Bupivacaine
Chemical
Amide local anaesthetic
Use
Local anaesthesia
Presentation
Clear colourless solution
Racemic (S- & R- enantiomers)
Concentrations of 0.25% and 0.5%
+/- Adrenaline 1:200,000 and preservative sodium metabisulphite
Hyperbaric solution of 0.5% contains 80mg/ml glucose (specific gravity 1.026)
Dose
1-2mg/kg up to a maximum of 150mg
Toxic Dose
Max dose 3mg/kg
Route
Peripheral n blocks, epidural, spinal
Onset
Slower cf lignocaine
DoA
T1/2b = 0.3-0.6hrs
MoA
Unionised diffuses across neuronal cell memb
Becomes ionized within cell
Binds and OPENS Na+ ch → blocks them
↓depol of membrane →Cardiac myocyte, Motor & sensory n fibre APs blocked
Bupi is x4 more potent cf lignocaine & prolonged DoA, but slower onset
PD
CNS
- Reversible neural blockade
- Levobupi produces less motor block but longer sensory block following epidural administration
CVS
- Reduces SVR
- Negative inotropy
- Cardiotoxic: binds myocardial proteins & blocks Na ch to ↓rate of increase Ph0 cardiac AP
- Levobupi has less cardiotoxicity
PK
A
Dose & concentration dependant
IC > Caudal > Epidural > Brachial Plx > Subcut
+Adr = delayed absorption
Highly lipid soluble, take up into fat is rapid
Drug has direct vasodilatory effect
D
95% PPB to a1 glycoprotein
Vd 1L/kg
M
Low extraction ratio drug => less influence by HBF cf lignocaine
Primarily liver metabolised via conjugation w glucuronic acid
Main metabolic is 2,6 pipecoloxylidine (catalysed by P450 3A4)
E
Clearance 7ml/min/kg
T1/2b = 0.3-0.6hrs
Metabolites in urine. 16% unchanged
Adverse Effects
Drug interactions: propranolol
Cardiotoxicity
Systemic toxicity of LAs → neurotoxicity, cardiotoxicity, death