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PA 2 (RESP 262) > Mod 2 - Neurolgical Assessment of the Critically Ill > Flashcards

Mod 2 - Neurolgical Assessment of the Critically Ill Flashcards

1
Q

3 common sources of error from equipment?

A

artifact (external factor aka patient moving)

factious event (real but not accurate to the overall pic)

instrument drift (something happens to the device)

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2
Q

LOC is usually asses by oriented x3, what is the most important point to emphasis about the test?

what would you do if the patient can’t respond (i.e intubated?)

A

Check how the patient responds to stimuli

-Central stimulation
-peripheral stimulation

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3
Q

what is a basic assessment of a neurological assessment?

A

LOC

Motor examination

Posturing

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4
Q

4 common levels of LOC

A

full consciousness
Obtunded
Stupor
Coma

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5
Q

what would you score the verbal response for a patient that is intubated for GCS?

A

Default 1 for no response with a “T” placed after the score

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6
Q

Gagging and swallow reflex is protective reflex, which nerve is it apart of?

A

Glossopharyngeal (Cranial nerve 9)

-sensory, taste is also included

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7
Q

Which nerve is mostly associated with a cough?

A

Vagus (cranial nerve 10)

It is a protective motor reflex

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8
Q

On a unconscious patient, how do you check for a cough reflex?

A

Poke the carina during suction (trigger it)

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9
Q

How would you perform a: Motor examination?

A

Central stimulation is the most common way to check (aka eternal rub, pain stimulation).

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10
Q

Posturing is a response to what?

A

noxious stimulus, the decorticate and decelerate position are responses the we gauge for GCS

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11
Q

What is noxious stimuli?

A

A stimulus strong enough to threaten the bodies integrity (cause damage to tissue)

Usually serves as a test response to pain

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12
Q

What do you look for when evaluating brainstem reflexes?

Who do we check brainstem reflexes for?

A

Evaluated for stuporous or comatose patients to determine if the brain stem is intact

if not intact, evaluated to determine if brain death has occurred.

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13
Q

what factor can affect reflexes?

A

sedatives, analgesics, and paralytics can interfere with the ability to assess motor function and reflexes

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14
Q

Pupil/pupillary reflex: Anisocoria

A

One pupil is larger than the other

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15
Q

Why do you give people anti cholinergic drugs with someone who is breathing normally?

A

Anticholinergics:

relax and enlarge (dilate) airways in the lungs, making it easier to breath (bronchodilator).

Protect the airways from spasms that can suddenly cause the airway to become narrower (bronchospasm).

Reduce mucus production in airways

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16
Q

Pupil/pupillary reflex: Anisocoria

A

One pupil is larger than the other

ometimes the first sign people notice of a life-threatening underlying condition like a stroke or aneurysm

TLDR; could indicate a brain bleed

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17
Q

Pupil/pupillary reflex: myosin

A

pontine hemorrhage, narcotics

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18
Q

Pupil/pupillary reflex: mydriasis

A

brain injury, anticholinergics

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19
Q

Pupil/pupillary reflex: mid-position fixed pupils

A

severe cerebral damage

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20
Q

how are pupil/pupillary reflex’s tested?

A

passing a bright light in front of both open eyes and watching for over movement

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21
Q

Pupil/pupillary reflex: what is a ominous sign?

A

Eyes are fixed and dilated -> could indicate brain death.

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22
Q

what do we test for during oral care and suctioning?

A

gag and cough

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23
Q

Which nerves are checked for with someone with a spinal injury?

A

Patellar reflex - deep tendon reflexes

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24
Q

What reflexes are tested in a comatose patient or someone with a lower spinal chord injury?

A

Plantar reflex - superficial reflexes

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25
Q

what stimulation type is bad motor reflex test?

A

peripheral stimulation (nail bed pressure), could indicate a reflex vs. motor function.

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26
Q

How many cranial and spinal nerves are there?

A

12 cranial nerves

31 spinal nerves

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27
Q

Add slide 6

A
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28
Q

Lemon determines what?

A

potential difficulty for intubation

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29
Q

why are do you log roll a patient?

