ropivacaine

ROPIVACAINEVerdah SabihHouse officerAnesthesiology 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.