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02. Cardiovascular > L35. Ischaemic Heart Disease > Flashcards

L35. Ischaemic Heart Disease Flashcards

1
Q

What is the definition of an ischaemia?

A

An imbalance between oxygen supply and demand

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2
Q

What is the difference between acute and chronic ischaemic heart disease?

A

Acute: unstable angina = MI or sudden cardiac death
Chronic: stable angina = chronic myocardial ischaemia

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3
Q

What are the four main factors limiting Coronary Blood Flow and thus Oxygenation?
Explain each factor

A
  1. Perfusion pressure: Systemic hypotension for example reduces this
  2. Coronary vascular resistance: atherosclerosis
  3. External Compression: the flow of blood/oxygenation to the heart only occurs in diastole
  4. Intrinsic Regulation: Endothelium derived factors (NO, Prostacyclin, Endothelin) and Metabolite (adenosine, lactate, hydrogen)
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4
Q

Why does perfusion/exchange to the heart only occur in diastole?

A

Because during systole (contraction) the heart muscles contract and compress the coronary vessels (which lie in the sulci of between the chambers). Thus the only times the vessels are patent (time able to conduct oxygenation) is during diastole

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5
Q

What are some examples of solid organs. Describe infarction of solid organs.

A

Solid Organs (lungs, liver, kidney, spleen)
They have a hilum and flow of blood goes in through there and spreads out from that point.
Hence when blockage occurs to these ‘end arteries’ they cause infarction to a section of solid tissue
= Wedged shaped infarction

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6
Q

What are some examples of hollow organs. Describe infarction of solid organs.

A 
Hollow Organs (heart, GIT, blood vessels)
They have a fatty external layer that contains all the vessels for the organ and flow of blood goes from outside the organ to inside it.
Hence when blockage occurs to these organs the infarction occurs on the INSIDE of the organ and spreads (because the inside is the last of the organ to receive blood from the supply).
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7
Q

Where is the most vulnerable part of the heart to infarction?

A

The SUB-ENDOTHELIUM is the first place and most vulnerable part for infarction. - because the heart is a hollow organ

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8
Q

Why is the endocardium of the heart largely spared in infarction?

A

Because it lines the inside of the chambers and hence is in constant contact with chamber blood

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9
Q

Draw the coronary arterial supply to the heart

A

Must include:

  • Left main coronary artery
  • circumflex
  • left anterior descending
  • right coronary artery
  • marginal artery
  • posterior descending artery
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10
Q

What are some general characteristics of the heart in cross section to help orientate transversly cut specimens. Draw a diagram

A

The posterior is more flatter and anterior rounder
The anterior is more fatty than the posterior
Can look at chordae tendinae direction for atria vs. ventricle

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11
Q

Describe which vessels supply which parts of the heart.

A

Left main coronary artery supplies the circumflex and the left anterior descending. Blockage here blocks both areas theses supply. Also part of the posterior descending.

  • Left anterior descending = Anterior 2/3 of the septa and the anterior wall of the heart
  • Circumflex = Anterior lateral (left) part of the heart

Right coronary artery supplies the marginal and the posterior descending

  • Right Coronary Artery = Right lateral side of the heart (RA and RV) and marginal artery
  • Marginal artery = the Inferior heart

Posterior descending artery supplies the posterior 1/3 of the septum and the posterior wall

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12
Q

What is a heart attack? What is the most common cause?

A

A myocardial infarction which is most commonly caused by an acute rupture or haemorrhage of atherosclerotic plaques = occlusive thrombus

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13
Q

What is the general step by step process of a myocardial infarction? [4 major steps]

A
  1. Necrosis
  2. Acute Inflammation
  3. Granulation Tissue
  4. Fibrosis/Scarring
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14
Q

What from the point of a blockage occurs in myocardial infarction and in what time scale? (Histologically)

A
  1. OCCLUSION: Angina and reversible injury [0-30mins]
  2. IRREVERSIBLE INJURY: [30min-2hr]
  3. COMPLICATIONS: arrhythmia and/or cardiac failure [4hours]
  4. INFARCTION: NSTEMI then to STEMI [12 hrs]
  5. NECROSIS and EARLY ACUTE INFLAMMATION [24 hrs]
  6. ACUTE INFLAMMATION: Heavy neutrophils, necrosis and pus [3 days] - peak of destruction
  7. EARLY GRANULATION TISSUE: [7 days]
    - rupture can occur in this stage
  8. LATE GRANULATION TISSUE: [8 weeks]
  9. FIBROSIS/SCARRING - healed infarction which can have its own complications
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15
Q

What happens during the reversible phase of MI?

A

No macro or microscopic changes are seen

Intracellular changes of mitochondrial swelling, myofibril relaxation = rapid loss of contractility

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16
Q

What is the major characteristic of the irreversible injury at 30mins -2 hours?