A

The patient has a C-spine injury (potentially)
To assess the patients back
or patient is vomiting

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30
Q

Complications with inadequate sedation

A
  1. Anxiety
  2. pain
  3. pt-vent dysynchrony
  4. agitation - self removal of tubes + catheters
  5. myocardia ischemia
    family dissatisfaction
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31
Q

Complications of excessive sedation

A
  1. Prolonged mech. ventilation and length of ICU stay
  2. Tracheostomy
    DVT, VAP
    Additional testing
  3. Inability to communicate
    Cannot evaluate for delirium
  4. Resp. depression: sedatives can slow down the rate of breathing = hypoxia + hypotension
  5. Delirium
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32
Q

Richmond agitation sedation scale (Rass) what sedation level do we ideally want patients at (in the ICU)

A

-3

most are kept at -3 to -5

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33
Q

What is delirium a sign of?

A

Brain failure:

  • loss of higher brain function.
  • Oversedation or other drugs
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34
Q
  1. what is delirium?
  2. what is the time frame of action.
A
  1. Acute brain dysfunction accompanied by reduced ability to sustain or shift attention.
  2. Developed over a short period of time and tends to fluctuate
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35
Q

Why is delirium a issue?

A

indicates a underlying medical problem

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36
Q

Why do we assess for delirium?

A

helps to optimize the delivery of sedatives and analgesics ( i.e can you ween off? )

-helps patient outcome

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37
Q

how do we assess delirium?

A
  1. The confusion assessment method for the ICU (CAM-ICU)
  2. Intensive care delirium screening checklist (ICDSC)
    -used in Calgary
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38
Q

What pneumonic is used to determine causes for delirium?

Edit

A

Think delirium - need to be able to list 5 causes

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39
Q

Think delirium pneumonic (slide 18)

Edit

A
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40
Q

what is “SAT”

A

spontaneous awakening trial

  • Evaluate a patient’s readiness to be weaned off sedation and mechanical ventilation.
  • less accumulation of sedative drug and metabolites…decreases risk of delirium
  • provides opportunity for more effective weaning from ventilation
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41
Q

Review and add slides 19 & 20 up to slide 23

A
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42
Q

Methods to assess a patients condition
(2)
hint unconscious vs. conscious

A

GCS - used to gauge responsiveness w/o much info for the first time. (outside ICU)

RASS - used w/o some info and target a level of responsiveness (for sedation)

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43
Q

We actively assess a look for what reflex to gauge airway protection?

A

Gag and cough reflex

Nerves 9 and 10

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44
Q

what is the target sedation for a patient?

A

-4

  • we aim keep it at -4 they’re still semi rousable/responsive
  • Give the min (not overdosing) to remain sedated.
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45
Q

What is delirium described as?

A

Acute brain dysfunction: has 2 hallmarks

  • indicator/marker of other issues.
  • inability to shift attention
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46
Q

Wake up safety screen?

A
  • no active seizures
  • no active alcohol withdrawal
  • no active agitation
  • no active paralytic use
  • no myocardial ischemia (24h)
  • normal intracranial pressure
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47
Q

Breathe safety screen?

A

No active agitation
oxygenation saturation > 88%
FiO2 <50%
PEEP < 7.5 cmH2O
no active myocardial ischemia (24hr)
no significant vasopressor use

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48
Q

What is the ABCDE protocol?

A

help break the cycle of over sedations and prolonged ventilation

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49
Q

Breakdown of ABCDE protocol?

A

ABC = awakening and breathing coordination
(wake up and breath)

D = delirium management/intervention

E = early exercise and mobility

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50
Q

Normal (ICP) - intraranial pressure

A

10-15 mmHg

small fluctuations are normal
> 20 is considered intracranial hypertension

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51
Q

CPP = MAP - ICP

what relation does this describe?

A

describes cerebral perfusion in relation to mean arterial pressure and intracranial pressure.

If ICP is within 40-50 mmhG of MAP (the difference).

when ICP is approx. = to MAP -> Perfusion stops and brain dies.

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52
Q

Placements for diagnostic measures/interventions of ICP (monitoring) (5)

needs edit

A

1.intraparenchymal
2. subarachnoid
3. ventricular
4 subdural
5. epidural

Mainly via pascals principle?

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53
Q

membranes that line the brain (3)

A

meninges
deramater - outer most membrane of brain
subarachnoid matter? -
peamater

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54
Q

2 types of ICP monitoring systems

A

fluid filled systems

solid-state systems

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55
Q

what is SjVO2? what is its normal value?

