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SPM- Cardiology > Acute Coronary Syndrome > Flashcards

Acute Coronary Syndrome Flashcards

1
Q

What three conditions make up ACS?

A

STEMI
NSTEMI
Unstable Angina

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2
Q

What is the difference between ischaemia and infarction?

A

Infarction is when there is death of tissue due to low oxygen supply
Ischaemia is when there is a low oxygen supply but not tissue death

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3
Q

What causes the pain in ischaemia?

A

Production of lactic acid leads to the pain experienced

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4
Q

What is the underlying pathology in a myocardial infarction?

A

Rupture of an atherosclerotic plaque causes thrombus formation, this then obstructs the flow of blood leading to ischaemia distally

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5
Q

Briefly describe the blood supply to the heart

A

RCA and LCA are the first branches of the Aorta and arise from the aortic sinus
LCA divides into Circumflex and LAD
RCA sometimes gives off Posterior Descending Artery (80%) or this may come from the Circumflex (15%) or from both (5%). Termed left/right or co dominant.

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6
Q

What does the RCA supply?

A

Right atrium and ventricle

If Posterior descending- Inferior and posterior walls

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7
Q

What are the inferior leads?

A

II, III, aVF (think F in inferior)

RCA/Posterior descending

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8
Q

What does the LAD supply?

A

Anterior aspect of LV
Anterior aspect of septum
Apex

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9
Q

What does the circumflex supply?

A

Lateral wall of LV

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10
Q

What are the lateral leads?

A

V5 and V6 and aVL and I-

Circumflex Artery

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11
Q

What are the anterior leads?

A

V3 and V4

LAD

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12
Q

What are the septal leads?

A

V1 and V2-

LAD and RCA

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13
Q

What is the blood supply to the SA node?

A

RCA gives sinoatrial node off in 60%

Can arise from left circumflex

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14
Q

What is the blood supply to the septum?

A

LAD- Anterior septum

RCA- Posterior Septum

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15
Q

Which group of patients might have an atypical presentation for an MI?

A

Diabetic and elderly

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16
Q

How might patients with an atypical presentation present?

A 
Dyspnoea- due to pulmonary oedema
Epigastric pain
N and V
Pallor
Sweating
Syncope- poor cerebral perfusion
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17
Q

How do the three ACS presentations differ from each other?

A

Unstable Angina- No troponin rise, ECG normal or ischaemic changes
NSTEMI- Troponin rise, ECG normal or ischaemic change
STEMI- Troponin rise and ST elevation on ECG

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18
Q

What is a troponin rise indicative of?

A

Myocardial infarction and the death of myocytes

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19
Q

Which troponins are measured?

A

Troponin T and I

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20
Q

What are some other causes of a raised troponin?

A 
Renal failure
Sepsis
Anaemia
PE
Aortic dissection
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21
Q

Why can a single troponins not be used in isolation?

A

It is the troponin rise that is important, baseline is taken and then another 6-12 hours apart

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22
Q

For patients presenting with an ACS picture, what immediate investigations would you request and why?

A

Bloods-
Troponins
FBC Anaemia, Infection
U and Es Renal Function, Important for anti-hypertensive meds too
LFTs- before starting statins
Lipids- risk factor profile
HBA1c/Fasting Glucose- risk factor profile
TFTs- Tachycardia from hyperthyroidism can trigger chest pain

ECG- Ischaemic Changes
Minutes- Hyper acute T Waves
Hours to Days to Weeks- ST Depression/ST Elevation/T Wave Inversion
Days- Pathological Q Waves

ECHO-
Assess myocardial function and for valve disease if suspected

CXR-
Rule out other causes of acute chest pain

CT Angiogram- Gold standard for investigating vessel disease in the heart

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23
Q

What are some signs of ischaemia on ECG?

A

ST Elevation
ST Depression
T wave inversion
Pathological Q Waves

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24
Q

What would you check for on examination of an ACS patient?

A

This is a medical emergency so requires an A to E approach

A- Airway
B- Auscultate- bi-basal crackles, percussion and palpation for chest expansion
C- Blood pressure, HR, Heart Sounds, CRT, JVP, Temperature, Pulse, Urine output

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25
Q

How many leads must ST elevation be present in for it to be classed as a STEMI?

A

At least two or more sister leads

26
Q

What are some features that suggest pain is more cardiac in origin?

A

Central- behind the sternum
Poorly localised (if they can point to a specific point it is more likely to be MSK)
Radiation down the L arm and into the jaw/neck
Crushing/Dull in nature
Associated dyspnoea, N+V, pallor, sweating
Risk factors present- FHx, Diabetes, Smoking, HTN, Hyperlipidaemia, Male gender

27
Q

What type of cardiac pathology pain eases with leaning forward?

A

Pericarditis

28
Q

What type of cardiac pathology pain feels like a tearing sensation with radiation to the back?

A

Aortic dissection

29
Q

What ECG findings might be seen for a NSTEMI?

A

ST Depression
T Wave Inversion
Or may be normal

30
Q

Can both STEMIs and NSTEMIs be localised to an anatomical area?

A

No only acute STEMIs can be localised

NSTEMIs cannot as the ischaemia changes do not correspond to the ischaemic vascular territory

31
Q

What areas are infarcted in NSTEMIs and STEMIs?

