Sedation / analgesia Flashcards

1
Q

3 core features of delirium

A
  1. A disturbance of consciousness (i.e. reduced awareness of the environment, with reduced
    ability to focus, sustain or shift attention)
  2. A change in cognition (i.e. impaired problem solving or memory) or a perceptual
    disturbance
  3. Onset within hours or days, with a tendency to fluctuate
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2
Q

Name 3 critical illness factors that may contribute to delirium

A

Acidosis.
• Hypoxaemia: anaemia, pulmonary or cardiac failure.
• Sepsis/Fever.
• Hypotension.
• Metabolic and electrolyte disturbances.
• Hepatic and renal failure.
• Poisons: carbon monoxide, metabolic blockade, pesticides, solvents, mercury, lead.
• CNS pathology: abscesses, haemorrhage, hydrocephalus, subdural haematoma, infections,
seizures, stroke, tumours, metastases, vasculitis, encephalitis, meningitis.

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3
Q

Name an assessment tool for delirium in ICU

A
  1. The Confusion Assessment Method in the ICU (CAM-ICU).

2. The Intensive Care Delirium Screening Checklist

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4
Q

How to assess CAM-ICU ? When is it positive

A
  1. Acute onset or fluctuating course.
  2. Inattention.
  3. Altered level of consciousness.
  4. Disorganised thinking.

The patient is considered to be CAM-ICU Positive or DELIRIOUS when Features 1 AND 2 and
EITHER Feature 3 OR 4 are present.

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5
Q

Non-pharmacological management of Delerium - name 3

A

Orientation
• Provide visual and hearing aids.
• Encourage communication and re-orientate the patient repetitively.
• Have the same nurse caring for the patient where possible.
• Display familiar objects from patient’s home, in the room.
• Allow television during the day, with daily news.
• Non-verbal music.

Environment
• Sleep aids: lights on during the day, off at night.
• Control excess noise at night.
• Ambulate and mobilise patient early and often.

Clinical parameters.
• Maintain systolic pressure > 90 mmHg.
• Maintain oxygen saturations > 92%.
• Treat underlying metabolic derangements and infections.

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6
Q

Sedation/analgesia in delerium - how can you reduce delerium

A

• Assess the need for all current medications, especially sedatives, analgesics and
anticholinergic drugs.

  • Daily sedations breaks to titrate appropriate sedative/analgesic requirements.
  • Adequate analgesia will reduce the risk of delirium if the pain is a problem.
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7
Q

Approved med for acute hyperactive delirium in critical care

A

haloperidol

quetiapine also used

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8
Q

Name 3 complications of inadequate sedation/analgesia

A

Stress response -> reduced immunity, increased catabolism, hypercoagulopathy

sleep deprivation -> prolonged recovery

worsened pulm function

inadvertent removal of lines/tubes

anxiety - and PTSD

FAILURE TO COMPLY WITH TREATMENT

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9
Q

Name 3 complications of excessive sedation/analgesia

A

difficult to assess neuro function

increased duration of mechanical ventilation

Increased cardiovascular depression and increased vasoactive agent use

agitated / disorientated patient

increased length of stay

delusional memories an -> PTSD

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10
Q

2 ways of assessing pain

A

patient reported

pain observation tools Eg - Critical Care Pain Observation tool CPOT

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11
Q

Tool for assess sedation/agitation

A

Richmond agitation sedation scale RASS

Sdation-agitation scale - SAS

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12
Q

Propofol usual dose in adults for sedation

A

Propofol is available in a 1% and 2% preparation

sedation in adults is run between 1 and 20ml/hr of 1% with titration to a pre-defined end point.

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13
Q

Name 3 side effects propofol

A

 Respiratory depression and suppression of laryngeal reflexes, requiring caution with its use in patients with unsecured airways.

 Cardiovascular depression with a negative inotropic and chronotropic effect and a reduction in systemic vascular resistance.
=hypotension + bradycardia
Great care must therefore be taken with hypovolaemic or cardiovascularly unstable patients, and inotropes/vasopressors should be to hand if propofol boluses are being administered.

 Pain when administered peripherally.

 Hypertriglycerideaemia and Propofol Infusion Syndrome

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14
Q

Bar sedation name another use of propofol

A

refractory status epilepticus

as part of a treatment regimen for raised intracranial pressure, e.g. in traumatic brain injuries.

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15
Q

What is propofol infusion syndrome?

