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NURS 412 Midterm #2 > Increased ICP > Flashcards

Increased ICP Flashcards

1
Q

Normal ICP

A

Pressure exerted from total volume of 3 components within the skull - brain tissue, blood and CSF

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2
Q

Relationship between 3 components within the skull

A

If volume of any of 3 components increases without corresponding decrease in another component the result is increased ICP (Monroe-Kelly Hypothesis)

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3
Q

Measure of ICP and normal and abnormal values

A

In ventricles, subarachniod space, subdural space, epidural space, or brain tissue using a pressure transducer
normal ICP: 5-15 mmHg
sustained ICP > 20 mmHg = abnormal

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4
Q

Compensatory Mechanisms to resist increased ICO by: (3)

A
  1. Changes in CSF volume
  2. Altering intracranial blood volume
  3. Brain tissue volume

However, compensatory adaptation are finite. only going to last so long and then they will cause brain damage

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5
Q

Compensatory Mechanism: changes in CSF volume

A

By displacement of CSF (into spinal subarachnoid space) or altering production and absorption rates of CSF

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6
Q

Compensatory Mechanisms: Altering intracranial blood volume

A

By compression of veins, or vasoconstriction/vasodilation, or changes in venous outflow

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7
Q

Compensatory Mechanism: Brain Tissue

A

Distension of dura, or compression of brain tissue

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8
Q

Cerebral Blood Flow (CBF) definition

A

Amount of blood (ml) passing through 100 gms of brain tissue/min -> approx 750ml/min

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9
Q

Brain and glucose

A

brain is unable to store oxygen and glucose means you always have to have blood flow and supply of glucose and oxygen

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10
Q

CBF: Autoregulation

A

Brain has ability to autoregulate its own blood flow in response to metabolic needs.
- automatic alteration in diameter of cerebral flow to maintain constant blood flow
autoregulation does not work in extreme hypo/hypertension

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11
Q

MAP and Autoregulation of CBF

A

If MAP< 50, CBF is decreased and cerebral ischemia occurs
If MAP>150, cerebral vessels are maximally constricted and further response is lost

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12
Q

Other Factors Affecting CBP
- PaCO2
- PaO2

A

Increased Carbon Dioxide in the blood (increased PaCO2) causes cerebral vasodilation, decreased vascular resistance, and increased cerebral blood flow. If carbon dioxide is decreased in the blood this is reversed and CBF is decreased
PaO2 < 50 - vascular dilation, increasing CBF. In acidotic environment, further vasodilation in attempt to increased blood flow
CBF can be indirectly reflected by calculating cerebral perfusion pressure (CPP)

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13
Q

What is CPP (cerebral perfusion pressure)

A

CPP is the pressure needed to ensure adequate perfusion to brain tissue
CPP does not reflect perfusion pressure in ALL parts of the brain

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14
Q

Calculation of CPP

A

CPP = MAP - ICP

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15
Q

Calculation of MAP

A

MAP = SBP + 2(DBP)/3
Imperative to maintain MAP when ICP is increased

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16
Q

Normal CPP

A

70-100 mmHg

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17
Q

Min CPP required for adequate cerebral perfusion

A

50-60 mmHg

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18
Q

CPP meaning cerebral ischemia

A

CPP < 50 mmHg

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19
Q

CPP incompatible with life

A

CPP < 30 mmHg

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20
Q

What causes increased ICP (4)

A
  1. Cerebral edema
  2. Contusion (bruise - can cause bleeding and swelling)
  3. Cerebral abscess (pocket of pus and infected fluid in the brain)
  4. Cerebral neoplasm
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21
Q

Causes of cerebral abscess

A

surgery, ear infection, sinus infection, brain injury, meningitis, hx of IV drug use, HIV/AIDS, immunocompromised

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22
Q

Crucial factor of increased ICP

A

preservation of brain tissue by maintaining cerebral blood flow

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23
Q

Cerebral Edema - different types

A

Increased accumulation of fluid in extravascular spaces of brain tissue
Different types:
- vasogenic cerebral edema
- cytotoxic cerebral edema
- interstitial cerebral edema

