L48 – Myocardial Ischaemia Flashcards Preview

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Flashcards in L48 – Myocardial Ischaemia Deck (49):
1

Anatomy of the myocardium.
Describe cardiac muscle cells? (B,A,S)

Branching
Anastamosing
Striated

2

Compare the amount of mitochondria in cardiac muscle cell vs skeletal muscle. Why?

Contain 10x more mitochondria per muscle cell than skeletal muscles

extremely dependent on aerobic metabolism > need
constant supply of a lot of energy

3

How do coronary arteries penetrate myocardium?

arise from aorta > runs
epicardially > branches penetrate myocardium as
intramural arteries

4

During which phase of the cardiac cycle does blood flow to myocardium?

Blood flow to myocardium occurs only during ventricular diastole:

When microcirculation in myocardium not compressed by cardiac contraction

5

How does elevated HR protect the heart from overworking?

Faster heart rate > shorter diastolic time (needs more
blood supply for oxygen, energy; but actually getting less) > stops heart from overworking

6

Which part of endocardium has limited supply?

endocardium in direct contact with oxygenated blood in left ventricle

7

Branches of Left coronary artery?

Left marginal, Left circumflex, Left anterior descending (LAD)

8

Branches of Right coronary artery?

Right marginal, Posterior interventricular Artery, Sinoatrial nodal artery

9

What structures do Left anterior descending artery supply?

 Most of heart apex
 Anterior wall of left ventricle
 Anterior 2/3 of ventricular septum

10

What structure does Left circumflex supply?

Lateral wall of LV

11

What structures does right coronary artery (dominant) supply?

 Right ventricle
 Posterior 1/3 of ventricular septum
 Posterior-basal wall of left ventricle

12

What method is used to detect which CA is blocked in heart?

Angiogram

13

Define Ischaemic heart disease (IHD)?

a group of closely-related syndromes that result from myocardial ischaemia

14

What is the most likely cause of IHD?

Due to Coronary obstruction > reduction in coronary blood supply

15

What classifies as coronary obstruction?

One or more leasions that causes at least 75% reduction of cross sectional area of at least one of the major epicardial arteries

16

What is the effect of ischaemia on myocytes within seconds of MI?

Onset of ATP depletion

17

What is the effect of ischaemia on myocytes within minutes of MI?

<2 mins = loss of contractility

continuous reduction of ATP

Irreversible damage within 20-40 mins

18

What is the effect of ischaemia on myocytes after one hour of MI?

Microvascular injury (capillary network in heart is damaged)

19

How does MI change the rhythm of heart beat within minutes?

1) Cardiac arrhythmias

2) Asystole (heart ceases to beat)/ ventricular fibrillation

20

How does MI cause contractile dysfunction in heart?

myocytes cannot successfully compensate lack of O2 > dead myocytes cannot conduct electrical impulses / lead to short-circuiting > contractile dysfunction

21

What is angina pectoris caused by?

symptom complex caused by transient myocardial ischaemia

22

Does Angina pectoris classify as MI?

Angina pectoris does not induce cellular necrosis > not defined as MI

23

What is stable angina?

Chronic stenosing coronary atherosclerosis (Fixed coronary obstruction) becoming critical > leave heart vulnerable to increased demand

24

What is stable angina typically relieved by>?

Rest

Vasodilator

25

What is unstable angina?

Pain occurs with progressively
increasing frequency

Tends to be more prolonged

26

What is unstable angina associated with?

Disruption of previously stenosing atherosclerotic plaque

Superimposed thrombosis, Embolism or Spasm

Predictor of MI

27

What 3 processes can lead to disruption of atherosclerotic plaque?

Hemorrhage into atheroma > expand plaque volume

Rupture / Fissure
or
Erosion / Ulceration

> Expose thrombogenic plaque constituents

28

What is the difference in coronary obstruction between stable angina and chronic IHD?

Stable angina = fixed coronary obstruction

Chronic IHD = SEVERE fixed coronary obstruction

29

What is the difference in coronary obstruction between unstable angina and acute transmural MI?

Unstable angina: Mural thrombus with variable obstruction

Acute transmural MI: Occlusive thrombus

30

How does vasoconstriction contribute to plaque fracture?

Increase local mechanical forces > contribute to plaque fracture

31

What is vasoconstriction stimulated by?

1) Circulating adrenal agonist
2) Locally-released platelet contents
3) Impaired secretion of endothelial cells relaxing factors
4) Mediators released from pervascular inflammatory cells

32

What is the clinical manifestation of angina pectoris progressing to sudden cardiac death?

Angina pectoris (stable or stable > unstable) > MI > either Chronic myocardial ischaemia or sudden death

33

What are the biomarkers of MI?

Lactate dehydrogenase (LDH)

Creatine kinase + isoenzymes (CK, CK-MB)

Troponin I & T

Myoglobin

Aspartate aminotransferase (AST)

34

What ECG changes can be observed in MI?

ST elevation (in STEMI )
T wave inversion
Enlarged Q wave

35

Apart from angiogram, ECG, what other diagnostic tools are there for MI?

MRI, Radioistope studies
Cardiac catheterisation
Echocardiogram

36

What does Echocardiogram visualise?

Non-contracting part of ventricular wall + Ejection fraction in ventricle

37

Which 2 diagnostic tools are not used in acute MI?

MRI
Radioisotope studies

38

What is the extent of ischaemic necrosis in Transmural infarction?

Involves (nearly) full thickness of ventricular wall

39

What is the extent of ischaemic necrosis in Subendocardial infarction?

Limited to inner 1/3 - 1/2 of ventricular wall
(most distant from blood supply)

Recall: dominant artery gives rise to posterior
descending branch (i.e. supplies the posterior
1/3 of interventricular septum)

40

Compare the perfusion territory affected by transmural vs subendocardial infarction?

Transmural = perfusion territory in distribution of single coronary artery

Subendocardial = May extend laterally beyond perfusion territory of single coronary artery

41

What is transmural infarction caused by?

Chronic coronary atherosclerosis
> Acute plaque change
> Superimposed completely obstructive thrombosis

42

What is subendocardial infarction caused by?

Diffuse stenosing coronary atherosclerosis

43

How is MI caused in patients with normal coronary arterial supply? (uncommon)

Increased HR or increased heart size

> increased demand of energy from heart

44

What causes increased HR?

 Thyrotoxicosis > increased metabolic state
 Stress, anxiety states (shock)

45

How does chronic hypertension lead to change in heart size?

chronic hypertension (heart needs to work against higher pressure) > cardiomegaly, cardiomyopathies > hypertrophy

46

How does myocardial rupture arise from MI?

Infarct > zone of necrosis extends > replaced by dense collagenous/ fibrous scar > weakened myocardial wall bulges out > rupture

47

What are 3 distinctive microscopic changes oberved in MI 4-12 hours after?

 Early coagulative necrosis
 Oedema
 Haemorrhage

48

What are 3 distinctive microscopic changes oberved in MI 12-24 hours after?

 Pyknosis of nuclei (dense haematoxylinophilic mass of chromatin)
 Hypereosinophilia (different staining property: opaque “tombstone”)
 Early neutrophilic infiltrate

49

What are 2 distinctive microscopic changes oberved in MI 1-3 days after?

Coagulative necrosis

Dead tissue is yellow, firm, dull (fibrin, denatured cellular protein
(structural, enzymatic) block proteolysis of cell)

Interstitial infiltration of neutrophils (react to cellular death)

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