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LC Cardiology Week 5 > Heart Attack > Flashcards

Heart Attack Flashcards

1
Q

Describe roughly chronic stable angina?

A

Fixed stenosis of the vessel
Causing demand led ischaemia
Predictable and relatively safe

Stop, sit down (reduces CO) and use spray (improves coronary perfusion)

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2
Q

What is typical anginal pain?

A

Vague area over breastbone radiating down the arm

Heavy feeling
Weight on the chest
Pressure tightness

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3
Q

What is acute coronary syndrome?

A

Any acute presentation of coronary artery disease

Only a provisional diagnosis that covers a spectrum of conditions.

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4
Q

Describe the rough pathogenesis of acute coronary syndromes?

A 
Normal 
Fatty streak 
Atherosclerotic plaque 
Fibrous plaque 
Plaque rupture/fissure + thrombosis
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5
Q

What is Plaque rupture/fissure + thrombosis usually associated with?

A

ACS

  • unstable angina
  • MI
  • Sudden cardiac death
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6
Q

Roughly describe acute coronary syndromes ( unstable angina/MI)

A

Dynamic stenosis - an obstruction suddenly develops

Supply let ischaemia which is unpredictable and dangerous

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7
Q

What is the main pathogenesis of ACS?

A

Spontaneous plaque rupture

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8
Q

What are some of the factors affecting plaque rupture/fissure?

A

Lipid content of plaque
Thickness of fibrous camp
Sudden changes in intraluminal pressure or tone
Bending/twisting of arteries during contraction
Plaque share
Mechanical injury

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9
Q

What happens in PCI - in terms of the vessel wall damage?

A

A metal stent is fitted under high pressure
This disrupts the vessel wall and established the lumen
The vessel wall damage leads to exposed tissue elements (collagen and vWF)
Platelets react to these factors
They form a monolayer, starting the activation process and undergo a conformational change which encourages platelet clumping

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10
Q

What happens next in the platelet cascade - release of activators?

A

Platelets when activated release ADP ( from granules in the platelets) and thromboxane A2 (from cycloxygenase)
These bind to the platelets via receptors
Induces the conformational change
The platelet activation accelerates causing platelet aggregation
Inflammation is also set up - leukocytes are involved
Clotting network then forms the fibrin rich thrombus and blood clot

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11
Q

What happens in unstable plaque - in terms of platelets etc?

A

The plaque ruptures
Platelets react
Form a clump which further reduces the luminal AP causing restricted blood flow leading to ACS.

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12
Q

Briefly summaries the central pathway to platelet aggregation?

A

Activation
Activator release –> Aggregation –> Inflammation
Vascular blockage
Acute MI, stoke or death

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13
Q

What is management of ACS focused on?

A

Damping down the activation of platelets

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14
Q

What happens to the heart after an acute infarct if the patient survives?

A

The tissue downstream will die due to the blockage, leading to the acute infarct.
There will be scarring, loss of muscular function and dilatation.
Leading to a progressive reduction in blood that can be pumped by the centric;e
Eventually leading to cardiac failure

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15
Q

What would be a history diagnosis of STEMI?

A

Central crushing chest pain
Radiating to arm and jaw (left)
Like angina, but worse and not relieved by GTN
Nausea, sweating, vomitting

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16
Q

What would you look for on an ECG in a STEMI?

A

ST elevation

T wave inversion and Q waves

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17
Q

What are the values for ST elevation for diagnosis of a STEMI?

A 
>= to 1mm of ST elevation in 2 adjacent limb leads 
>= 2mm of ST elevation in 2 contiguous precordial leads

New onset of LEFT bundle branch block (hard to tell on ECG if new onset, so chest pain in the history is CRUCIAL to diagnosis)

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18
Q

What is the sign of a previous MI?

A

Q waves

+/- T wave inversion

19
Q

(?) What leads are inferior?

A

2, 3 AVF

20
Q

(?) What leads are anterior?

