Week 2: Acute coronary syndrome Flashcards

1
Q

Define acute coronary syndrome.

A

-group of clinical symptoms/signs compatible with acute myocardial ischemia and include: sudden death, unstable angina, non-ST elevation MI (Non-Stemi), ST elevation MI (STEMI)

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2
Q

Describe the mechanism of coronary thrombosis.

A

Atherosclerosis leading to:

  1. plaque rupture:
    - interplaque hemorrhage leads to decreased vessel diameter
    - release of tissue factor, activation of of coagulation cascade
    - exposure of sub endothelial collagen/turbulent blood flow leading to platelet activation and aggregation–>further vasoconstriction, and activation of coag cascade
  2. Dysfunctional endothelium
    - decreased vasodilator effect
    - decreased antithrombotic effect
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3
Q

What are the consequences of coronary thrombosis?

A
  1. small thrombus: non flow limiting
    - no ECG changes
    - healing and plaque enlargement
    - stable angina
  2. Partially occlusive thrombus
    - ST segment depression and/or T wave inversion–>
    - unstable angina if no serum biomarkers
    - non-ST segment elevation MI if +serum biomarkers
  3. occlusive thrombus
    - can have ST segment depression and/or T wave inversion (like above) if it recanalizes or has collateral flow.
    - reperfusion in less than 20mins–>unstable angina
    - reperfusion after 20min and before 2hrs->NSTEMI
    - can have ST elevation which w/ serum biomarkers indicates ST elevation MI
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4
Q

Other uncommon causes of ACS.

A

-suspected when ACS is in young person or person with no coronary risk factors
Severe coronary artery spasm ( primary or cocaine induced)
Coronary emboli ( endocarditis, prosthetic valves)
Coronary trauma
Increased blood viscosity ( polycythemia vera, thrombocytosis)
Markedly increased myocardial oxygen demand ( severe aortic stenosis or acute aortic regurgitation)
Vasculitis syndromes
Congenital coronary artery anomalies

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5
Q

Describe the clinical presentation of Unstable Angina.

A
  • crescendo pattern in which a patient with chronic stable angina experiences a sudden increase in frequency, duration, and/or intensity of ischemic episodes
  • episodes of angina that occur at rest, without provocation
  • new onset of anginal episodes, severe class III severity, without previous CAD symptoms
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6
Q

Describe the clinical presentation of myocardial infarction.

A
  • rapid in onset, rapid crescendo to feeling of doom
  • pain doesn’t go away with rest
  • maybe be little response to nitroglycerin
  • systemic signs from sympathetic response: sweating (diaphoresis), tachycardia, cool and clammy skin due to vasoconstriction
  • dyspnea (due to reduced LV contractility, causes decreased SV, rise in pressure in LV and EDV, conveyed to left atrium and pulmonary veins)
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7
Q

Describe ECG findings in ACS.

A

Unstable Angina and NSTEMI
-ST segment depression and/or T wave inversions. May be transient, occurring just during chest pain in UA, or may persist in patients with NSTEMI
STEMI
-acute: initial ST segment elevation
-hours: ST elevation, Q wave begins, decreased R wave
-1-2days: T wave inversion, Q wave deeper
-Days: ST normalizes, T wave inverted
-Weeks: ST and T normal, Q wave persists.

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8
Q

Assessment of ACS

A
  1. ECG
  2. cardiac biomarkers: Troponin is more sensitive than ck-mb. Onset 3-4 hrs, peak 18-36 hrs, persist up to 10-14 days
  3. Clinical hx and symptoms: chest pain
    If still uncertain, echocardiogram useful for assessing wall motion abnormalities in suspected region of ischemia or infarction
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9
Q

Approach to management after EKG, history, and physical exam of ACS.

A

ALL patients
1. anti-ischemic meds: beta blocker, nitrates, +/-Ca2+ channel blocker
2. General measures: oxygen, pain control
3. additional therapies: ACE inhibitor, statins
STEMI–Reperfusion approach
1. Aspirin
2. heprain
3. clopidogrel
4. reperfusion method: fibronlytic drug or primary PCI w/ GP iib/iiia inhibitor
NSTEMI/UA–antithrombotic approach
1. aspirin
2. heparin
3. clopidogrel
4. high risk patients: GP IIb/IIIa inhibitor, proceed to cardiac cath

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10
Q

Treatment goals and pharmocologic management after ACS.

A
  • relief is ischemia not just chest pain
  • prevent propagation of intracoronary thrombosis
  • ID high risk patients
  • cardiac cath and revascularization in high risk patients who fail medical therapy
  • Standard pharmacologic therapy following discharge from the hospital includes measures to reduce the risks of thrombosis (aspirin and clopidogrel), recurrent ischemia (a
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11
Q

Describe treatment strategies for ACS

A
  1. Conservative
    - stabilized by meds only initially
    - cardiac angiography done only if patients fail medical therapy or noninvasive risk assessment indicate high risk features
  2. early invasive strategy
    - diagnosis angiography with intent to revascularize
    - patients with high risk features
    - advantage of early ID and revascularization for high risk anatomy
    - but costly and potentially risky
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