local anesthetics Flashcards
more soluble a gas is
slower onset
less soluble
faster onset
if a drug has 1 I in the name it is an
Ester and is destoryed by esterase which is in every tissue in the body
if a drug has 2 I’s it is an
amide
esters are converted
in the plasma by esterase enzymes
SHORT ACTING and not widely use
why do amides take lober to biotransform
converted in the liver by amidase
compared to esters that are converted in the plamsa
molecules with a positive charge are what in terms of solubility
they are water soluble and this is a problem because you need to inject an dhope that it gets into the neuron through the neuronal sheath
if it is water soluble it will not enter
the target of all anesthetics is the
Na receptor on the axon
shut it down
keep it from firing
patient will never feel the knife
electrical conduction Na K Na K Na K
neuron goes to sleep
unionized is
not charge
which means you can go through lipid soluble layers and this is where we want the drugs at
need a buffer
why is a infx an issue
more acidic and not as infective because it is ionized right away
faovirng the charged form
buffering
makes i more basic so that you are in a state that will remain unionized and allow for a shorten onset time
charge all has to do with cell penetration
why would you use epinephrine w/ lidocaine
vasoconstriction will keep the local anesthetic at the site longer
DKA
ph at which half of the drug is ionized and half is onionized
you w
why doesn’t the second injc of lidocaine work as well as the first
because o the buffering capacity at the injection site
buffer it yourself and you won’t run into problems
all local anesthetics promote vasodilation except
cocaine
nasal surgey this is the drug of choice
this is why we use Brier’s block
epinephrine
reduces blood flow
co-administration with CO2 saturated solutions increases intracellular levels of local anesthetic because
high intracellular CO2 produces a local acidosis which causes intracellular accumulation of cationic anesthetics
reduced response from repeated dosing)
Tachyphylaxis (
at pH 7.5 drugs are
unionized and pass through lipid membranes
In extracellular fluids drugs are buffered from
6 (bottle) to 7.4
why can Intralipid be used to reverse bupivacaine toxicity?
lipid solluble and intraplipid sucks it up
IV anesthestics
barbs (thipental methohexital) benzo (midazolam, diazepam) GABA propofol ketamine opioid (morphine tanil) misc sedative (etomidate)
inhaled anesthetics
make it RANE =volatile (liquid at room temp)
nitrous oxide
remain the primary INHIBITORY ion channels considered legitimate candidates of anesthetic action.
Chloride channels (γ-aminobutyric acid-A [GABAA] and glycine receptors) ETOH
and potassium channels (K2P, possibly KV, and KATP channels)
Excitatory ion channel targets for general anesthesia
Excitatory ion channel targets include those activated by acetylcholine (nicotinic and muscarinic receptors), by glutamate (amino-3-hydroxy-5-methyl-4-isoxazol-propionic acid [AMPA], kainate, and N-methyl-D-aspartate [NMDA] receptors), or by serotonin (5-HT2 and 5-HT3 receptors). Figure 25– 1 depicts the relation of these inhibitory and excitatory targets of anesthetics within the context of the nerve terminal.
balanced anethesia
inhaled anestheis
sedative hypnotic
opioid for pain mngmt
neuromuscular blocking for relaxation
monitored anesthesia
used when you need the pt conscious
local plus a sedative allowing the pt to respond
low vapor pressure and high boiling points are characteristics of this gas
volatile
and the RANEs
allows for precision
gas works through (4)
CL
K channels
this means that
inside the neuron K is much higher
K flows out
brining up inhibition can be done by taking K out of the neuron
glutamate
aCH
all possible MOA
BLUE CYLINDER
Nitrous Oxide
The most important parameter that can be controlled by the anesthesiologist to change alveolar concentration quickly is
the inspired concentration or partial pressure.
stages of anesthesia
stage I analgesia without amnesia
stage II excitement delirious and vocalizing but amnesic
stage III surgical
stage IV medullary depression CNS depression and death
what can be used to determine whether a pt is in surgical anesthesia
pupil size
most reliable is loss of response to noxious stimuli (trapezius muscle squees) and restablishment of regular respiratory pattern
which stage of amnesthia do you want to skip
2!
most dangerous
MAC
minimum alveolar concentration
the alveolar concentration at one atmosphere that produced immobility in 50% of pts expose
this is how they measure potency
pharmakodynamis
drug does to the body
kinetics
body does to the drug
concentration for gas
partial pressure
concentration at sea level
factors that effect movement of the gas into the CNS
solubility- based on blood solubility
concentration in inspired air
pulmonary ventilation
arteriovenous concentration gradient
if gas is highly soluble
slow induction
halothane
if gas is poorly solluble
rapid induction
nitrous oxide induction is
rapid because it does not like the blood
why would you use nitrous oxide first and halothane second
balanced anesthesia
primary target of gasses
Cl
negative
FLUR toxicity of gas anasthetic
worry about the kidney
liver toxicity with this gas
halothane
may induce immune mediated cause of hepatitis
nurses that administer this start to make antibodies against it
malignant hypothermia toxicity is caused by
genetic disorder of skeletal muscle and can be induced by general anesthetics and succinylcholine
how to we tx malignant hypothermia caused by anesthetics
dantrolene
what are the sxs of malingnant hyperthermia
tachy HTN muscl rigidity hyperthermia hyperkalemia acidosis
chronic toxicity of general anesthetics
mutagenisity
carcinogenesity
reproductive organs
two most widly used barbiturates iv anesthetic
thiopental and methohexital
thiopental is used
for the induction of anesthesia
acts through GABA
blocks sodium gated ion channels
this benzo is most widly used benzo anesth
medazolam
drug blocks excitatory NT glutamic acid at NMDA receptors
Ketamine
dissociative anesthesia
vivd dreasm
5 desired effects of anesthesia
unconsciousness, amnesia, analgesia, inhibition of autonomic reflexes and skeletal muscle relaxation).
fosproprofol
prodrug that reduces incidence of injection site pain
removal of phosphate
what MUST be used with etomidate
opioid
no analgesic effect
but used
pre synaptic homeostatic biofeedback mechanism is utilized in this alpha 2 targeting drg
dexmedetomidine–> ALPHA 2
receptro on the nueron that is releasing the neurotransmitter
doubles back and bins to itself
raises blood pressure
alpha
succinylcholine is the DOC
for intubation in the ER
tubocurarine moa
neuromuscular blocking
antagonist and nondepolorizing
all that end in curarine
suzzinylcholine moa
excess depolarization leading to muscle paralysis
depolarizing
ONLY ONE THAT WORKS LIKE THIS
TOO MUCH KEEPS BINDING
Keeps the channel open
ADRs succinylchlinr
HYPERKALEMIA
muscle relaxant that can lead to what in hemiparaiasis pts
and neuronal injuries cause increase expression of NT receptors
and can lead to lifethreatenting hyperkalemia in pts with succinylcholine
spasmolytic for chronic use
diazepam
spasmolytic that acts on GABAb
baclofen
GABAa receptor agonist
diazepam
valieum
can be used for anxiety at low levels (less than 5)
and at 60 it’s a sedative
phase I blocking is
depolarizing
Phase II is
desnesitizing
what drugs enhance neuromuscular blockade
AG
