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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
How is Cell death caused by reperfusion
results from opening of mitochondrial | permeability transition pore and induction of cardiac myocyte hyper-contraction
26
Antioxidant system (electron donators)
-Superoxide dismutase -Catalase -Glutathione reductase (Protect heart from free radicals)
27
5’ nucleotidase system converts what?
Converts AMP-> adenosine | If adenosine nucleotide pool <50% full recovery is impossible
28
Mediators of Lethal Reperfusion Injury
``` Oxygen paradox Calcium paradox pH paradox Inflammation Myocardial edema ```
29
What is Oxygen paradox? | mediator of lethal reperfusion injury
Too much of a good thing: oxygen-derived free radical formation (reactive oxygen species (ROS))
30
What is Calcium paradox? | mediator of lethal perfusion
Large influx of calcium into the cell
31
What is pH paradox? | mediator of lethal perfusion
pH moves from acidic to normal–potentiates | many of the changes
32
Inflammation | mediator of lethal perfusion
Neutrophil activation
33
endogenous antioxidants (4)
superoxide dismutase catalase glutathione glutathione peroxidase
34
What happens to tissue stores of endogenous antioxidants during ischemia ?
they are depleted
35
Greatest risk to develop Oxygen free radicals is when?
when oxygen returned to myocardium
36
Factors that determine the amount of Oxygen Free Radicals produced? (4)
Severity of ischemic injury Activation and recruitment of neutrophils to myocardium Level of O2 in CPG solution Presence of endogenous scavengers and inhibitors
37
Results caused by Oxygen Free radicals? (4)
postischemic dysfunction dysrhythmias morphologic injury necrosis
38
What changes can Oxygen Free Radicals cause?
Peroxidation of lipid components of myocellular membranes (steal electrons from lipid membranes) Impairment of vascular endothelial function (produces vasoactive & antiinflammatory autocoids)
39
autocoids
act like local hormones, act near site of synthesis, short acting
40
Oxy Free Radicals induce opening of what?
Induce opening of mitochondrial permeability transition pore
41
Oxy Free Radicals chemoattract what?
Act as neutrophil chemoattractants
42
Oxy Free Radicals mediate what?
dysfunction of sarcoplasmic reticulum
43
Oxy Free Radicals overload what?
intracellular calcium overload
44
How do Oxy Free Radicals damage cell membrane?
Damage cell membrane by lipid peroxidation
45
Oxy Free Radicals induce denaturation of what?
Induce enzyme denaturation
46
How do Oxy Free radicals damage DNA
Cause direct oxidative damage to DNA
47
What is the Mitochondrial Permeability Transition Pore?
``` Nonselective channel (protein) of inner mitochondrial membrane ```
48
When the Mitochondrial Permeability Transition Pores open, what happens to permeability?
When open increases permeability of molecules <1500 Daltons
49
When are the Mitochondrial Permeability Transition Pores open? closed?
Closed during ischemia / open during | reperfusion
50
Why do the Mitochondrial Permeability Transition Pores open?
Opens in response to mitochondrial calcium overload, oxidative stress, restoration of physiologic pH, and ATP depletion
51
pharmacological agents that inhibit the formation of oxygen free radicals?
Anesthetic agents, Anti arrhythmics may eliminate hydroxyl radicals, Vit C->peroxides
52
pharmacological agents that scavenge / remove oxygen free radicals
Mannitol, N-acetylcysteine
53
Attack” The Oxygen Free Radical Problem
- 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
Accumulation in mitochondria kills ability to produce ATP, which affects what?
- Ability of cell to contract | - Ability of cell to move calcium out of the cell or back into the SR
55
Changes Are Caused By Myocyte Calcium Influx (4)
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
Activation of catalytic enzymes does what?
Increase cellular damage
57
Alteration of excitation-contraction coupling of actin-myosin-troponin - what happens to calcium (3)
Calcium into the cell causes the contraction sequence Calcium not removed (Stone heart syndrome) Calcium can enter by multiple pathways
58
Stone heart syndrome?
