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ZA - Cardio Diseases > ACS > Flashcards

ACS Flashcards

1
Q

What are the different acute coronary syndromes?

A

Step up from stable angina.

Involves Unstable angina, NSTEMI, STEMI and Sudden cardiac death

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2
Q

What causes an ACS?

A

Either the rupture of a plaque or thrombosis which makes the occlusion of vessel worse than in stable angina

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3
Q

What is the difference between unstable angina and NSTEMI?

A

An NSTEMI is an actual infarct which causes necrosis and a rise in serum troponins or creatine kinase-MBs due to that breakdown of muscle

Unstable angina is kind of like stable angina at rest but not enough to cause a MI

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4
Q

Non-modifiable risk factors for an ACS?

A

Age
Gender
Family/genetics

Previous angina, cardiac event or surgery

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5
Q

Modifiable risk factors?

A 
Smoking
Bad diabetic control leading to hyperglycemia
Hypertension
Hyperlipidaemia
Poor exercise/diet
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6
Q

What will you want to ask the patient about the angina pain?

A

Onset at rest

Relieving factors - does GTN spray help?

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7
Q

In a history - what would make you suspect unstable angina/NSTEMI?

A

Angina on rest

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8
Q

How does an NSTEMI typically start presenting - Angina getting progressively worse or angina on rest?

A

NSTEMI will show first as angina on rest

as it has reached that point and has been reclassified to an actal MI

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9
Q

Examination wise - will patients look very unwell on an end of bed inspection?

A

They can do, but not all the time

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10
Q

Is there any remarkable features to look for in an examination?

A

Not really

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11
Q

What should be checked in an examination anyway?

A

HR
BP
Auscultate for murmurs and crackles

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12
Q

What should you keep in mind when looking for symptoms for an ACS in different patients?

A

You always get atypical patients in which typical symptoms do not show

In this case - women, elderly or diabetics due to a reduced pain sensation

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13
Q

What symptoms should you keep your eye open for instead with atypical patients?

A

Breathlessness
Signs of heart failure
Nausea and vomiting
Epigastric (upper abdomen) pain

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14
Q

What to look for in an ECG?

A

Can have but not always;

ST segment depression
Transient ST segment elevation and/or T wave inversion

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15
Q

What happens to ECG changes in unstable angina when the pain subsides?

A

The ECG tends to return to normal

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16
Q

What happens to ECG changes in NSTEMI when the pain subsides?

A

Changes tend to persist

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17
Q

Should ECGs be done routinely?

A

Yes to detect any changes

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18
Q

What are some biomarkers which indicate a high risk of an adverse event?

A

Cardiac troponin - I and T proteins types

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19
Q

What is cardiac troponin?

A

Contractile apparatus unique to heart

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20
Q

Should cardiac troponin be detectable in normal instances?

A

No

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21
Q

Is troponin elevation always a sign of ACS?

A

No

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22
Q

What is the immediate treatment response to give to someone having an ACS?

A

MONA

Morphine/dimorphine
Oxygen
Nitrates - GTN spray or tablet
Aspirin - 300mg orally

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23
Q

What is the further medical treatment from someone with unstable ACSs?

A 
Anti-platelet
Anti-thrombotic (anticoagulants)
Glycoprotein llb/lllb inhibitor 
Beta blockers
Statins
ACEIs
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24
Q

What are the anti-platelet drugs and doses?

A

Aspirin - 75-100mg

Clopidogrel - 300mg initially then 75mg daily

Ticagrelor - 60mg initially then 10mg daily

Prasugrel - 180mg then 90mg daily

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25
Q

How does aspirin work?

A

Platelet thromboxane A2 production inhibitor

Stops platelet aggregation and vasoconstriction

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26
Q

How does ticagrelor/prasugrel work?

A

ADP receptor blocker - stops pathway reaching Glycoprotein llb/lllb pathway

In turn stops platelet aggregation and fibrin linking

27
Q

Should patients be on one or more than one of these antiplatelet drugs and for how long after an event should they be used?

A

Dual therapy for one year after event is best

28
Q

Name some glycoprotein llb/lllb receptor blockers?

A

Tirofiban

29
Q

What do these glycoprotein llb/lllb blockers do?

