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MBBS VI - SpC - Medicine > Cardiac - ACS > Flashcards

Cardiac - ACS 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

Acute MI Pathophysiology
Phases of myocardial response to AMI

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

ACS

Clinical presentation
Associated symptoms

A
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10
Q

Risk factors of ACS
Triggering factors of ACS

A

Triggers:
□ 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

Ddx cardiovacular cause of chest pain

A
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12
Q

Ddx of respiratory cause of acute chest pain

A
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13
Q

Ddx of gastro-intestinal cause of acute chest pain

A
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14
Q

Misc. ddx of chest pain

A
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15
Q

Compare the different acute chest pain due to cardiac causes

A
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16
Q

AMI

Investigations

A

Radiological Ix:
- ECG
- Echocardiogram: Regional wall motion abnormality, LVEF, complications such as MR/ VSD/ Pericardial effusion, Stress echo
- Coronary angioraphy: IVCA/ CTCA/ MRCA

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17
Q

AMI ECG

Areas of infarction seen on ECG

A
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18
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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19
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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20
Q

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

Changes in ECG findings after AMI

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

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21
Q

List serum cardiac markers

Function of markers

A

Biomarkers:
* Myoglobin
* CKMB
* Cardiac Troponin I
* Cardiac Troponin T
* BNP

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22
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)

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23
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

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

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/ loss of viable myocardium
  4. Cardiac biomarkers >99 percentile URL
26
Q

AMI

Diagnostic criteria

A
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

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

A
30
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
31
Q

Outline the TIMI risk score for NSTE-ACS stratification

A

Early risk assessment for UA/ NSTEMI
o All patients with UA/ NSTEMI should undergo risk assessment since it can determine prognosis and guide the timing of coronary angiography and possible revascularization
o Early risk stratification tools = TIMI/ GRACE risk score

32
Q

Outline the GRACE risk score scheme for NSTE-ACS stratification

A

Early risk assessment for UA/ NSTEMI
o All patients with UA/ NSTEMI should undergo risk assessment since it can determine prognosis and guide the timing of coronary angiography and possible revascularization
o Early risk stratification tools = TIMI/ GRACE risk score

33
Q

Right coronary artery

Origin
Branches
Supply territory
Areas of corresponding infarct

A
34
Q

Left coronary artery

Origin
Branches
Supply territory
Areas of corresponding infarct

A
35
Q

Troponin

Sources
Limit for MI
Confounding non-MI causes

A

Source:
- Myocardial
- Skeletal muscles

cTn reference decision limit for MI
- Any troponin elevation > 99th percentile (URL) = myocardial damage

cTnT and cTnI
- Sensitive and specific
- Cardiac specific but NOT specific for the cause

36
Q

Creatine kinase

Sources
Isoenzymes
Function
Confounding factors

A
37
Q

5 principles of management of ACS

Outline treatment plan

A

General management:
- ABC, bed rest with continuous ECG monitoring
- Support: Analgesics with morphine, Anxiolytics
- First line investigations

Acute:
- Anti-thrombotic therapy: Anti-platelet + Anti-coagulants
- Anti-ischmeic therapy: BB, CCB, Nitrates
- Support: Analgesics with morphine, Anxiolytics
- Coronary revascularization with fibrinolysis: tPA, rPA, Streptokinase
- Coronary revascularization with PCI

Long-term therapy and secondary prevention:
- Lifelong aspirin +/- warfarin
- ACEi/ARB
- Aldosterone antagonist
- Beta-blockers
- Statin
- Lifestyle modification

38
Q

Anti-thrombotic therapy for ACS

Drug choices
MoA

A

Aspirin
- Non-selective COX-1 and COX-2 inhibitors
- ↓ Thromboxane A2 (TXA2) production from COX-1 by platelets
- Inhibits platelet aggregation

Thienopyridine (P2Y12) antagonist
- P2Y12 is a component of ADP receptor
- ADP is stored in platelet dense granules and released upon platelet activation
- Amplifies the initial signal for platelet activation and facilitate platelet aggregation

GP IIb/IIIa antagonist
- bind to the receptor and prevent fibrinogen and von Willebrand factor (vWF) from binding to the receptors
- protection from ischemic events in patients undergoing percutaneous coronary intervention (PCI)

39
Q

Thienopyridine (P2Y12) antagonist

Choice of P2Y12 antagonist
Use with PCI, fibrinolysis or without fibrinolysis/PCI

A
40
Q

GP IIb/IIIa antagonist

Drug choice
Benefit
Contraindications

A

GP IIb/IIIa antagonist
- bind to the receptor and prevent fibrinogen and von Willebrand factor (vWF) from binding to the receptors
- protection from ischemic events in patients undergoing percutaneous coronary intervention (PCI)

41
Q

Anti-coagulant for ACS

Drug choice
MoA
S/E

A
42
Q

Anti-coagulant for ACS

Advantage of unfractionated heparin vs LMW heparin

A
43
Q

Anti-ischemic therapy for ACS

Drug choices
Indications for each drug
Contraindication
MoA

A
44
Q

ACS

Supportive medication (apart from anti-thrombotic and anti-ischemic therapy)

A
45
Q

Coronary revascularization via fibrinolytic therapy
- Indications
- MoA
- Drug choices
- Major complication

A
46
Q

Coronary revascularization via fibrinolytic therapy
Absolute contraindications
Relative contrainfications

A
47
Q

Coronary revascularization via PCI

Indications in STEMI
Access
Stent choices
Subsequent therapy

A
48
Q

PCI

Complications

A
49
Q

ACS

Signs of successful reperfusion

A
50
Q

Factors indicating early invasive strategy or ischemia-guided strategy in NSTE-ACS

A
51
Q

STEMI treatment flowchart

A
52
Q

STEMI PCI choice flowchart

A
53
Q

Long-term post-MI management

A
54
Q

Structural and conductive complications of AMI

A
55
Q

Circulatory complications of AMI

A

MBBS VI - SpC - Medicine (80 decks)

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