A

acute bradycardia resistant to treatment and progressing to asystole associated with prolonged (>48hrs) high dose (>5mg/kg/hr) propofol infusion

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16
Q

Who is susceptible to propofol infusion syndrome?

How to avoid?

A

avoid using prolonged high dose infusions of propofol, but rather use alternative agents alone or in combination

Dont use propofol alone in children for long term

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17
Q

Uses of benzos - name 3

A
sedation,
 hypnosis, 
anxyiolysis, 
anterograde amnesia,
muscle relaxation
 anti-epileptic.
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18
Q

Benzo mechanism

A

GABA-mediated inhibition

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19
Q

Main 2 complications of benzos

A

hypotension in haemodynamically unstable patients

hypoventilation

Paradoxical agitation

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20
Q

Usual dose midazolam

A

1mg/ml solution and run between 1 and 10mls/hr

with titration to a pre-determined end point

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21
Q

Midazolam onset offset time ? accumulation ?

A
rapid onset (0.5-2.5 mins) and a reasonably rapid offset (30 to 60 mins)
 It, therefore, tends to be given by infusion.

 Minimal accumulation occurs with short infusions (< 24hours) but is seen thereafter.

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22
Q

Diazepam onset off set time ?

A

very long terminal elimination half-life and active metabolites.
Intravenously diazepam has a reasonably rapid onset of action (within 2-3 mins) with repeat
doses every 2-4 hours.
Enterally diazepam takes approximately 30-60 minutes for onset of action

only really administered intermittently to minimise accumulation.

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23
Q

Usual dose diazepam

A

0.5-5mg intravenously

2-10mg enterally

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24
Q

Lorazepam duration

A

long duration of action (6-10hours)

making it less titratable

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25
Q

Lorazepam benefit vs midazolam ? why?

A

wake-up has been found to be more predictable than midazolam’s with prolonged infusion.

lorazepam’s metabolism is less influenced by other factors (e.g. drugs),
its metabolites are inactive and it has a more stable context-sensitive half time

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26
Q

Rare issue with lorazepam

A

hyperosmolar, lactate acidaemia with

acute tubular necrosis associated with prolonged, very high-dose lorazepam infusion

27
Q

Key side effects antidopaminergics eg haloperidol

A

hypotension, QT prolongation, ventricular arrhythmias
(including torsade de pointes with an incidence of up to 3.6%) and
extrapyramidal effects
(e.g. dystonias, akathisia, parkinsonism, neuroleptic malignant syndrome).

28
Q

Eg of alpha-2-adrenoreceptor agonists? Effects?

Key uses

A

Clonidine and dexmedetomidine

sedation, anxiolysis, analgesia,
reduced sympathetic output and an anti-sialogogue

Sedation
Management of hypertension
Opiate withdrawal (augments spinal cord to produce endogenous opiates)

29
Q

Clonidine and dexmedetomidine Benefit vs other sedatives

A

providing both sedation and analgesia but

with MINIMAL respiratory depression.

30
Q

main side effects Clonidine and dexmedetomidine

A

bradycardia and hypotension from the reduced sympathetic output,

Rebound hypertension on the abrupt withdrawal of these agents has been described,
necessitating its tapered withdrawal.

31
Q

clonidine dosing

A

 Loading dose: 1-2mcg/kg over 10 mins

 Maintenance: Infusion of 0.1-2mcg/kg/hr

32
Q

When do you get accumilation of clonidione

A

AKI / CKD

Clonidine is 50% metabolised to inactive metabolites in the liver but with the remaining 50%
being excreted unchanged in the urine, accumulation will occur in renal dysfunction.

33
Q

Ketamine mechanism

A

NMDA-receptor antagonist

34
Q

Name 3 side effects ket

A

Unpleasant dreams, emergence delirium, hallucinations.
 Increased cerebral metabolic rate (contraindicated in raised ICP)
 Increased myocardial oxygen consumption (cautious use in patients with coronary artery
disease)

35
Q

How often do patients get sedation breaks ? Why

A

daily
bar in patients with neuromuscular blockade EG Neuro ICU , HF with critical ventricular funciton

Reduce LOS and number of investigations required

36
Q

3 Non pharmacological methods of reducing pain

A
proper positioning 
Temperature 
hydration 
bowel / bladder care 
physio / regular turning 
massage 
music therapy
37
Q

Accumulation midazolam usually in

A

Liver failure, renal failure, elderly

38
Q

Benzo reversal

A

FLUMAZENIL

39
Q

DEXMEDETOMIDINE
Mechanism?
Side effects?
Why useful?

