11/4 Ischemic Heart Disease (ACS) - Moreyra Flashcards Preview

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Flashcards in 11/4 Ischemic Heart Disease (ACS) - Moreyra Deck (28):

myocardial oxygen supply vs. myocardial oxygen demand

factors affecting oxygen supply

  1. oxygen content
    • in clinical practice, anemia/low Hb doesn't really hold as a cause of oxygenation imbalance bc compensation kicks in
  2. coronary blood flow
    • depends on perfusion pressure and resistance
    • resistance is the major determinant of flow; influenced by several addt'l factors:
      1. external compression: incr resistance/decr flow during systole
      2. arterial tone
      3. metabolic factors: hypoxia? ATP→ADP→AMP, releasing ADENOSINE (powerful coronary vacodilator). also lactate, acetate, H, CO2
      4. endothelial factors: vasodil via cGMP
      5. neural factors: SNS alpha, beta2 receptors

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endothelial factor induced relaxation

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endothelial vasoactive factors

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myocardial oxygen supply vs. myocardial oxygen demand

factors affecting oxygen demand

  1. wall stress: S = P*r/2h [h = thickness]
  2. heart rate
  3. contractility

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atherosclerosis timeline

newer theory about heart ischemia

  • not just obstruction of coronary vessels via ischemia
  • combo of atherosclerosis AND increased tone of coronary vessels
    • both together: DECREASED FLOW OF BLOOD 

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relationship between stenosis and flow

increasing stenosis decreases the change in flow that will result from vasodilation

  • eventually, mismatch in supply and demand

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interaction between platelets and endothelial cells

recall: in general, when platelets aggregate, they stimulate sm muscle contraction (vasoconstriction)


endothelial cells produce vasoactive substances: prostacyclin and NO

  1. cause vasodilation via relaxation of sm muscle
  2. prevent platelets from aggregating

implication: damage to the endothelium leads to vasoconstriction (directly and indirectly) → contributes to ischemic heart disease along with any existing obstructions

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ischemic heart disease

most common cause of ischemia: atherosclerosis

risk factors:

  • existing conditions: HTN, diabetes, hypercholesterolemia
  • modifiable: lifestyle, smoking, diet
  • fixed factors: male sex, age, genetics



cellular composition of atherosclerotic plaques

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manifestations of myocardial ischemia

chest pain

decreased contractility

  • necrosis (MI)
  • stunned myocardium
  • hibernating myocardium

congestive heart failure


sudden death


ischemic syndromes

  1. stable angina: chest pain occuring in a predictable fashion
    • pt knows what will trigger, can avoid
  2. unstable angina: chest pain with an unpredictable pattern
    • pt cannot predict/avoid
  3. myocardial infarction: lack of blood flow → infarct
  4. variant angina: decrease in blood flow WITHOUT increase in demand! due to transient coronary spasm
  5. silent ischemia: ischemia minus the pain warning system
  6. syndrome X: no obstruction, but yes ischemia/pain
    • poss obstruction at capillary level (which can't be seen in imaging)


effect of nitroglycerine on chest pain (due to decr blood flow)

nitroglycerine is a powerful vasodilator, dilates everything

  • dilates coronary artery → incr flow to heart
  • dilates peripheral veins → decr venous return → overall decrease in heart size (aka decr in radius) → less tension → less oxygen demand!


aortic dissection pain vs ischemic pain

aortic dissection: TEARING, RIPPING, 10/10 pain, radiating to front/back

ischemic pain: heaviness, tightness, choking, toothache, burning, etc.



lab diagnosis

  • creatinine kinase
  • CK - isoenzymes
    • MM: muscles (cardiac and skeletal)
    • MB: cardiac muscle only
    • troponins: I & T (specific to myocardium)
  • LDH (long lasting, when originating from myocardium)
  • myoglobin (impractical and expensive)


treatment of ischemic heart disease



medical treatment for acute angina, recurrent angina, acute events


  1. decrease angina attacks
  2. prevent progression to ACS
  3. prolong survival

meds for:

1. acute angina 

  • nitroglycerine

2. prevention of recurrent angina

  • organic nitrates
  • beta blockers
  • Ca channel blockers

3. prevention of acute events

  • ASA
  • clopidogrel
  • prasugrel
  • ACE inhibitors
  • statins


myocardial revascularization techniques

  • percutaneous coronary intervention (PCI)
  • coronary artery bypass graft (CABG)


acute coronary syndromes

  • characterized by thrombus formation
  • with increasing severity, see ST elevation


there are lots of factors produced by the endothelium to prevent unnecessary clotting

  • atherosclerosis increases the chances of aberrant clotting due to endothelial dysfx


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mechanisms of coronary thrombus formation

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histo signs of infarction

MI 18-24hr

  • loss of nucleus
  • contraction bands
  • coagulation necrosis

MI 3-4d

  • hemorrhage
  • inflammation

MI 1-2w

  • granulation tissue

MI 2-4w

  • resorption
  • fibrosis

MI >4-6w

  • collagen scar


mechanisms of cell death in MI

hypoxia → no ATP made and switch to anaerobic metabolism

1. no ATP made

  • function of Na/K ATPase is altered → extracellular K, intracellular Na, intracellular Ca
    • altered membrane potential → arrythmia
    • intracellular edema

2. anaerobic metabolism

  • intracellular H → chromatin clumping, protein denaturation

overall, intracellular Ca and damage to chromatin/proteins/lipids/etc →→→ cell death

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consequences of coronary thrombosis




1. small thrombus (non flow-limiting)

  • no ECG changes
  • outcome: healing, plaque enlargement

2. partially occlusive thrombus

  • ST segment depression and/or T wave inversion
    • neg serum biomarkers → unstable angina
    • pos serum biomarkers → non-STE MI

3. occlusive thrombus

  • transient ischemia → ST segment depression and/or T wave inversion
    • neg serum biomarkers → unstable angina
    • pos serum biomarkers → non-STE MI
  • prolonged ischemia → ST elevation (Q waves appear later)
    • pos serum biomarkers → STEMI

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MI chart



serum biomarkers?

EKG initial findings

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likelihood for ACS secondary to CAD


acute coronary syndrome: high, intermed, low likelihood

  • history
  • exam
  • EKG
  • cardiac markers

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pattern of CK-MB and troponin rise following STEMI (w/ and w/out reperfusion)

  • with reperfusion: peak and washout earlier than without reperfusion
  • CK-MB returns to normal sooner than cardiac troponin


components of TIMI Risk Score

  • age >65yr
  • presence 3+ risk factors (DM, HTN, smoking, etc)
  • known CAD (stenosis >50%)
  • ASA use in last 7 days (aspirin)
  • 2+ episodes of angina in last 24h
  • ST seg changes >0.05nV
  • pos cardiac markers


how does streptokinase work


diff between SK and tPA

leads to formation of plasmin → breaks down fibrin clots

  • can cause systemic lytic state (bc it binds to all plasminogen, not just that which is bound to the clot already)
    • do not see systemic lytic state with tPA


both tPA and SK have complications: bleeding!

  • 1% intracranial bleeding, can be fatal

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strategies to treat MI

how do you choose what type of strategy to use? (invasive vs conservative)

  • risk score
  • pt/physician preference in low risk situations

both of these suggest conservative tx


invasive strategies indicated if..

  • hemodynaimcally unstable
  • electrically unstable
  • high risk score
  • elevated TnT or TnI
  • reduced LV (LVEF under 40%)
  • 'new' ST seg depression
  • PCI within 6mo/prior to CABG

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platelet mediated thrombosis targets

1. adhesion: no currently approved antiplatelent agents targeting

2. activation: most agents affect this step by blocking ADP and P2Y-12 receptors

  • prasugrel
  • clopidogrel
  • ticlopidine
  • aspirin

3. aggregation: GP IIb/IIIa inhibitors inhibit "final common pathway"

  • abciximab
  • eptifibatide
  • tirofiban