When calcium is not removed
59
What starts the activation of Neutrophils
Receptor molecules will be activated / exposed | Start attachment process to the endothelium
60
Three types of receptor molecules
``` selectins (P, L, E) beta2 integrins (CD11/CD18 complex) immunoglobulin superfamily (ICAM-1) ```
61
selectins (P, L, E)
Initial binding processes with endothelial | wall of neutrophils
62
beta2 integrins (CD11/CD18 complex)
Mediate firmer contact with wall (of Neutrophils)
63
immunoglobulin superfamily (ICAM-1)
Mediates final surface adherence of neutrophils
64
P-selectin (endothelial cells) is triggered by what?
triggered by proinflammatory mediators
65
Proinflammatory mediators that can trigger P-selectin
oxygen-derived free radicals (Hydrogen Peroxide etc) thrombin complement components histamine
66
Neutrophil recruitment triggered by similar | proinflammatory mediators to what
to P-selectin inhibitors
67
Causes Myocardial Edema
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
Increased intracellular osmotic pressure
accumulation metabolic end-products of anaerobic glycolysis, lipolysis, ATP hydrolysis
69
Disruption of electrical potential across cell membrane
sodium / chloride accumulate inside the cell –attract water
70
Increased what can cause myocardial edema? (3)
Increased microvascular permeability Increased intracellular osmotic pressure Increased interstitial osmotic pressure
71
High pressure where can cause myocardial edema?
High Cardioplegia delivery pressure
72
Hypothermia induced changes to sodium-potassium pump can cause what?
cause myocardial edema
73
Disruption of electrical potential across cell membrane can cause what?
cause myocardial edema
74
Myocardial Edema results in what two things?
increased microvasculature resistance | increased diffusion distance to myofibril
75
What conditions can we modify of cardioplegia during bypass?
hydrodynamics temperature route
76
What elements of the composition of cardioplegia can we modify ?
``` pH metabolic substrate hypocalcemia oxygen pharmaceuticals ```
77
Off-Pump cases how do we minimize effects of ischmia?
IV administration of drugs?
78
Dysrhythmias we see as a result of RPI
PVC’s, fibrillation, non-spontaneous return of sinus rhythm, dysrhythmia persistence
79
Systolic dysfunction caused by the result of RPI are what?
contractile function / stroke volume | View by TEE or measure a Cardiac Output
80
Result of RPI (3)?
Dysrhythmias Systolic dysfunction Diastolic dysfunction (compliance / relaxation)
81
What is the Diastolic dysfunction (compliance / | relaxation) that is the result of RPI
impaired filling
82
Clinical results we see as a result of RPI? (3)
Myocardial necrosis Endothelial dysfunction No reflow phenomenon
83
No reflow phenomenon (5)
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
Active vasoconstriction from loss of endothelium derived vasodilators caused by what?
No reflow phenomenon
85
Release of neutrophil derived vasoconstrictors caused by what result of RPI?
No reflow phenomenon
86
Capillary plugging by adhering neutrophils caused by what result of RPI?
No reflow phenomenon
87
Post ischemic tissue edema caused by what result of RPI?
No reflow phenomenon
88
When can Myocardial Injury occur during bypass? (3)
``` Before bypass (think “lines”) During cardioplegic arrest (think XC ON) During reperfusion (think XC off) ```
89
“prebypass window” is what?
Pre-bypass / before delivery of cardioplegia | Period of unprotected ischemia
90
During Phase one "prebypass window" when Period of unprotected ischemia, what cause myocardial injury? (3)
- coronary artery or other disease process - hypotension due to dysrhythmia and/or cardiogenic shock - coronary spasm
91
Myocardial Injury, Phase 2, During cardioplegic arrest (think XC ON)
Cross-clamp applied / cardioplegia delivered
92
What can cause ischemia during period of protected ischemia, during phase 2 of possible myocardial injury (7)
- 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
During phase 3, reperfusion, time of possible myocadial injury Ischemic injury also possible due to what? (5)
- 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
After cross-clamp removed, when can myocardial injury can occur when/how? Phase 3 of time of possible myocardial injury
- 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
Goal of Myocardial Protection
Initiate rapid myocardial arrest Keep the heart quiet, no electrochemical activity Minimize ischemia Control Reperfusion
96
4 main objectives of hypothermic cardioplegia
Immediate/Sustained electromechanical arrest Rapid Sustained homogenous cooling Maintenance of therapeutic additives in effective concentrations Periodic washouts of metabolic inhibitors
97
Goals of Myocardial Protection (4)
Control Reperfusion Initiate rapid myocardial arrest Minimize ischemia Keep the heart quiet, no electrochemical activity
98
4 main objectives of hypothermic cardioplegia
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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