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Year 3 > Acute coronary syndromes (CV) > Flashcards

Acute coronary syndromes (CV) Flashcards

1
Q

What does ACS refer to?

A

A spectrum of acute myocardial ischaemia and/or infarction

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2
Q

What are the types of ACS? (3)

A
  • unstable angina
  • NSTEMI
  • STEMI
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3
Q

How can you remember LBBB?

A

WiLLiaM

  • W in V1
  • M in V5/V6
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4
Q

What are some causes of LBBB? (1 + 5)

A

Always pathological:

  • MI
  • hypertension
  • aortic stenosis
  • cardiomyopathy
  • hyperkalaemia
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5
Q

What does new onset LBBB prompt?

A

Investigation for ACS –> troponin levels

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6
Q

What type of MI is LBBB most likely to be?

A

Anterior-anteroseptal MI

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7
Q

How can you remember RBBB?

A

MaRRoW

  • M in V1
  • W in V5/V6
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8
Q

What are some causes of RBBB? (3)

A
  • can be normal - more common with increasing age (vs LBBB - always pathological)
  • RVH
  • chronically increased RV pressure (cor pulmonale)
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9
Q

How can you differentiate between LBBB and RBBB on ECG?

A
  • LBBB: WiLLiaM (W in V1, M in V5/V6)
  • RBBB: MaRRoW (M in V1, W in V5/V6)
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10
Q

What does ACS result in?

A

Angina pectoris due to partial/total occlusion of a coronary artery due to plaque rupture (thrombosis), embolus or dissection –> necrosis

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11
Q

What are some clinical features of ACS? (10)

A
  • acute central chest pain
    • dull, squeezing tightness
    • radiates to left chest, arm, shoulder, neck, jaw
    • crushing
  • dyspnoea (SOB)
  • sweating
  • pallor
  • nausea and vomiting
  • palpitations
  • syncope and dizziness
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12
Q

What do you check on examination of ACS to rule out aortic dissection?

A

Check both radial pulses

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13
Q

What may develop and be seen on examination in later stages of ACS?

A

A pericardial friction rub or peripheral oedema

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14
Q

What is an atypical presentation of ACS?

A

Painless in elderly and diabetics - presentation includes syncope, pulmonary oedema, epigastric pain and vomiting

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15
Q

How can an MI cause mitral regurgitation and what would you see on examination?

A
  • due to rupture of the tendinous cords that usually hold the valve in place
  • flash pulmonary oedema seen in patient
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16
Q

What is a complication of MI that causes S3 + S4 heart sounds?

A
  • left ventricular aneurysm - due to significant damage to part of the ventricular muscle –> weakening
  • patients present with tiredness and breathless
  • persistent ST elevation on ECG (still there from previous MI)
  • can lead to left ventricular thromboembolism –> embolic stroke or other systemic embolisms
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17
Q

What do S3 and S4 heart sounds suggest?

A
  • S3 - LV is larger than normal (as S3 represents sloshing of blood into large ventricle during diastole)
  • S4 - LV is stiffer than normal (as S4 represents the forceful atrial push of blood against a hard ventricular wall)
  • therefore S3+S4 = LV is larger than usual, with stiff walls and causing pulmonary congestion
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18
Q

What do you see on ECG of left ventricular aneurysm (complication of MI)?

A
  • persistent ST elevation in V1-6 on ECG
  • as fibrosis and dead tissue is not able to properly move as expected
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19
Q

What are the symptoms of left ventricular free wall rupture post-MI? (3)

A
  • raised JVP
  • pulsus paradoxus
  • diminished heart sounds
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20
Q

How do we treat left ventricular free wall rupture post-MI?

A

Urgent pericardiocentesis and thoracotomy

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21
Q

Compare unstable angina vs NSTEMI vs STEMI.

A
  • unstable angina - no biochemical evidence of myocardial damage, no raised troponin
  • NSTEMI - ischaemic ECG changes, elevation of troponin/CK
  • STEMI - ST elevation on initial ECG, elevation of troponin/CK, complete occlusion, transmural infarction
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22
Q

What are the risk factors for ACS? (10)

A
  • male
  • diabetes mellitus
  • Fx
  • hypertension
  • hyperlipidaemia
  • smoking
  • age
  • obesity
  • sedentary lifestyle
  • cocaine use
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23
Q

What are the 1st-line investigations for ACS? (5)

A
  • 12-lead ECG - best initial test to differentiate STEMI & NSTEMI
  • cardiac biomarkers - troponin & CK-MB
  • bloods
  • CXR
  • exercise ECG (patients with troponin -ve ACS or stable angina with high pretest probability of coronary heart disease)
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24
Q

What is seen on an ECG in NSTEMI? (2)

A
  • ST depression
  • T wave inversion
  • (transient ST elevation)
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25
Q

What is seen on an ECG in STEMI? (5)

A
  • persistent (>20min) ST elevation in 2+ contiguous leads:
    • leads V2-3: men<40=2.5mm, men>40=2mm, women=1.5mm
    • 1mm in other leads (II, III, avF, aVL)
  • new LBBB (WiLLiaM)
  • hyperacute T-waves
  • T-wave inversion
  • pathological Q-waves
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26
Q

What is PAIL (ECG)?

