Sedation / analgesia Flashcards

(64 cards)

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
Lorazepam benefit vs midazolam ? why?
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
26
Rare issue with lorazepam
hyperosmolar, lactate acidaemia with | acute tubular necrosis associated with prolonged, very high-dose lorazepam infusion
27
Key side effects antidopaminergics eg haloperidol
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
Eg of alpha-2-adrenoreceptor agonists? Effects? Key uses
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
Clonidine and dexmedetomidine Benefit vs other sedatives
providing both sedation and analgesia but | with MINIMAL respiratory depression.
30
main side effects Clonidine and dexmedetomidine
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
clonidine dosing
 Loading dose: 1-2mcg/kg over 10 mins |  Maintenance: Infusion of 0.1-2mcg/kg/hr
32
When do you get accumilation of clonidione
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
Ketamine mechanism
NMDA-receptor antagonist
34
Name 3 side effects ket
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
How often do patients get sedation breaks ? Why
daily bar in patients with neuromuscular blockade EG Neuro ICU , HF with critical ventricular funciton Reduce LOS and number of investigations required
36
3 Non pharmacological methods of reducing pain
``` proper positioning Temperature hydration bowel / bladder care physio / regular turning massage music therapy ```
37
Accumulation midazolam usually in
Liver failure, renal failure, elderly
38
Benzo reversal
FLUMAZENIL
39
DEXMEDETOMIDINE Mechanism? Side effects? Why useful?
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
paralytic drug mechanism
acetylcholine blockers
41
difference between depolarising and non depolarising paralytics
depolarising. Bind to Ach receptor -> depolarise then stay bound preventing further depolarisation non depolarising - don't activate receptor - just bind
42
Eg of depolarising paralytic
succinylcholine
43
succinylcholine. onset / offset time ? When is is commonly used?
fast 60s onset offset 5 min for breathing, 10 min for total reversal Makes very useful for intubation of patient
44
3 key side effects succinylcholine. in what populations might this make it contraindicated
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
2 examples of intermediate acting non depolarising paralytics
rocuronium vecuronium cisatracurium
46
Rocuronium onset / offset when is it commonly used
onset 1-3mins offset 30-90mins Often used for RSI - rapid sequence induction
47
cisatracurium onset offset ? when is commonly used ?
onset 5mins offset 30 mins used in liver / kidney failure
48
Why cisatracurium not atracurium
atracurium -> | Histamine release -> hypotension, tachy, flushing
49
Long-acting non-depolarising paralytic?
pancuronium
50
pancuronium onset offset? key side effect
3 mins 60-120mins vagolytic -> suppress vagus -> tachycardia
51
how to monitor paralytic
peripheral nerve stimulation
52
How does peripheral nerve stimulation in monitoring paralytics work? name a common site use?
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
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
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
Key things to think about in paralysed patients
need to be heavily sedated and no analgesic effect require eye care (pupils are not effected)
55
Mechanism of paralytic reversal meds? | Eg of one?
Inhibit acytlcholinesterase -> less break down of Ach -> increased Ach availability and compete with neuromuscular blockers Neostigmine pyridostigmine endrophonium
56
Key side effects of paralytic reversal agents eg neostigmine? How to prevent this?
``` 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
eg of antimuscarinic/anticholinergic med?
Atropine scopolamine - sedating glycopyrrolate
58
Which antimuscarinic most commonly used
glycopyrrolate - doesn't cross blood brain barrier
59
Medication that directly binds to rocuronium and stops it working?
sugammadex -> complete reversal in 2-4 mins
60
Why do we sedate in ICU
``` Amnesia ventilator tolerance and effective ventilation anxiety / fear agitation sleep deprevation delerium ```
61
Medication for head injury and raised icp / bursts of seizures ?
pentobarbital Lowers ICP decreases cerebral blood flow and oxygen consumption Issues excessive sedation respiratory depression myocardial deprssion
62
Key sedative for short term sedation or if you require rapid offset
propofol
63
dexmedetomidine why useful
no respiratory depression , minimal amnesia , easier to arouse and keep alert -> can use while extubating
64
Which paralytic in renal failure
atracurium