A

jugular venous oxygen saturation

Normal value is 50-75%

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56
Q

jugular venous oxygen saturation

A

approximates amount by the amount that goes into the brain.

measured via specialized catheter

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57
Q

what does jugular venous oxygen saturation (SjvO2) reflect?

A

the balance between cerebral oxygen therapy delivery and the cerebral metabolic rate of oxygen

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58
Q

Decreased jugular venous oxygen saturation (SjvO2) can indicate?

A

decreased cerebral blood flow; cerebral hypoperfusion and possible ischemia.

increased cerebral metabolic rate (febrile, seizure)

arterial hypoxemia

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59
Q

Increased jugular venous oxygen saturation (SjvO2) indicates?

A

reduced cerebral metabolic rate
-hypothermia, sedatives, brain death

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60
Q

What is metabolic rate a reflection of

A

increased O2 consumption

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61
Q

Head injuries for jugular venous oxygen saturation (SjvO2) patients can diagnosis early what?

A

ischemia

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62
Q

why do you cool the body down to reduce metabolic rate?

A

To cause hypothermia, to slow the bodies metabolic rate.

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63
Q

What is cerebral oximetry

A

a non-invasive method to determine saturation or determine cerebral oxygenation (or other locations)

can indicate underlying conditions

mostly used in the OR

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64
Q

what is a Licox monitor?

A

is a monitor connected to a catheter that is inserted in the brain tissue.

measures brain tissue oxygenation (PbtO2)

for patients w/trauma/neuro brain injury

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65
Q

what can develop regardless of a normal ICP and CPP?

A

cerebral hypoxia can still develop

66
Q

peripheral nerve stimulator: train of four monitoring

A

small electric shock is delivered to sites (on the wrist)
-zaps 4 times.

-checking for the amount of times the patient responds to zaps.

67
Q

what is the purpose of peripheral nerve stimulator?

A

To test and aim for certain levels of paralysis before you put someone out.

68
Q

What is the purpose of electroenecephalography (EEG)

A

measures the brain for seizure activity

also gauges comas or brain death.

69
Q

Go to mod 2 core and read ICP article

A

than write test

70
Q

Therapeutic interventions

A

Ventilation therapies

Therapeutic hypothermia

extra-ventricular drain (EVP)

Hyperosmolar therapy

decompressive therapy

pharmacological therapy

71
Q

Therapeutic interventions:
Therapeutic hyperventillation (now ventilation therapies)

A

Targeting the low end of normal.

Increasing minute volume with the goal of decreasing PaCO2

72
Q

Therapeutic interventions: why do you target the lower end of PaCO2 (35-40) for ventilation therapies?

A

results in vasoconstriction of the cerebral arteries, reducing blood in the… and thus reducing intracranial pressure.

reducing ICP is the goal.

73
Q

Therapeutic interventions:
why is ventilation therapy problematic?

A

decreased blood flow to the brain results in decreased O2 delivery and anoxic brain injury

74
Q

low CO2 results in constriction, what does high CO2 do?

A

dilates the blood vessels

75
Q

Therapeutic interventions: describe extraventricular drains (EVD)

A

Putting a catheter into a ventricle of the brain to monitor ICP and removal of fluids/blood from ventricular space

76
Q

Therapeutic interventions: indicators for extra-ventricular drains (EVD)?

A

Allow monitoring of ICP

reduce ICP

relieve hydrocephalus (fluid/blood in the intracranial cavity)

77
Q

Therapeutic interventions: what is therapeutic hypothermia and why is it referred to as protective hypothermia?

A

lowering patients body temp to help reduce the risk of ischemic injury after a period of insufficient blood flow.

Goal is to reduce the metabolic demand of the brain and tissue. It helps stabilize ….?

78
Q

What is a heart arrythmia?

A

Irregular heartbeat; problems with electrical signals that coordinate the hearts beat (don’t work properly)

-fault signals cause tachycardia or bradycardia

79
Q

What is the purpose of a pressure transducer?

A

measures the hemodynamics w/a actual value for ICP

80
Q

At 15-20mmHg, is ICP normal?

A

No.

Capillary bed is compressed and microcirculation is compromised

81
Q

At 30-35mmHg, what can be predicted about ICP?

(3)

A
  1. venous drainage is impeded and leads to edema -> develops in uninjured tissue
  2. ICP > 20 is considered IC hyper
    (cap. bed is compressed and microcirculation is compromised)
  3. Fluid buildup/swelling generally speaking
82
Q

why does premedication come before paralysis?