A

V3,4

21
Q

(?) What leads are septal?

A

V1,2

22
Q

(?) What leads are lateral?

A

1, AVL, V5,6

23
Q

Describe cardiac enzymes and protein markers in diagnosis of MI?

A

May be normal at presentation

May not have time to wait for results in STEMI

24
Q

Describe the cardiac enzyme CK?

A

Creatinine kinase
Peaks in 24h
Also in skeletal muscle and brain

Not used so much

An elevated level of creatine kinase is seen in heart attacks, when the heart muscle is damaged, or in conditions that produce damage to the skeletal muscles or brain

25
Q

Describe the protein marker Tn?

A

Troponin
Highly specific for cardiac muscle damage
Can detect tiny amounts of myocardial necrosis

Used most commonly

26
Q

What does the early treatment of STEMI include?

A

Trying to dampen down platelet activation
Do this by blocking the ADP receptors and the cyclooxyrgenase cycle

Aspirin = ADP receptor blockage 
Clipodogrel = Cyclooxygenase
27
Q

What should you treat patients with ASC with immediately?

A

300mg of aspirin

28
Q

What should you treat patients with ECG changes or cardiac marker changes with?

A

300mg Aspirin

300mg Clopidogrel

29
Q

What is the aim of thrombolysis?

A

to break down the clot and re establish the blood flow

30
Q

What do fibronlytic agents do?

Give an example

A

the break down the fibrin inside the clot itself but not the thrombus, therefore leaving the contents of the thrombus active

Example is streptokinase

31
Q

What is an example of a thrombolytic drug?

A

(Heparin)

32
Q

Describe the treatment of STEMI?

A 
M - diamorphine + anti emetic 
O - oxygen (if hypoxic)
N - GTN (if BP >90mmHg (not clinically shocked))
A - aspirin (300mg)
\+
C - clopidogrel (300mg)
33
Q

What are the conditions for PCI in STEMI?

A

PCI - if within 40mins of PCI lab

Thrombolysis otherwise

34
Q

What are the complications of an acute MI?

A

Death
Arrhythmias - ventricular fibrillation
Structure complications
Functional complications

35
Q

Describe arrhythmias in terms of a complication of MI?

A

Ventricular fibrillation is the most common arrhythmia post MI

Disorganised, dangerous and life threatening, reduces CO and can cause cardiac arrest

36
Q

Describe structural complications in terms of a complication of MI?

A 
Cardiac rupture 
VSD 
Mitral valve regurgitation 
LV aneurysm formation 
Mural thrombus +/- systemic emboli 
Inflammation 
Acute pericarditis
37
Q

Describe functional complications in terms of a complication of MI?

A

Acute ventricular failure - L, R and both
Chronic cardiac failure
Cariogenic shock

38
Q

What is the difference between a STEMI and NSTEMI?

A 
STEMI = due to complete blockage of the coronary artery 
NSTEMI = coronary artery partially blocked and there is severe reduced blood flow
39
Q

What might you see on an ECG in NSTEMI?

A

Might be normal
May see ST depression
May see T wave inversion

40
Q

What is troponin?

A

Protein on the actin and myosin chain helps muscles contract

41
Q

Describe how measuring troponin tells you about the myocardial cell damage?

A

Clots are broken down and the emboli are sent downstream to clog up the micro vessels and they nip off small and isolated pockets of myocytes - this myocyte damage be detected

42
Q

If there is troponin increased in the body but no history of acute chest pain is it an MI?

A

No, likely to be another cause such as CCF, renal failure, Sepsis, PE, stroke

43
Q

What should be the goal in treating a NSTEMI?

A

Blocking the activation of factor 10 to factor 10a. This prevents clotting which prevents an NSTEMI going to a STEMI

44
Q

What other treatment options are there for NSTEMI?

A

They should undergo early coronary angiography

  • looking for partially stenosed arteries to then perform a balloon or stent

LC Cardiology Week 5 (2 decks)

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