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CV Perf Tech II > Ischemia/Reperfusion- Exam 2 > Flashcards

Ischemia/Reperfusion- Exam 2 Flashcards

1
Q

Ischemia

A

Blood supply problem

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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

What will the EKG show with myocardial ischemia?

A

Depressed ST segment

Inverted T wave

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5
Q

What causes myocardial ischemia?

A 
Not enough blood
atherosclerosis
vasospasm
thrombosis
embolism
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6
Q

What will the EKG show for myocardial infarction?

A

Pathologic Q waves; permanently

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7
Q

What is released with myocardial infarction?

A

Troponin

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8
Q

What will the EKG show for myocardial injury?

A

Elevated ST segment

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9
Q

Oxygen Free Radicals

A

Reactive Oxygen Species (ROS)

Altered O2 molecules created; at XC and reperfusion; reactions add unpaired electrons to outer orbit

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10
Q

5 reactions leading to O2 Radical Formation

A
  1. NADPH + O2 = Superoxide O2-
  2. Superoxide Dismutase O2- -> Hydrogen Peroxide H2 O2
  3. Hydrogen peroxide + myeloperoxidase= hypochlorite HOCL
  4. Hydrogen peroxide + Catalase = O2 + H20
  5. Hydrogen peroxide + Fe++ = Hydroxyl Radical OH
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11
Q

How are reactive oxygen species created?

A

Xanthine oxidase releases in endothelial cells; catalyze: hypoxanthine to xanthine to uric acid

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12
Q

What enzyme is important in purine breakdown path?

A

Xanthine oxidase

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13
Q

Total depletion of O2; complete lack of O2

A

Anoxia

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14
Q

Lack of oxygen delivered to tissues

A

Hypoxia

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15
Q

Lack of blood supply

A

ischemia

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16
Q

Restoration of circulation

A

Reperfusion; can result in inflammation and oxidative damage through inducing oxidative stress rather than restoration of normal funcion

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17
Q

What abrupt biochemical and metabolic changes occur resulting in reperfusion injury?

A 
Mitochondrial reenergization
Generative of reactive oxygen species
Intracellular calcium overload
Rapid restoration of physiologic pH
Inflammation
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18
Q

What does cell death result from? (related to reperfusion injury)

A

Opening of mitochondrial permeability transition pore and induction of cardiac myocyte hyper-contraction

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19
Q

What protects the heart from free radicals?

A

Antioxidant system (electron donators)

20
Q

What are the three antioxidant system components?

A

Superoxide dismutase
Catalase
Glutathione reductase

21
Q

What is the 5’ nucleotidase system?

A

Converts AMP to adenosine

22
Q

When is full recovery impossible?

A

If adenosine nucleotide pool <50% full recovery

23
Q

What are the mediators of lethal reperfusion injury?

A 
Oxygen paradox
Calcium paradox
pH paradox
Inflammation
Myocardial edema
24
Q

oxygen paradox

A

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

25
calcium paradox
large influx of calcium into the cell
26
pH paradox
pH moves from acidic to normal- potentiates many of hte changes
27
inflammation
neutrophil activation
28
What is depleted during ischemia?
Tissue stores of endogenous antioxidants - Superoxide dismutase - catalase - glutathione - glutathione peroxidase
29
What factors determine the amount of oxygen free radicals produced?
Severity of ischemic injury actiavtion and recruitment of neutrophils to myocardium Level of O2 in the cardioplegic solution presence of endogenous scavengers and inhibitors
30
What changes are caused my oxygen free radicals?
Peroxidation of lipid components of myocellular membranes (steal electrons from lipid membranes) Impairment of vascular endothelial function; produces vasoactive and autoinflammatory autocoids
31
Autocoids
act like local hormones, act near sites of synthesis, short acting
32
What are the results of oxygen free radicals? (Know this)
Postischemic dysfunction Dysrhythmias morphologic injury necrosis
33
How do Oxygen free radicals cause injury?
Induce opening of mitochondrial permeability transition pore act as neutrophil chemoattractants mediate dysfunction of SR contribute to intracellular calcium overload damage cell membrane by lipid peroxidation induce enzyme denaturation cause direct oxidative damage to DNA
34
What is the mitochondrial permeability transition pore?
Nonselective channel (protein)of inner mitochondrial membrane when open increases the permeability of molecules <1500 daltons when open oxidative phosphorylation is uncoupled (results in decrease in atp and cell death)
35
When is the mitochondrial permeability transition pore closed?
During ischemia
36
When is the mitochondrial permeability transition pore open?
During reperfusion; opens in response to mitochondrial calcium overload oxidative stress, resotration of physiologic pH, and ATP depletion
37
How can we combat the oxygen free radical problem?
Drugs that inhibit their formation (anesthetic agents, antiarrythmics may eliminate hydroxyl radicals, vitamin C peroxides) ``` Drugs that scavenge/remove them Antineutrophil agents (decrease ischemia reperfusion injury) ```
38
What drugs remove oxygen free radicals?
Mannitol, N-acetylcysteine
39
What changes are cause by myocyte calcium influx?
Depletion of high-energy phosphate stores; Accumulation of mitochondria kills ability to produce ATP Activation of catalytic enzymes Alteration of excitation-contraction coupling of actin-myosin-tropnin
40
Inability to produce ATP affects what?
Ability of the cell to contract | Ability of the cell to move calcium out of hte cell or back into the SR
41
What does activation of catalytic enzymes do?
increase cellular damage
42
Stone heart syndrome
calcium not removed after going onto the cell causing contraction sequence; can enter by multiple pathways
43
What are the three types of receptor molecules that activate neutrophils?
``` selectins (P, L, E)- inital binding Beta2 integrins (CD11/CD18 complex)- firmer contact Immunoglobulin superfamily (ICAM-1)- final surface adherance ```
44
Diapedesis
once bound to receptor molecule, blood goes through capillaries
45
What starts the activation of neutrophils?
P-selectin (endothelial cells) triggered by proinflammatory mediators (oxygen-derived free radicals/hydrogen peroxide) thrombin, complement components, histamine
46
What causes myocardial edema?
Increased intracellular osmotic pressure disruption of electrical potential across membrane increased microvascular permeability increased intersitial osmotic pressure high cpg delivery pressure hypothermia induced changes to sodium potassium pump

CV Perf Tech II (17 decks)

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