JC 07 (Medicine) - Acute Coronary Syndrome Flashcards
(46 cards)
Differentiate Unstable Angina, NSTEMI and STEMI
□ 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
4 major clinical presentations of ACS
Mechanism of Myocardial Ischaemic pain
Causes of exertional chest pain vs resting chest pain
Classification of ACS
- Unstable angina
- Plaque rupture with thombus formation > partial occlusion of vessel with No infarction - NSTEMI
- Plaque rupture with thrombus formation > partial occlusion of vessel > subendocardial myocardial injury and infarct - STEMI
- Plaque rupture with thrombus formation > complete occlusion of 1 of 3 major coronary arteries > Transmural myocardial injury and infarct
Outline diagnostic criteria for ACS (4)
- Clinical presentation
- ECG: Acute ischemic changes
- Biochemical: Biomarkers for myocardial injury
+/- 4. Imaging: ECHO or CT coronary angiogram show regional wall motion abnormality
Describe the 4 types of chest pain in ACS
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)
Differentiate ACS and MI
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
Associated symptoms of ACS
□ 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
Triggering factors of ACS
□ Unusual heavy exercise
□ Emotional stress
□ Progression from Unstable Angina
□ Surgical procedures
□ Infections, eg. pneumonia
□ Circadian (peak incidence between 6am to 12pm)
5 ddx of Cardiac-cause chest pain
3 Ddx of respiratory-cause acute chest pain
6 ddx of gastro-intestinal cause of acute chest pain
3 causes of acute chest pain that is not cardiac, respiratory or GI in origin
Compare the different acute chest pain due to cardiac causes
ECG features of STEMI, NSTEMI and Unstable Angina
ECG features of NSTEMI
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)**
Ddx ST elevation on ECG
- 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
Other ECG features suggestive of acute MI other than ST segment changes
□ 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
List serum cardiac markers
Myoglobin
CKMB
Cardiac Troponin I
Cardiac Troponin T
BNP
Compare the time course of each serum cardiac biomarker
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)
Compare the function of Cardiac troponin T or I vs CKMB monitoring
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
Confounding non-MI causes of cardiac troponin increase in serum
5 types of MI
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)
