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MBBS IV - Junior Clerkship WCS > JC 07 (Medicine) - Acute Coronary Syndrome > Flashcards

JC 07 (Medicine) - Acute Coronary Syndrome Flashcards

1
Q

Differentiate Unstable Angina, NSTEMI and STEMI

A

□ Unstable angina (UA): severe ischaemia at rest without infarction

□ NSTEMI: partial occlusion of coronary arteries (usually due to critical narrowing) → some myocardial necrosis but not transmural

□ STEMI: complete occlusion of coronary arteries (usually due to acute plaque disruption leading to complete thrombosis) → transmural myocardial necrosis

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2
Q

4 major clinical presentations of ACS

A
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3
Q

Mechanism of Myocardial Ischaemic pain

A
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4
Q

Causes of exertional chest pain vs resting chest pain

A
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5
Q

Classification of ACS

A
  1. Unstable angina
    - Plaque rupture with thombus formation > partial occlusion of vessel with No infarction
  2. NSTEMI
    - Plaque rupture with thrombus formation > partial occlusion of vessel > subendocardial myocardial injury and infarct
  3. STEMI
    - Plaque rupture with thrombus formation > complete occlusion of 1 of 3 major coronary arteries > Transmural myocardial injury and infarct
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6
Q

Outline diagnostic criteria for ACS (4)

A
  1. Clinical presentation
  2. ECG: Acute ischemic changes
  3. Biochemical: Biomarkers for myocardial injury

+/- 4. Imaging: ECHO or CT coronary angiogram show regional wall motion abnormality

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7
Q

Describe the 4 types of chest pain in ACS

A

Clinical presentation: can be a new phenomenon or on top of background stable angina

□ Angina at rest: prolonged >20min angina at rest (due to accumulation of toxic metabolites)

□ New-onset angina: transient ectopic beats, pain

□ Increasing angina: previous angina w/ ↑frequency, ↑duration

□ Post-infarct angina: recurrent angina after recent MI

(complete infarct and totally ischemic muscles do not produce toxic metabolites that cause rest pain anymore)

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8
Q

Differentiate ACS and MI

A

ACS = clinical term referring to patients with suspicion or confirmation of acute myocardial ischaemia or infarction

MI = acute myocardial injury (as evidenced by ↑cTn) in the setting of clinical evidence of acute myocardial ischaemia (as evidenced by chest pain or ECG changes)

MI = all tests done and confirmed

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9
Q

Associated symptoms of ACS

A

□ Breathlessness: may be the only symptom in ‘silent MI’ (esp in elderly or DM)

□ Syncope: co-existing arrhythmia or profound hypotension

□ Vomiting, sinus bradycardia: due to vagal stimulation (esp in inferior MI) or opiates

□ Sudden death: often within the first hour, due to VF or asystole

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10
Q

Triggering factors of ACS

A

□ Unusual heavy exercise
□ Emotional stress
□ Progression from Unstable Angina
□ Surgical procedures
□ Infections, eg. pneumonia
□ Circadian (peak incidence between 6am to 12pm)

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11
Q

5 ddx of Cardiac-cause chest pain

A
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12
Q

3 Ddx of respiratory-cause acute chest pain

A
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13
Q

6 ddx of gastro-intestinal cause of acute chest pain

A
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14
Q

3 causes of acute chest pain that is not cardiac, respiratory or GI in origin

A
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15
Q

Compare the different acute chest pain due to cardiac causes

A
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16
Q

ECG features of STEMI, NSTEMI and Unstable Angina

A
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17
Q

ECG features of NSTEMI

A

Non-ST-elevation ACS (NSTE-ACS):
□ Indicates: partial occlusion of major vessels(or complete occlusion of minor vessels) → unstable angina or subendocardial MI

  • *□ ECG features:**
  • *→ ST depression**
  • *→ T wave changes**
  • *→ ± some loss of R waves (if infarcted)**
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18
Q

