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562 - Perfusion Technology II > Exam 4 - Ischemia & Reperfusion Injury > Flashcards

Exam 4 - Ischemia & Reperfusion Injury Flashcards

1
Q

Ischemia

A
  • Inadequate tissue perfusion to sustain aerobic metabolism at a given level of cardiac performance
  • Imbalance between O2 supply and demand
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2
Q

Normal perfusion

A

Supply / Demand > 1

  • must increase supply (flow) to increase ratio
  • Ischemia occurs when ratio < 1
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3
Q

Anoxia

A
  • flow to tissue ok, but no O2 delivery

- O2 extraction problem

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4
Q

Hypoxia

A
  • Flow to tissue ok, but insufficient O2 delivery

- [O2] not high enough to meet demand

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5
Q

Reperfusion

A
  • Restoration of flow after period of ischemia
  • Happens after x-clamp, cardioplegia, or blocked vessel
    - we can control first two
  • Ischemic injury may be accelerated / extended by reperfusion phase
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6
Q

Reperfusion injury

A
  • extends / accelerates damage from ischemia
  • Ischemia sets stage… reperfusion continues injury process
  • Perfusionists can create optimal / protected conditions for reperfusion to minimize injury
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7
Q

Why should be concerned with reperfusion injury

A
  • CAD
  • Treatment of MI leads to reperfusion (opens artery)
  • CPB w/ x-clamp
  • Off pump procedures
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8
Q

Cells most affected by ischemic injury

A
  • Cardiac myocyte
    • no buffer periods of low flow like other cells
    • high levels of aerobic metabolism (no anaerobic)
  • Coronary vascular endothelium
    • active tissue / release vasoactive substances (dilators/mediators)
    • release NO… NO is good free radical scavenger
    • free radicals hurt membranes / homeostasis of cells
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9
Q

Good vasoactivators

A
  • NO
  • Adenosine
  • Prostacyclin
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10
Q

Bad vasoactivators

A
  • Platelet activating factor
  • Endothelin-1
  • Superoxide anion
  • Histamine
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11
Q

What determines myocardial O2 demand

A
  • Work of chambers (pressure and stroke work)
  • Passive stretch (minimized by vent)
  • HR (CPB stops heart…so 0)
  • Basal metabolism
  • Inotropic state
  • Ionic homeostasis (energy needed to maintain)
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12
Q

Stroke work on CPB

A
  • Minimal / zero

- Stroke work is shown by area under P-V curve

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13
Q

How does CPB affect O2 demand

A
  • Total bypass and diastolic arrest
    • drop demand 50% or more
  • Myocardial cooling
    • drop 50% per 10 degree C drop
    • Normal drift to 34 = 25% drop in demand
  • Vent decompression
  • All these decrease demand AND slow ischemic injury
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14
Q

Biggest factor in ischemic injury

A
  • time

- 30-45 min before bad damage occurs

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15
Q

Global myocardial ischemia (GMI)

A
  • occurs during x-clamp or widowmaker (LAD coronary)
  • no flow to entire heart
  • 45 min ischemia w/ no modified reperfusion….50-60% drop in systolic function but no necrosis
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16
Q

Regional myocardial ischemia (RMI)

A
  • No flow to part of heart
  • Off pump cases / coronary blockage
  • 45 min of ischemia…subendocardial infarction / contractile dysfunction of ischemic area
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17
Q

Consequences of myocardial ischemia

A
  • decreased contractile function
  • endothelial damage and decreased function
  • decreased blood flow
  • neutrophil accumulation
  • Apoptosis
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18
Q

Factors affecting ischemic injury

A
  • duration of ischemia (biggest)
  • collateral flow (more collateral…less injury)
  • baseline health of tissue
  • Ca influx (too much causes stone heart)
  • Intracellular Na increase and K decrease (ionic homeostasis)
  • stimulation of activators (cytokines, etc)
19
Q

Factors affecting time to permanent damage

A
  • severity of ischemia
  • heart temperature (cooler the better)
  • tissue energy demand
  • collateral flow
  • necrosis can occur w/ 30 min of occlusion
20
Q

RPI damage

A
  • extend postishchemic injury
  • myocardial stunning
  • no-reflow phenomenon (neutrophils stuck on vessel wall…block)
  • reperfusion arrhythmia (ST changes…caused by air emboli)
  • lethal perfusion injury (O2 free radicals)
21
Q

Myocardial stunning

A
  • mechanical dysfunction after reperfusion
    • without necrosis
  • occurs even with normal coronary flow
  • days/weeks to recover
  • pacing after surgery helps prevent
22
Q

