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Perf Tech II (exam 2) > Tpoic 9 and 10: Myocardia Ischemia and Reperfusion > Flashcards

Tpoic 9 and 10: Myocardia Ischemia and Reperfusion Flashcards

1
Q

Problems that lead us to Surgery and Cardioplegia? (3)

A

Ischemia
Injury
Infarction

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2
Q

Infarction (necrosis)

A

(necrosis):

cell death

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3
Q

Mycardial infarct causes what ECG waves ?

A

Pathologic Q waves

Permanent pathological Q waves– Troponin released

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4
Q

Myocardial Ischemia is caused by what things ? (5)

A 
Not enough blood flow
artherosclorosis
Vasospasm
Thrombis
Embolism
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5
Q

Myocardial Ischemia has what kind of ECG wave?

A

depressed ST

inverted T wave

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6
Q

Myocardial Injury caused by what?

A

No blood flow

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7
Q

Myocardial Injury ECG waves?

A

elevated ST

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8
Q

Oxy Free Radicals-

Altered O2 molecules created when?

A

At XC and reperfusion

Reactions add unpaired electrons to outer orbit

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9
Q

Oxygen Free Radicals are what?

A

Reactqive Oxygen Species (ROS)

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10
Q

what are Constantly manufactured and removed

A

Oxygen Free Radicals

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11
Q

A missing electron can create what?

A

Free radical, highly reactive

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12
Q

How are ROS created?

A

Xanthine oxidase releases in endothelial cells
Enzyme important in purine breakdown path
Catalyze: hypoxanthine to xanthine to uric acid
Process generates hydrogen peroxide (H2O2)

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13
Q

Anoxia

A

Total depletion of O2

Complete lack of Oxygen

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14
Q

hypoxia

A

Lack of oxygen delivered to the tissues

Insufficient supply of O2

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15
Q

Ischemia

A

Restriction in blood supply to an organ

Results from a restriction

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16
Q

How can Reperfusion result in inflammation?

A

Results in oxidative damage through Inducing oxidative stress rather than restoration of normal function

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17
Q

Reperfusion

A

Restoration of the circulation

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18
Q

How does Myocyte hypercontracture cause Reperfusion Injury?

A

Increase intracellular Ca

Reoxygenation of myocytes

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19
Q

How do Oxy free Radicals cause reperfusion injury ?

A

Alters membrane proteins and phospholipids
Increase oxidative stress
increase inflammation
Leukocyte activation and aggregation

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20
Q

How does mitochondrial dysfucntion cause reperfusion injury ?

A

Decrease mitochondrial Ca concentration

Decrease ATP and apoptosis

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21
Q

How does Activation of coagulation cause Reperfusion injury ?

A

Platelet activation

Complement activation leading to microvascular and endothelial dysfunction

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22
Q

Reperfusion Injury is an independent mediator of what?

A

cardiomyocyte death separate from ischemic injury

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23
Q

Abrupt biochemical and metabolic changes

occur during reperfusion how? (5)

A 
Mitochondrial reenergization
Generation of reactive oxygen species
Intracellular calcium overload
Rapid restoration of physiologic pH
Inflammation
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24
Q

Reperfusion can cause two things?

A

Abrupt biochemical and metabolic changes

Cell death

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25
Q

How is Cell death caused by reperfusion

A

results from opening of mitochondrial

permeability transition pore and induction of cardiac myocyte hyper-contraction

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26
Q

Antioxidant system (electron donators)

A

-Superoxide dismutase
-Catalase
-Glutathione reductase
(Protect heart from free radicals)

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27
Q

5’ nucleotidase system converts what?

A

Converts AMP-> adenosine

If adenosine nucleotide pool <50% full recovery is impossible

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28
Q

Mediators of Lethal Reperfusion Injury

A 
Oxygen paradox
Calcium paradox
pH paradox
Inflammation
Myocardial edema
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29
Q

What is Oxygen paradox?

mediator of lethal reperfusion injury

A

Too much of a good thing: oxygen-derived free radical formation (reactive oxygen species (ROS))

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30
Q

What is Calcium paradox?

mediator of lethal perfusion

A

Large influx of calcium into the cell

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31
Q

What is pH paradox?

mediator of lethal perfusion

A

pH moves from acidic to normal–potentiates

many of the changes

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32
Q

Inflammation

mediator of lethal perfusion

A

Neutrophil activation

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33
Q

endogenous antioxidants (4)

A

superoxide dismutase
catalase
glutathione
glutathione peroxidase

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34
Q

What happens to tissue stores of endogenous antioxidants during ischemia ?

A

they are depleted

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35
Q

Greatest risk to develop Oxygen free radicals is when?

A

when oxygen returned to myocardium

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36
Q

Factors that determine the amount of Oxygen Free Radicals produced? (4)

A

Severity of ischemic injury
Activation and recruitment of neutrophils to myocardium
Level of O2 in CPG solution
Presence of endogenous scavengers and inhibitors

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37
Q

Results caused by Oxygen Free radicals? (4)

A

postischemic dysfunction
dysrhythmias
morphologic injury
necrosis

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38
Q

What changes can Oxygen Free Radicals cause?

