Ropivacaine is a long-acting local anesthetic similar to bupivacaine that provides both anesthesia and analgesia. It has decreased cardiotoxicity compared to bupivacaine. Ropivacaine is metabolized in the liver and excreted renally. It works by reversibly blocking sodium ion influx in nerve fibers, inhibiting impulse conduction. It can be used for epidural, spinal, infiltration, and peripheral nerve blocks for surgical anesthesia, C-sections, and postoperative or chronic pain management. Side effects include central nervous system and cardiovascular toxicity at high doses.

1. ROPIVACAINE
Verdah Sabih
House officer
Anesthesiology dept. HFH

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.