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M2 Cardio > 11/4 Ischemic Heart Disease (ACS) - Moreyra > Flashcards

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

1
Q

myocardial oxygen supply vs. myocardial oxygen demand

A

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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2
Q

endothelial factor induced relaxation

A
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3
Q

endothelial vasoactive factors

A
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4
Q

myocardial oxygen supply vs. myocardial oxygen demand

A

factors affecting oxygen demand

  1. wall stress: S = P*r/2h [h = thickness]
  2. heart rate
  3. contractility
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5
Q

atherosclerosis timeline

A

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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6
Q

relationship between stenosis and flow

A

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

  • eventually, mismatch in supply and demand
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7
Q

interaction between platelets and endothelial cells

A

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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8
Q

ischemic heart disease

A

most common cause of ischemia: atherosclerosis

risk factors:

  • existing conditions: HTN, diabetes, hypercholesterolemia
  • modifiable: lifestyle, smoking, diet
  • fixed factors: male sex, age, genetics
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9
Q

cellular composition of atherosclerotic plaques

A
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10
Q

manifestations of myocardial ischemia

A

chest pain

decreased contractility

  • necrosis (MI)
  • stunned myocardium
  • hibernating myocardium

congestive heart failure

arrhythmias

sudden death

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11
Q

ischemic syndromes

A
  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)
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12
Q

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

A

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!
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13
Q

aortic dissection pain vs ischemic pain

A

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

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

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14
Q

lab diagnosis

A
  • 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)
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15
Q

treatment of ischemic heart disease

goals

medical treatment for acute angina, recurrent angina, acute events

A

goals:

  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
  1. prevention of acute events
  • ASA
  • clopidogrel
  • prasugrel
  • ACE inhibitors
  • statins
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16
Q

myocardial revascularization techniques

A
  • percutaneous coronary intervention (PCI)
  • coronary artery bypass graft (CABG)
17
Q

acute coronary syndromes

A
  • 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
18
Q

mechanisms of coronary thrombus formation

A
19
Q

histo signs of infarction

A

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
20
Q

mechanisms of cell death in MI

A

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
  1. anaerobic metabolism
    * intracellular H → chromatin clumping, protein denaturation

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

21
Q

consequences of coronary thrombosis

algorithm/flowchart

A

possibilities:

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
22
Q

MI chart

sx

serum biomarkers?

EKG initial findings

A
23
Q

likelihood for ACS secondary to CAD

acute coronary syndrome: high, intermed, low likelihood

  • history
  • exam
  • EKG
  • cardiac markers
A
24
Q

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

A
  • with reperfusion: peak and washout earlier than without reperfusion
  • CK-MB returns to normal sooner than cardiac troponin
25
Q

components of TIMI Risk Score

A
  • 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
26
Q

how does streptokinase work

diff between SK and tPA

A

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
27
Q

strategies to treat MI

A

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
28
Q

platelet mediated thrombosis targets

A
  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
  1. aggregation: GP IIb/IIIa inhibitors inhibit “final common pathway”
  • abciximab
  • eptifibatide
  • tirofiban

M2 Cardio (22 decks)

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