A
83
Q

What is the purpose of Licox monitoring

A

regional oxygenation (mmHg)

Partial pressure of oxygen at brain tissue

84
Q

What does jugular venou oxygena saturation (SjvO2) typically measure?

A

How much of oxygen is in the blood as it comes out of the brain

85
Q

what is responsible for a low SjvO2 or what does it indicate?

A

high metabolic rate

Increased oxygen consumption

decreased cerebral blood flow

86
Q

what does a high SjvO2 indicate/cause?

A

reduced metabolic rate

the brain is not using the oxygen (sedation or paralysis)

tissue death

increased cerebral flow (blood is flowing faster but not offloading O2 fast enough)

87
Q

Stages of general anesthesia

A

induction
excitement
surgical
overdose

88
Q

characteristics of general anesthesia?

A

unconsciousness
analgesia
muscle relaxation
depression of reflexes

89
Q

non-depolarizing vs depolarizing blocking agents?

A

some stimulate muscle contraction before paralytic affect.

90
Q

Benzodiazepines function

A

Sedation, hypnotic, anxiolytic

used to treat:
anxiety, agitation,
insomnia/seizures/status epilepticus,
muscle spasms,
Alcahol withdrawal (DTS)

91
Q

What are some complications with benzos?

A

can cause loss of airway reflexes at high doses and decreased tidal volume at lower doses

92
Q

What is a typical reversal agent for Benzos?

A

Flumazenil (Romazicon)

93
Q

Short acting vs. long acting benzodiazepines?

A

Short is usual the sedative or hypnotic

Long acting = anti-anxiety

94
Q

Dexmedetomidine (Precedex)

A

Expensive sedative in ICU w/o resp. System depression

Less delirium, shortened time to extubation, reduce icy stay

95
Q

Barbiturates

A

no reversal agents

sedative drug;largely replaced by benzo’s
can be used as anaesthetics (thiopoental) or hypnotics.

phenobarbital used for seizure control

96
Q

General use, pros, and cons of: propofol

A

Anesthetic w/hypno + sedative properties

recovery is rapid and clear; is not a analgesic.

Cons: hypotension, resp. depression

97
Q

What is the general use of Propofol in the ICU?

A

used for induction and maintenance of gen. anesthesia sedation for mechanically ventilated conscious patients procedural sedation

98
Q

Narcotics: Opioid Analgesic effects?

A

Analgesia
Sedation (secondary affect)
Decreased preload and afterload on the left ventricle antitussive qualities (cough suppression)

99
Q

Signs of narcotic overdose?

A

pinpoint pupils
coma
resp. depression

100
Q

Side effects of opioid analgesics?

A

-Release of histamine; can lead to bronchospasm (sounds like wheezing)

constipation
tolerance/addiction
nausea + vomitting

101
Q

Reversal agents for Opioid analgesics (narcotics)?

A

Nalaxone (Narcan) or naltrexone(Revia)

reversal agent doesn’t last as long as the drug; redosing may be needed.

102
Q

NSAID effects

A

primary use is for anti-pyretic or anti-flammatory effect.

But, they also have analgesic affects.

103
Q

what are the affects of Neuromuscular Blocking Agents (NMBA)?

A

paralytic or muscle relaxant.

-there is no amnesiac, analgesic, or sedative afffect.

-must have use w/sedative and analgesic otherwise patient will be locked in and awake.

104
Q

What’s the difference between Non-depolarizing or depolarizing NMBA?

A

non-depolarizing = slow onset w/longer duration (maintain paralysis)

depolarizing = rapid onset; short duration
-for short procedures (intubation)

105
Q

What is the mechanism of action for neuromuscular blocking agents (NMBA)?

A

blocks acetylcholine binding to. its receptors preventing depolarizing the muscle fibres (stops muscle contractions)

106
Q

What are examples of some NMBAs?

hint the middle of the names typically have “cur” in it?

A

Atacurium (tracrium)

Pancuronium (Pavulon)

Rocuronium (zemuron)

Tubocuraine

107
Q

Side of effects of NMBAs?

A

cardiovascular effects (tachycardia, vasoconstriction, and hypertension) - pavulon is the worst.

can release histamine

need to provide ventilation

108
Q

Reversal agent for NMBAs?

