ACS Flashcards

(63 cards)

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
How does aspirin work?
Platelet thromboxane A2 production inhibitor Stops platelet aggregation and vasoconstriction
26
How does ticagrelor/prasugrel work?
ADP receptor blocker - stops pathway reaching Glycoprotein llb/lllb pathway In turn stops platelet aggregation and fibrin linking
27
Should patients be on one or more than one of these antiplatelet drugs and for how long after an event should they be used?
Dual therapy for one year after event is best
28
Name some glycoprotein llb/lllb receptor blockers?
Tirofiban
29
What do these glycoprotein llb/lllb blockers do?
Stop the protein undergoing a conformational change and binding fibrinogen and activating platelets
30
Adverse effects of glycoprotein llb/lllb blocker therapy?
Bleeding
31
What are some anti-thrombotic (anti-coagulant) agents?
Unfractionated heparin Low molecular weight heparin Fondaparinux - a LMWH like drug
32
Which ones IV administered?
Unfractionated heparin
33
How is LMWH given?
Sub/c
34
Which one of the 2 heparins has a better clinical outcome and why?
LWMH Easier to give No need to be monitored
35
Name some IV beta blockers used to treat unstable angina/NSTEMI.
Atenolol | Metoprolol
36
Should oral beta blockers be started?
Yes - shown to reduce morality
37
How do beta blockers work?
Rate limiting | Reduce myocardial O2 consumption
38
B/Blocker contraindications?
Asthma Heart failure Bradycardia/Heart block
39
What type of patients have been shown to die if given beta blockers?
``` Over 70s HR is below 110bpm S. BP is below 120 Coronary vasospasm Cocaine use ```
40
Should stains be used?
Yes -acutely and chromically to reduce risk of further events
41
In who should ACEIs be used for a ACS?
Abnormal LV function, unstable angina or an MI
42
What are the 2 surgical ways to treat an ACS?
PCI | CABG
43
Why is a STEMI treated differently?
The occlusion is larger and needs to be reduced rapidly (I think)
44
What are the 2 main treatments for a STEMI?
Primary PCI (Surgical) Fibrinolysis/Thrombolysis (medical)
45
Features of PCI.
Better than fibrinolytic therapy Used to unblock artery and save muscle cells so time is muscle
46
When is fibrinolysis used?
When PCI not an option
47
What is fibrinolysis?
Drugs that thin out the thrombus that has grown on top of plaque and blocked artery even more
48
How does fibrinolysis work?
Serine proteases convert plasminogen to plasmin Plasmin works to lyse a clot by breaking down fibrinogen and fibrin
49
2 types of fibrinogen agents?
Fibrin specific | Non fibrin specific
50
Name some fibrin specific agents?
Alteplase Reteplase Tenecteplase
51
Name the non-fibrin specific agent
Streptokinase
52
Contraindictions of fibrinolysis
Suspected aortic dissection Bleeding due to HYPOcoagubiltiy Brain tumours/bleeds/stokes
53
What increases the risk of an intra-cranial bleed in fibrinolysis therapy?
``` Over 75 Female Previous stroke history Low body weight Severe hypertension INR of over 4 Chronic kideny disease and elevated creatine ```
54
What is some secondary prevention regarding lifestyle after an ACS event?
Stop smoking Better diet/exercise Control co-morbities - BP/glycemia
55
What is some further medical therapy to use after an ACS?
``` Aspirin/clopidogrel for 1 year Beta blocker (if tolerable_ ``` ACEIs if LV dysfuntion
56
What investigations should be done post ACS?
An echocardiogram for myocardial dysfunction
57
What is the most important determinant for an MI survival?
Age | LV ejection fraction
58
Sudden cardiac death - survival rate?
~2% are get past resus and survive
59
In those resus'd - what do they end up with?
about 80% have V-tachy or V-fib
60
How is sudden cardiac death seen?
Seen as V-fib. multiple wavelets on ecg - rapidly progresses to asytole
61
How to treat SCD?
Defib only way to treat a V-fib arrest If progresses to asytole then prognosis isn't good
62
List the major trials which have proven the advantage of thrombolytic therapy
local GREAT study
63
Describe rehabilitation following myocardial infarction
build up easy exercise and keep bp low