Q

What are the light microscopy features 3-7 days after an MI? (4)

A
  • Dead myofiber disintegration
  • Dying neutrophils
  • Dead cell phagocytosis by macrophages at infarct border
32
Q

What are the light microscopy features 7-10 days after an MI? (2)

A
  • Well developed dead cell phagocytosis

- Fibrovasccular granulation tissue early formation at margins

33
Q

What are the light microscopy features 10-14 days after an MI? (2)

A

Well established granulation tissue with blood vessels and collagen deposition

34
Q

What are the light microscopy features 2-8 weeks after an MI? (2)

A
  • Increased collagen deposition

- Decreased cellularity

35
Q

What are the light microscopy features 12-24 hours after an MI? (5)

A
  • Ongoing coagulation necrosis
  • Nuclei pyknosis (chromatin condensation)
  • Mycocyte hypereoisophilia
  • Marginal contraction band necrosis
  • Early neutrophilic infiltrate
36
Q

What are the light microscopy features more than 2 months after an MI? (2)

A

Dense collagenous scar

37
Q

Summarise how heart tissue changes afer an MI microscopically (3)

A
  • 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
Q

What are the 2 types of treatment for an MI?

A
  • Medical therapy

- Revascularisation

39
Q

What are the 2 types of revascularisation treatment for an MI?

A
  • Percutaenous coronary intervention (PCI)

- Coronary artery bypass graft (CABG)

40
Q

When is PCI used as a revascularisation treatment for an MI? (2)

A
  • Localised obstruction

- Expand blood vessel to repurfuse specific damaged area

41
Q

What happens in PCI? (3)

A
  • Stent inserted into vessel
  • Guided into coronary artery with wire
  • Progressively expanded to full size with balloon inserted with catheter
42
Q

When is CABG used as a revascularisation treatment for an MI? (2)

A

Widespread coronary disease - multiple areas of obstruction affecting different coronary arteries

43
Q

What does a CABG involve? (2)

A
  • Bypass area of obstruction by making connection between subclavian artery and aorta
  • With stem from saphenous vein/mammary artery/intercostal artery
44
Q

Where is the stem for a CABG taken from? (3)

A
  • Saphenous vein
  • Mammary artery
  • Intercostal artery
45
Q

What is a common complication of CABG? (2)

A
  • Atherosclerosis building up in bypass graft

- Vein not adapted to increased pressure in arterial system

46
Q

How can repurfusion cause more damage than the original obstruction? (2)

A
  • Limits necrosis area

- But causes shock to issue as was limited in perfusion so has accumulated metabolites

47
Q

When must restoration of coronary flow occur to salavage ischaemic myocardium and prevent all necrosis?

A

15-20 mins

48
Q

What occurs in lethally injured cells on repurfusion?

A

Contraction bands

49
Q

How can reperfusion lead to a lack of reflow? (7)

A
  • Leukocytes in reperfused blood
  • Myocytes apoptosis
  • Microvascular injury
  • Haemorrhage
  • Endothelial swelling
  • Occludes capillaries
  • Prevents local repurfusion = no flow
50
Q

What used to be as cardiac biomarkers but have found to be non specific? (3)

A
  • Creatinine kinase MB (CK-MB)
  • Aspatate transaminase (AST)
  • Lactate dehydrogenase (LDH)
51
Q

What biomarkers are most specific to cardiac muscle damage? And which isomer is the most common? (2)

A
  • Troponin T (most common)

- Troponin I

52
Q

What is CK-MB? How is it different to (2) CK?

A
  • CK = rhambdomyolysis = skeletal muscle damage

- CK-MB = iso-enzyme specific to cardiac muscle damage

53
Q

What is the advantage to using troponin over CK-MB as a cardiac biomarker?

A
  • 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
Q

How is tropononin used as a cardiac biomarker?

A

Specific to heart, detected in blood after myocardial injury

55
Q

Why is troponin alone not enough to diagnose an MI?

A

Not specific to ischaemia e.g can be due to blood trauma, physical damage to heart

56
Q

What are the similarities between a STEMI and nSTEMI in terms of diagnosis? (4)

A
  • 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
Q

What are the differences between a STEMI and nSTEM? (4)

A
  • 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
Q

What is the difference between stable angina and ACS? (6)

A
  • 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
Q

What are the disadvantages of using high sensitivity troponin? (2)

A
  • More sensitive = picks up smaller damages to heart
  • But less specific = misdiagnosing small damages as something serious
  • More interventions - NHS on budget
60
Q

What is infarction?

A

Tissue death (necrosis) due to insufficient blood supply (ischaemia)

Cardiology (18 decks)

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