Pharmacology of intravenous induction agents
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1 Pharmacology of intravenous induction agents Ákos Csomós MD, PhD Professor, Head of Department Medical Centre, Hungarian Defence Force, Budapest
2 What do we have in the market? Thiopental Metohexital Etomidate Ketamine Propofol
3 Uptake and redistribution of an iv. bolus of thiopental Published in 1974 by Eger. Similar pharmacokinetic mechanism apply to the other iv. anaesthetics.
4 Properties of induction agents
5 Effect of lignocaine and ph on propofol induced pain Traditional teaching was that local anaesthetics have an effect on the vascular endothelium. The ph of 1% Diprivan decreased after mixing with 1% lignocaine, compared to saline. CONCUSION: mixing lignocaine with propofol is more efficient than injection of licnocaine followed by propofol. Br J Anaesth 1997;78:502.
6 Cardiovascular, respiratory and CNS effect of iv. anaesthetics
7 Intravenous anaesthetics primarily act on receptor proteins Antagonists on GABA A Agonists on NMDA Propofol, etomidate, barbiturates, benzodiazepines Ketamine
8 Effect of propofol on GABA A receptors in brain Flumazenil is selective GABA antagonist. Radioactive 11C-flumazenil was used as the PET tracer. Propofol 9.0 ±3.0 μg/ml BIS 28±8 Salmi L, Anesth Analg 2004
9 News on GABA A receptors Etomidate acts at multiple sites on GABA synopses Anesth Analg 2012;115:270.
10 Ketamine and NMDA receptors Ketamine is noncompetitive NMDA receptor antagonist. Agonist of this NMDA receptor are excitatory amino acids (EAA), like: glutamic acid, aspartic acid, glycine
11 Ketamine
12 Ketamine pharmacology
13 Ketamine pharmacology
14 Ketamine pharmacology Elimination half-life 2.17 hrs, redistribution halflife 4.68 hrs. Water soluble; but fat solubility 10x thiopentone. pka 7.5 permits iv, im, oral, intranasal, rectal adm. Major metabolite norketamine. Produces cataleptic unconscious state with complete amnesia and analgesia. Produces dose- and age-dependent behavioral effects resembling schizophrenia. Emergence characterized by vivid dreams.
15 Ketamine mechanism of action Non-competitive NMDA receptor antagonist. Ketamine blocks sensory input and impairs limbic functions. Agonist at α and β adrenergic receptors. Antagonist at muscarinic receptors of the central nervous system. Blocks reuptake of cathecolamines. Agonist at opioid sigma receptor.
16 Ketamine practical pharmacology How fast is ketamine ( pharmacokinetics )? Onset of action: after 2 mg/kg iv. injection: 45 seconds after 3 mg/kg im. Injection: 4 minutes Recovery times: 18 minutes and 25 minutes respectively After iv. bolus: distribution half-life: 24.1 sec redistribution half-life: 4.68 min elimination half-life: 2.17 hrs Cotsen MR, Am J Roentgenol 1997 Domino EF, Clin Pharmacol Ther 1984
17 Ketamine pharmacology
18 Ketamine for mood disorders? Ketamine causes a surge in glutamate release and cycling, through a blockade of tonic GABAergic inhibition. Rapid onset antidepressant effect can be achieved with a single administration of ketamine Sanacora G, Neurophsychopharm 2015
19 Etomidate 1972
20 Etomidate pharmacology Carboxylated imidazole compound (2xnitrogen). ph 8.1, 75% protein bound. Rapid onset, lasting for 8 min. Elmination half-life 70 min. Interferes with adrenal corticosteroid synthesis. inhibits 11-β-hydoxylase and 17-α-hydroxylase. Increases the incidence of PONV. Induction of anesthesia with etomidate results in dose-dependent myoclonus in 50 80% of patients without premedication.
21 Etomidate and myoclonus 4 Groups: 1) NP = no pretreatment; 2) F = fentanyl 1 µg/kg; M = midazolam 0.03 mg/kg; 4) FM fentanyl 0.5 µg/kg and midazolam mg/kg. Myoclonus movements were observed for 2 min. Myoclonus incidence was NP=85%, F=40%, M=70%, and FM=25%; significantly lower in Group F and Group FM.
22 Pharmacokinetics of etomidate After 3 mg/kg iv. bolus. There are 3 distinct decline phases with half-times: 2 min 21 min 3.9 hrs Adrenal suppression is prolonged! Forman SA, Anaesthesiology 2011
23 Propofol
24 2.6-Diisopropylphenol Propofol pharmacology Oil-water emulsion in 1% and 2%, containing 10% soya-bean oil, 1.2% egg-phosphatide and 2.25% glycerol and 0.005% EDTA. pka 11, 98% protein bound. Distribution half life 1-2 min. Elimination half-life 1-5 hrs. CSHT 20 min/ 2 hrs, 30 min/6 hrs, 50 min/9 hrs. Metabolised in liver, excreted renally.
25 Neuroprotective properties of propofol Propofol is a global CNS depressant: activates GABA A receptors, inhibits NMDA receptors and modulates calcium-influx. reduces cerebral blood flow and ICP lab studies showed it might protect brain from ischaemic injury. Recently EDTA has been reported to exert a neuroprotective effect. CNS NeurSc 2008;14:95.
26 TTPE: propofol vs. midazolam (10.4 min)
27 Dose-response curves for hypnosis Steep curve implies that a small increase in dose results in large increase in response.
28 OUR OWN STUDY: Does the type of music affects the volume of TCI propofol used during endoscopies?
29 No of cases Effect of listening to music during TCI propofol for endoscopies Jazz Classic Rock Romantic No music Age (yrs) 42 (13)** 54 (14) 44 (10)** 48 (11) 50 (17) BMI 24,6 (4,1) 26,5 (4,8) 26,9 (4,9) 25,2 (4,9) 25,7 (4,3) Length (min) Propofol dose (mg) 21,5 (8,9) 20,5 (8,1) 20,6 (7,2) 18,2 (6,8) 20,9 (8,8) 401 (154) 333 (106) 386 (99) 355 (121) 382 (127)
30 Any new iv. medications?
31 New benzodiazepine receptor agonist: CNS7056 esterase-hydrolysed, rapid onset and short duration. recovery within 10 min (vs. 40 min with midazolam). Carboetomidate removal of binding nitrogen atom from etomidate reduces adrenocortical inhibitory potency by 3 magnitude. May be used for maintenance.
32 Fospropofol phosphate pro-drug for propofol; converted to propofol within few minutes. longer TTPE and slower recovery. water soluble, no pain at injection. FDA approved. Sedasys Propofol with automated ECG, SaO2, exhaled CO2 and patient responsivesess analysis.
33 Our own brain can NOT be replaced! Downloaded: 16th March 2016
34 Thanks for your attention!
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