A

Neostigmine; is a cholinesterase inhibitor.

cholinesterase is the enzyme that breaks down AcH

109
Q

NMBAs: depolarizing

what is the mech of action?

A

depolarizers the muscle fibre and prolongs the depolarized state to repolarization

results in fasiculation; wide spread uncoordinated skeletal muscle contraction (tremoring) = flaccid muscles

110
Q

What is the onset of depolarizing NMBAs?

A

30-60 seconds, lasting about 3-5

111
Q

What is the generic name of Anectine?

A

Succinylcholine; its a depolarizing NMBA

112
Q

why does high amounts of potassium result in the stopping of the heart?

why is hyperkalemia a problem?

A
113
Q

Side effects of succinylcholine? is there a reversal agent?

A

No reversal agent.

Side effects:

114
Q

When are NMBAs used?

A

Intubation

  • reduce ICP in intubated patients with uncontrollable ICP
  • To achieve patient-ventilator synchrony
  • To reduce O2 consumption
  • stop epilepticus or shivering
    (therapeutic hypothermia)
  • Paralyze; for those who must remain still.
115
Q

Mannitol function and use

edit

A

osmotic diuretic - increases osmotic pressure and draws fluid from interstitial spaces.

What does it do?
-reduces ICP when cerebral edema is present due to TBI

116
Q

What is tier 2 of AHS TBI protocol?

A

ICP consistently > 20mmHg but SjvO2 > 60%

or

PbtO2 > 20 mmHg

117
Q

TBI protocol tiers?

A
118
Q

What is the function of a anti-pyretic?

A

used to prevent or treat fever

119
Q

What is a complication of ASA?

A

asthmatics can be sensitive to aspirin resulting in bronchospasm

120
Q

What does quality does ASA and Ibuprofen have in common that acetaminophen doesn’t?

A

ASA and Ibuprofen can be given for acute coronary syndromes because they both inhibit platelet aggregation.

Acetaminophen does not inhibit platelet aggregation nor does it have a anti-inflammatory quality.

121
Q

4 types of ICP monitoring (methods)

A

Jugular venous oxygen saturation (SjvO2)
-fluid-filled system
-use external pressure transducer

Cerebral oximetry
-non invasive

Licox monitoring
-catheter in brain tissue

Peripheral nerve stimulator: (train of 4 monitoring)
-delivers shocks
-observes reaction to stim.

122
Q

Differentiate between the CNS and PNS

A

CNS: Brain and spinal cord
-Brain = (cerebrum + cerebellum + brainstem)

PNS: 12 pairs of cranial nerves (most originate in brainstem), 31 pairs spinal nerves

123
Q

which cranial nerves are significant for RTs?

and, how do we test for their functionality?

A

cranial nerve 9 (glossopharyngeal): sensory for gag
-innervated the carotid sinus

cranial nerve 10 (vagus): motor for gag + cough
-stimulation can result in brady

124
Q

Where in the brain does the control of respiration reside?

A

Brainstem
-> primary medulla (dorsal and ventral groups)
-> pons (apneustic and pneumotaxic centre)

also, there is chemical control respiration (chemoreceptors)

125
Q

In the pons, what do the apneustic and pneumotaxic centres do?

A

fine tunes the main controls of breathing, but does not stimulate it on its own.

126
Q

Where does the phrenic nerve arise from?

A

C3 to C5 (branches at each level)

127
Q

what 3 categories does the GCS access?

A

motor/verbal and eye opening responses

128
Q

A decreased PaCO2 level has what impact on cerebral blood flow

A

Decreased PaCO2 levels in the brain cause vasoconstriction; this decreases cerebral blood flow

129
Q

Define delirium

A

An acute brain dysfunction that involves altered LOC and inattention or disorganized thinking.

Tends to fluctuate via the day

130
Q

Why is evaluating for delirium important in critically ill patients?

A

bc it points to underlying medical problems (infection/sepsis, organ failure, electrolyte problems, acid-base imbalances, need for non-pharmological interventions)

Helps optimize sedation and improve patient care.

131
Q

What are the different features that are assessed to define delirium (4)

A
  1. Acute change or fluctuating mental status
  2. Inattention
  3. Altered LOC
  4. Disorganized thinking
132
Q

List 5 specific causes of delirium

hint
Toxic and delirious pneumonic

edit

A

-CHF, shock, dehydration, meds, new organ failure, electrolyte problems

-drugs, labs, environmental factors

133
Q

What type of ICP monitor allows for concurrent EVD?

