Local anaesthetics. Dr JM Dippenaar
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1 Local anaesthetics Dr JM Dippenaar
2 Chemical structure Lipophilic phenol ring + Amide/Ester bridge + Hydrophilic chain
3 Local anesthetic drugs Amides Esters Lignocaine Cocaine Bupivacaine PABA esters Ropivacaine Procaine Levobupivacaine Chloroprocaine mepivacaine
4 Local anesthetic drugs Amides Liver metabolism Esters Pseudocholine esterase
5 Local anesthetic drugs Lignocaine Cocaine
6 Local anesthetic drugs Bupivacaine Ropivacaine
7 Chemical & physical characteristics Lipid solubility = potency onset of action pka onset of action
8 pka
9 Chemical & physical characteristics Lipid solubility = potency, onset of action pka onset of action Protein binding = duration of action Isomerism L= duration, potency, toxicity Local factors spinal vs. peripheral Nerve anatomy Diameter, myelinated or not, activity
10 Physico-chemical properties Drug Lipid pka Protein Potency solubility binding Lignocaine Bupivacaine Levo-bupiva Ropivacaine
11 Mechanism of action
12 Mechanism of action
13 Mechanism of action
14 Mechanism of action
15 Mechanism of action
16 Mechanism of action
17 Cocaine Ester derivative Intense vasoconstriction Indirect sympathomimetic release NA Block reuptake of NA and dopamine S/E Euphoria, paranoia, seizures, Hypertension, tachcardia
18 Prilocaine Emla cream Eutetic Mixture of Local Anaesthetic Added to lignocaine in equal quantities Changes the melting point of the drugs Skin analgesia within 60 min Methaemoglobinaemia
19 Lignocaine Amide, pka = 7.7 Low lipid solubility Metabolism Liver 99% (1% unchanged via kidneys) CYP 2D6 and 3A4 Monoethylglycinexilidide (MEGX) Active metabolite Additive to CNS side effects
20 Bupivacaine pka 8.1 Slow onset of action Very potent Highly lipid soluble Long duration of action CVS toxicity Refractory ventricular fibrillation
21 Lignocaine vs. bupivacaine Drug Lignocaine Bupivacaine Potency 4 16 Onset Short Prolonged Duration Short Prolonged Protein binding 64% 95% Toxicity manifesting: CVS CNS
22 Additives to bupivacaine Glucose 80mg (8%) added to spinal bupivacaine Increase the baricity of bupivacaine Heavier than CSF Gravitates to lower spinal regions Smaller dose for denser block.
23 Spinal anaesthesia: Heavy bupivacaine
24 Spread of heavy bupivacaine
25 Additives to local anaesthetics Vasoconstrictor = Adrenaline Decreased absorption Increased safe dose Increased duration of action Opioids = morphine, fentanyl, sufentanil Neuraxial = morphine vs fentanyl. Increased duration of action.
26 Additives to local anaesthetics Alkalinize = NaHCO3 Increased non-ionized fraction Faster onset of action Precipitation of adrenaline no premix!!! Anticholinergics = Neostigmine Α2 agonists = clonidine, dexmedetomidine Denser sensory blockade Prolonged duration of action
27 Dosage Lignocaine = 1% 1g in 100ml 1000mg in 100ml 10 mg/ml Bupivacaine = 0.5% 0.5g in 100ml 500mg in 100ml 5mg/ml
28 Maximum dose for infiltration Lignocaine 3-4mg/kg without adrenaline 7mg with adrenaline Bupivacaine / L-bupivacaine 2mg/kg irrespective of adrenaline Maximum of 150mg Ropivacaine 2mg/kg irrespective of adrenaline
29 Dosage calculation Child of 20kg for suture laceration. How many mls of 2% lignocaine with adrenaline may he receive? Toxic dose with adrenaline = 7mg/kg Total dose - 20kg x 7mg/kg = 140mg Each 2% vial has 20mg/ml of lignocaine Therefore 140mg / 20 mg/ml = 7ml of 2%
30 Dosage calculation Child of 20kg for suture laceration. How many mls of 0,5% bupivacaine with adrenaline may he receive? Toxic dose with adrenaline = 2mg/kg Total dose - 20kg x 2mg/kg = 40mg Each 0,5% vial has 5mg/ml of bupivacaine Therefore 40mg / 5 mg/ml = 8ml of 0,5% bupivacaine!
31 Toxicity: Classification Local toxicity Neurotoxicity Transient neurological symptoms Myotoxicity Systemic toxicity CNS CVS
32 Systemic toxicity Intravascular injection Increased absorption plasma concentration Distribution Vessel rich organ group
33 Toxicity: absorption Excessive dose Site of injection Intercostal>caudal>epidural>brachial plexus Physico-chemical properties Lipid solubility } Protein binding } absorption Potency } Vasoconstrictor
34 Toxicity CNS (Lignocaine 7x more) Convulsions CVS (Bupivacaine 3x more) Refractory ventricular fibrillation
35 CNS toxicity Initial phase Circumoral paresthesia, tinnitis, confusion Excitatory phase Convulsions Depressive phase Los of consciousness Coma Respiratory arrest
36 CVS toxicity Initial phase Hypertension, tachycardia Intermediate phase Myocardial depression CO Hypotension Terminal phase Vasodilatation, hypotension, bradycardia Conduction defects, dysrhythmias
37 Bupivacaine cardiac toxicity
38 Toxicity To complications due to bupivacaine Ropivacaine Levo-bupivacaine
39 Ropivacaine Amide, pka = 8.1 Lower lipid solubility Metabolism Liver 99% (1% unchanged via kidneys) CYP 1A2 (fluvoxamine metabolism 16%)
40 Ropivacaine Biphasic vascular effect Low[ ] = vasoconstriction High [ ] = vasodilatation Faster dissociation from cardiac Na+ channels than bupivacaine Higher threshold for CNS symptoms
41 Ropivacaine: clinical uses Pain relief: Epidural for labour, post op: Surgery: 0.75%-1% up to 12ml bolus Well differentiated block Good sensory blockade Much less motor blockade
42 L-bupivacaine L isomer of bupivacaine pka 8.1 As potent as racemic mixture Potentially less CVS toxicity L-isomer less direct cardiotoxic effects
43 Rx of toxicity Convulsions BZ Thiopentone Propofol Ventricular fibrilation Bretilium Intralipid K+ channel openers
44 Rx of toxicity Ventricular fibrilation Bretilium Intralipid K+ channel openers
45 Bretilium tosylate Class III anti arrhythmic Slows phase 3 repolarisation Prolongs refractory period release of NA Not manufactured currently
46 K+ channel openers Pinacidil, bimakalim Opens K+ATP channels Shorten action potential in Purkinje fibers Prolongs plateau phase Hyperpolarise resting membrane potential
47 K+ channel openers: side effects Shorten action potential = Ca++ influx Reduced contractility Excessive coronary vasodilatation Coronary steal with steal prone anatomy
48 K+ channel openers Improve AV conduction But Myocardial depression
49 Intralipid Lipid emulsion Soya oil Egg phospholipids Glycerol TPN, Propofol effective antidote Bupivacaine induced CVS collapse
50 Intralipid : proposed actions Lipid sink Draws Bupivacaine from plasma Decreased free fraction High lipid concentration Forced lipid influx into myocyte Overwhelms L-CAT FFA for energy production susceptibility for resuscitation
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