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Perf Tech Exam 2 > Topic 9 and 10 > Flashcards

Topic 9 and 10 Flashcards

1
Q

Ischemia=

A

blood supply problem—wounded

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2
Q

Injury=

A

cellular damage

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3
Q

Infarction (necrosis)=

A

cell death

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4
Q

myocardial ischemia causes

A 
not enough blood
athersclerosis
vasospasm
thrombosis
embolism
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5
Q

myocardial ischemia- ekg

A

depressed ST wave

inverted T wave

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6
Q

myocardial infarct- ekg

A

deep Q wave

- Troponin released

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7
Q

myocardial injury- ekg

A

elevated ST wave

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8
Q

Oxygen Free Radicals/Reactive Oxygen Species (ROS)=

A

Altered O2 molecules created

  • -At XC and reperfusion
  • -Reactions add unpaired electrons to outer orbit
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9
Q

Cardioplegia goal is to protect and

A

create scavengers to make them harmless

–Constantly manufactured and removed

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10
Q

What do free radicals do?

A

They attack and steal energy from other cells

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11
Q

What creates a free radical?

A

missing electron

–highly reactive

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12
Q

Free radical damage:

A

After a cell looses an electron- it creates a chain reaction on the cell membrane. Erosion of the cell membrane then occurs

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13
Q

What neutralizes free radicals?

A

antioxidants- it donates an electron to the free radical

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14
Q

NADPH+ O2 (n the presence of NADPH oxidase)=

A

Superoxide O2-

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15
Q

Superoxide O2- (in the presence of superoxide dismutase)=

A

Hydrogen peroxide H2O2

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16
Q

Hydrogen peroxide H2O2 (n the presence of Fe++)=

A

Hydroxyl radical OH-

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17
Q

Hydrogen peroxide H2O2 (n the presence of Myeloperoxidase)=

A

Hypochlorite HOCl

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18
Q

Hydrogen peroxide H2O2 (n the presence of catalase)=

A

O2 + H2O

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19
Q 
How Reactive Oxygen Species (ROS) are created:
\_\_\_\_\_\_\_\_\_ releases in endothelial cells.
Enzyme important in \_\_\_\_\_ breakdown path
Catalyze:  \_\_\_\_\_\_\_
Process generates \_\_\_\_\_\_\_
A

Xanthine oxidase
purine
hypoxanthine to xanthine to uric acid
hydrogen peroxide (H2O2)

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20
Q

How Reactive Oxygen Species (ROS) are created:

Re-energized electron transport chain in

A

myocyte mitochondria

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21
Q

How Reactive Oxygen Species (ROS) are created:

Hours later additional released from

A

neutrophil s from NADPH oxidase

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22
Q

Anoxia=

A
  • Total depletion of O2

- Complete lack of Oxygen

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23
Q

Hypoxia=

A
  • Lack of oxygen delivered to the tissues

- Insufficient supply of O2

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24
Q

Ischemia=

A
  • -Restriction in blood supply to an organ

- -Results from a restriction

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25
Q

Reperfusion=

A

Restoration of the circulation

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26
Q

Reperfusion can result in

A
  • -Can result in inflammation

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

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27
Q

Reperfusion injury from: Myocyte hypercontracture

A
  • increased intracellular calcium

- reoxygenation from myocytes

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28
Q

Reperfusion injury from: mitochondrial dysfunction

A
  • decreased mitochondrial calcium cencentration

- decreased ATP and apoptosis

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29
Q

Reperfusion injury from: free oxygen radicals

A
  • alters membrane proteins and phospholopids
  • increased oxidative stress
  • increased inflamation
  • leukocyte activation and aggravation
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30
Q

Reperfusion injury from: activation of coagulation

A
  • platelet activation

- complement activation leading to microvascular and endothelial dysfunction

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31
Q

Reperfusion injury: Independent mediator of

A

cardiomyocyte death

–separate from ischemic injury

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32
Q

Reperfusion injury: Abrupt biochemical and metabolic changes occur–(compound injury after ischemia) [5]

A 
Mitochondrial re-energization
Generation of reactive oxygen species
Intracellular calcium overload
Rapid restoration of physiologic pH
Inflammation
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33
Q