A

Peroxidation of lipid components of myocellular membranes
(steal electrons from lipid membranes)
Impairment of vascular endothelial function
(produces vasoactive & antiinflammatory autocoids)

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39
Q

autocoids

A

act like local hormones, act near site of synthesis, short acting

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40
Q

Oxy Free Radicals induce opening of what?

A

Induce opening of mitochondrial permeability transition pore

41
Q

Oxy Free Radicals chemoattract what?

A

Act as neutrophil chemoattractants

42
Q

Oxy Free Radicals mediate what?

A

dysfunction of sarcoplasmic reticulum

43
Q

Oxy Free Radicals overload what?

A

intracellular calcium overload

44
Q

How do Oxy Free Radicals damage cell membrane?

A

Damage cell membrane by lipid peroxidation

45
Q

Oxy Free Radicals induce denaturation of what?

A

Induce enzyme denaturation

46
Q

How do Oxy Free radicals damage DNA

A

Cause direct oxidative damage to DNA

47
Q

What is the Mitochondrial Permeability Transition Pore?

A 
Nonselective channel (protein) of inner
mitochondrial membrane
48
Q

When the Mitochondrial Permeability Transition Pores open, what happens to permeability?

A

When open increases permeability of molecules <1500 Daltons

49
Q

When are the Mitochondrial Permeability Transition Pores open? closed?

A

Closed during ischemia / open during

reperfusion

50
Q

Why do the Mitochondrial Permeability Transition Pores open?

A

Opens in response to mitochondrial calcium
overload, oxidative stress, restoration of
physiologic pH, and ATP depletion

51
Q

pharmacological agents that inhibit the formation of oxygen free radicals?

A

Anesthetic agents, Anti arrhythmics may eliminate hydroxyl radicals, Vit C->peroxides

52
Q

pharmacological agents that scavenge / remove oxygen free radicals

A

Mannitol, N-acetylcysteine

53
Q

Attack” The Oxygen Free Radical Problem

A
  • Administer pharmacological agents that inhibit the formation of oxygen free radicals
  • Admin pharmacological agents that scavenge / remove oxygen free radicals
  • Administer anti-neutrophil agents
54
Q

Accumulation in mitochondria kills ability to produce ATP, which affects what?

A
  • Ability of cell to contract

- Ability of cell to move calcium out of the cell or back into the SR

55
Q

Changes Are Caused By Myocyte Calcium Influx (4)

A

Depletion of high-energy phosphate stores
Accumulation in mitochondria kills ability to produce ATP
Activation of catalytic enzymes
Alteration of excitation-contraction coupling of actin-myosin-troponin

56
Q

Activation of catalytic enzymes does what?

A

Increase cellular damage

57
Q

Alteration of excitation-contraction coupling of actin-myosin-troponin - what happens to calcium (3)

A

Calcium into the cell causes the contraction
sequence
Calcium not removed (Stone heart syndrome)
Calcium can enter by multiple pathways

58
Q

Stone heart syndrome?

A

When calcium is not removed

59
Q

What starts the activation of Neutrophils

A

Receptor molecules will be activated / exposed

Start attachment process to the endothelium

60
Q

Three types of receptor molecules

A 
selectins (P, L, E)
beta2 integrins (CD11/CD18 complex)
immunoglobulin superfamily (ICAM-1)
61
Q

selectins (P, L, E)

A

Initial binding processes with endothelial

wall of neutrophils

62
Q

beta2 integrins (CD11/CD18 complex)

A

Mediate firmer contact with wall (of Neutrophils)

63
Q

immunoglobulin superfamily (ICAM-1)

A

Mediates final surface adherence of neutrophils

64
Q

P-selectin (endothelial cells) is triggered by what?

A

triggered by proinflammatory mediators

65
Q

Proinflammatory mediators that can trigger P-selectin

A

oxygen-derived free radicals (Hydrogen Peroxide etc)
thrombin complement components
histamine

66
Q

Neutrophil recruitment triggered by similar

proinflammatory mediators to what

A

to P-selectin inhibitors

67
Q

Causes Myocardial Edema

A

Increased intracellular osmotic pressure
Disruption of electrical potential across cell membrane
Increased microvascular permeability
Increased interstitial osmotic pressure
High cardioplegia delivery pressure
Hypothermia induced changes to sodium-potassium pump

68
Q

Increased intracellular osmotic pressure

A

accumulation metabolic end-products of anaerobic glycolysis, lipolysis, ATP hydrolysis

69
Q

Disruption of electrical potential across cell membrane

A

sodium / chloride accumulate inside the cell –attract water

70
Q

Increased what can cause myocardial edema? (3)

A

Increased microvascular permeability
Increased intracellular osmotic pressure
Increased interstitial osmotic pressure

71
Q

High pressure where can cause myocardial edema?