A

Stop the protein undergoing a conformational change and binding fibrinogen and activating platelets

30
Q

Adverse effects of glycoprotein llb/lllb blocker therapy?

A

Bleeding

31
Q

What are some anti-thrombotic (anti-coagulant) agents?

A

Unfractionated heparin
Low molecular weight heparin

Fondaparinux - a LMWH like drug

32
Q

Which ones IV administered?

A

Unfractionated heparin

33
Q

How is LMWH given?

A

Sub/c

34
Q

Which one of the 2 heparins has a better clinical outcome and why?

A

LWMH

Easier to give
No need to be monitored

35
Q

Name some IV beta blockers used to treat unstable angina/NSTEMI.

A

Atenolol

Metoprolol

36
Q

Should oral beta blockers be started?

A

Yes - shown to reduce morality

37
Q

How do beta blockers work?

A

Rate limiting

Reduce myocardial O2 consumption

38
Q

B/Blocker contraindications?

A

Asthma
Heart failure
Bradycardia/Heart block

39
Q

What type of patients have been shown to die if given beta blockers?

A 
Over 70s
HR is below 110bpm
S. BP is below 120
Coronary vasospasm
Cocaine use
40
Q

Should stains be used?

A

Yes -acutely and chromically to reduce risk of further events

41
Q

In who should ACEIs be used for a ACS?

A

Abnormal LV function, unstable angina or an MI

42
Q

What are the 2 surgical ways to treat an ACS?

A

PCI

CABG

43
Q

Why is a STEMI treated differently?

A

The occlusion is larger and needs to be reduced rapidly (I think)

44
Q

What are the 2 main treatments for a STEMI?

A

Primary PCI (Surgical)

Fibrinolysis/Thrombolysis (medical)

45
Q

Features of PCI.

A

Better than fibrinolytic therapy

Used to unblock artery and save muscle cells so time is muscle

46
Q

When is fibrinolysis used?

A

When PCI not an option

47
Q

What is fibrinolysis?

A

Drugs that thin out the thrombus that has grown on top of plaque and blocked artery even more

48
Q

How does fibrinolysis work?

A

Serine proteases convert plasminogen to plasmin

Plasmin works to lyse a clot by breaking down fibrinogen and fibrin

49
Q

2 types of fibrinogen agents?

A

Fibrin specific

Non fibrin specific

50
Q

Name some fibrin specific agents?

A

Alteplase
Reteplase
Tenecteplase

51
Q

Name the non-fibrin specific agent

A

Streptokinase

52
Q

Contraindictions of fibrinolysis

A

Suspected aortic dissection
Bleeding due to HYPOcoagubiltiy

Brain tumours/bleeds/stokes

53
Q

What increases the risk of an intra-cranial bleed in fibrinolysis therapy?

A 
Over 75
Female
Previous stroke history
Low body weight
Severe hypertension
INR of over 4
Chronic kideny disease and elevated creatine
54
Q

What is some secondary prevention regarding lifestyle after an ACS event?

A

Stop smoking
Better diet/exercise

Control co-morbities - BP/glycemia

55
Q

What is some further medical therapy to use after an ACS?

A 
Aspirin/clopidogrel for 1 year
Beta blocker (if tolerable_

ACEIs if LV dysfuntion

56
Q

What investigations should be done post ACS?

A

An echocardiogram for myocardial dysfunction

57
Q

What is the most important determinant for an MI survival?

A

Age

LV ejection fraction

58
Q

Sudden cardiac death - survival rate?

A

~2% are get past resus and survive

59
Q

In those resus’d - what do they end up with?

A

about 80% have V-tachy or V-fib

60
Q

How is sudden cardiac death seen?

A

Seen as V-fib. multiple wavelets on ecg - rapidly progresses to asytole

61
Q

How to treat SCD?

A

Defib only way to treat a V-fib arrest

If progresses to asytole then prognosis isn’t good

62
Q

List the major trials which have proven the advantage of thrombolytic therapy

A

local GREAT study

63
Q

Describe rehabilitation following myocardial infarction

A

build up easy exercise and keep bp low

ZA - Cardio Diseases (36 decks)

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