206 - MI Flashcards

1
Q

What part of the heart do leads II, III, aVF show?

A

Inferior surface

Mainly L ventrical

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2
Q

What part of the heart do leads I and aVL show?

A

Lateral wall

  • L Ventrical
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3
Q

What part of the heart do leads V1- V6 show?

A

Anteroseptal - lateral surface

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4
Q

What part of the heart do V1 and V2 show?

A

Anteroseptal

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5
Q

What part of the heart do V3 and V4 show?

A

Apex / anterior inferior surface

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6
Q

What part of the heart do V5 and V6 show?

A

Lateral wall

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7
Q

What does this ECG show?

A

Inferior STEMI (II, III, aVF)

with reciprical changes

eg. R coronary artery occlusion

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8
Q

What does this ECG show?

A

STEMI - V1, V2, V3, V4

Inverted T wave -> hours post MI

eg. L anterior decending artery

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9
Q

What does this ECG show?

A

STEMI II, III, aVF

Inferior leads

? V2 in mirror -> ? posterior infarct too

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10
Q

What does this ECG show?

A

Atrial Fibrillation

+ Tenting of T waves V2, V3

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11
Q

What does this ECG show?

A

STEMI - V2, V3, V4

+ Pathological Q waves in V2, V3, shows heart attack days ago, so if not in pain no intervention, he has had and survived MI.

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12
Q

What does this ECG show?

A

Tombstoning - STEMI V2, V3

Large anterior MI

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13
Q

What does this ECG show?

A

nSTEMI

ST depression in V2, V3, V4, V5, V6

Medical mamagement

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14
Q

This ECG is of a young, fit person with a fever. What could it show?

A

ST elevation V2-V6

Acute pericarditis

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15
Q

What is the difference between ischaemia and infarction?

A

Ischaemia - Reversible, no harm done

Infarction - irreversible, cell death, troponin release

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16
Q

What 3 things are used to diagnose an MI?

A

Myocardial pain

ECG alteration

Troponin T levels

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17
Q

What signs can be seen in an MI?

A

Sweating, anxiety, pale, high HR, high BP

or sometimes excessive parasympathetic tone - bradycardia, low BP, nausea, belching

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18
Q

What signs could suggest a severe MI?

A

Impaired LV function - crackles in lung, murmur - 3rd heart sound

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19
Q

There are many differentials for chest pain, what are some?

A

Resp - PE, pneumothorax, plurisy

MSK - chostochondritis, fracture, nerve compression

GI - Oseophagitis, spasm , rupture

Vascular - Aortic dissection

Cardiac - Angina, Pericarditis

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20
Q

What may you see on an ECG of a suspected MI?

A

Dynamic ST segment change

Evidence of previous MI (Q wave, ST depression)

Arrythmias

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21
Q

Describe the dynamic ST changes you may see in an MI

A

1st - loss of clear ST segment

2nd - ST elevation

3rd - development of Q waves

4th - ST depression - later stage/incomplete occlusion

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22
Q

Why are troponin levels used?

A

A marker for myocardial damage

  • higher trop = bigger infarct
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23
Q

What are the limiting factors of using troponin?

A

Might not elevate until 4-6hrs after MI

Highest levels 1 day later - so retrospective diagnosis?

Not cardiac specific:

renal dysfunction

PE

Arrythmias

Hypertensive crisis

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24
Q

What is the immediate management of an MI?

A

MONAC

Morphine

O2

Nitrates

Aspirin

Clopidogrel

25
Q

How can coronary blood flow be restored post MI?

A

STEMI - reperfusion therapy - PCI (primary angioplasty) or Throbolytic therapy

Nitrates

Elective angioplasty/CABG

26
Q

What are the MI5 drugs given post MI?

A

Aspirin

Clopidogrel

Beta Blocker - metoprolol

ACE inhibitor - ramipril

Statin - atorvostatin

27
Q

Platelet activation involves many pathways - name 5 things/molecules that initiate platelet activation

A

ADP

Thrombin

Collagen

Adrenaline

Thomboxane

28
Q

How does Aspirin work as an antiplatelet?

A

Permenant acylation of COX in platelets which stops thromboxane A2 synthesis - reduced activation

29
Q

How does clopidogrel work as an antiplatelet?

