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Y1 Cardiology > Acute MI > Flashcards

Acute MI Flashcards

1
Q

Atheromatous plaque causes…

A

luminal narrowing, reducing space for blood flow.

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2
Q

Whats is Chronic Stable Angina?

A

Fixed stenosis causes demand led ischaemia, exacerbations on exertion, relieved with GTN/rest

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3
Q

Characteristics of typical anginal pain

A

Often affects vague area over the breast bone
Often radiates to left arm, sometimes to right arm and jaw.
Posterior infarcts can affect epigastrium or the back.
Pressure, weight or tightness.

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4
Q

Causes of exacerbations of stable angina

A 
Exercise (tolerance varies)
After eating (increased cardiac workload as intestine require increased perfusion) 
Cold wind
Smoking 
Stress
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5
Q

ACS (name and def.)

A

Acute Coronary Syndrome - any acute presentation of coronary artery disease, spectrum of conditions.

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6
Q

Three subgroups of ACS

A

Unstable angina
acute NSTEMI
STEMI

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7
Q

What causes ACS (i.e. common pathogenesis that causes movement from stable to unpredictable)

A

spontaneous plaque rupture

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8
Q

Causes of plaque rupture (or increased likelihood of plaque rupture)

A

Thinning of fibrous cap (young plaque more likely to rupture)
Sudden changes in intraluminal pressure or tone
Bending or twisting of artery during heart contraction
Plaque shape
Mechanical injury

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9
Q

Angina vs Acute MI

A

Demand led ischaemia vs blood supply led ichaemia
Exertion vs rest
Short (10mins) vs longer (30mins+)
GTN relief in angina only
More sever pain in MI
Ohter associated symptoms of MI = sweating, nausea and vomiting.

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10
Q

Damage to the endothelial lining exposes…

A

sub-endothelial collagen (which platelets adhere to via von Willebrand factor)

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11
Q

Sub-endothelial collagen initiates…

A

the platelet cascade - platelet recruitment, adhesion, activation and aggregation.

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12
Q

Two adhesion receptors for leukocytes on activated platelets

A

CD40 ligand
P-selectin

(recruitment to injury site, forms platelet-leukocyte conjugates)

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13
Q

Series of events leading to thrombus formation

A
  1. Plaque rupture
  2. Platelet cascade
  3. Aggregation
  4. Inflammation cascade
  5. Thrombus formation and occlusion
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14
Q

Acute Infarct (def.)

A

tissue downstream from occluded artery does not receive sufficient blood flow therefore infarcts and dies. This results in scarring and loss of muscular function.

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15
Q

How does acute MI lead to HF?

A

The loss of muscular function causes a reduction in the blood volume the ventricle is able to pump. This leads to cardiac failure, left ventricular in particular.

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16
Q

Symptoms of (LV) Heart Failure

A 
Breathlessness
Cough
Orthopnea 
Paroxysmal nocturnal dyspnoea 
Cyanosis
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17
Q

Examples of differential diagnosis for chest pain

A

Sudden onset pneumothorax
Bronchopneumonia
Musculoskeletal chest pain
Heartburn

REMEMBER- CHEST PAIN DOES NOT NECESSARILY MEAN CARDIAC ISSUE

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18
Q

ECG changes in STEMI

A

ST segment elevation (1mm or greater in 2 adjacent limb leads, 2mm in at least 2 contiguous precordial leads)
Later result in T wave inversion and Q waves
New onset bundle branch block also sometimes seen

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19
Q

ECG patterns and region/naming of MI

A

Inferior - II, III, avF (bottom left corner)
Anterior- V1 and V2
Anterioseptal- V3 and V4
Anterolateral- I, avL, V5 and V6

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20
Q

Cardiac enzyme and protein marker assay tests for the presence of….

A

Troponin- in particular TnT or TnI

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21
Q

Why is identifying the presence of troponin a useful test?

A

Highly specific for cardiac muscle damage and can detect tiny amount of myocardial necrosis

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22
Q

What is the downfall of the cardiac enzyme and protein marker tests?

A

May be normal at presentation
Not always time to wait for results if patient suffered a STEMI.

TIME IS MUSCLE

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23
Q

Why is early treatment essential in STEMI?

A

Avoid muscle damage that will result at heart failure, and to reduce risk of MI complications that can be fatal.

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24
Q

What are the gold standard drugs used for the treatment of an acute STEMI?

A

MONA+C

Morphine 
Oxygen 
Nitrates (GTN) 
Aspirin 
Clopidogrel
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25
Q

Why are aspirin and clopidogrel used for treatment of acute STEMI?

