Acute Coronary Syndrome Flashcards

1
Q

What is ACS usually a cause of?

A

A thrombus from an atherosclerotic plaque blocking a coronary artery

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2
Q

Why are anti-platelet medications mainstay of treatment in ACS?

A

When a thrombus forms in a fast flowing artery it is made up mostly of platelets

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3
Q

What are the three types of ACS?

A

Unstable Angina
ST Elevation Myocardial Infarction (STEMI)
Non-ST Elevation Myocardial Infarction (NSTEMI)

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4
Q

What symptoms suggest ACS?

A

Chest pain - the classical presentation can be considered in terms of the SOCRATES mnemonic:

Site - Central/left sided

Onset - Often sudden

Character - Crushing (‘like someone is sitting on your chest’)

Radiation - Left arm, neck and jaw

Associated symptoms - Nausea, sweating, clamminess, shortness of breath, sometimes vomiting or syncope

Timing - Constant

Exacerbating/relieving factors - Worsened by exercise/exertion and may be improved by GTN

Severity - Often extremely severe

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5
Q

What should you do if a patient presents with possible ACS?

A

Perform an ECG

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6
Q

What is a myocardial infarction?

A

When there is a blockage in blood supply to the heart that cuts off oxygen to the heart, causing the heart muscle to die

Most MIs are due to atherosclerosis

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7
Q

How can a STEMI be diagnosed?

A

ST elevation or new left bundle branch block on an ECG

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8
Q

What should you do is ACS is suspected but the ECG shows no ST elevation?

A

Perform troponin test

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9
Q

How can NSTEMI be diagnosed?

A

Raised troponin levels
ECG changes - ST depression or T wave inversion or pathological Q waves

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10
Q

What is the diagnosis if ACS is suspected but troponin levels and ECG are normal?

A

Unstable angina or another cause such as MSK chest pain

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11
Q

What is the treatment in acute STEMI?

PROCEDURES

A

Patients with STEMI presenting within 12 hours of onset should be discussed urgently with local cardiac centre for either:

Primary PCI (if available within 2 hours of presentation and within 12 hours of symptom onset)
Thrombolysis (if PCI not available within 2 hours)

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12
Q

Acute NSTEMI treatment

A

B – Beta-blockers unless contraindicated

A – Aspirin 300mg stat dose

T – Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative if higher bleeding risk)

M – Morphine titrated to control pain (IV morphine/diamorphine)

A – Anticoagulant: Fondaparinux (unless high bleeding risk)

N – Nitrates (e.g. GTN) to relieve coronary artery spasm

Give oxygen only if their oxygen saturations are dropping (i.e. <95%).

Start antithrombin therapy such as treatment dose low molecular weight heparin or fondaparinux if they are for an immediate angiogram

Patients with high 6 month risk of mortality should be offered an angiogram within 96 hours of symptom onset.

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13
Q

What is used to assess for PCI in NSTEMI?

A

GRACE score

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14
Q

What does the GRACE score tell us?

A

6 month risk of death or repeat MI after having an NSTEMI

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15
Q

What are the different outcomes of a GRACE score?

A

<5% Low Risk
5-10% Medium Risk
>10% High Risk

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16
Q

Who is considered for early PCI (within 4 days of admission) to treat underlying coronary artery disease?

A

Medium or high risk

17
Q

What are the complications of MI?

A

THINK: DREAD

Death
Rupture
Edema (heart failure)
Arrhythmia and Aneurysm
Dressler’s Syndrome

18
Q

What is dressler’s syndrome?

A

AKA Post-myocardial infarction syndrome.

It usually occurs around 2-3 weeks after an MI.

It is caused by a localised immune response and causes pericarditis

It is less common as the management of ACS becomes more advanced.

19
Q

How does Dressler’s syndrome present?

A

Pleuritic chest pain
Low grade fever
Pericardial rub on auscultation.

20
Q

How is dressler’s syndome diagnosed?

