Multimodal Flashcards
Gabapentin (Neurontin)- MOA
Binds VG Ca++ channels; inhibits glutamate release in the dorsal horn of the spinal cord
Gabapentin (Neurontin)- Doses
300 - 1200 mg prior to OR
Gabapentin (Neurontin)- Side Effects
Can exacerbate MG & myoclonus
Gabapentin (Neurontin)- Misc
GABA ANALOGUE WITH NO GABANERGIC ACTIVITY
Dexamethasone (Decadron) -MOA
Inhibits phosolipase & cytokines; stabilizes membrane
Dexamethasone (Decadron): Dose
8-10 mg
Dexamethasone (Decadron): Side Effects
Can elicit a vomit reflex if given RIVP; Perineal burning/Itching
Celecoxib (Celebrex)- MOA
1st COX-2 specific Inhibitor; decreases PG synthesis (inducible)
Celecoxib (Celebrex)- Doses
200 - 400 mg PO QD.
Peak 3 hours
Acetaminophen (Ofirmev): MOA
Decreases prostaglandin metabolites
Acetaminophen (Ofirmev): Doses
1 Gm IV/PO
Onset: 30 - 60 mins IVOnset: 1 - 3 hours
PO Max: 3 Gm (24 hrs) Duration: 6 - 8 hours
Acetaminophen (Ofirmev): Misc
Can have hepatic effects; toxic > 3 Gm/Day
Ketorolac (Toradol): Doses
30 or 60 mg IM Q6 hours Elderly: 1/2 dose. Peak: 45 to 60 mins IV
Ketorolac (Toradol): MOA
Inhibits COX-1/COX-2; Decreases PG synthesis
Ketorolac (Toradol): S/E
Can be extremely renal toxic; 1/2 doses in elderly & renal pts
Ketorolac (Toradol): Misc
C/I: Severe renal impairment, significant risk for bleeding, CAD, CABG, pregnancy; decrease dose in. elderly, NSAID allergy
Ibuprofen (Caldolor, Neoprofen): MOA
Inhibits COX-1/COX-2;
Ibuprofen (Caldolor, Neoprofen): Doses
200 - 800 mg IV Max: 3200 mg (24 hrs)
Ibuprofen (Caldolor, Neoprofen): S/E
Allergies to NSAIDs; bleeding, CABG, ulcers
excretion: urine and bile
Lidocaine: MOA
Amide - Local Anesthetic
Lidocaine: Doses
1 - 2 mg/kg IV Q 2 - 4 mins
gtt: 1 - 2 mg/kg/hr
terminated 12 - 72 hours
Magnesium: MOA
NMDA receptor non-competitve antagonist
Magnesium: Dose
Pre-op: 50 mg IV Intra-op (gtt): 8 mg/kg/hr
Be prepared to treat bradycardia and/or hypotension.
Magnesium: S/E
C/I in Myasthenia Gravis (MG) and renal failure
Magnesium: Misc
SIGNIFICIANTLY DECREASES FENTANYL REQUIRMENTS
Limited passage across BBB
Cox-1
ubiquitous
“physiologic”
Inhibition is responsible for many adverse affects
“constitutive”
COX-2
“pathophysiologic”
Expressed at sites of injury
Not protective…oncogenic processes
Sensitization, “wind-up”
Inducible
√√√ COX-2 Selective √√√
vs.
Nonspecific Inhibitors
Comparable analgesia
Lack effects on platelets
May be assoc. with ↓ GI effects
Possible ↑ in MI and CVA
Dosage ceiling
↑ in side effects
Types of NSAIDS
Non-specific
Ibuprofen, naproxen, aspirin, acetaminophen, ketorolac