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Increased ICP Flashcards

1
Q

Definition of increased intracranial pressure

A

Sustained increase of > 20 mmHg for at least 5 minutes

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2
Q

What is normal ICP range?

A

0-15 mmHg

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3
Q

What is the Monro-Kellie Hypothesis?

A

ICP is made up the pressure exerted by the combined volume of blood, brain, and CSF.

When the volume of any one of these increases, one or both of the other 2 must decrease to prevent ICP

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4
Q

What is CPP?

A

Cerebral perfusion pressure - estimate of cerebral blood flow

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5
Q

How to calculate CPP:

A

MAP-ICP

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6
Q

What is normal CPP?

A

Range: 70-100 mmHg
Average: 85 mmHg

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7
Q

CPP amt to prevent cerebral anoxia

A

Must be > 60 mmHg

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8
Q

Most important step for increased ICP

A

*Always alter ICP first if it’s high with *Mannitol
Then give fluids

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9
Q

Names of the compensatory mechanisms for increased ICP

A

Autoregulation
Accommodation

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10
Q

What is autoregulation

A

Compensatory mechanism for ICP
*A NORMAL bodily function

Ability of cerebral vessels to dilate or constrict in response to arterial pressure changes in the brain

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11
Q

How does autoregulation occur with hypertension?

A

Carotids constrict to decrease blood flow to the brain

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12
Q

How does autoregulation occur with hypotension?

A

The carotids dilate to increase blood flow to the brain

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13
Q

What is accommodation?

A

An ABNORMAL compensatory mechanism to ICP in which intercranial contents shift

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14
Q

What occurs during accommodation?

A

1st: CSF is reabsorbed or displaced to subarachnoid space
2nd: blood returned to venous sinuses and pushed down
3rd: shifting of brain tissue (starts the herniation process)

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15
Q

How does autoregulation try to compensate for hypercapnia?

A

High CO2 means decreased O2, so carotids dilate to increase blood flow which increases O2

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16
Q

How does autoregulation try to compensate for hypoxia?

A

Decreases O2 causes carotids to dilate to increase blood flow to brain, which increases amt of O2

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17
Q

Example of nursing intervention that could cause hypoxia

A

*Suctioning

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18
Q

How does autoregulation try to compensate for volume overload?

A

Increased BP causes carotids to constrict to decrease blood flow to brain

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19
Q

How does autoregulation try to compensate for an aneurysm?

A

Takes up more room in the head than there is, causing increased ICP
Carotids will constrict to decrease amt of blood flowing to the brain

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20
Q

How does autoregulation try to compensate for arteriovenous malformation?

A

Takes up more room in the head than there is, causing increased ICP
Carotids will constrict to decrease amt of blood flowing to the brain

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21
Q

Examples that could cause jugular drainage obstruction

A

Neck flexion, hyperextension (need to control with positioning)
Neck swelling (constricts carotids)
Tight tracheostomy (leave 2 finger with between tie and pt’s neck)
Coughing (ICP already increased, will increase it too much)
Vomiting
Valsalva’s maneuver (teach pt not to bear down)
Positive pressure ventilation/PEEP (constant pressure of vent to keep airway open makes neck tighter. Need to keep as low as possible)

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22
Q

Examples of situations that would cause increased oxygen (—> increased blood flow)

A

Seizure activity - anti-seizure drugs to prevent
Hyperthermia - causes increased energy demand
Shivering - usually in post op patients as reaction to anesthesia
Hyperactivity - increased movement causes increased brain waves (need to monitor and treat)
Pain - use drugs and positioning to help

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23
Q

Two types of cerebral edema

A

Cytotoxic ( most dangerous: life threatening event )
Vasogenic (usually from brain injury itself)

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24
Q

What causes Cytotoxic cerebral edema?

