ACS, angina, UA, STEMI, NSTEMI Flashcards

1
Q

List the modifiable and unmodifiable RFs for ischaemic heart disease

A

Unmodifiable risk factors:
Increasing age
Male gender
Family history

Modifiable risk factors:
Smoking
Diabetes mellitus
Hypertension
Hypercholesterolaemia
Obesity

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2
Q

Explain the pathophysiology of ischaemic heart disease listing some of the cells involved

A
  1. ENDOTHEILIAL DYSFUNCTION triggered by smoking/HTN/DM
  2. fatty infiltration of subendothelial space by LDL particles [low-density lipoproteins]
  3. Monocytes migrate over from blood and differentiate into macrophages
  4. Macrophafes phagocytose oxidised LDLs –> become large foam cells fomring fatty plaques. Death of macrophages increases inflammation.
  5. Smooth muscle cells migrate from tunica media –> intima and form fibrous capsules around the fatty plaques
  6. Plaques cause narrowing of coronay arteries (angina), and can also rupture and occlude the cornary artery (MI)
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3
Q

Signs and symptoms of ACS

A
  • left-sided chest pain
  • radiating to jaw or left arm
  • heavy, crushing
  • dyspnoea
  • sweating
  • N+V
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4
Q

Which patients may have ACS without chesy pain?

A

elderly, DM, females

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5
Q

What are the 2 most important Ix for someone presenting with chest pain?

A
  • ECG
  • Troponin
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6
Q

Which leads are associated with which territors of the heart? (HINT: visualise 3D model of heart)

A

Anterior: V1-V4

Inferior: ll. aVF, lll

Lateral: l, V5-V6, aVL

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7
Q

Which leads are associated with which coronaty arteries? (HINT: visualise 3D model of heart)

A

V1-V4: left ANTERIOR descending

ll. lll. aVF: right coronary

l. V5-V^: left circumflex

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8
Q

Expected Ix results for angina, unstable angina, STEMI and NSTEMI

A

Angina: changes only seen in exercise ECG

UA: ECG changes but normal trop

NSTEMI: increased trop, widespread ST depression and/or inverted T-waves

STEMI: increased trop, persistent ST elevation in leads V2-V3 + new LBBB

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9
Q

Common management in all patients presenting with ACS (with key dose)

A

MONA
1. Morphine (if pt is in severe pain)
2. Oxygen (Only if sats are <94%)
3. Nitrates (cautious if Pt is hypotensive)
4. aspirin 300mg

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10
Q

Drugs used in longterm Mx of pt with ACS

A

aspirin + statins for all
sublingual GTN to abort attacks

1st line: BB/CCB monotherapy
2nd line: BB/CCB combination therapy
3rd line: atypical drugs

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11
Q

Which CCB should be used as monotherapy for angina and which can be used with a BB?

A

Alone: verapamil, diltiazem (will cause complete block if used with BB)

With BB: long-acting dihydropyridine like amlododipine, nifedipine

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12
Q

if a patient is on monotherapy and cannot tolerate the addition of a calcium channel blocker or a beta-blocker then consider less common antianginals like:

A
  • a long-acting nitrate(isobromide mononitrate)
  • ivabradine (reduced HR)
  • nicorandil (vasodilator)
  • ranolazine
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13
Q

Mx of STEMI once confirmed by ECG

A
  1. Is pt presenting with 12h of onset of symptoms?
  2. Can PCI be done in 120 min?

If yes, do PCI.

If PCI cannot be done in 120 min, do fibrinolysis

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14
Q

What drugs are used for fibronlysis?

A

tPA (good mortality outcomes!)e.g alteplase, streptokinase

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15
Q

Drugs given to pt prior to PCI (for pts on/not on anticoag)

A

Prior: needed to do dual antiplatelet therapy (aspirin has been given already under MONA)

if the patient is not taking an oral anticoagulant: prasugrel (higher bleeding risk)

if pt is taking anticoag: clopidogrel

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16
Q

Which acceess is prefered for PCI?