A
  • Posterior-Anterior-Inferior-Lateral
  • ST elevations in these leads most commonly create reciprocal ST depressions in the corresponding leads of the next letter of the pnemonic
27
Q

In which types of ACS are cardiac troponin levels raised?

A
  • NSTEMI
  • STEMI
  • (not ACS)
28
Q

How often do you repeat cardiac troponin levels after MI?

A

After 1-6 hours

29
Q

When do cardiac troponin levels begin to rise after MI?

A

3 hours after MI begins

30
Q

How long do cardiac troponin levels remain elevated for post-MI?

A

10 days after infarction

31
Q

How long does CK-MB remain elevated for post-MI?

A

3-4 days after infarction - useful to look for reinfarction since troponin may since be elevated from initial MI (10 days)

32
Q

What leads are affected in an anteroseptal/anterior MI, and what artery is affected?

A
  • V1-V4
  • (depression in II, III, aVF)
  • left anterior descending artery
33
Q

What leads are affected in an inferior MI, and what artery is affected?

A
  • II, III, aVF
  • right coronary artery
34
Q

What leads are affected in a lateral MI, and what artery is affected?

A
  • I, aVL +/- V5, V6
  • (depression in III, aVF)
  • left circumflex artery
35
Q

What leads are affected in an anterolateral MI, and what artery is affected?

A
  • V1-V6, I, aVL
  • (depression in III, aVF)
  • proximal LAD artery
36
Q

What leads are affected in a posterior MI, and what artery is affected?

A
  • changes in V1-V3
  • reciprocal changes of STEMI usually seen:
    • horizontal ST depression
    • tall, broad R waves (V1-2)
    • upright T waves
  • confirmed by ST elevation and Q waves in posterior leads V7-9
  • usually left circumflex, also right coronary artery
37
Q

What does deep and widespread ST depression signify?

A

Associated with very high mortality, as it signifies severe ischaemia usually of LAD

38
Q

What might AST and LDH be like in MI?

A

Raised 24hrs and 48hrs post-MI respectively

39
Q

What is associated with a false positive result for exercise ECG?

A

Digoxin

40
Q

What are some differential diagnoses for ACS? (11)

A
  • aortic dissection (check radial pulses)
  • PE
  • pneumothorax
  • pneumonia
  • pericarditis
  • myocarditis
  • GORD
  • acute pancreatitis
  • oesophageal spasm
  • costochondritis
  • anxiety/panic attack
41
Q

What is the initial management for acute ACS? (4)

A

MONA

  • Morphine - patient with severe pain
  • Oxygen - if sats<94
  • Nitrates - contraindicated if hypotensive <90mmHg
  • Aspirin - 300mg
42
Q

What do individuals with NSTEMI require after initial management?

A

GRACE score calculated

43
Q

How would we treat patients with ACS with Hb<80g/L?

A

Transfusion of packed red cells

44
Q

What is the 1st line initial management for STEMI?

A

Aspirin 300mg and continue indefinitely

45
Q

What are the two types of coronary reperfusion therapy for STEMI?

A
  • percutaneous coronary intervention (PCI) - presentation within 12h of symptom onset + PCI possible within 2h
  • fibrinolysis (considered if significant delay in being able to provide PCI) - within 12h of symptoms if PCI cannot be given within 2h
46
Q

How do you manage a STEMI patient with symptoms <12h and PCI possible in 2h? (4)

A
  • angiography
  • unfractionated heparin + bailour GPIIb/IIIa inhibitor before PCI
  • PCI (aka coronary angioplasty) with a drug eluting stent
  • dual antiplatelet therapy with aspirin + prasugrel (if not on anticoagulant)/clopidogrel (if on anticoagulant)
47
Q

What do we do if a patient has pain or haemodynamic instability after PCI?

A

Urgent CABG

48
Q

What is the preferred site for PCI insertion?

