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Y1 Cardiovascular > Acute MI > Flashcards

Acute MI Flashcards

1
Q

what happens to the lumen of an artery in atherosclerosis?

A

it becomes narrowed so less blood passes through to adequately supply the heart + other organs

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2
Q

what causes chronic stable angina?

A

fixed stenosis in a coronary artery

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3
Q

when does pain from stable angina come on?

A

only when demand is put on the heart i.e. during exercise

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4
Q

what should patients do when the pain from stable angina comes on?

A

sit down and use their GTN spray

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5
Q

how does GTN spray relieve chest pain in angina?

A

lowers BP
reduces afterload
can cause vasodilation

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6
Q

is stable angina an acute coronary syndrome?

A

no

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7
Q

where does cardiac chest pain radiate?

A

down the left arm and up the jaw

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8
Q

what is an acute coronary syndrome?

A

any acute presentation of coronary artery disease

STEMI, NSTEMI, unstable angina

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9
Q

what are the two types of MI?

A

non st elevation = NSTEMI

st elevation = STEMI

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10
Q

what is the pathogenic trigger for acute MI?

A

spontaneous plaque rupture causing thrombosis, resulting in occlusion of a vessel

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11
Q

what is the response to a plaque rupture by the circulating blood?

A

the blood starts to clot as it reacts like this is a vascular injury

platelets form a monolayer over the rupture and encourage the adhesion of more and more platelets

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12
Q

what do platelets release that activates more platelets and how?

A

ADP and other activators via degranulation

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13
Q

what do activated platelets express and what does this ultimately cause?

A

they express adhesion receptors for leukocytes

this allows WBC’s to bind and the coagulation cascade starts

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14
Q

what intracellular enzyme system helps activate more platelets during clotting and how?

A

cyclooxygenase

produces thromboxane A2, which activates platelets and promotes thrombosis

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15
Q

how does aspirin stop platelet aggregation?

A

it stops the cyclooxygenase system, halting production of thromboxane A2

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16
Q

name three ADP receptor antagonists

A

clopidogrel
prasugrel
ticagrelor

17
Q

how do ADP receptor antagonists stop platelet aggregation?

A

they stop ADP binding to platelets and activating them

18
Q

describe the chest pain associated with an MI

A

severe, crushing, central chest pain

radiates to the jaws and arms (especially the LA)

19
Q

what can pain from MI often be associated with?

A

sweating

nausea and vomiting

20
Q

what ECG changes can be seen in acute STEMI?

A

ST elevation
T wave inversion
pathological Q waves

21
Q

how is ST elevation in a STEMI defined

A

> 1mm in two adjacent limb leads

>2mm in at least two contiguous precordial leads

22
Q

what may be seen on ECG if a patient has had a previous MI?

A

Q waves

T wave inversion

23
Q

ST elevation in which leads suggests an inferior MI?

A

II
III
AVF

24
Q

ST elevation in which leads suggests an anterior MI?

A

V1-V6

25
Q

what enzyme may be used as a marker for MI?

A

creatinine kinase (CK)

26
Q

what protein marker is used in MI?

A

troponin

27
Q

why is troponin a good marker for MI?

A

it is highly specific for cardiac muscle damage

28
Q

what should be given IMMEDIATELY to patients with ECG changes/elevated troponin?

A

aspirin and ticagrelor

29
Q

how should aspirin be taken in MI?

A

should be chewed to make it work faster

30
Q

what does thrombolysis do?

A

breaks up a clot

31
Q

what is the initial management of an MI?

A 
morphine + anti-emetic 
oxygen if hypoxic 
nitrate (GTN) 
aspirin 
clopidogrel etc.
32
Q

when is thrombolysis done in MI?

A

if primary angioplasty is not available in the first 120 mins

33
Q

what is PCI?

A

percutaneous coronary intervention (angioplasty)

34
Q

name an arrhythmic complication of MI

A

ventricular fibrillation

35
Q

how is ventricular fibrillation treated?

A

defibrillation

36
Q

what two types of troponin are cardiac specific?

A

T and I

Y1 Cardiovascular (22 decks)

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