A

STEMIs- Transumaral infarcts

NSTEMIs- Subendocardial infarcts- this is the first area to undergo ischaemia when the blood supply is reduced

32
Q

What features on an ECG indicate STEMI?

A

ST Elevation

Or NEW ONSET LBBB

33
Q

What is the initial approach for suspected ACS?

A

Medical Emergency so A to E approach

ECG confirms if STEMI or NSTEMI/Unstable Angina

34
Q

What is the initial treatment if STEMI?

A

Follow ACS Protocol for Trust

Aspirin 300mg
Another Anti-platelet- Clopidogrel/ Ticagrelor
Morphine 5-10mg IV repeat and titrate after 5 minutes
Anti-emetic- metoclopramide 10mg IV (cyclizine increases HR)
GTN
Oxygen- only if their oxygen saturations are below 95%
LMWH- Enoxaparin treatment dose
Beta blockers- Bisoprolol
ACEi- Started within 24 hours

Cardiac Reperfusion- PCI or if not available within 120min thrombolysis

35
Q

Within what time frame of symptom onset must patients with STEMI have presented to be considered for PCI?

A

12 hours

36
Q

What is a contra indication to giving nitrates?

A

Hypotensive

37
Q

What are some side effects of nitrates?

A

Flushing
Headache
N and V
Hypotension

38
Q

What is the mechanism of action of aspirin?

A

COX inhibitor that prevents platelet aggregation

39
Q

What dose of aspirin is given if ACS is suspected?

A

300mg Stat

40
Q

What does of aspirin is given for long term secondary prevention?

A

75mg OD

41
Q

What is a side effect of aspiring, how could this be reduced?

A

Increased risk of gastric ulcers and upper GI bleeds- therefore a PPI may be given too

Also it is nephrotoxic so close monitoring of renal function is required

42
Q

What second anti-platelet (in-addition to aspirin) is now commonly used?

A

Ticagrelor

Clopidogrel may also be used if there is a higher risk of GI bleeding as it has a reduced risk

43
Q

What is the mechanism of action of Ticagrelor?

A

P2Y12 receptor antagonist

44
Q

What are the doses of ticagrelor, loading and daily?

A

180mg loading dose

90mg BD

45
Q

What is the management for NSTEMI?

A

As with STEMI and other ACS

BATMAN

Beta blockers- unless CI- asthma, bradycardia, never with verapamil or diltiazem
Aspirin 300mg
Ticagrelor 180mg
Morphine + Metoclopramide
Anticoagulants- Enoxapain treatment dose
Nitrates- relieve coronary artery spasm

Then Risk assess for consideration of PCI to treat the underlying coronary artery disease

46
Q

What score is used to risk assess NSTEMIs? What is it a risk of?

A

GRACE Score- 6 month risk of repeat MI or death

47
Q

What agents are used for thrombolysis?

A

TPAs- Tissue Plasminogen Activator
Streptokinase
Alteplase
Tenectaplase

48
Q

What are some complications from MI?

A

DREAD

Death
Rupture- Myocardium/Papillary Muscles
Edema- Heart Failure
Arrthymia and Aneurysm
Dresslers Syndrome
49
Q

What is Dresslers syndrome?

A

Pericarditis that occurs after MI due to the ongoing inflammation. Presents with chest pain and a low grade fever. A pericardial rub may be head on auscultation.

50
Q

What is the treatment for a pericardial effusion caused by Dressler syndrome?

A

Pericardiocentesis

An ECHO confirms the presence of an effusion

51
Q

What features are seen on the ECG for Dressler syndrome?

A

Global ST elevation and T wave inversion

52
Q

What is the management of Dressers syndrome?

A

NSAIDs
Severe cases Prednisolone

Pericardiocentesis if there is an effusion

53
Q

What medicines are used in the secondary prevention of MIs?

A

6 As

Aspirin 75mg OD
Another Anti platelet- Ticagrelor or Clopidogrel for up to 12 months
Atorvastatin- 80g OD
ACEi- e.g. Ramipril
Atenolol (Beta Blocker, more commonly bisoprolol)
ARB- Eplerenone

54
Q

Why are ACEi or ARBs particularly useful to start post MI?

A

They reduce ventricular re-modelling after an MI

55
Q

What are some side effects of ACEi?

A

Hypotension

Cough

56
Q

Why are beta blockers (e.g. bisoprolol, atenolol) given after MI?

A

Increase cardiac perfusion during diastole by reducing the HR

Not to be given if bradycardia, heart block, asthma, COPD

57
Q

What ARB is useful to give post MI?

A

Eplerenone - proven mortality benefit in heart failure and prevents ventricular remodelling like ACEi. Initiated if LVEf less than 40%

58
Q

What must be checked before starting someone on a a statin>

A

LFTs

59
Q

What blood test can check for an important complication of statins?

A

CK

Rhabdomyolysis is the complication, monitor renal function too as myoglobin is nephrotoxic.

60
Q

What is a leading side effect of statins?

A

Muscle aches- consider reducing the dose from 80mg to 40mg.

61
Q

When is eplerenone started in patients after MI?

A

If there is evidence of heart failure- LVEF <40%

SPM- Cardiology (4 decks)

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