Cardiac - ACS Flashcards
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
Acute MI Pathophysiology
Phases of myocardial response to AMI
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
ACS
Clinical presentation
Associated symptoms
Risk factors of ACS
Triggering factors of ACS
Triggers:
□ Unusual heavy exercise
□ Emotional stress
□ Progression from Unstable Angina
□ Surgical procedures
□ Infections, eg. pneumonia
□ Circadian (peak incidence between 6am to 12pm)
Ddx cardiovacular cause of chest pain
Ddx of respiratory cause of acute chest pain
Ddx of gastro-intestinal cause of acute chest pain
Misc. ddx of chest pain
Compare the different acute chest pain due to cardiac causes
AMI
Investigations
Radiological Ix:
- ECG
- Echocardiogram: Regional wall motion abnormality, LVEF, complications such as MR/ VSD/ Pericardial effusion, Stress echo
- Coronary angioraphy: IVCA/ CTCA/ MRCA
AMI ECG
Areas of infarction seen on ECG
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
Changes in ECG findings after AMI
□ 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
Function of markers
Biomarkers:
* 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
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)
