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ROPIVACAINE
Verdah Sabih
House officer
Anesthesiology dept. HFH
INTRODUCTION:
 Long acting amide local anesthetic with both
anesthetic and analgesic effects.
 Similar to bupivacaine & etidocaine in duration of
activity.
 Structurally similar to mapivacaine & bupivacaine.
 Decreased cardiotoxicity
 Used for regional nerve block.
 At high doses it produces surgical anesthesia and
at lower doses it produces analgesia (sensory
block) with limited motor block..
STRUCTURE:
 belongs to the group of local
anaesthetics, the
pipecoloxylidides and has a
propyl group on the
piperidine nitrogen atom
(compared to bupivacaine,
which has a butyl group)
 Enantiomer of propivacaine (S
stereoisomer)
PHARMACOKINETICS
 Onset time : 15 mins
 Duration :2-6 hrs
 Bioavailability:87%–98% (epidural)
 Metabolism: Hepatic (CYP1A2-mediated)
 Biological half-life:1.6–6 hours (varies with
administration route)
 Excretion: Renal 86%
 less lipophilic than bupivacaine less likely to
penetrate large myelinated motor fibres selective
action on the pain-transmitting A β and C nerves rather
than Aβ fibres, which are involved in motor function.
 bound to plasma proteins to an extent of 94%, mainly to
α1-acid glycoprotein.
MODE OF ACTION
 reversible inhibition of sodium ion influx, and
thereby blocks impulse conduction in nerve fibre.
 potentiated by dose-dependent inhibition of
potassium channels.
DOSAGE AND ADMINISTRATION
 Max.dose= 3mg/kg
TECHNIQUES:
 Epidural block
 Spinal block
 Infiltration anesthesia
 Peripheral nerve block
INDICATIONS
 Local Surgical anesthesia
 C-section
 Hip or lower limb surgery
 Peripheral nerve blocks
 Post operative pain management
 Labour pain management
 Chronic pain management
CONTRAINDICATIONS
 Use as intravenous regional anaesthesia (IVRA).
CLINICAL SIDE EFFECTS
 CNS toxicity:usually occur at lower blood plasma
concentrations
 CNS excitation,(nervousness, tingling around the
mouth, tinnitus,tremor, dizziness, blurred vision,
seizures) followed by depression(drowsiness, loss
of consciousness), respiratory depression and
apnea).
 CVS toxicity:
 hypotension, bradycardia, arrhythmias, and/or
cardiac arrest
INTERACTIONS WITH OTHER DRUGS
 Anti-arrhythmics: increased myocardial
depresssion
 Antidepressants:meabolism of ropivacaine
inhibited by fluvoxamine(strong inhibitors of
cytochrome P4501A2).
 other local anaesthetics or agents : (structurally
related to amide-type local anaesthetics)toxic
effects of these drugs are additive.
TREATMENT OF OVERDOSE:
 Celepid, a commonly available intravenouslipid
emulsion, can be effective in treating severe
cardiotoxicity.
ropivacaine-160113161602.pdf

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ropivacaine-160113161602.pdf

  • 2. INTRODUCTION:  Long acting amide local anesthetic with both anesthetic and analgesic effects.  Similar to bupivacaine & etidocaine in duration of activity.  Structurally similar to mapivacaine & bupivacaine.  Decreased cardiotoxicity  Used for regional nerve block.  At high doses it produces surgical anesthesia and at lower doses it produces analgesia (sensory block) with limited motor block..
  • 3. STRUCTURE:  belongs to the group of local anaesthetics, the pipecoloxylidides and has a propyl group on the piperidine nitrogen atom (compared to bupivacaine, which has a butyl group)  Enantiomer of propivacaine (S stereoisomer)
  • 4. PHARMACOKINETICS  Onset time : 15 mins  Duration :2-6 hrs  Bioavailability:87%–98% (epidural)  Metabolism: Hepatic (CYP1A2-mediated)  Biological half-life:1.6–6 hours (varies with administration route)  Excretion: Renal 86%  less lipophilic than bupivacaine less likely to penetrate large myelinated motor fibres selective action on the pain-transmitting A β and C nerves rather than Aβ fibres, which are involved in motor function.  bound to plasma proteins to an extent of 94%, mainly to α1-acid glycoprotein.
  • 5. MODE OF ACTION  reversible inhibition of sodium ion influx, and thereby blocks impulse conduction in nerve fibre.  potentiated by dose-dependent inhibition of potassium channels.
  • 6. DOSAGE AND ADMINISTRATION  Max.dose= 3mg/kg TECHNIQUES:  Epidural block  Spinal block  Infiltration anesthesia  Peripheral nerve block
  • 7. INDICATIONS  Local Surgical anesthesia  C-section  Hip or lower limb surgery  Peripheral nerve blocks  Post operative pain management  Labour pain management  Chronic pain management
  • 8. CONTRAINDICATIONS  Use as intravenous regional anaesthesia (IVRA).
  • 9. CLINICAL SIDE EFFECTS  CNS toxicity:usually occur at lower blood plasma concentrations  CNS excitation,(nervousness, tingling around the mouth, tinnitus,tremor, dizziness, blurred vision, seizures) followed by depression(drowsiness, loss of consciousness), respiratory depression and apnea).  CVS toxicity:  hypotension, bradycardia, arrhythmias, and/or cardiac arrest
  • 10. INTERACTIONS WITH OTHER DRUGS  Anti-arrhythmics: increased myocardial depresssion  Antidepressants:meabolism of ropivacaine inhibited by fluvoxamine(strong inhibitors of cytochrome P4501A2).  other local anaesthetics or agents : (structurally related to amide-type local anaesthetics)toxic effects of these drugs are additive.
  • 11. TREATMENT OF OVERDOSE:  Celepid, a commonly available intravenouslipid emulsion, can be effective in treating severe cardiotoxicity.