A

Clopidogrel is used to block the ADP receptors.
Aspirin is used to block cyclooxygenase enzyme system that produces thromboxane A2.
This dampens down platelet activation (see platelet cascade).

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26
Q

When should patients begin aspirin and for how long should they continue? (SIGN 93)

A

Aspirin should be immediate in ACS. ECG changes or elevated cardiac markers should instigate immediate combination therapy, long term aspirin and 4 weeks clopidogrel (STEMI).

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27
Q

Why is Aspirin started immediately?

A

Antiplatelet drug- blood thinner.

TIME IS MUSCLE

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28
Q

Two methods of revascularisation (STEMI treatment)

A

Thrombolysis

Percutaneous Coronary Intervention (PCI)

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29
Q

Thrombolysis works best within what period of time after onset of pain?

A

Within the first two hours. Outcomes are quite poor if pain has been established for a long time.

30
Q

Where should thrombolysis be delivered?

A

Pre-hospital (has a chance to work while being transported, paramedics make appropriate decision)

31
Q

Indications for reperfusion (Thrombolysis or PCI)

A
  1. Chest pain suggestive of acute MI, more then 20 mins, less than 12 hours.
  2. ECG changes, acute ST elevation or new LBBB.
  3. No contraindications.
32
Q

Why is there reluctance to use Thrombolysis?

A

Risk of intracerebral haemorrhage- 0.5-2% of patients will suffer this, causing long term disability or fatality.
Other risks include other haemorrhage, hypersensitivity and failure to reprefuse.

33
Q

Probability of reopening of vessel after thrombolysis with streptokinase?

A

50% - is fails or acute reocclusion recurs, long term mortality risk is doubled.

34
Q

PCI (name and def.)

A

Percutaneous Coronary Intervention/Primary angioplasty -

Fine wire down coronary artery, reestablishes blood flow to distal muscle (balloon + stent).

35
Q

Optimal reperfusion time (PCI)

A

Angioplasty balloon within 90 mins of the diagnostic ECG- patient must be within 40 minutes of cath lab for PCI to better option than thrombolysis.

36
Q

MONA+C

A

Early treatment of STEMI:
MORPHINE- analgesia diamorphine (IV) for pain and to reduce afterload, bp, tachycardia, oxygen demand (antiemetic may be given to battle nausea)
OXYGEN- treat hypoxia
NITRATES- GTN administered if BP >90 mmHg
ASPIRIN- 300mg asap
+
CLOPIDOGREL- 300mg initially, often administer an additional 300mg near cath lab (PCI)

37
Q

Complications of acute STEMI

A

Death (often through immediate complications below)
Arrhythmic complications
Structural complications
Functional complications

38
Q

Arrhythmic complication of STEMI

A

Ventricular Fibrillation

39
Q

Ventricular Fibrillation (def.)

A

Chaotic, rapid and disorganised ventricular activity causing loss of cardiac output.
Results in death in not treated.
Arrhythmic complication of STEMI.

40
Q

Treatment for Ventricular Firbillation

A

Defibrillation is the only treatment- electric energy delivered to heart to repolarise all of the cells immediately, hope SA node is the first to recover, to restore normal sinus rhythm.

41
Q

Structural complications of STEMI

A 
Cardiac rupture 
Ventricular septal defect 
Mitral valve regurgitation
Left ventricular aneurysm 
Mural thrombus +/- systemic emboli 
Acute pericarditis (from inflammation) 
Dressler's Syndrome
42
Q

Dressler’s Syndrome

A

Autoimmune disease that can cause long term pain if developed post MI

43
Q

Functional Complications of STEMI

A

Acute ventricular failure (R, L or Both)
Chronic HF
Cardiogenic Shock
(see Killip classification)

44
Q

Killip Classification of In-Hospital Mortality

A

I - no signs of HF - 6%
II - crepitations <50% lung fields = 17%
III - crepitations >50% lung fields (Po Oedema) = 38%
IV - Cardiogenic shock = 81%

45
Q

Cardiogenic Shock

A

the heart pump has been damaged to the extent it cannot support body needs. HF and hypotension lead to renal failure and organ shut down.

46
Q

Routine observations in CCU

A

Cardiac monitor for rhythm (react to VF quickly)
How does the patient feel?
BP and pulse - check for tachycardia and hypotension (HF)
Heart sounds - added sounds may indicate mitral regurgitation or septal defects
New murmurs
Pulmonary crepitations (another sign of HF)
Fluid balance

47
Q

NSTEMI (def.)

