Sedation / analgesia Flashcards
3 core features of delirium
- A disturbance of consciousness (i.e. reduced awareness of the environment, with reduced
ability to focus, sustain or shift attention) - A change in cognition (i.e. impaired problem solving or memory) or a perceptual
disturbance - Onset within hours or days, with a tendency to fluctuate
Name 3 critical illness factors that may contribute to delirium
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.
Name an assessment tool for delirium in ICU
- The Confusion Assessment Method in the ICU (CAM-ICU).
2. The Intensive Care Delirium Screening Checklist
How to assess CAM-ICU ? When is it positive
- Acute onset or fluctuating course.
- Inattention.
- Altered level of consciousness.
- 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.
Non-pharmacological management of Delerium - name 3
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.
Sedation/analgesia in delerium - how can you reduce delerium
• 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.
Approved med for acute hyperactive delirium in critical care
haloperidol
quetiapine also used
Name 3 complications of inadequate sedation/analgesia
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
Name 3 complications of excessive sedation/analgesia
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
2 ways of assessing pain
patient reported
pain observation tools Eg - Critical Care Pain Observation tool CPOT
Tool for assess sedation/agitation
Richmond agitation sedation scale RASS
Sdation-agitation scale - SAS
Propofol usual dose in adults for sedation
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.
Name 3 side effects propofol
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
Bar sedation name another use of propofol
refractory status epilepticus
as part of a treatment regimen for raised intracranial pressure, e.g. in traumatic brain injuries.
What is propofol infusion syndrome?
acute bradycardia resistant to treatment and progressing to asystole associated with prolonged (>48hrs) high dose (>5mg/kg/hr) propofol infusion
Who is susceptible to propofol infusion syndrome?
How to avoid?
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
Uses of benzos - name 3
sedation, hypnosis, anxyiolysis, anterograde amnesia, muscle relaxation anti-epileptic.
Benzo mechanism
GABA-mediated inhibition
Main 2 complications of benzos
hypotension in haemodynamically unstable patients
hypoventilation
Paradoxical agitation
Usual dose midazolam
1mg/ml solution and run between 1 and 10mls/hr
with titration to a pre-determined end point
Midazolam onset offset time ? accumulation ?
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.
Diazepam onset off set time ?
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.
Usual dose diazepam
0.5-5mg intravenously
2-10mg enterally
Lorazepam duration
long duration of action (6-10hours)
making it less titratable
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
Rare issue with lorazepam
hyperosmolar, lactate acidaemia with
acute tubular necrosis associated with prolonged, very high-dose lorazepam infusion
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).
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)
Clonidine and dexmedetomidine Benefit vs other sedatives
providing both sedation and analgesia but
with MINIMAL respiratory depression.
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.
clonidine dosing
Loading dose: 1-2mcg/kg over 10 mins
Maintenance: Infusion of 0.1-2mcg/kg/hr
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.
Ketamine mechanism
NMDA-receptor antagonist
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)
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
3 Non pharmacological methods of reducing pain
proper positioning Temperature hydration bowel / bladder care physio / regular turning massage music therapy
Accumulation midazolam usually in
Liver failure, renal failure, elderly
Benzo reversal
FLUMAZENIL
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
paralytic drug mechanism
acetylcholine blockers
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
Eg of depolarising paralytic
succinylcholine
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
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
2 examples of intermediate acting non depolarising paralytics
rocuronium
vecuronium
cisatracurium
Rocuronium
onset / offset
when is it commonly used
onset 1-3mins
offset 30-90mins
Often used for RSI - rapid sequence induction
cisatracurium
onset offset ?
when is commonly used ?
onset 5mins
offset 30 mins
used in liver / kidney failure
Why cisatracurium not atracurium
atracurium ->
Histamine release -> hypotension, tachy, flushing
Long-acting non-depolarising paralytic?
pancuronium
pancuronium
onset offset?
key side effect
3 mins
60-120mins
vagolytic -> suppress vagus -> tachycardia
how to monitor paralytic
peripheral nerve stimulation
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
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
Key things to think about in paralysed patients
need to be heavily sedated and no analgesic effect
require eye care
(pupils are not effected)
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
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
eg of antimuscarinic/anticholinergic med?
Atropine
scopolamine - sedating
glycopyrrolate
Which antimuscarinic most commonly used
glycopyrrolate - doesn’t cross blood brain barrier
Medication that directly binds to rocuronium and stops it working?
sugammadex -> complete reversal in 2-4 mins
Why do we sedate in ICU
Amnesia ventilator tolerance and effective ventilation anxiety / fear agitation sleep deprevation delerium
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
Key sedative for short term sedation or if you require rapid offset
propofol
dexmedetomidine why useful
no respiratory depression , minimal amnesia , easier to arouse and keep alert
-> can use while extubating
Which paralytic in renal failure
atracurium