A

Hypoxia - ischemia from CVA, cardiac arrest, asphyxiation, severe SIADH (water intoxication)

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25
What is vasogenic cerebral edema?
Breakdown in the blood brain barrier allowing proteins to penetrate, pulling water into cells
26
What causes vasogenic cerebral edema?
Head injuries Brain tumors Meningitis Abscesses
27
Definition of herniation
Shifting of brain tissue resulting in neurological deficits and eventually death
28
Types of herniation
Supratentorial: - cingulate - central - uncal Infratentorial - cerebellar tonsil
29
What is cingulate herniation?
Unilateral herniation of cerebral hemisphere across the midline Compresses cerebral vessels and brain tissue
30
Symptoms of cingulate herniation
Change in LOC and mental status
31
What is central herniation
Downward displacement of cerebral hemisphere through tentorial notch onto brain stem, compressing vital centers
32
Manifestations of central herniation
Early: Change in LOC & respiration pattern Motor weakness and increased muscle tone Small pupils (a factor, but not indicative) Positive Babinski reflex Late: Decortecate posturing Cheyne-stokes respirations
33
What is uncal herniation?
Herniation of uncal portion of temporal lobe through tentorial notch, compressing midbrain, causing dysfunction of CN III (Oculomotor)
34
Manifestations of uncal herniation
CN III: ipsilateral dilated pupil Contra lateral hemiplegia Worsening (moving further down brainstem): - fixed midposition pupils (wide and non-reactive) - altered respiration pattern (depending on where they are in process) - decerebrate posturing Quick progression to coma if not treated (Can treat symptoms and slow progress, but will always result in coma)
35
What is cerebellar tonsil herniation?
Compression of brainstem by cerebellar tonsils displaced through Foramen magnum
36
Manifestations of cerebellar tonsil herniation
Cardio-respiratory compromise
37
What does the glasgow coma scale measure?
Motor and verbal response: -eye opening - motor response to verbal commands / painful stimulus - verbal response
38
Scoring of Glasgow coma scale
3-15 points possible 3 = bad, 15 = wnl 8 = not good, 6 = bad
39
What do you assess in critically ill patients to assess their cranial nerves
Pupillary response Corneal check Cough, gag, and swallow reflexes
40
Types of posturing and what they each mean
*Decorticate = abnormal flexion (toward core) - arms flexed, wrists flexed, legs extended *Decerebrate = extension (away from core) - arms extended, external rotation of wrists, legs extended, internal rotation of feet Flaccid = brain death - no response in any extremity to noxious stimuli (Spinal cord injury must be ruled out as cause of flaccidity before pt is considered brain dead)
41
How to perform babinski reflex check
Use moderately sharp object, stroke later aspect of the foot, curving medially across the ball Negative (normal) = plantar flexion (toes go in) Positive (abnormal) = dorsiflexion (spreading of toes)
42
Late signs of brain damage
*Vital sign changes - changes to HR or BP So, never trust these vital signs to tell us what’s going on
43
Respiratory changes that occur as brain death progresses, in order
Cheyne-Stokes breathing - bilateral, deeper and faster (considered normal) Central neurogenic hyperventilation - very deep and rapid, > 25/min (considered normal) Apneusis = deep gasping with pauses at inspiration (1st abnormal breathing pattern) Cluster breathing - clusters of panting with a pause (abnormal) Ataxic breathing - irregular/uncoordinated (abnormal) Then, death rattle, then guppy breathing, then death
44
Important info for dolls eyes test
*Never do this on a normal patient * Normal = positive dolls eyes: eyes move in direction opposite of head movement *Abnormal = negative dolls eyes: eyes move in same direction as head moves = severe brain damage
45
What is an oculovestibular test? And when would you do it?
Ice water injected into ear only in neuro compromised patients Normal = eyes deviate toward ear with ice water
46
*Symptoms of Increased ICP