No-reflow phenomenon causes

A
  • neutrophils plugging up caps
  • air emboli / debris
  • vasoconstriction
  • post ischemic edema
23
Q

Reperfusion arrhythmias treatment

A
  • pace patient
  • drugs
    • mannitol - O2 free radical scavenger
    • lidocaine
    • Mg
24
Q

Lethal reperfusion injury

A
  • separate from ischemic injury….2nd part
  • cardiomyocyte death
  • cell death results from opening of mitochondrial permeability transition pore (mPTP) and hypercontraction
25
Q

Mediators of lethal perfusion injury

A
  • O2 paradox
    • too much O2 leads to free radicals (most from dissolved O2)
    • reactive oxygen species (ROS)
  • Calcium paradox
    • influx of Ca into cell
  • pH paradox
    • moves from acidic to normal
  • Inflammation
    • Neutrophil activation
  • Myocardial edema (blood cpg helps reduce this)
26
Q

When are ROS generated

A
  • periods of ischemia
  • tissue antioxidants are depleted during ischemia
  • O2 not available until reperfusion
  • GREATEST production is when O2 returned to myocardium
    • happens a lot during “hot shot”
27
Q

Pathway of ROS production

A
  • Xanthine oxidase is enzyme for purine breakdown
  • in endothelial cells
  • this process makes H2O2
  • H2O2 disrupts cell membranes
28
Q

Two ways H2O2 produced

A
  • Re-energized ETC in mitochondria

- NADPH oxidase

29
Q

What determines amount of free radicals

A
  • severity of ischemic injury
  • neutrophils
  • levels of O2 in cardioplegia
  • status of scavengers / inhibitors
30
Q

What changes are caused by free radicals

A
  • disruption of cell membrane
  • poor endothelial function
    • production of autocoids (like hormones/short living)
  • causes:
    • post-ischemic dysfunction
    • dysrhythmias
    • injury
    • necrosis
31
Q

How do free radicals cause injury

A
  • Open mPTP
  • attract neutrophils
  • disrupt Sarcoplasmic reticulum
  • Cell Ca overload
  • damage cell membrane (H2O2)
  • enzyme denaturation
  • damage to DNA
32
Q

mPTP

A
  • nonselective
  • when open…<1500 dalton molecules can enter
  • when open…ATP depletion and cell death
  • closed during ischemia / open during reperfusion
  • opening of pore is bad
33
Q

How to treat free radical problem

A
  • drugs that block free radical formation
  • drugs that scavenge free radicals
  • anti-neutrophil agents
34
Q

What changes caused by Ca influx

A
  • depletion of energy stores
  • stops ability to make aTP
  • activates catalytic enzymes
  • disruption of actin-myosin-troponin
  • opens up mPTP
35
Q

What starts activation of neutrophils

A
  • Pro-inflammatory mediators triggers P-selectin
  • Pro-inflammatory mediators recruit neutrophils
  • Neutrophils ultimately create free radicals
36
Q

What causes myocardial edema

A
  • increased intracellular osmotic pressure
  • disruption of membrane electrical potential
    • Na/Cl accumulate inside cells
  • increased permeability
  • high cpg delivery pressure
  • hypothermia changes Na/K pump
  • results in no-reflow phenomenon and poor O2 delivery
37
Q

How can we target perpetrators of injury during CPB

A
  • IV
  • Cardioplegia
  • Can alter conditions or reperfusion (route, temp, dynamics)
  • Can alter composition of cpg solution
38
Q

How can we target off-pump

A
  • IV administration
    • No cpg
    • No hypothermia
    • minimal cardiac work reduction
39
Q

Clinical results of RPI

A
  • Dysrhythmias (PVC, fib, etc.)
  • Systolic dysfunction
  • Diastolic dysfunction (impaired filling)
  • Necrosis
  • Endothelial dysfunction
  • No-reflow phenomenon
40
Q

When can myocardial injury occur

A
  • Three phases
    1 - before bypass (uncontrolled)
    2 - during cpg arrest (x-clamp)
    3 - during reperfusion
41
Q

Phase 1 - Pre-bypass window

A
  • unprotected ischemia
  • coronary artery or other disease
  • hypotension
  • coronary spasm
  • RPI possible
42
Q

Phase 2 - CPG

A
  • cpg delivery / x-clamp on
  • protected ischemia
  • unresolved coronary stenosis
  • obstruction of graft
  • poor distribution of cpg / not enough delivery
  • RPI possible
43
Q

Phase 3 - Peperfusion

A
  • after x-clamp removal
  • Ischemic injury possible
  • during weaning of CPB
  • dysrythmias
  • vasospasm of graft
  • hypotension (mannitol and K drop BP)

562 - Perfusion Technology II (9 decks)

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