A

Fluid filled system where catheter is inserted into the brain ventricle

134
Q

what is the relationship between SjvO2, cerebral metabolic rate, and cerebral oxygen delivery (math wise)?

A

SjvO2 = cerebral O2 delivery / cerebral metabolic rate

135
Q

What is EVD?

A

External ventricular drain (EVD): A temporary system that allows drainage of cerebral spinal fluid (CSF) from the ventricles to an external closed system.

136
Q

Describe how CO2 impacts cerebral blood flow?

A

Increased CO2 levels in the brain causes vasodilation; which increases cerebral blood flow

137
Q

What happens when there are increased CO2 levels in the brain?

A

Vasodilation; increasing cerebral blood flow

138
Q

What three categories does GCS assess?

A

motor/verbal and eye opening responses

139
Q

Oral and tracheal suction assess which of the cranial nerves?

A

Glossopharyngeal (9)
-sensory for gag (innervates the carotid sinus)

Vagus (10)
-motor for gag, sensory for cough
-laryngeal nerve; branch of the vagus and glottis closure is due to vagal innervation

140
Q

Is the pherenic nerve/spinal nerve apart of the diaphragm contraction part of the cough?

A

Yes.

141
Q

A decreased PaCO2 level has what impact on cerebral blood flow?

A

Vasoconstriction; decreasing cerebral blood flow.

142
Q

Complications of over-sedation?

A

-Prolonged mech. ventilation and length of ICU stay

-Additional testing/cost

-Inability to communicate

-cannot evaluate for delirium

143
Q

What are some complications that come with extended mech. ventilation?

A

-Tracheostomy

-Deep vein thrombosis (DVT) ; clots in vein

-Ventilator-associated Pneumonia (VAP)

144
Q

Define delirium

A

An acute brain dysfunction (not chronic, like dementia) that involves ““altered LOC and inattention or disorganized thinking.””

Tends to fluctuate through the day.

145
Q

what does the following measure, where does it measure, and is it a continuous or a spot-check monitor: SjvO2

A

SvjO2 monitors: SvjO2

gives a global approximation.

Both continuous and spot-check monitor

146
Q

what does the following measure, where does it measure, and is it a continuous or a spot-check monitor: Cerebral oximetry

A

Measures: SO2

Area: SO2 of underlying tissue

Continuous OR spot check

147
Q

Licox:

  1. what does Licox monitoring measure?
  2. where does it measure?
  3. Is it a continuous or a spot-check monitor
A

Measures: PO2

Area: PO2 of underlying tissue

Continuous monitor

148
Q

Function of Anticholinergic drugs?

A

Block AcH

Meaning:
Inhibits nerve impulses responsible for involuntary muscle movements and various bodily functions

149
Q

Pupils/pupillary reflex: PERRLA

A

Pupils are round reactive to light and accommodation

150
Q

Pupils/pupillary reflex: myosis

A

pontine hemorrhage; narcotics

151
Q

Pupils/pupillary reflex: mydriasis (dilation)

A

Brain injury or anticholinergics

152
Q

Pupils/pupillary reflex: mid-position fixed pupils

A

Severe cerebral damage

153
Q

Which nerves are you assessing when checking pupillary reflexes?

A

Cranial nerves II and III

154
Q

Affect of increasing/decreasing ICP

edit

A
155
Q

What is the function of ASA [Aspirin]?

A

NSAID w/Anti-coagulation properties

156
Q

What are commonly used non depolarizing NMBA?

A

Rocuronium

Vercuronium

Tubocuarine

157
Q

Reversal agent of non depolarizing NMBAs?

A

Neostigmine

158
Q

Side of affect of depolarizing NMBA?

A

increased systemic vasculature

K+ increase

159
Q

Do depolarizing NMBAs have reversal agents?

A

Nah bro

160
Q

What drug reduces ICP?

A

Mannitol, it is a osmotic diuretic

used when cerebral edema is present.

161
Q

How do NMBA’s reduce ICP?

A
  • Reduce metabolic cerebral oxygen demand
  • Reduces agitation = better ventilation
162
Q

What therapy can be used to decrease delirium?

A

Analgesia, adequate paint control may lower delirium.

  • Only considered if narcotics are feasible, assess with an objective tool.

PA 2 (RESP 262) (14 decks)

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