A

radial over femoral

17
Q

Drugs given to Pt during PCI (radial/femoral access)

A

patients undergoing PCI with radial access:
unfractionated heparin with bailout glycoprotein IIb/IIIa inhibitor (GPI) - this is the action of using a GPI during the procedure when it was not intended from the outset, e.g. because of worsening or persistent thrombus. GPI prevents platelet aggregation and thrombus formation.

patients undergoing PCI with femoral access:
bivalirudin with bailout GPI

18
Q

When would you do a CABG?

A

Mulltivessel coronary arterty disease

19
Q

What should be given along with and following fibrinolysis?

A

Along with: antithrombin (fondaparinux, edoxaban)

Following: tricagrelor (antiplatelet)

20
Q

antiplatelets vs anticoagulants

A

Both classes of medications are antithrombotic agents.

Plarelets are the primary mediators that trigger the mechanical pathway of the coagulation cascade. Platelets + fibrin (product of CC) form the clot in a vascular wall.

Anticoagulants disrupt the CC and include Vitamin K antagonists (warfarin), DOACs and LMWH.

Antiplatelets prevent platelet formation and include clopidogrel, ticagrelor, prasugrel.

21
Q

Mx once NSTEMI/UA is confirmed (including score)

A
  1. Aspirin 300mg
  2. Fondaparinux if no immediate PCI
  3. Calculate GRACE Score

If <3% - Give tricagrelor

If >3% - coronary angiography + PCI within 72h if necessary

22
Q

What are the criteria of the GRACE Score?

A

Gold standard biomarker: troponin
Renal (serum creatinine) and cardiac (killip class) function
Age
Cardiac arrest on presentation
ECG findings

23
Q

Pt comes in with NSTEMI/UA, GRACE score <3% but hypotensive - what is the mx?

A

immediate CA + PCI

24
Q

clopidogrel vs ticagrelor - how do you decide which to use?

A

higher bleeding risk = use clopidogrel

25
Q

What are Killip classes + what are the classes?

A

Killip class - system used to stratify risk post myocardial infarction

I No clinical signs heart failure
II Lung crackles, S3
III Frank pulmonary oedema
IV Cardiogenic shock

26
Q

What is the referral criteria for a Pt who comes in with chest pain?

A

current chest pain or chest pain in the last 12 hours with an abnormal ECG: emergency admission

chest pain 12-72 hours ago: refer to hospital the same-day for assessment

chest pain > 72 hours ago: perform full assessment with ECG and troponin measurement before deciding upon further action

27
Q

Patient with suspected ACS has normal ECG, OR Pt has ECG changes but no clinical symptoms - what do you do?

A

1st line: CT coronary angiography

2nd line: non-invasive functional imaging (SPECT, sress echocardiography)

3rd line: invasive coronary angiography

28
Q

How long after an MI can PDE5 inhibitors (sildenafil/viagra) be used? When must they be avoided?

A

6 months

Pts who are on a nitrate or nicorandil

29
Q

How long after MI must dual antiplatelet therapy be followed?

A

12 months

30
Q

What class of drugs is prescribed for patients with acute MI who also have Sx of HF/LVF? When is it started?

A

Aldosterone antagonist (like eplerenone, spironolactone). Start 3-14 days after MI, after ACE-I.

31
Q

How do you manage a patient with ACS who is also having hyperglycaemia?

A

dose-adjusted insulin infusion with regular monitoring of blood glucose levels to glucose below 11.0 mmol/l

32
Q

G ive tw o cardiac enzym es th at com m only rise follow ing cardiac
dam age

A

Troponin (I/T), CK-MB, CK, AST, LDH.

33
Q

Man hasSTEMI - tw o abnorm alities th a t
m ay be seen on his E C G p rio r to discharge

A

Inverted T waves, pathological Q waves.

34
Q

safe for pt to drive after STEMI?

A

Not allowed to drive for 4 weeks, can drive from then on so long
as not otherwise disqualified, DVLA do not need to be informed.