076 - Cardiac Ischemia - Unstable Angina_NSTEMI

Definition: Myocardial infarction without ST elevations on the surface ECG.
Cause: Plaque rupture with thrombus formation.
Vessel Occlusion: Subtotal or less than 100% occlusion.
- Allows some blood flow beyond the obstruction.
- Myocardium is not completely deprived of oxygen.
Ischemia Type: Subendocardial ischemia.
- The subendocardium is the layer just below the endocardium.
- Most vulnerable to ischemia due to being furthest from coronary vessels (which are in the epicardium) and needing to rely on them for oxygen, unlike the endocardium which can get oxygen from ventricular blood.
- Different from STEMI, which typically causes transmural ischemia (entire wall develops ischemia due to complete blood flow loss).

Symptoms: Ischemic chest pain (similar to STEMI).
ECG:
- No ST elevations (key differentiator from STEMI, due to subtotal occlusion).
- Possible changes: ST depressions, T wave inversions.
- These ECG signs indicate subendocardial ischemia.

Clinical Suspicion: Ischemic chest pain + T wave inversions or ST depressions on ECG.
Cardiac Biomarkers (normally in myocytes, spill into blood with injury):
- Troponin (I or T):
  - Increases 2-4 hours after NSTEMI.
  - Remains elevated for several weeks.
- CK-MB (Creatinine Kinase - Myocardial Band):
  - Increases 4-6 hours after MI.
  - Normalizes within 2-3 days.
  - CK Forms:
    - CKMM: Predominant in skeletal muscle.
    - CKMB: Predominant in cardiac cells.
    - CKBB: Predominant in brain.
  - Issue: Elevated CK can occur from non-cardiac sources (e.g., rhabdomyolysis, which has high CK, including some CKMB).
  - Solution: Use the ratio of CK-MB to total CK.
    - MI: High proportion of total CK is CK-MB.
    - Rhabdomyolysis: Very little of total CK is CK-MB, ratio is helpful.
- AST (Aspartate Aminotransferase):
  - Typically used for liver problems.
  - Isolated increase can indicate MI, especially if patient presents with abdominal pain as an anginal equivalent. Always check EKG for abdominal pain.

Nature: Thrombotic and ischemic problem.
Urgency: Not an emergent situation with a "ticking clock" like STEMI.
- Subtotal occlusion allows some distal blood flow.
- Emergency angioplasty usually not performed.
- Thrombolysis not administered.
Typical Medical Therapy (STAT):
- Aspirin: Reduces thrombus burden.
- Beta blockers: Reduce myocardial oxygen demand.
- Heparin: Reduces risk of clot formation.
Angioplasty: Non-emergent; can wait hours or a day until the patient is stabilized.

Similarity to NSTEMI: Very similar clinical syndrome.
Cause: Plaque rupture with thrombus formation and subtotal vessel occlusion.
Blood Flow: Some blood flow beyond the occlusion to the myocardium.
Symptoms: Ischemic chest pain.
Key Differentiator from NSTEMI: Normal cardiac biomarkers (troponin, CK-MB).
- If biomarkers are elevated, it's NSTEMI.
- If biomarkers are normal, it's unstable angina.
Underlying Process: Same at the blood vessel level as NSTEMI.

Primary Basis: Largely dependent on patient's history due to normal biomarkers.
History Features:
- Chest pain increasing in frequency and intensity (e.g., multiple episodes per day, growing severity).
- Chest pain at rest.
- These features are not typically seen in stable angina.
ECG Changes:
- May show ST depressions or T wave inversions (similar to NSTEMI).
- However, these are not always present.

Consistency: Same treatment as NSTEMI.
Clinical Grouping: Often grouped with NSTEMI in clinical trials (e.g., "UA/NSTEMI").
Reasoning: Both syndromes share the same pathologic process (plaque rupture with subtotal occlusion) and respond to the same therapeutic strategies.