*Change in LOC *Headache (because of increased pressure) Pupillary changes Nausea/projectile vomiting Papilledema (red reflex) Seizures (with tumor only) Changes in vital signs = late (Cushing’s triad)
47
What is Cushing’s triad?
Changes in vital signs with brain death: - slow, bounding pulse - irregular respirations - depends on level of lesion - increased SBP with widening pulse pressure
48
Important info for ICP monitoring using a monitor
Measured at the level of the ear *Recorded on flow sheet, only paying attention to trends over several hours
49
Types of ICP monitoring sensors
Intraparenchymal sensor Epidural sensor Subarachnoid bolt Intra ventricular catheter Ventriculostomy
50
Risks for all ICP monitoring
*bleeding *infection
51
What is the gold standard for ICP monitoring?
*Ventriculostomy
52
Important info about Ventriculostomy ICP monitoring
Can also be used for CSF drainage Disposable kit, so most common in regular hospitals that don’t have a lot of neuro patients
53
Important info about intraventricular catheter ICP monitoring
Catheter goes into lateral ventricle on non dominant side *Most accurate monitoring device
54
*Nursing care for ICP monitoring (SATA question)
- Maintain closed system - Monitor for infection - Change dry sterile gauze according to protocol - Level with ventricles (ear) - Zero and calibrate frequently (using square test) - Record ICP and CPP (usually every hour) - Report changes to physician
55
Types of waveforms for ICP monitoring and what they mean
Normal: 0-15 mmHg Others (need trending to view) - *A waves - 50-100 (dangerous, need immediate intervention) - B waves - < 50 mmHg (warning signs of potential increased ICP) - C waves - 16-20 mmHg (small change with BP or respiration, not significant)
56
Gold standard for diagnosing neurological conditions
CT b/c it’s timely, easy, and doesn’t need a lot of prep
57
Medical management of increased ICP Goals for ICP and CPP
*First decrease ICP, then identify and treat the cause *ICP < 20 mmHg (no time frame) *CPP of 70 mmHg
58
Treatment for airway and goals for oxygenation in a pt with increased ICP
Intubate and ventilate as needed Goals: - PaO2 80-100 mmHg (*low O2 leads to ICP elevation, need to decrease CO2 slowly though, so you don’t cause rebound increase in ICP)
59
Diuretics given fir increased ICP
Osmotic diuretics - *Mannitol Loop diuretics - furosemide
60
Treatment for ICP using mannitol
Want to withdraw fluid from normal tissue: - Works in 20 minutes (draws water into plasma so it can be reabsorbed and drawn out) May cause rebound cerebral edema and hypotension Use hypertonic saline (3% NS) with diuretics to pull water out of blood stream
61
Treatment for ICP using furosemide
Reduces rate of CSF production Removes sodium and water from injured brain cells Can use hypertonic solution with diuretics
62
Goal for blood pressure in a pt with ICP
Avoid hyper- and hypo- tension Keep systolic BP <160 mmHg and MAP 70-90 mmHg
63
Treatment for increased MAP or decreased MAP
Increased = Diuretics, BP control meds Decreased = give fluids
64
When would the goals of BP control for a pt with ICP not be the same?
In management of vasospasms associated with subarachnoid hemorrhage, higher blood pressure may be required
65
Treatment for vasospasms associated with subarachnoid hemorrhage
Nicardipine (CCB)
66
Fluid restriction guidelines for increased ICP
Goal = 75-100 mL/hr (NS) Except in management of SA spasms, may need more or less, would look at order
67
How to control cerebral metabolism
Treat fever - controlled hypothermia Seizure prophylaxis Analgesics Sedation (propofol) Neuromuscular blockade (always sedate as well)
68
What are the disadvantages of sedating the neurological patient?
Can’t see changes in monitoring
69
Actions of giving phenobarbital to a pt to control cerebral metabolism
Puts pt in barbiturate coma - decreases metabolism - decreases cerebral edema - better CBF
70
Surgical intervention for increased ICP
Surgery called an evacuation - open skull and scoop out problem (mass, lesion, hematoma) - causes damage, sometimes worse than leaving it alone

Critical Care (35 decks)

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