A

Irreversible blocks ADP receptor - inhibits ADP dependant activation

30
Q

Why does clopidogrel not work in all people?

A

It is a prodrug, needs cytrochrome P-450 to work

Genetic deficiencies exist

31
Q

How does presugrel work as a antiplatelet?

A

Similar to clopidogrel - blocks ADP receptor

Stronger effect - more prolonged

Higher risk of bleeding

needs hepatic activation

32
Q

How does ticagrelor work as an antiplatelet?

A

Similar to clopidogrel

Reversibly blocks ADP receptor

Not a prodrug

No higher bleeding risk - good

33
Q

How does dipyridomole work as an antiplatelet?

A

Reversibly binds to platelet phosphodiesterase - so increases cAMP concentration - reduced activity

34
Q

What 3 antiplatelets act directly on the fibrinogen/CPIIbIIIa receptor?

A

Abciximab (Reo-pro)

Eptitibratide

Tirofiban

35
Q

What is an atheroma?

A

Degredation of walls of the arteries due to formation of fatty plaques and scar tissue - predisposes the artery to thrombosis

36
Q

Where do atheromas usually form?

A

Elastic arteries

  • large and medium sized
  • not in veins (too low presure)
37
Q

Describe the structure of a atheromatous plaque

A

Cap - connective tissue, lots of collagen and preoteoglycans, fibronectin and elastic fibres

Core - made up of extracellular lipid and macrophages, smooth muscle cells, T lymphocytes and dendritic cells

38
Q

What thrombogenic substances are found in an atheromatous plaque?

A

Fibrin and platelets

39
Q

The hallmark of atheromatous disease is ………?

A

Endothelial dysfunction

40
Q

What do the endothelial cells of a plaque produce?

A

Nitric oxide

  • has anti-atherogenic actions
  • inhibits WBC adhesion
  • promotes macrophage apoptosis
  • inhibits lipid oxidation
41
Q

What do the inflammatory cells in a plaque produce?

A

Cytokines

Growth factors

Metalloprotienases

42
Q

What do vascular smooth muscle cells in a plaque produce?

A

Proteinases

growth factors

collagen

elastin

  • their role becomes reparative rather than contractile
43
Q

What occurs when an atheromatous plaque ruptures?

A

The subendothelial collahen is exposed

This activates a coagulation cascade via intrinsic and extrinic pathways

Cross linking of platelets by fibrin

Plaque englarges, can cause thrombosis…

44
Q

As what do lipids and cholesterol travel in the blood as?

A

Lipoprotein

45
Q

What influences a lipoproeitns role in metabolism?

A

The density of lipid and proetin making it up

46
Q

What are chylomicrons?

A

How FA and cholesterol are carried from the SI and absorbed into the lymphatics

47
Q

Where are FAs aborbed into as they enter the blood stream from the lymphatics

A

Muscles

fat cells

Liver

48
Q

In the liver, unburnt food metabolites (FA + cholesterol) are converted into what substances?

A

VLDL - IDL + LDL

HDL

49
Q

What are VLDLs and what happens to them?

A

Very Low density lipoproteins

Secreted into plasma

Then converted into IDL - intermediate density

and LDL + fatty acids - Low density

These are then absorbed into body tissues

50
Q

What are HDLs and what happens to them?

A

High density lipoproteins

Transport cholesterol back to the liver for excretion

51
Q

Which type of lipoprotein is seen as good?

A

HDL

In health - high levels of HDL

In atheromatous disease - Low levels seen

52
Q

Which type of lipoprotein is seen as Bad cholesterol?

A

LDL

In atheroma you get many small, dense LDL particles in arteries - sdLDL

53
Q

What is the role of cholesterol in the body?

A

Needed for membranes and source of steroid hormones

BUT if high levels - plaque formation and growth - atheroscleroisis

54
Q

What is hyperlipideamia?

A

High lipid levels in the blood

55
Q

What in high levels leads to a high level of triglyceride?

A

Chylomicrons or VLDL

56
Q

What in high levels leads to an increase in cholesterol in the blood

A

LDL/IDL

57
Q

What classification can be used to measure hyperlipidaemia?

A

Fredrickson classification

Used to use: Average overnight serum

58
Q

What is high in FH: Familial hypercholesterolaemia?

A

High LDL levels

But triglyceride levels normal