A

a2 agonist with sedative effects
Hypotension, bradycardia
May require breakthrough boluses of other sedatives

Does not cause resp depression -> can use when extubating
Also easy to arouse / wake up pt

40
Q

paralytic drug mechanism

A

acetylcholine blockers

41
Q

difference between depolarising and non depolarising paralytics

A

depolarising. Bind to Ach receptor -> depolarise then stay bound preventing further depolarisation

non depolarising - don’t activate receptor - just bind

42
Q

Eg of depolarising paralytic

A

succinylcholine

43
Q

succinylcholine.
onset / offset time ?
When is is commonly used?

A

fast 60s onset
offset 5 min for breathing, 10 min for total reversal

Makes very useful for intubation of patient

44
Q

3 key side effects succinylcholine.

in what populations might this make it contraindicated

A

initially fasciculations
hyperkalemia due to initial muscle activation
risk of malignant hyperthermia

Due to hyperkalemia from damaged muscles
-trauma with skeletal muscle damage
-burns
spinal cord injury

45
Q

2 examples of intermediate acting non depolarising paralytics

A

rocuronium
vecuronium
cisatracurium

46
Q

Rocuronium
onset / offset
when is it commonly used

A

onset 1-3mins
offset 30-90mins
Often used for RSI - rapid sequence induction

47
Q

cisatracurium
onset offset ?
when is commonly used ?

A

onset 5mins
offset 30 mins
used in liver / kidney failure

48
Q

Why cisatracurium not atracurium

A

atracurium ->

Histamine release -> hypotension, tachy, flushing

49
Q

Long-acting non-depolarising paralytic?

A

pancuronium

50
Q

pancuronium
onset offset?
key side effect

A

3 mins
60-120mins
vagolytic -> suppress vagus -> tachycardia

51
Q

how to monitor paralytic

A

peripheral nerve stimulation

52
Q

How does peripheral nerve stimulation in monitoring paralytics work?
name a common site use?

A

train of 4 - 4 quick electrical shocks to see muscle twitching

ulnar nerve -> watch thumb / fingers
facial nerve -> eyelid / brow
posterior tibial neve -> big toe

53
Q

in peripheral nerve stimulation (train of 4) how does the number of twitches correlate to neuromuscular blockade? what do you normally want?

2 factors that reduce effect of stimulation

A

1 twitch - 90%
2 twiches - 80%
3 twitches 75%

usually 2-3 twitches

length of time n meds
oedema
- may need to increase voltage of stimulation

54
Q

Key things to think about in paralysed patients

A

need to be heavily sedated and no analgesic effect
require eye care
(pupils are not effected)

55
Q

Mechanism of paralytic reversal meds?

Eg of one?

A

Inhibit acytlcholinesterase -> less break down of Ach -> increased Ach availability and compete with neuromuscular blockers

Neostigmine
pyridostigmine
endrophonium

56
Q

Key side effects of paralytic reversal agents eg neostigmine?

How to prevent this?

A
As increase globally level of Ach for neuromuscular receptors  
->activate parasympathetic system 
bradycardia
 pupil constriction
 salivation
 bronchoconstriction
 increased urine output
 increased peristalsis 

Give antimuscarinic (anticholinergic) drug

57
Q

eg of antimuscarinic/anticholinergic med?

A

Atropine
scopolamine - sedating
glycopyrrolate

58
Q

Which antimuscarinic most commonly used

A

glycopyrrolate - doesn’t cross blood brain barrier

59
Q

Medication that directly binds to rocuronium and stops it working?

A

sugammadex -> complete reversal in 2-4 mins

60
Q

Why do we sedate in ICU

A
Amnesia 
ventilator tolerance and effective ventilation 
anxiety / fear 
agitation 
sleep deprevation 
delerium
61
Q

Medication for head injury and raised icp / bursts of seizures ?

A

pentobarbital
Lowers ICP

decreases cerebral blood flow and oxygen consumption

Issues
excessive sedation
respiratory depression
myocardial deprssion

62
Q

Key sedative for short term sedation or if you require rapid offset

A

propofol

63
Q

dexmedetomidine why useful

A

no respiratory depression , minimal amnesia , easier to arouse and keep alert
-> can use while extubating

64
Q

Which paralytic in renal failure

A

atracurium