Viva - Sedation Flashcards

1
Q

What is remi

A

Synthetic phenylpiperidine derivative of fentanyl

Pure u agonist

White powder, 1,2,5mg reconstituted in saline

Metab - non-specific plasma and tissue esterases (but unlike sux, no affected by cholinesterase deficiency)
Duration is by elimination and not distribution

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2
Q

Remi side effects

A

Resp - depression, chest wall rigidity

CVS - Brady and hypotension

Can be reversed by naloxone

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3
Q

What receptor does remi act on

A

Pure u (mu) opioid receptor

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4
Q

Remi metabolism

A

Non specific tissue and plasma esterase

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5
Q

Why would you use remi in ICU

A

Rapid predictable offset once turned off due to short CSHT (3 minute)

Used in Neuro—crit care to assess neurology rapidly

Useful in difficult to wean patients, patients expected to extubate quickly, or to facilitate procedures

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6
Q

Problems with remi use

A

Wears off rapidly - need alternative analgesia

Hyperalgesia intra-op, therefore need more opioids post op

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7
Q

What is context sensitive half time

A

Time taken for plasma conc to halve, after an infusion designed to maintain constant blood levels is STOPPED

Context - duration of infusion (half time changes as duration progresses)

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8
Q

What influences the range of CSHT

A

Ratio of:

Clearance due to redistribution to clearance due to elimination

Predicts how long a patient will wake up from steady state infusion

Fent - redistributes quickly, elimination is 20% of distribution. Therefore CSHT increases rapidly with infusion to 300 minutes max

Propofol - redistribution = elimination. Concentration falls rapidly. 20 mins CSHT

Remi - distribution lower the elimination (opp of fent). Elimination dictates clearance and is low and constant

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9
Q

Propofol

A

2-6 di-iso-propylphenol
1 to 2% lipid emulsion. Soya bean oil and egg phosphatic
Lipid soluble. Not water soluble

Unionised at physiology (pKa = 11)
98% protein bound
Vd 4litres/kg

Rapid distribution so wears off after quick bolus

Hepatic metabolis to quinol - sulphate and glucuronide

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10
Q

Adverse effects of propofol

A

Resp - depression and apnoea

CVS - Low SVR, hypotension
Brady
Reduced sympathetic activity

Met - PRIS

Other - green urine

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11
Q

PRIS

A

Refractory bradycardia leading to asystole plus:

Unexplained met acidosis (BE > -10
Rhabdo /high CK, high K, AKI or myoglobinuruea
Lipaemic plasma (triglycerides)
Fatty liver/hepatomegaloy/liver dysfunction
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12
Q

Patho phys of PRIS

A

Impaired mitochondrial fatty acid metabolism

Direct inhibition of mitochondrial function

Impaired oxygen utilisation, anaerobic resp and lactate production

Also myocardial depression and accumulation of unutilised fatty acid

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13
Q

Risk for PRIS

A

High dose infusion >4mg/kg/hour

Young age (low glycogen stores, depend on lipid metab)

CI in ICU under 16

Brain injury
Low carb high lipid intake, TPN
Catecholamine, and steroids
Inborn mitochondrial disease

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14
Q

PRIS presentation

A
Brady
Varying heart blocks
RBBB
Arrhythmia
Brigade - concave ST V1-3

Unexplained cardiovascular instability

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15
Q

PRIS treat

A

Stop propofol
Start alternative agent - midaz

Support oxygen and haemodynamic
Treat rhabdo - urine to 2-3mls/hour, alkalinisation, diuretics, treat K)
RRT if AKI
Carbohydrate intake

Temporary pace
VA ECMO???

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16
Q

Ways to assess sedation

A

Richmond Agitation Sedation Score (RASS)
Ramsey Sedation Scale

Richmond:
+4 to -5
+4 combative, -5 unrousable
0 alert and calm, 1 restless, -1 drowsy

Ramsey
1 to 6
1- anxious agitated restless
2 - cooperative
3 - commands only
…
6 no respond to glabellar tap
17
Q

What level of sedation?

A

Titration to clinical need and should be set as part of daily ward round

3 C rules - Calm, co-operative and comfy

RASS 0 to -1

Or -3 to -5:
Brain injury, raised ICP
Use of paralysis
ARDS
Vent dysynchrony
Immolbisation - spinal #
Status epilepticus