Ddx ST elevation on ECG

A
  • Acute STEMI (Convex ST, III>II)
  • Acute pericarditis (Concave ST, II>I/III/aVF)
  • LVH with strain pattern (Concave ST, V1-2)
  • Early repolarization (J point elevation follows S wave, Concave ST, No reciprocal ST depression)
  • LBBB
  • Ventricular aneurysm
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19
Q

Other ECG features suggestive of acute MI other than ST segment changes

A

□ Hyperacute T wave: occurs within minutes of acute MI

□ Pseudonormalization of T wave: transient normalization of T wave from an inverted form (transient recanalization of coronary artery)

□ Wellens syndrome: deeply inverted or biphasic T waves in V2-3 (High LAD stenosis)

□ ST elevation in aVR: usually indicates left main stem occlusion

20
Q

List serum cardiac markers

A

Myoglobin

CKMB

Cardiac Troponin I

Cardiac Troponin T

BNP

21
Q

Compare the time course of each serum cardiac biomarker

A

1st: Myoglobin

2nd: Creatine kinase MB isoform (CKMB):
Course: rise (4-6h) → peak (12h) → normalize (48-72h)

3rd: Cardiac troponin T or I (cTnT, cTnI):
Course: rise (4-6h) → elevated for up to 2 weeks

Creatinine kinase - muscles, non-specific

Troponin - specific for cardiomyocyte, very sensitive (may have false positive)

22
Q

Compare the function of Cardiac troponin T or I vs CKMB monitoring

A

Cardiac Troponin:

□ Advantages: not normally present → ↑sensitivity ↑specificity
□ Use: detection of first infarct event

CKMB:

□ Caveat: not sensitive or specific
(esp consider skeletal muscle damage eg. IM injection)
□ Use: mainly to detect early re-stenosis

23
Q

Confounding non-MI causes of cardiac troponin increase in serum

A
24
Q

5 types of MI

A

Type 1: MI caused by Atherothrombotic CAD, preciputated by Atherosclerotic plaque disruption (rupture or erosion)

Type 2: MI secondary to ischemia due to imbalance between oxygen demand and supply (no atherothrombosis) eg. coronary spasm, anaemia or hypotension

Type 3: Sudden cardiac death - MI with typical symptoms and new ischemic ECG changes, but died before blood biomarker diagnosis

Type 4: MI related to PCI (procedural complication)

Type 5: MI related to CABG (procedural complication)

25
Q

3 investigations to confirm type 4 and 5 MI

A
  1. New ECG changes
  2. Angiography: evidence of new coronary artery occlusion
  3. Imaging: evidence of new loss of regional wall movement/ new coronary artery occlusion
26
Q

Diagnostic criteria for Type I MI

A

Detection of ↑/↓cardiac biomarker values (preferably cTn) with ≥1 value above 99th URL; plus ≥1 of

  1. Symptoms of ischaemia
  2. New or presumed new significant ST-T changes or new LBBB
  3. Development of pathological Q waves
  4. Imaging evidence of new loss of viable myocardium or new regional wall motion abnormality
  5. Identification of an intracoronary thrombus by angiography or post-mortem
27
Q

Diagnostic criteria of type II MI

A

Detection of ↑/↓cardiac biomarker values (preferably cTn) with
≥1 value above 99th URL; plus ≥1 of

  1. Symptoms of ischaemia
  2. New or presumed new significant ST-T changes or new LBBB
  3. Development of pathological Q waves
  4. Imaging evidence of new loss of viable myocardium or new
    regional wall motion abnormality

Same as Type 1 criteria but NO EVIDENCE OF CORONARY ATHEROTHROMBOSIS

28
Q

List some causes of Type II MI

A

Type 1 = atherosclerosis + thrombus; Type 2 = oxygen supply and demand mismatch, no thrombus

Causes of increased coronary oxygen demand in type 2:

  1. Coronary spasm
  2. Coronary microvascular dysfunction
  3. Coronary embolism
  4. Coronary artery dissection
  5. Severe HTN and LVH
  6. Respiratory failure, severe anaemia, hypotension, shock
29
Q