A

Non-ST elevation MI
dynamic narrowing leading to symptoms at rest that are predictable and dangerous. Occurs when thrombosis or haemorrhage due to unstable/ruptured plaque.

48
Q

What prevents acute occlusion of the vessel in NSTEMI?

A

intravascular thrombolysis aspect of the clotting system where the plasminogen activator binds with plasminogen, creating plasmin which then breaks up clots, resulting in fibrin degradation products.

49
Q

Mortality in NSTEMI

A

Immediate outcome is good, long term outcome is poor.
ST depression in ACS has worse outlook than STEMI.

Note- importance in identification for differentiating which drug treatment req’d.

50
Q

New ACS treatments impose the risk of…

A 
Minor bleeding (24%) 
Major bleeding (3.3%) 
Allergic reactions (2.3%) 
Acute MI 
Death
51
Q

Diagnosis of NSTEMI

A

History - does this sound like cardiac pain?

ECG - important as this is where the main differences of STEMI and NSTEMI occur.

52
Q

Why can’t ECG be relied on alone for NSTEMI diagnosis?

A

It may be normal- this does not exclude NSTEMI

53
Q

What MAY be seen on ECG in NSTEMI?

A

ST depression

T wave inversion in the absence of ST elevation

54
Q

Troponin (def.)

A

Protein on the actin-myosin chain involved in sliding filament contraction. TnT and TnI have almost absolute specificity to cardiac muscle.

55
Q

Other conditions in which Troponin is elevated

A 
CCF 
Hypertensive crisis 
Renal failure 
Pulmonary Embolism 
Sepsis 
Stroke/TIA 
Pericarditis/myocarditis 
Post arrhythmia
56
Q

Type 1 vs Type 2 MI

A

1- MI related to ischaemia due to coronary event e.g. plaque rupture
2- secondary to ischaemia due to imbalance of oxygen supply and demand, e.g. from spasm, embolism, anaemia, arrhythmias, hypertension or hypotension.

57
Q

Treatment of NSTEMI aims to block the coagulation cascade at

A

Factor X activation- where the intrinsic and extrinsic pathways meet

58
Q

How can Factor X activation (coagulation cascade) be blocked?

A

Use of low molecular weight heparin and fondaparinux in addition to aspirin and clopidogrel

59
Q

How long should clopidogrel be administered alongside long term aspirin in NSTEMI?

A

three months

60
Q

Three types of thienopyridines

A

Clopidogrel
Prasugrel
Ticagrelor

61
Q

Role of GP IIb-IIIa inhibitors in NSTEMI

A

reduce aggregation and thus reduce chance of development of NSTEMI into STEMI

62
Q

Treatment of NSTEMI

A

Aspirin and clopidogrel Heparin and fondaparinux
GP IIb-IIIa inhibitors
Non-emergency revascularisation

63
Q

Why treat vulnerable plaque with a stent?

A

blood flow can be improved and the chances of clot less likely (virchow’s triad)

64
Q

How long would clopidogrel be used alongside aspirin where patient has a DRUG ELUTING stent?

A

1 year

Note- normal 3 months for patients using medication only, bare metal stent or elective PCI.

65
Q

Bare metal stent will re-endothelialise within…

A

28 days.

66
Q

If the patient is aspirin intolerent…

A

clopidogrel prescribed indefinitely

67
Q

Acute Stent Thrombosis (def.)

A

when aspirin an clopidogrel stopped prematurely, platelet activation within a stent is possible causing acute stent thrombosis.

68
Q

Predischarge check after MI

A

Is the patient well?
Do they know what has happened?
Do they know what to expect over the next few weeks?
Do they understand their drug therapy?

69
Q

Secondary prevention (def)

A

moving “back the way” from a vulnerable plaque/rupture to the stable condition and possibly restore vigor

70
Q

Methods of secondary prevention

A 
Healthier lifestyle 
Smoking cessation 
Control of BP 
Control of Diabetes 
Control of cholesterol (lowering)
71
Q

4 Phases of cardiac rehabilitation

A
  1. In-patient
  2. Early post discharge period
  3. Structured exercise programme
  4. Long term maintenance
72
Q

Targets for cardiac rehabilitation

A

Avoid smoking
Healthy diet
Regular aerobic exercise
Optimal drug therapy
Cholesterol < 4.0 mmol/l - statin therapy
BP < 140/85 mmHg (90 for a diabetic)
Diabetes, renal disease, target organ damage <130/80 mmHg

Y1 Cardiology (9 decks)

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