Local anesthetics and muscle relaxants Flashcards
Local anesthetics that are esters
procaine
tetracaine
benzocaine
breakdown easy due to esterases
Local anesthetics that are amides
Lidocaine Mepivacaine Bupivacaine Atricaine Ropivacaine
explain things to consider with inflamed tissue
- Local anesthetics are weak bases .
- low pH in inflammed tissue
- Low pH will ionize weak base-more water soluble
- in order to increase penetration, must increase pH to let it be in its more nonionized form .
- in the cell, the nonionized form is then ionized in order to block sodium
Overdose on Locals will affect which tissues
those with voltage gated sodium channels
Stages of overdose with local
- numbness, metalic flavor, dysgeusea
- Tremor, tinnitus, nystagmus, clouding of conscious
- Convulsions
- * at this stage of convulsions: also; indirect cardiac depression including:HTN, tachy, arrythmia. - CNS depression
- * also cardiac arrest, hypotension, ischemia, AV-dissociation, ECG -widening, low output.
Ach binds only to
alpha subunits
Delta and gamma subunits are in
NM junction–binding of ACh is still Ach binding to alpha
characteristic feature of muscle relaxants
Quaternary amine
Succinylocholine
Highly resembles Ach, results in the relaxation of skeletal muscles.
tubocurarine
polar and cannot penetrate the BBB.
Atracurium
derivative of tubocurarine -used in the clinic
Muscle relaxants with a steroidal skeleton
Pancuronium (clinic)
Rocuronium (history of used to kill people)
Vecuronium
Succinylocholine is a depolarizing blocker which means
1st step actually causes contraction, but later it prevents sodium channels from closing.
this drug opens sodium channels then leaves sodium channels and they are not allowing it to depolarized
All other drugs and molecules are termed as
nondepolarizing blockers-these dont allow depol
Trio of going under anesthesia
inducer (benzo, barb)
anelgesic
muscle relaxor
general anesthesia mechanism is not fully understood, but thought to
increase GABA and decrease glutamate
Certain gen anethetics have been shown to
block NMDA
Two groups of general anesthetics
inhaled , IV
Inhaled anesthetics
Nitrous oxide Xenon Halothane* Enflurane* Isoflurane* Sevoflurane* Desflurane * *= volatile liquid anesthetics
Pharmokinetics of inhaled anesthetics
gets into lungs which are high perfused and gets dissolved into the blood
then to brain and gets redistributed very quickly
Minimum alveolar concentration
concentration of a vapor in the lungs that is needed to prevent motor response in 50% of subjects in response to pain. Lower = more potent.
Pharmacodynamics and toxic effects of inhaled anesthetics
- decreased cerebreal metabolic rate
- 4 stages of increasing depth of CNS depression
- analgesia
- excitement (unsure of situation)
- surgical anesthesia (unconscious)- Medullary depression (breathing and cardio)
- analgesia
- Nephrotoxicity
- Hematotoxicity -careful with nitrous oxide
- Malignant hyperthermia- mutation specific - leads to uncontrolled release of calcium from ER which causes an increase in temp which leads to death
- Hepatotoxicity-be careful with halothane
Propofol/Fospropofol
hypnotic but no analgesia
water insoluble , formulated as an emulsion
**potentiation of GABAergic transmission
Rapidly metabolized in the liver
leads to drop in bld pressure and is potent respiratory depressant
antiemetic effect
Fospropofol is water soluble
Thipental and methohexital
GABAergic neurotransmission –penetrates BBB then redistribution
IV benzos
Diazepam, Lorazepam, Midazolam – these induce anesthesia
Etomidate
hypnotic but no analgesia
endocrine side effects
potentiation of gabaergic transmission
Ketamine
Inhibition of NMDA receptors
Low protein binding compared to other intravenous anesthetics
unpleasant emergence reactions