Reperfusion injury: Cell death results from opening of

A

mitochondrial permeability transition pore and induction of cardiacmyocyte hyper-contraction

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34
Q

Ionic homeostasis can be disrupted: all designed to keep balance of

A

electrolytes in the extracellular and intracellular fluids

35
Q

Enzyme system: (2)

A 
Antioxidant system (electron donators)
5’ nucleotidase system
36
Q

Antioxidant system (electron donators)=

A

Protect heart from free radicals

  • -Superoxide dismutase
  • -Catalase
  • -Glutathione reductase
37
Q

5’ nucleotidase system=

A

Converts AMP- > adenosine

-If adenosine nucleotide pool <50% full recovery is impossible

38
Q

What Are The Mediators of Lethal Reperfusion Injury? (5)

A 
Oxygen paradox
Calcium paradox
pH paradox
Inflammation paradox
Myocardial edema
39
Q

Oxygen paradox=

A

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

40
Q

Calcium paradox=

A

Large influx of calcium into the cell

41
Q

pH paradox=

A

pH moves from acidic to normal–potentiates many of the changes

42
Q

Inflammation paradox=

A

Neutrophil activation

43
Q

Myocardial ischemia favors

A

oxygen free radical generation

44
Q

Tissue stores of endogenous ______ depleted during ischemia

A

antioxidants

  • -superoxide dismutase
  • -catalase
  • -glutathione
  • -glutathione peroxidase
45
Q

Oxygen not available until reperfusion after

A

clamp off

46
Q

When Are Oxygen Free Radicals Generated? Greatest risk (i.e. greatest production) occurs when

A

oxygen returned to myocardium

47
Q

What Factors Determine The Amount of Oxygen Free Radicals Produced? (4)

A
  1. Severity of ischemic injury
  2. Activation and recruitment of neutrophils to myocardium
  3. Level of O2 in the cardioplegic solution
  4. Presence of endogenous scavengers and inhibitors
48
Q

What Changes Are Caused By Oxygen Free Radicals?

A
  1. Peroxidation of lipid components of myocellular membranes (steal electrons from lipid membranes)
  2. Impairment of vascular endothelial function (produces vasoactive & antiinflammatory autocoids)
    - -autocoids: act like local hormones, act near site of synthesis, short acting
49
Q

Results from Changes Caused By Oxygen Free Radicals?

A

postischemic dysfunction
dysrhythmias
morphologic injury
necrosis

50
Q

How Do Oxygen Free Radicals Cause Injury?

Induce opening of

A

mitochondrial permeability transition pore

51
Q

How Do Oxygen Free Radicals Cause Injury?

Act as neutrophil

A

chemoattractants

52
Q

How Do Oxygen Free Radicals Cause Injury?

Mediate dysfunction of

A

sarcoplasmic reticulum

53
Q

How Do Oxygen Free Radicals Cause Injury?

Contribute to intracellular

A

calcium overload

54
Q

How Do Oxygen Free Radicals Cause Injury?

Damage cell membrane by

A

lipid peroxidation

55
Q

How Do Oxygen Free Radicals Cause Injury?

Induce enzyme

A

denaturation

56
Q

How Do Oxygen Free Radicals Cause Injury?

Cause direct oxidative damage to

A

DNA

57
Q

What is the Mitochondrial Permeability Transition Pore?

A

Nonselective channel (protein) of inner mitochondrial membrane

58
Q

When the Mitochondrial Permeability Transition Pore it open increases permeability of molecules _____ Daltons

A

<1500 daltons

59
Q

Mitochondrial Permeability Transition Pore: When open oxidative phosphorylation is uncoupled= Results in

A

decreased ATP and cell death

60
Q

Mitochondrial Permeability Transition Pore: Closed during ______ / open during ______

A 
closed=  ischemia
open= reperfusion
61
Q

Mitochondrial Permeability Transition Pore Opens in response to

A

mitochondrial calcium overload
oxidative stress
restoration of physiologic pH
ATP depletion

62
Q

How Can We “Attack” The Oxygen Free Radical Problem? (3)