A

ECG (global ST elevation and T wave inversion), echocardiogram (pericardial effusion) and raised inflammatory markers (CRP and ESR).

21
Q

What is the management of Dressler’s syndrome?

A

NSAIDs (aspirin / ibuprofen) and in more severe cases steroids (prednisolone).

May need pericardiocentesis to remove fluid from around the heart

22
Q

Secondary prevention (6 A’s) of MI

A

Aspirin 75mg once daily

Another antiplatelet: e.g. clopidogrel or ticagrelor for up to 12 months
Atorvastatin 80mg once daily

ACE inhibitors (e.g. ramipril titrated as tolerated to 10mg once daily)

Atenolol (or other beta blocker titrated as high as tolerated)

Aldosterone antagonist for those with clinical heart failure (i.e. eplerenone titrated to 50mg once daily)

23
Q

Secondary prevention lifestyle

A

Stop smoking
Reduce alcohol consumption
Mediterranean diet
Cardiac rehabilitation (a specific exercise regime for patients post MI)
Optimise treatment of other medical conditions (e.g. diabetes and hypertension)

24
Q

How many types of MI are there?

A

4

25
Q

What is a type I MI?

A

Traditional MI due to an acute coronary event

26
Q

What is type II MI?

A

Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension)

27
Q

What is type III MI?

A

Sudden cardiac death or cardiac arrest suggestive of an ischaemic event

28
Q

What is type IV MI?

A

MI associated with PCI / coronary stunting / CABG

29
Q

What is troponin and when is it released?

A

A myocardial protein released into the bloodstream when cardiac myocytes are damaged.

Serum levels typically rise 3 hours after myocardial infarction begins.

30
Q

What does a low troponin level mean in regards to ACS?

A

Definitely no myocardial cell death.

The patient is not having an MI although they may be experiencing unstable angina.

31
Q

What does a mildly raised troponin level mean in regards to ACS?

A

These patients usually need a 6-12 hour repeat test.

If repeat troponin is raised on the repeat they are having an MI.

If repeat troponin is stable or falling then they are unlikely to be having an MI.

32
Q

What does a highly raised troponin level mean in regards to ACS?

A

MI confirmed (be aware of the possibility of a Type 2 MI)

33
Q

What is a rise in troponin related to?

A

A rise in troponin is consistent with myocardial ischaemia as the proteins are released from the ischaemic muscle.

They are non-specific, meaning that a raised troponin does not automatically mean ACS.

34
Q

Other than ACS, what can cause a raise in troponin levels?

A

Chronic renal failure
Sepsis
Myocarditis
Aortic dissection
Pulmonary embolism
Pericarditis
Myocarditis
Arrythmias
Defibrillation
Acute heart failure
Pulmonary embolus
Type A aortic dissection
Chronic kidney disease
Prolonged strenuous exercise

35
Q

What is the treatment for STEMI?

Medication

A

Targeted oxygen therapy (aiming for sats >90%)

Loading dose of PO aspirin 300mg

Note that some hospital protocols will also call for a loading dose of another anti-platelet agent such as clopidogrel (300mg) or ticagrelor (180mg)

Sublingual GTN spray - for symptom relief

IV morphine/diamorphine - in addition this causes vasodilation reducing preload on the heart

36
Q

What five drugs should al patients be started on post-MI?

A

Aspirin 75mg OM + second anti-platelet (clopidogrel 75mg OD or ticagrelor 90mg OD)

Beta blocker (normally bisoprolol)

ACE-inhibitor (normally ramipril)

High dose statin (e.g. Atorvastatin 80mg ON)

37
Q

Who should all patients be referred to post-MI?

A

Cardiac rehab

38
Q

What should all patients have post-MI?

A

ECHO performed to assess systolic function and any evidence of heart failure should be treated.

39
Q

What is an echocardiogram?

A

A type of ultrasound.

Checks structure of heart and surrounding vessels, analysing how blood flows through them, and assessing the pumping chambers of the heart.