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Elsa AACN > Ch 28 Hypoxic and Ischemic brain injury > Flashcards

Ch 28 Hypoxic and Ischemic brain injury Flashcards

1
Q

Definition of anoxia

A

Complete lack of oxygen in blood due to profound and sudden medical events such as cardiac arrest, loss of perfusion pressure

Hanging, strangulation

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2
Q

Definition of hypoxia

A

Deficient amount of oxygen available in the blood supply to the brain.

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3
Q

Hypoxemia definition

A

Reduced partial pressure of oxygen in blood.
(Low levels of oxygen in blood)
Hypoxemia can lead to hypoxia

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4
Q

Ischemia definition

A

Failure of perfusion of blood through the cerebral vessels to tissue.

Ischemia and anoxia are usually involved in sudden cardiac arrest

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5
Q

What is the partial pressure of arterial oxygen and healthy adults?

A

95 to 100 mm Hg

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6
Q

What happens when partial pressure of arterial oxygen drops or is disrupted?

A

Homeostatic protective mechanisms are triggered

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7
Q

Which parts of the brain regions are more vulnerable to hypoxia and ischemia?

A

Brain regions with high metabolic demands

Those that are at the distal end of cerebral arteries, watershed regions

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8
Q

Sample of brain regions that are highly vulnerable to hypoxia and Ischemia?

A 
Neo cortex
Hippocampus
Basal ganglia
Cerebellar regions
Visual cortex
Thalamus
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9
Q

What is a common response of the brain following anoxic or hypoxic insult?

A

Edema

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10
Q

What else may happen during anoxia and hypoxia?

A

Edema, a series of metabolic events which lead to
Wallerian degeneration
Accelerated apoptosis
Atrophy

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11
Q

Does atrophy and degeneration happen acutely or span over a longer period?

A

It evolves over the course of many weeks and months

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12
Q

Neural imaging findings in apraxia or hypoxia

A

Loss of distinction between white and gray matter in the cortex
Damage of basal ganglia in neo cortex regions

Results that come later-

Hippocampal damage
Diffuse atrophy
White matter tracks vulnerable to carbon monoxide poisoning

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13
Q

What used to be considered the hallmark feature of hypoxic damage

A

Hippocampal damage.

This has been refuted in studies.

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14
Q

Other areas that are frequently damaged?

A

Watershed cortex

basal ganglia

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15
Q

Most energy required by neurons is derived from hydrolysis of what chemical

A

Adenosine triphosphate ATP

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16
Q

Does the brain have any inherent energy stores?

A

No, so it’s critically dependent on uninterrupted flow of oxygen and glucose

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17
Q

When there is a critical shortage of oxygen and glucose supply to neurons, what would result

A

Neuronal death

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18
Q

Describe the secondary toxic process that is triggered as a result of neuronal death?

A

Sodium and calcium pumps fail

depolarization of neuronal membrane and release of excessive glutamate.

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19
Q

How is glutamate related to toxic process in hypoxia and anoxia

A

Glutamate is the most common excitatory neurotransmitter, but at excessive levels it could be toxic to neurons

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20
Q

What else is involved in the toxic process?

A

Lactic acidosis
Wallerian degeneration
Necrosis
Apoptosis

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21
Q

Additional potential sources of damage to the brain after circulation is restored?

A

Secondary hypoxia
-after circulation returns, blood flow may go through a period of 30 to 50% reduction

Reperfusion injury
-After re-perfusion, some processes happen that may cause further damage such as
1 free radical formation
2 nitric oxide toxicity,
3 additional glutamate release,
4 edema and micro hemorrhages,
5 impaired ability to remove toxic metabolic stuff

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22
Q

What shares many of the same affects as hypoxia and ischemia?

A

Carbon monoxide poisoning

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23
Q

Carbon monoxide has a very high for affinity for binding with what

A

Hemoglobin

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24
Q

After carbon monoxide binds with hemoglobin, what would be formed?

A

Carboxyhemoglobin

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25
Q

Once carboxyhemoglobin rises above 20 to 30% of total hemoglobin in the blood, what happens

A

Levels above 50% will result in coma and other severe CNs effects

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26
Q

What else happens with carbon monoxide poisoning?

A

Delayed neurologic deterioration which happens 1 to 3 weeks after severe exposure.

Basal ganglia damage

Hippocampal atrophy and generalized brain atrophy

Neuropsych deficits including attention, processing, executive functions, memory

27
Q

Incidence rates for hypoxia and ischemia

A

Extremely difficult to estimate

28
Q

Percentage of people surviving with permanent brain damage after anoxic or hypoxic injury

A

50%

29
Q

Hypoxia that does not involve collapse or cessation of functioning of the circulatory system will typically result in less or more damage?

A

If it does not involve the collapse of circulatory system, damage is less

30
Q

Under what circumstance is hypoxia not going to damage CNS?

A

If it is not severe enough to disrupt consciousness

31
Q

Examples of severe hypoxia cases

A

Sudden cardiac arrest

Acute respiratory distress syndrome

32
Q

What happens after a loss of consciousness happens?

A

Once the brain is deprived of oxygen for several minutes, damage progresses rapidly, and if the underlying condition is not quickly reversed, brain death or minimally conscious state would result.

33
Q

What happens when someone wakes up from a prolonged coma after hypoxia or ischemia?

A

Long lasting cond of functional disability

extrapyramidal syndrome’s such as parkinsonism

34
Q

What environmental factor can help reduce likelihood of permanent damage the brain after hypoxia?