A

Disruption of the cell membranes of the cardiac muscles = leakage of cardiac proteins
Troponin (appears 3-4 hours post MI)
Creatine Kinase
… and leakage of current (ECG changes develop)

17
Q

What are the ECG changes seen?

A

ST elevation STEMI or ST depression NSTEMI

T wave insertion

18
Q

What does ST elevation suggest?

A

The infarction is Transmural and severe occlusion. The infarction is through the full thickness of the wall

19
Q

Describe the two major complications of infarction in the early stages

A

Arrhythmia due to damaged and unstable myocytes

Dyfunction with contractility leading to cardiac failure

20
Q

What is the difference between a non-transmural and a transmural infraction?

A

Non-transmural is when the infarction is transient or there is a partial obstruction leading to an infarction that is limited to the subendothelium NSTEMI

Transmural is when the blockage is severe or prolonged leading to a much larger infarction that spans an area further than the subendothelium (the full thickenss of the wall)

21
Q

What kind of necrosis occurs in MI?

A

A contraction band necrosis after about 24 hours which leads to high neutrophil infiltration leading to a mottled looking, haemorrhagic myocardium: Coagulative necrosis (ghost cells)

22
Q

What does early granulation (after about 7 days) mark? What happens in this stage?

A

The end of acute inflammation.
Macrophages dominate and ingest the debris
Fibroblasts and granulation tissue begins to appear
Angiogenesis occurs and a red rim is seen macroscropically
Collagen starts to build up - macroscopically looks gelatin like

23
Q

What are the three outcomes of this early granulation tissue stage?

A

The wall is necrotic and very weak = rupture
The Damaged wall doesn’t change = mural thrombus
Inflammation becomes too much = pericarditis

24
Q

Why is rupture of the infarct area very most likely in the early granulation stage?

A

Because collagen being laid down is yet mature and thus is weak and prone to rupture

25
Q

What are the three types of rupture than can occur following an MI?

A
  1. Rupture into the ventricular wall = blood in the pericardium. This means haemopericardium (blood in pericardium) and this pushes back on the heart = CARDIAC TAMPONADE
  2. Rupture of the paillary muscle leading to new onset murmur, mitral regurgitation and cardiac failure
  3. Rupture of the IV septum leading to a ventricular septal defect, a new onset murmur and cardiac failure
26
Q

What is important about a rupture of the papillary muscle or the IV septum?

A

It can lead to acute, severe cardiac failure or CARDIOGENIC SHOCK

27
Q

What are the features of late granulation tissue?

A

Occuring after 8 weeks
Loss of the cellularily and vascularity of the granulation tissue
Large increase in collagen (with interspersed fibroblasts). This gets stronger and becomes more fixed in position

28
Q

What is a major problem that can occur when collagen is laid down?

A

The flexibility of the wall may stretch out under the pressures generated by the heart leading it to thin and cause an aneurysm and may cause a mural thrombus (thrombus in the wall)

29
Q

What are the complications of the fibrous scar?

A

Arrhythmia due to islands of isolated myocytes
Cardiac failure due to remodelled LV or decompensation
Aneurysm/Mural Thrombus (due to static blood) which doesn’t regress and may increase in size

30
Q

What are some other causes of MI (other than atherosclerotic narrowing)

A

Coronary artery disease, thrombosis due to vasculitis (inflammation), thromboembolism from the heart (very rare)

Also Reduced flow or oxygenation to the heart in general:
Hypotension (shock), hypoxaemia, very rapid tachycardia (not enough time spent in diastole for patent vessels)

31
Q

What is angina?

A

A transient ischaemia with chest pain with NO cell death or necrosis

32
Q

What is the difference between stable and unstable angina?

A

Stable is a chest pain (that can occur multiple times) and occurs with exertion. It is due to atherosclerotic narrowing of a vessel

Unstable is a a chest pain occurs either at rest or upon exertion. And occurs with an unreliable pattern. It is often caused by an acute plaque event with coronary artery thrombosis that resolves WITHOUT permanent damage

33
Q

What is a chronic MI?

A

An ongoing, atherosclerotic narowing if the vessels which causes small patches or areas of subendothelial ischaemia due to patchy myocyte necrosis and replacement by fibrosis

34
Q

Does chronic MI have a smaller or larger risk of cardiac failure and arrhythmia compared to acute MI?

A

It has a similar risk

35
Q

What is sudden cardiac death?

A

An unexpected, cardiac related death within a short time period when the person has no previous diagnosis of a fatal condition.

36
Q

What are the majority of cases of Sudden Cardiac Death due to?

A

Ischaemic Heart Disease: First Presentation, which is frequently an early arrhythmic event or can be due to a silent MI.
Can be due to Marfan’s syndrome and others in young children

02. Cardiovascular (43 decks)

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