A
  1. Administer pharmacological agents that inhibit the formation of oxygen free radicals
  2. Administer pharmacological agents that scavenge / remove oxygen free radicals
  3. Administer anti-neutrophil agents
63
Q

Pharmacological agents that inhibit the formation of oxygen free radicals=

A

Anesthetic agents and Antiarrhythmics

–may eliminate hydroxyl radicals, Vit C- >peroxides

64
Q

Pharmacological agents that scavenge / remove oxygen free radicals=

A

Mannitol

N-acetylcysteine

65
Q

anti-neutrophil agents do what

A

Decrease ischemia reperfusion injury

66
Q

What Changes Are Caused By Myocyte Calcium Influx? (4)

A
  1. Depletion of high energy phosphate stores
  2. Accumulation in mitochondria kills ability to produce ATP
  3. Activation of catalytic enzymes
  4. Alteration of excitation-contraction coupling of actin-myosin-troponin
67
Q

What Starts The Activation of Neutrophils?

A
  1. Receptor molecules will be activated / exposed
    - -Start attachment process to the endothelium
  2. Once bound–Diapedesis
    - (blood goes thru capillaries)
68
Q

3 types of receptor molecules

A
  1. selectins (P, L, E)= Initial binding processes with endothelial wall
  2. beta2 integrins (CD11/CD18 complex)= Mediate firmer contact with wall
  3. immunoglobulin superfamily (ICAM-1)= Mediates final surface adherence
69
Q

What Starts The Activation of Neutrophils?

A
  1. P-selectin (endothelial cells) triggered by proinflammatory mediators
  2. Neutrophil recruitment triggered by similar proinflammatory mediators
70
Q

Neutrophil products= (5)

A 
Oxygen derived free radicals
platelet activating factor
hypoclorous acid
proteases
cytokines
71
Q

What Causes Myocardial Edema? (6)

A
  1. Increased intracellular osmotic pressure
  2. Disruption of electrical potential across cell membrane
  3. Increased microvascular permeability
  4. Increased interstitial osmotic pressure
  5. High cardioplegia delivery pressure
  6. Hypothermia induced changes to sodium-potassium pump
72
Q

Myocardial edema results=

A

increased microvasculature resistance

increased diffusion distance to myofibril

73
Q

How Can We Target The Perpetrators During Bypass?

A

Cardioplegia

Ability to modify conditions of reperfusion and the composition of the solution

74
Q

modifiable conditions=

A

hydrodynamics
temperature
route

75
Q

modifiable compositions=

A 
pH
metabolic substrate
hypocalcemia
oxygen
pharmaceuticals
76
Q

How Do We Target The Perpetrators During Off-Pump Cases?

A

IV administration
NO cardioplegia
NO hypothermia
MINIMAL cardiac work -load reduction

77
Q

What Clinical Results Do We See As a Result of RPI?

A
  1. Dysrhythmias
  2. Systolic dysfunction
  3. Diastolic dysfunction (compliance / relaxation)
  4. Myocardial necrosis
  5. Endothelial dysfunction
  6. No reflow phenomenon
78
Q

When Can Myocardial Injury Occur?

A 
Before bypass (think “lines”)
During cardioplegic arrest (think XC ON)
During reperfusion (think XC off)
79
Q

Pre-bypass / before delivery of cardioplegia –“prebypass window”=Period of

A

unprotected ischemia

  • -coronary artery or other disease process
  • -hypotension due to dysrhythmia and/or cardiogenic shock
  • -coronary spasm
80
Q

Cross-clamp applied / cardioplegia delivered=Period of

A

protected ischemia

  • -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
81
Q

After cross-clamp removed= period of

A

Reperfusion
–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

82
Q

Ischemic injury also possible (5)

A

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

83
Q

Objectives for hypothermic cardioplegia administration (4)

A
  1. immediate/sustained electromechanical arrest
  2. rapid/sustained homogenous myocardial cooling
  3. maintenance of therapeutic additives in effective concentrations
  4. periodic washouts of metabolic inhibitors
84
Q

Goals for Myocardial Protection (4)

A
  1. initiate rapid myocardial arrest
  2. keep the heart quiet- no electromechanical activity
  3. minimize ischemia
  4. control re-perfusion

Perf Tech Exam 2 (3 decks)

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