A

High Cardioplegia delivery pressure

72
Q

Hypothermia induced changes to sodium-potassium pump can cause what?

A

cause myocardial edema

73
Q

Disruption of electrical potential across cell membrane can cause what?

A

cause myocardial edema

74
Q

Myocardial Edema results in what two things?

A

increased microvasculature resistance

increased diffusion distance to myofibril

75
Q

What conditions can we modify of cardioplegia during bypass?

A

hydrodynamics
temperature
route

76
Q

What elements of the composition of cardioplegia can we modify ?

A 
pH
metabolic substrate
hypocalcemia
oxygen
pharmaceuticals
77
Q

Off-Pump cases how do we minimize effects of ischmia?

A

IV administration of drugs?

78
Q

Dysrhythmias we see as a result of RPI

A

PVC’s, fibrillation, non-spontaneous return of sinus rhythm, dysrhythmia persistence

79
Q

Systolic dysfunction caused by the result of RPI are what?

A

contractile function / stroke volume

View by TEE or measure a Cardiac Output

80
Q

Result of RPI (3)?

A

Dysrhythmias
Systolic dysfunction
Diastolic dysfunction (compliance /
relaxation)

81
Q

What is the Diastolic dysfunction (compliance /

relaxation) that is the result of RPI

A

impaired filling

82
Q

Clinical results we see as a result of RPI? (3)

A

Myocardial necrosis
Endothelial dysfunction
No reflow phenomenon

83
Q

No reflow phenomenon (5)

A

Post ischemic tissue edema
Interstitial hemorrhage
Active vasoconstriction from loss of endothelium derived vasodilators
Release of neutrophil derived vasoconstrictors
Capillary plugging by adhering neutrophils

84
Q

Active vasoconstriction from loss of endothelium derived vasodilators caused by what?

A

No reflow phenomenon

85
Q

Release of neutrophil derived vasoconstrictors caused by what result of RPI?

A

No reflow phenomenon

86
Q

Capillary plugging by adhering neutrophils caused by what result of RPI?

A

No reflow phenomenon

87
Q

Post ischemic tissue edema caused by what result of RPI?

A

No reflow phenomenon

88
Q

When can Myocardial Injury occur during bypass? (3)

A 
Before bypass (think “lines”)
During cardioplegic arrest (think XC ON)
During reperfusion (think XC off)
89
Q

“prebypass window” is what?

A

Pre-bypass / before delivery of cardioplegia

Period of unprotected ischemia

90
Q

During Phase one “prebypass window” when Period of unprotected ischemia, what cause myocardial injury? (3)

A
  • coronary artery or other disease process
  • hypotension due to dysrhythmia and/or cardiogenic shock
  • coronary spasm
91
Q

Myocardial Injury, Phase 2, During cardioplegic arrest (think XC ON)

A

Cross-clamp applied / cardioplegia delivered

92
Q

What can cause ischemia during period of protected ischemia, during phase 2 of possible myocardial injury (7)

A
  • unresolved coronary stenosis
  • obstruction within vascular graft (kink, tight anastomosis, emboli)
  • maldistribution of cardioplegia
  • inadequate cardioplegia delivery (inadequate -pressure or volume, inappropriate composition)
  • between infusions of intermittent cardioplegia
  • unintentional interruption of continuous cardioplegia
93
Q

During phase 3, reperfusion, time of possible myocadial injury

Ischemic injury also possible due to what? (5)

A
  • Ischemic injury also possible
  • hypotension post clamp release (think “neo”)
  • during weaning/termination CPB (do not distend)
  • vascular graft thrombosis or mechanical obstruction
  • Dysrhythmias(watch EKG)
  • vasospasm of grafted vessel
94
Q

After cross-clamp removed, when can myocardial injury can occur when/how?

Phase 3 of time of possible myocardial injury

A
  • early phase: <4 hours
  • late phase: 4 to 6 hours
  • resolution of hypotension /dysrhythmia restores blood flow
  • cardioplegia infused at high pressures or with improper composition
  • coronary blood flow restored with unmodified blood after clamp removal
95
Q

Goal of Myocardial Protection

A

Initiate rapid myocardial arrest
Keep the heart quiet, no electrochemical activity
Minimize ischemia
Control Reperfusion

96
Q

4 main objectives of hypothermic cardioplegia

A

Immediate/Sustained electromechanical arrest
Rapid Sustained homogenous cooling
Maintenance of therapeutic additives in effective concentrations
Periodic washouts of metabolic inhibitors

97
Q

Goals of Myocardial Protection (4)

A

Control Reperfusion
Initiate rapid myocardial arrest
Minimize ischemia
Keep the heart quiet, no electrochemical activity

98
Q

4 main objectives of hypothermic cardioplegia

A

Immediate/Sustained electromechanical arrest
Rapid Sustained homogenous cooling
Maintenance of therapeutic additives in effective concentrations
Periodic washouts of metabolic inhibitors

Perf Tech II (exam 2) (6 decks)

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