Explain why cardiac troponin levels rise and fall after infarction

A

Infarction due to total blockage of artery and causing complete cardiomyocyte death

>> dead cardiomyocytes cannot release any more troponin

>> Troponin rise and fall

30
Q

Outline the ddx if troponin levels rise/ fall vs stabilize over time

A
31
Q

Indication for cardiac imaging

Types of cardiac imaging

A

Indication: in patients with low-to-intermediate risk for ACS to rule out ACS

Types:

  • Echocardiography
  • CT coronary angiogram
  • Stress imaging: ETT, MPI, stress echo/MRI
32
Q

Outline the TIMI risk score for NSTE-ACS stratification

A

10x difference in mortality between low risk and high risk*** remember this criteria

33
Q

Outline the GRACE risk score scheme for NSTE-ACS

A
34
Q

5 principles of management of ACS

A
35
Q

First-line immediate management of NSTE-ACS (6)

A
  1. Bed rest with continuous ECG monitoring
  2. Supplemental O2, correct precipitating factors e.g. anemia, hypoxia, arrhythmia
  3. Anti-thrombotic therapy/ Anti-coagulants
  4. Revascularization procedure
  5. Anti-ischemic therapy - nitrates, BB, CCB
  6. Analgesia
36
Q

List 4 Anti- Ischemic drugs for ACS

A

Nitrate: sublingual or IV

B-blocker: metoprolol, atenolol

CCB: verapamil, diltiazem, nifedipine

Morphine: severe angina

37
Q

List 3 types of antiplatelet for ACS

Define DAPT

A

Aspirin (300mg loading and daily 100 doses)

P2Y12 inhibitor e.g. clopidogrel, ticagrelor

GPIIb/IIIa receptor antagonist e.g. abiciximab, tirofiban

DAPT- Dual antiplatelet therapy

  • Maintenance dose of P2Y12 receptor inhibitor for 1 YEAR + Aspirin daily
38
Q

List 3 type of anticoagulants for ACS

A

Unfractionated Heparin

LMW Heparin/ Pentasaccharides

Warfarin or NOAC

39
Q

Types of P2Y12 inhibitors and which one is indicated for STEMI

A

Ticagrelor

Onset time is shortest - 30 min

Add-on therapy with aspirin reduces mortality rate

40
Q

List all drugs/ treatment for long-term management after ACS

A

Antiplatelet:

    • Aspirin forever
    • Dual anti-platelet therapy for at least 1 year after PCI

Anticoagulant: Only warfarin

Reperfusion: CABG or PCI

Long-term Cardioprotective:

  1. ACEi/ ARB
  2. High intensity statin: Crestor, Lipitor
  3. Mineralocorticoid antagonist: Eplerenone
41
Q

Indications for invasive surgery for ACS

A

Urgent/ deadly:

  • Haemodynamic shock
  • Dangerous arrhythmia/ cardiac arrest

Refractory ACS:

  • Failed medical treatment, recurrent angina
  • Heart failure with refractory angina/ STEMI

Mechanically complicated MI

42
Q

Criteria for early invasive strategy for ACS (<24h)

A
  • Troponin profile compatible with MI
  • Dynamic ST changes
  • GRACE score >140
43
Q

Criteria for delayed invasive strategy against ACS (<72 hours)

A
  • DM
  • Renal failure
  • LVEF <40% or CHF
  • Previous PCI/ CABG
  • Grace score >109 and <140
44
Q

Criteria for choosing CABG over PCI

A

CABG only if:

  1. Left main coronary artery disease, or
  2. 3 or 2 vessels disease with proximal LAD involvement with LV dysfunction
45
Q

List 3 long-term cardioprotective drugs after ACS

A

ACEI or ARB

Statins e.g. Crestor, Lipitor

Mineralocorticoid antagonist (MRA) e.g. Eplerenone

46
Q

Secondary prevention of ACS

A

MBBS IV - Junior Clerkship WCS (131 decks)

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