24
Q

Vasogenic Cerebral Edema

A
  • most common type
  • from changes in endothelial lining of cerebral capillaries
  • increase in permeability of blood-brain and increase extracellular fluid volume
  • occurs mainly in white matter
25
Cytotoxic edema
From disruption of integrity of cell membrane Results from destructive lesions or trauma to brain tissue, leading to cerebral hypoxia/anoxia, Na+ depletion, syndrome of inappropriate antidiuretic hormone Fluid and protein shift from extracellular space into cells Most often in grey matter
26
Interstitial cerebral edema
Result of diffusion of ventricular CSF in an uncontrolled hydrocephalus
27
Clinical Manifestations of increased
- headache - confusion - decreased LOC
28
Three categories of clinical manifestations
Change in LOC Change in Vital Signs Ocular signs
29
Change in LOC
flattened affect, confusion, voice changes, talking different than they were before
30
Changes in Vital Signs: Cushings Triad
- irregular or decreased respirations - decreased HR - widening pulse pressure (difference between systolic and diastolic)
31
Ocular Signs
Dilation of the pupils epsilateral (on the same side of the lesion), sluggish or unresponsive to light. inability to move the eyes upward, or drooping of the eyelid. Fixed unilaterally dilated pupil is an emergency and a indication of herniation of the brain
32
Clinical Manifestations: decreased motor function
- Decorticate (flexor) - Decerebrate (extensor) - more serious damage - Headache from compression of intracranial structures (arteries, veins, nerves) - Pain is continuous
33
Clinical Manifestations: vomiting
Not proceeded by nausea From direct pressure on vomiting center in 4th ventricle in medulla Vomiting associated with increased ICP is projectile
34
Early Signs of Increased ICP (6)
Altered LOC - unilateral pupil changes in size, equality, and/or reactivity - altered respiratory pattern, bradypnea or irregular - unilateral hemiparesis (weakness to one side of the body) - focal findings (speech difficulty) - papiledema (swelling of the optic nerve) - vomiting, headache, seizures
35
Late Signs of increased ICP
decreased LOC (stupor) - unilateral or bilateral pupillary changes i.e. size, equality, and/or reactivity - cheyne-stokes respiration - decorticate or decerebrate posturing
36
Terminal Signs(4)
- coma - bilaterally fixed and dilated pupils - resp. arrest - absence of motor response
37
Pathophysiology of increased ICP
Insult to brain -> tissue edema -> increased ICP -> compression of ventricles -> compression of blood vessels -> decreased cerebral blood flow -> decreased oxygen with death of brain cells -> edema around necrotic tissues -> increased ICP with compression of brain stem and respiratory center -> accumulation of CO2 -> vasodilation -> increased ICP resulting from the increase in blood volume -> death
38
Causes of cerebral edema (6)
Mass lesions Head injuries Cerebral infections Brain Surgery Vascular insult Toxic or metabolic encephalopathic conditions
39
Mass lesions
Brain abscess, brain tumor Hematoma hemorrhage
40
Head injuries
Contusion Diffuse axonal injury Hemorrhage Post-traumatic brain swelling
41
Cerebral infections
Meningitis Encephalitis
42
Vascular insult
Anoxic & ischemic episodes Cerebral infarction (thrombotic or embolic) Venous sinus thrombosis – blood clot forms in the sinus and causes blood to fill in the ventricles and it can’t drain from the blood
43
Toxic or metabolic encephalopathic conditions
Hepatic encephalopathy (toxin build up from liver failure) Lead or arsenic intoxication Uremia
44
Complications of increased ICP
Inadequate cerebral perfusion Cerebral herniation
45
Cerebral herniation types (6)
- cingulate herniation - tentorial herniation - cerebellar tonsillar herniation (move downwards) - falx cerebri (brain tissue is pushed across to the other side from the damage. a midline shift) - tentorium cerebelli - tentorial incisura Brain herniation occurs as the brain is shifted from the compartment of higher pressure to the compartment of lower pressure.
46
Diagnostic Studies
- MRI - CT scan - MRA (magnetic resonance angiography) - CTA (computed tomographic angiography) - Above tests are used to differentiate many conditions that can cause increased ICP and to evaluate therapeutic options
47
Goal of care for a patient with increased ICPC
identify and treat the underlying cause of increased ICP and to support brain function
48
Drug Therapy
mannitol (diuretic osmotic - fluid moves into the blood vessels and is excreted) hypertonic saline (3% draws fluid out and into the vein) Corticosteroids to reduce swelling
49
Nutritional Therapy
pts with increased ICP are in hypermetabolic & hypercatabolic state -> increased need for glucose or fuel among other considerations
50
Significant part of interprofessional care
Pain Control
51
Supportive Therapy
Metabolic demands such as fever, agitation, shivering, pain and seizures can increased ICP. - address these with induced coma. dont want brain to be active. want the brain resting and sleeping so it can heal. decreases the oxygen and metabolic demands of the brain. Inducing hypothermia to suppress cerebral metabolism. This is often done for several days but extended hypothermia makes the patient susceptible to systemic infections and hypotension
52
Glasgow Coma Scale
Three areas tested: eye opening, motor response, verbal response) not able to use it when pt is in a coma or sedated from pain management Change: is key in determining what is happening neurologically
53
low glasgow coma number
Score less than or equal to 8 at 6 hours post injury - 50% die
54
Neurological Assessment
pupils compared for size, movement, and response (use penlight) evaluate cranial nerves for unconscious patients, observe their spontaneous movement If no spontaneous movement, painful stimuli are applied VS
55
Nursing Implementation (7)
Respiratory Function Fluid & Electrolyte balance Monitoring ICP Body position - elevated at least 30 degrees Protect from injury - confusion, agitation, seizures. give seizure precautions. turn slowly, keep head midline, avoid unnecessary stimulation Coughing, straining and the valsalva maneuver should be avoided Psychological consideration

NURS 412 Midterm #2 (18 decks)

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