Viva - Sedation Flashcards
What is remi
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
Remi side effects
Resp - depression, chest wall rigidity
CVS - Brady and hypotension
Can be reversed by naloxone
What receptor does remi act on
Pure u (mu) opioid receptor
Remi metabolism
Non specific tissue and plasma esterase
Why would you use remi in ICU
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
Problems with remi use
Wears off rapidly - need alternative analgesia
Hyperalgesia intra-op, therefore need more opioids post op
What is context sensitive half time
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)
What influences the range of CSHT
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
Propofol
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
Adverse effects of propofol
Resp - depression and apnoea
CVS - Low SVR, hypotension
Brady
Reduced sympathetic activity
Met - PRIS
Other - green urine
PRIS
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
Patho phys of PRIS
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
Risk for PRIS
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
PRIS presentation
Brady Varying heart blocks RBBB Arrhythmia Brigade - concave ST V1-3
Unexplained cardiovascular instability
PRIS treat
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???