Acute Coronary Syndrome Flashcards

1
Q

Whats is ischaemic heart disease all about

A

plaque formations from fatty streaks

If these rupture then they can cause thrombosis

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2
Q

What symptoms/effects can people get if arteries start to narrow?

A
  • TIA’s
  • Angina
  • leg ischaemia
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3
Q

What happens if a plaque ruptures?

A
  • platelets clump together to cause a sudden partial or total occlusion of the artery and an acute coronary syndrome develops.
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4
Q

what risk assessment tool do we use for CHD?

What does it assess?

A

QRISK2

10 year CVD risk

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5
Q

What modifiable risk factors do we have for ACS

A
  • diet
  • smoking
  • exercise
  • HTN - each 2mmHg rise incurs a 7% increase in CHD and a 10% increase in stroke risk.
  • alcohol
  • lipid control - offer 20mg atorvastatin to patients with QRISK score > 10%.
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6
Q

How can we monitor for primary preventions?

A

Keep reassessing the QRISK2 score

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7
Q

What do we check when starting statins?

- primary prevention

A
  • baseline lipids
  • LFT’s
  • No secondary cause of dyslipidaemia e.g. thyroid disease
  • repeat after 3 months and check compliance side/effects
  • Aim for >40% reduction in HDL cholesterol.
  • Consider increasing dose again if not maximal effect
  • Repeat LFT’s 12 months but not again unless indicated
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8
Q

What do we check if statin antihypertensives?

- primary prevention

A
  • Bloods: albumin creatinine ration (ACR), blood sugar, u&E, eGFR, lipids
  • ace/arb - U&E’s, eGFR 1-2 weeks after dose titration and then annually unless indicated.
  • diuretics - recheck (u&e, eGFR) 4-6 weeks then annually
  • check BP response to treatment and compliance/side effects
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9
Q

Is QRISK2 score used for primary or secondary prevention?

A

Primary

All patients that have had an event are high risk. All modifiable/non-modifiable lifestyle factors are still relevant in secondary prevention.

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10
Q

Patients with CHD who feel pain on exertion because the heart required more oxygen but this resolves on rest and GTN spray can be diagnosed with….

A

Angina

It is important to note that this resolves on rest because if it doesn’t and the patient feels pain on rest then they could be having an ACS

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11
Q

Management of Angina….

A
  • diet & lifestyle
  • education on what it is, what provokes it (cold, stress, exertion)
  • aspirin 75mg OD (clopidogrel if aspirin is C/I)
  • Evaluate bleeding risk and start PPI omeprazole 20mg to cover for long term aspirin
  • rationalise medicines - try to avoid NSAIDS for example.
  • Start atorvastatin 80mg regardless of lipid levels. 20mg in CKD.
  • antihypertensives if high BP
  • GTN spray - monitor frequency of use and if still symptomatic add in

1) BB or rate limiting CCB (verapamil or diltiazem)
2) BB + CCB (switch to non rate limiting)
3) nicorandil, ISMN, ranolazine, ivabradine (lowers HR with little effect on pulse)

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12
Q

How do we treat post-MI

A
  • CVD risk factor modification
  • diet/lifestyle advice
  • antiplatelets (aspirin + clopidogrel, ticagrelor or prasugrel) Usually dual therapy for 12 months then mono.
  • ace-inhibitor - start low and up titrate
  • beta-blocker - start low and up titrate
  • atorvastatin 80mg
  • GTN spray
  • rationalise meds - avoid NSAIDS
  • minimise bleeding risk > 65 years offer PPI e.g., concurrent steroids or SSRIS. Ensure second anti platelet is stopped at the correct time.
  • cardiac rehab - recommended to start 10 days post discharge
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13
Q

What is the difference between an NSTEMI (non ST elevation myocardial infarction|) and a STEMI. (ST elevation myocardial infarction)

A

STEMI - total occlusion of an artery - ECG picks up ST wave elevation and troponin rise is evident.

NSTEMI - partial occlusion of artery. ECG shows ischemic changes ( T wave inversion and ST segment depression) and troponin rise is evident

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14
Q

How do we treat a STEMI

A

1) PPCI - primary percutaneous coronary intervention (angioplasty) treatment of narrowed arteries. Favoured over thrombolysis due to more effective revascularisation, lead re-occlusion, less bleeding, decreased length of stay.
2) Thrombolysis - not used as much due to PPCI but may be needed if ‘delay to balloon time’
3) oxygen - hypoxic
4) morphine/diamorphine to relieve pain or anxiety
5) metoclopramide
6) GTN
7) Aspirin 300mg stat - if PPCI then further 300mg stat then loading dose of clopidogrel, ticagrelor or prasgruel.
8) IV beta-blocker (optional)
9) parenteral anticoagulation (heparin) if giving thrombolysis.

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15
Q

Treatment of NSTEMI

A

Review the GRACE score

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16
Q

What does a GRACE score predict?

A

Predicts the mortality risk due to CVD

17
Q

Some facts about ivabridine?

A
  • it has minimal effect on BP (only really effects HR)
  • It should be avoided inpatients with AF as only works on sinus node (sinus rhythm)
  • It should be avoided with clarithromycin.
18
Q

What can be used to treat a STEMI but not an NSTEMI

A

tenectaplase

19
Q

Facts about fondaparinux

A
  • dose is 2.5mg daily

- studies have shown a lower bleeding risk compared to enoxaparin

20
Q

A patient has an NSTEMI on the background of AF - how do we treat

A

Anticoagulation plus aspirin for 12 months then anticoagulation long term.

21
Q

Which of the following is no longer recommended post STEMI

A

omacor

22
Q

Can amitiptyline be used post MI?

A

No - contraindicated

23
Q

Digoxin should not be used in the management of paroxysmal AF because it has a negative chronotropic effect ?

A

True