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3.23 > Lecture 12: Acute Myocardial Infarction > Flashcards

Lecture 12: Acute Myocardial Infarction Flashcards

1
Q

What is myocardial infarction?

A

The interuption of blood supply to part of the heart, causing some heart cells to die

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2
Q

Where do thrombus form?

A

At the site of an atherosclerotic lesion, obstructing blood flow to the myocardial tissues

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3
Q

What can provide resistance to rupture?

A

Presence of smooth muscle cells in fibrous cap

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4
Q

What plaques are rupture prone?

A

Plaques rich in soft extracellular lipids

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5
Q

What is the triggering mechanism for the development of thrombus in patients with myocardial infarction?

A

Plaque rupture

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6
Q

What is infarct expansion?

A

A disproportionate thinning and dilation of the infarct zone

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7
Q

What is ventrical remodelling?

A

A disproportionate thinning and dilation of the ventricle resulting in an enlarged heart

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8
Q

What are the cellular changes associated with the initial myocardial infarction?

A
  • The development of infarct extension
  • Infarct expansion
  • Ventricular remodelling
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9
Q

What is a NSTEMI?

A

A complete occlusion of a minor coronary artery or a partial occlusion of a major coronary artery previously by atheroclosis.

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10
Q

What does a NSTEMI cause?

A

Causes a partial thickness damage of heart muscle

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11
Q

What is STEMI?

A

Occurs by developing a complete occlusion of a major coronary artery previeoisly affected by atherosclerosis

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12
Q

What does a STEMI cause?

A

Full thickness damage of heart muscle

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13
Q

What are the symptoms of myocardial infarction? (5)

A
  • Chest pain
  • Nausea
  • Vomiting
  • Sweating
  • Pain can radiate to neck, jaw, left arm, back
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14
Q

How do patients describe myocardial infarction?

A
  • Squeezing
  • Smothering
  • Choking sensations
  • Someone sitting on their chest
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15
Q

Is pain of myocardial infarction relieved by rest and sublingual GTN?

A

No

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16
Q

What causes GI complaints from myocardial infarction?

A

Due to sensitivity of pain and resulting vagal stimulation

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17
Q

How is acute MI diagnosed?

A
  • Biochemical markers
  • Laboratory tests
  • ECG
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18
Q

What are the biochemical markers used to diagnose MI

A
  • Rise and fall in troponin
  • Rapid rise and fall in creatine kinase
19
Q

What laboratory tests are used to diagnose MI?

A
  • Troponin I levels
20
Q

What is troponin?

A

Troponin T and I are components of the myofilament troponin complex. Released from damage

21
Q

Describe troponin I levels during a myocardial infarction

A
  • Rise in 3 hours
  • Peak at 14 to 18 hours
  • Remain elevated for 5-7 days
22
Q

Describe troponin T levels during MI

A

Rise in 3-5 hours and stay elevated for 10-14 days

23
Q

What are the iso forms of creatine kinase?

A
  • CK MB1
  • CK MB2
24
Q

Where is CK MB1 found?

A

Plasma

25
Q

Where is CK MB2 found?

A

Tissues

26
Q

When does CK-MB appear in the serum?

A

6-12 hours

27
Q

When does CK-MB peak?

A

Between 12 and 28 hours

28
Q

When do CK-MB levels return to normal?

A

72 to 96 hours

29
Q

What is myoglobin?

A

Oxygen binding protein

30
Q

Where is myoglobin found?

A

Skeletal and cardiac muscle

31
Q

When do myoglobin levels elevate?

A

Within 1-2 hours of MI

32
Q

When do myoglobin levels peak?

A

3-15 hours

33
Q

What is lactate dehydrogenase LDH?

A

A tetrametric protein, made up of two types of proteins

34
Q

What happens to LDH during MI?

A

Levels elevate

35
Q

Describe ECG during the early stage of MI?

A
  • T waves become tall and narrow
  • This stage is referred to as hyper-acute or peaked T waves
36
Q

What happens to the ST segment of an ECG during MI?

A

ST levels elevate

37
Q

What do Q waves represent?

A

Flow of electrical forces towards the septum

38
Q

What can a persistent elevation of ST segment indicate?

A

Presence of a ventricular aneurysm

39
Q

What will always indicate previous myocardial infarction

A

Q waves - they never disappear

40
Q

How does myocardial ischaemia affect ECG?

A
  • ST segment depression
  • With or without T wave inversion as result of altered reploarizarion
41
Q

How does myocardial injury affect ECG?

A

Causes ST segment elevation with or without loss of R wave

42
Q

How does myocardial infarction affect ECG?

A

Causes deep Q waves of absence of depolarization current from dead tissue and receding currents from opposite side of heart

43
Q

How long do Q waves take to develop?

A

Hours to days

44
Q

What do Q waves show?

A

Presence of dead tissue and provide ECG evidence of a previous MI

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