A

If event Occurs in a hospital setting and receives rapid and effective resuscitation

35
Q

Examples of chronic disease related to chronic hypoxic an ischemic conditions

A

Obstructive sleep apnea and COPD

36
Q

Chronic obstructive pulmonary disease COPD symptoms

A

Emphysema, neural muscular weakness, fibrosing lung disease

Persistent respiratory acidosis with reduced oxygen saturation an elevator carbon dioxide

Cognitive deficits may not occur in mild cases they do not produce persistent hypoxia

Severe COPD cases result in cognitive impairment

37
Q

Obstructive sleep apnea symptoms

A

Recurrent episodes of blood oxygen desaturation due to total apnea or partial apnea breathing cessation

38
Q

Neurological correlates of COPD

A

Greater risk for a white matter hyperintensities and cognitive impairment.

39
Q

How does CPAP machine help with COPD

A

Reduces episodes of breathing disruption
Reduces oxygen desaturation during sleep
Improves daytime sleepiness

40
Q

Factors that are associated with poor outcome after hypoxic and ischemic event

A

GCS score of 3 to 5 after 24 hours post onset
No pupillary response on Day 3 post injury
Sustained abnormal EYE functions
Lower cranial nerve or brainstem dysfunction
Seizures or Myoclonus
Alpha coma EEG pattern

41
Q

Relationship between Age and recovery after hypoxic or anoxic event

A

Negatively correlated

42
Q

Do patients with severe hypoxic ischemic injury return to independence?

A

No, recovery curves are flat

43
Q

Delayed Post hypoxic leukoencephalopathy DPHL

A

Condition that is sometimes seen after anoxia or hypoxia.

Commonly seen after CO poisoning

Can occur due to any etiology producing prolonged hypo oxygenation

Patient initially makes a good recovery and could resume normal functioning followed by an abrupt onset of progressive neurologic decline involving parkinsonism or akinetic mutism with prominent cognitive impairment.

44
Q

What can you expect on imaging studies for delete posts hypoxic leukoencephalopathy?

A

Prominent white matter demyelination in frontal parietal region

45
Q

Comparison of outcomes between TBI and Hypoxia anoxia

A

Difference
Amount of tissue loss is more critical in anoxia (than TBI) in determining outcome

Hypoxia cases are more likely to be referred to residential care than TBI

Hypoxia cases perform worse on all measures of functional outcome than TBI

Hypoxia cases have significantly lower FIM gains relative to TBI

Same

Measures of memory correlate with hippocampal atrophy in both conditions

Intelligence correlates with whole brain volume in both

46
Q

Assessment of hypoxia anoxia

A

CT, MRI of the brain do not reveal significant changes initially.

Abnormalities often take weeks or months to show on scans:

White matter changes
Corpus callosum atrophy
Cortical edema
Cerebellar lesions
Basal ganglia lesions
Thalamic lesions
Hippocampal atrophy
47
Q

Which cognitive domain is less likely a problem for anoxia

A

Aphasia

48
Q

Outcomes of sudden cardiac arrest and ARDS

A

More than 30% With sudden cardiac arrest and ARDS show generalized cognitive impairment

Memory, attention, processing speed

49
Q

Outcomes of severe hypoxia and anoxia

A

More than 50% of people have changes in memory,

30% show personality changes

50
Q

What percent of people can regain full independence after hypoxia ischemia

A

<50%

51
Q

Neuropsychological assessment results in hypoxic ischemic injury

A 
Memory is most common
Attention
Executive dysfunction
Visual spatial deficits
Overall decline
52
Q

Do pure amnestic syndromes happen often following anoxia hypoxia?

A

No, rarely happens

Cognitive impairment is typically more extensive due to diffuse cerebral injury

53
Q

Do all patients suffer from memory impairment?

A

No a subset of patients do not have memory impairment but display motor or cognitive impairments and other domains

54
Q

Which parts of the brain are at high-risk for injury in hypoxia and anoxia?

A

Basal ganglia and cerebellum

55
Q

Describe sensorimotor functioning after hypoxia and anoxia

A

Severe hypoxic injury can cause spastic Quadripareais
Ataxia
Parkinsonism syndromes

56
Q

Emotion and personality changes after hypoxic an anoxic injury?

A

Anosognosia, self awareness impairment

Depression
Emotional and behavioral dysregulation

PTSD may be seen in mild hypoxia and anoxia injuries following traumatic event

57
Q

Example of medication for hypoxia anoxia

A

Methylphenidate
Stimulants
Acetylcholinesterase inhibitor (aricept)
SSRIs or anti-convulsant for mood stabilization

58
Q

Brains of infants and children require higher or lower percentage of oxygen than adults?

A

Infants to kids age 4 need

> 30% total body oxygen consumption in their brains

59
Q

Outcomes of perinatal anoxic hypoxic injury?

A

Later development of ADHD

60
Q

Outcome of neonatal hypoxia

A

Developmental disorder and impaired cognition

61
Q

What is the strongest predictor of long-term outcome in brain injury in neonates?

A

If there is injury in basal ganglia and thalamus

62
Q

 Are older brains more or less able to recover from hypoxic brain injury?

A

Older people are less likely to repair or recover from hypoxic brain injury,

permanent and severe cognitive deficits due to reduce cerebral reserve

63
Q

Definition of acute respiratory distress syndrome ARDS

A

Severe, life-threatening medical condition in which lungs are compromised or damaged and are unable to supply enough oxygen to arterial blood.

Result in anoxic hypoxic damage to the brain

Elsa AACN (35 decks)

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