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Cardio Path > Myocardial Infarction > Flashcards

Myocardial Infarction Flashcards

0
Q

What is the most common cause of death in adults?
Age?
What age is the no. of men and women equal for MI?
What percentage of MIs are unrecognised?

A

MI @ adults
40–65 years
>65 years men = women phone number + risk
25% of acute MI = recognised

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1
Q

Histologically what is the myocardial infarction

A

Necrosis of cardiac myocytes

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2
Q

Explain pathophysiology of MI

A

CA atheromatous plaque = disrupted –>

Subendothelial collagen + thrombogenic necrotic material exposed – >

Platelets adhere to expose material – >

form occlusive platelet thrombus –>

release ThxA2 (vasoconstrictor+spasm) = platelet aggregation --> complete occlusion = 
Necrosis with thrombosis
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3
Q

Causes of MI?

A

DisCo VET

Dissection of blood in to CA wall
Cocaine
Vasculitis, Embolisation, Thrombosis syndrome

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4
Q

What are the types of MIs

A

STEMI - transmural full thickness wall necrosis
new Q-waves

NonSTEMI - subendocardial inner 1/3 myocardium Ischaemia < 50% wall –
No Q-waves

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5
Q

Explain the symptoms you get with acute MI

A

Pain = Crushing retrosternal/ Left arm/ Jaw> 20 mins

Diaphoresis
Dyspnoea – heart not pump well –> pulmonary congestion/Edema

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6
Q

Explain the timeframes for MI

A

0–4 hrs
4–12 hrs
12–24 hrs

1–3 days
3-14 days
14+days

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7
Q

Explain what happens in 0 to 4 hours in terms of:

gross appearance, light microscopy, complications

A

Nothing, nothing,

Cardiogenic shock - ⬇️ blood flow

Heart fail = blood back up + not pump forward = ⬇️EF

Arrhythmia - Damage conducting system
Ventricular premature contraction = most common
MOST important cause of death BEFORE reach hospital - @ first few days

Death

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8
Q

Explain what happens in 4 to 12 hours in terms of:

gross appearance, light microscopy, complications

A

dark MOTTLING + pale with tetrazolium stain

Wavy fibres
Edema
Necrotic cell contents release into blood
Coagulative necrosis
Haemorrhage

Complications = CHADS

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9
Q

Explain what happens in 12 - 24 hrs in terms of:

gross appearance, light microscopy, complications

A

dark MOTTLING + pale with tetrazolium stain

Neutrophils migrate
Reperfusion injury – > free radical damage – > contraction bands

CHAD

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10
Q

Explain what happens in 1 - 3 days in terms of:

gross appearance, light microscopy, complications

A

Yellow pallor + hyperaemia

Coagulative necrosis extensive
Tissue around infarct = AI + neutrophils

Fibrinous pericarditis – Friction Rub
@Transmural infarction neutrophils arrive + inflame wall – > ⬆️ VESSEL PERM. –>
ACUTE inflammatory exudate go into pericardial pericarditis –> auscultate –> PREcordial friction rub

Relieved by leaning forward
Worse by leaning backwards

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11
Q

Explain what happens in 3 - 14 days in terms of:

gross appearance, light microscopy, complications

A

Red hyperaemic border
Central yellow brown softening
@Day 10 = maximally yellow + soft

Macrophages + granulation tissue

MaP|L|PaT

Macrophage mediated degradation/LAD block –>
IVS rupture –> (L –> R shunt)

Pseudoaneurysm LV = mural thrombus plug hole in myocardium = timebomb –> ⬇️CO, Arrythmia, EMBOLUS = greatest risk post MI

RCA+ LAD block – >
(Papillary muscle rupture – >mitral regurg+LHF)
(Free ANT wall ruptured – >Tamponade)
Respectively

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12
Q

Explain what happens in 14+ days in terms of:

gross appearance, light microscopy, complications

A

Gross = Recanalised artery + grey-white

Microscopy = Contracted scar fibrosis

White scar = WEAK –> TCW

  1. True aneurysm dilation of vent. wall -> bulge out @ contraction -> DYSKINESIA + ant chest wall move
  2. ⬇️contractile tissue –> systolic HF
  3. ⬇wall ️movement –> stasis along wall –> mural thrombus along scar = embolise

TRANSMURAL infarction – >
pericardium inflammation = Pericarditis – >
expose pericardial antigens to immune system –>

6–8 weeks from Ab against pericardium = AUTOIMMUNE pericarditis - Dressler syndrome HSR2 –> Auscultate –> PREcordial friction rub

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13
Q

Explain the progression from subendocardial to transmural necrosis

A

Less than 50% of my cardio fitness necrosis ST depression – >

ISCHEMIA CONTINUE–>

full thickness transmural necrosis = ST segment elevate

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14
Q

Explain how the cardiac enzymes leak out

A

Irreversible cell damage – >membrane damage – >

Enzymes @ myocytes leak out –>

Troponin I + T
CK-MB

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15
Q

Explain the timings for troponin + CKMB

A

Troponin @ heart
Rise 2–4 hours after infarct
Return to normal after 7–10 days

CK – MB = recurrence @ heart + skel. muscle
Rise 4–6 hours after infarct
Return to normal after 72 hours

BOTH PEAK @ 24 hrs

16
Q

Patient has an MI, five days later he has another MI. What cardiac enzymes do you need to look at

A

CK – MB

17
Q

Treatment for MI

A

FAB MONA

Fibrinolysis/angioplasty

  • return bloodflow = Ca influx from blood into dead cell – > HYPERcontract = contraction band necrosis
  • Reperfusion injury
Ace inhibitor
⬇️Angiotensin II – > 
1*. Prevent peripheral arterioles v.constriction-->
⬇️afterload 
2*.  Prevent water retention

1+2 –> prevent LV dilation

Beta blockers = ⬇️ heart rate = ⬇️ O2 demand

Morphine – dimorphine
O2 for ischaemia
Nitrates = dilate veins + CA’s
Aspirin/heparin

18
Q

An infarct @Anterior wall Causes what reading on ECG?

A

LAD infarct

Q-waves @ V1 – V4

19
Q

An infarct @Anteroseptal part Causes what reading on ECG?

A

LAD infarct -

Q-waves @sign V1 – V2

20
Q

Infarct @ anterolateral wall causes what reading on ECG

A

LAD/Left circumflex infarct

Q-wave @ V4-V6

21
Q

Infarct @ lateral wall causes what reading on ECG

A

Left circumflex infarct

Q-waves @ aVL + I

22
Q

Infarct @ inferior wall causes what reading on ECG

A

RCA infarct

Q-waves @ lead II, III, aVF

23
Q

Clinical findings for MI

A

PENDD NAH

Pain @ crush chest/inner left arm/shoulder/Jaw
Nerves T12345 = to heart
Nerves T1 = to arm + shoulder
Nerves T45 = epigastrium

> 30 minutes
Diaphoresis + dyspnoea

Hypotension, anxiety, not relieved by GTN

24
Q

Which infarctions death occurs more,

STEMI or Non-STEMI

A

STEMI > non STEMI

25
Q

What percentage of people of silent MIs

A

20%

Diabetes mellitus – neuropathy
High pain threshold

26
Q

What exactly do the ST segments and Q-waves represent

A

Elevated ST segment =
injured myocytes AROUND area of necrosis

New Q-waves = area of coagulation necrosis

Inverted T waves = area of ischaemia @periphery of infarct

Cardio Path (18 decks)

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