A

Radial artery - if this does not work then femoral artery

49
Q

How do you manage a STEMI patient with symptoms <12h and PCI NOT possible in 2h? (5)

A
  • fibrinolysis:
  • antithrombin e.g. fondaparinux should be given, then:
  • thrombolysis –> alteplase (t-PA)
  • ticagrelor (antiplatelet) given after this (clopidogrel if bleeding risk)
  • must do ECG after 60-90 minutes & transfer for urgent PCI if ST elevation not resolved from fibrinolysis
50
Q

What is the 1st-line management for NSTEMI/angina? (5)

A
  • admit to CCU
  • aspirin - 300mg initially –> 75mg indefinitely
  • clopidogrel - 300mg initially –> 75mg for at least 1 year if troponin +ve or high risk
  • fondaparinux (activates antithrombin III) - given unless high bleeding risk/PCI planned
  • if immediate angiography planned or creatinine>256umol/L –> unfractionated heparin
51
Q

What do you calculate for NSTEMI/angina after initial management to inform further treatment?

A

GRACE (Global Registry of Acute Coronary Events) –> estimated 6 month mortality

  • <1.5% = lowest risk
  • 1.5-3% = low risk
  • 3-6% = intermediate risk
  • 6-9% = high risk
  • > 9% = highest risk
52
Q

How is a NSTEMI/angina patient with low risk (GRACE<3%) managed? (2)

A
  • aspirin
  • dual antiplatelet therapy: aspirin + ticagrelor (low bleeding risk)/clopidogrel (high bleeding risk)
53
Q

When should patients with NSTEMI/angina have coronary angiography (with follow-on PCI if necessary)? (5)

A
  • immediate: patients who are clinically unstable e.g. hypotensive
  • within 72h: patients with GRACE score>3% (intermediate, high or highest risk)
  • coronary angiography considered for patients if ischaemia subsequently experienced after admission
  • unfractionated heparin given before PCI regardless of if patient has had fondaparinux or not (due to easier reversibility with protamine sulfate)
  • aspirin + ticagrelor / prasugrel (no anticoagulant) / clopidogrel (on anticoagulant)
54
Q

What is the long-term management of MI?

A

He had an MI, now he DABS

  • Dual antiplatelet therapy (aspirin + ticagrelor/clopidogrel if already on anticoagulation)
  • ACEi (ramipril)
  • Beta-blocker (bisoprolol) - can reduce awareness of hypoglycaemic events
  • Statin (atorvastatin 80mg for secondary prevention dose, 20mg primary prevention dose)
55
Q

What are some side effects of ACEi (post-MI)? (4)

A
  • angioedema
  • cough
  • hyperkalaemia especially when also on potassium-sparing diuretic e.g. amiloride
  • 1st-dose hypotension
56
Q

What is DVLA advice post-MI?

A

Cannot drive for 4 weeks

57
Q

How are patients who have had MI secondary to cocaine use managed?

A

IV benzodiazepines e.g. lorazepam

58
Q

What are some complications of ACS?

A
  • increased risk of MI and other vascular disease
  • cardiac injury from MI –> HF and arrhythmias
  • early complications e.g. death, cardiogenic shock, HF, ventricular arrhythmias, heart block, pericarditis, myocardial rupture, thromboembolism
  • late complications e.g. ventricular wall rupture, valvular regurgitation, ventricular aneurysms, tamponade, Dressler’s syndrome, thromboembolism
  • pulmonary oedema
59
Q

Mnemonic for common complications of MI

A

DARTH VADER:

  • Death
  • Arrhythmias
  • Rupture - of septum or outer walls
  • Tamponade
  • Heart failure
  • Valve disease
  • Aneurysm
  • Dressler’s syndrome (AI pericarditis 2-10wk after MI)
  • Embolism
  • Reinfarction
60
Q

What is an indicator of poor prognosis in ACS?

A
  • cardiogenic shock (30d mortality 81%)
  • lung crackles heard on auscultation –> HF occurred with secondary pulmonary oedema
61
Q

What classification system is used in acute MI to determine mortality risk?

A

Killip class:

  • Killip class I - no clinical signs of HF
  • Killip class II - lung crackles + S3
  • Killip class III - frank pulmonary oedema, 30d mortality 38%, HF
  • Killip class IV - cardiogenic shock - tissue hypoperfusion, oliguria, systolic BP<90mmHg with hypovolaemic shock
62
Q

What is a common complication post-MI?

A
  • heart block
  • RCA commonly blocked - AV node infarction –> loss of normal conduction pathway from atria to ventricles
63
Q

What is the most common cause of death post-MI?

A

Ventricular fibrillation

Year 3 (80 decks)

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