Acute Coronary Syndrome Flashcards

1
Q

What is Acute Coronary Syndromes (ACS)?

A

ACS

  • Any array of clinical symptoms resulting from underlying acute myocardial ischemia
    • i.e. - mismatch of demand vs supply
  • Most often caused by ruptuture of atherosclerotic plaque and partial/complete thrombosis
    • i.e. - includes unstable angina , NSTEMI & STEMI – (not stable angina)
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2
Q

ACS Epidemiology

  1. How many Americans per year suffer from ACS?
  2. What precentage of people will die from ACS?
A

ACS Epidemiology

  1. 1.7 million people per year (note the decimal point)
  2. Approx 38% will die from ACS
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3
Q

What is the main cause of ACS?

A

Atheroscleoritc plaque rupture with thrombus

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4
Q
  1. What is transmural ischemia?
  2. What is subendocardial ischemia?
A
  1. Transmural: ischemia spans the entire thickness of the myocardium
    • Most often due to occlusion
  2. Subendocardial: ischemia involves the innermost layers of the myocardium only
    • Most often due to partial occlusion

If ischemia is prolonged results in myocyte death and tissue necrosis - i.e. M.I.

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5
Q

Transmural infarcts

  1. What is the clinical name for it?
  2. What are the ECG findings c/w it?
  3. What would the serum biomarkers look like?
A

Tranmural Infarcts

  1. Otherwise known as STEMI
  2. ST-segment elevation
  3. Positive Troponin-I/T & CK-MB
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6
Q

Subendocardial Infarcts

  1. Clinical name?
  2. ECG findings?
  3. Serum markers?
A

Subendocardial infarcts

  1. Otherwise known as NSTEMI
  2. ST-segment depression and/or T-wave inversion
  3. Positive Troponin-I/T & CK-MB
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7
Q

Troponins vs Creatine Kinase-MB

  1. Which is more sensitive/specific for myocardium?
  2. When do Troponins/CK-MB rise?
  3. When do Troponins/CK-MB peak?
A
  1. Troponin
  2. Troponin rise after 3-4 hr after onset of pain/ischemia
    • CK-MB begin to rise 3-8hr after
  3. Troponin peak at 18-36 hrs
    • CK-MB peaks at 24 hrs
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8
Q

Describe the physiology behind elevated troponin levels in the blood during/after an M.I.

A

Troponin

  • Regulatory protein in muscle cells that controls interactions between myosin and actin
    • Disruption of sarcolemma -> leak of intracellular molecules into cardiac interstitium -> blood
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9
Q

What are the clinical symptoms of stable vs unstable angina?

A

Stable Angina

  • Present when there is increased demand for myocardial O2 in a reproducible fashion

Unstable Angina

  • Increase in duration, intensity, or frequency
  • Less provocation/can occur at rest
  • New onset
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10
Q

Unstable Angina

  1. Amount of vessel occlusion?
  2. Serum biomarkers?
  3. ECG findings?
A

Unstable Angina

  1. Partial vessel occlusion
  2. Negative Troponin/CK-MB
  3. ST-depression
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11
Q

Treatment of ACS–STEMI

What is the treatment algorhythm?

A

Algorhythm:

  • Access to a cath lab w/in 90 min?
    • Yes
      • Cath lab -> Primary PCI (i.e. angioplasty/stent)
    • No
      • Fibrinolytic therapy (e.g. tPA)
  • Add beta blockers/nitrates as adjuvant therapy
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12
Q

Treatment of ACS–UA/NSTEMI

What is the treatment algorhythm for unstable angina and NSTEMI?

A
  • Halt the progression of the clot using both
    • Anti-platelet agent
      • Aspirin + P2Y12 inhibitor (Clopidogrel)
    • Anticoagulant
      • Unfractionated heparin or enoxaparin
  • Reduce myocardial oxygen demand
    • Beta blockers & nitrates
  • Catheterization for percutaneous coronary intervention (PCI) – at some point
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