Anesthesia Flashcards
5 primary effects of anestheisa
unconsciousness amnesia analgesia inhibition of automatic reflexes skeletal muscle relaxation
Remifentanil is what class of drug
remifentanil
thiopental is what class of drug
thiopental
stages of anesthesia
induction, maintenance, recovery
what is induction
time from initiation of anesthesia until desired concentration is achieved in brain
What drug and what route used for induction
propofol IV
when are opioids administered during anesthesia (ie what stage)
maintenance
which opioid commonly administered during anesthesia
fentanyl
what route for maintenance of anesthesia
inhaled and IV
Excitatory ion channel targets for general anesthesia
ACh (nic and mus receptors), Glutamate, serotonin
what is lipid theory?
correlate anesthetic potency w/ lipid solubility
2 factors influencing inhaled anesthetics effiacy
concentration of agent in inspired gas and gas pressure, alveolar ventilation
time to onset and time to recovery relationhipo to solubility
inversely related ie lower solubility= faster onset and recovery
least soluble inhaled anesthetic
NO
Most soluble anesthetic
halothane
sevoflurane solubility range
low
isoflurane solubility range
mid range
alveolar-venous partial pressure pressure effect on anesthesia
larger the difference, the more anesthetic will be taken up by tissues and venous blood will have lower concentration than arterial blood which means that it will take to achieve equilibrium between general circulation and the brain
which inhaled anesthetics is metabolized the most by the liver
halothane
Minimal alveolar concentration (MAC) measures what?
potency
which inhaled anesthetic is more potent
halothane
which inhaled anesthetic is least potent
NO
rate anesthetics according to potency
Halothane 0.74%
isoflurane
sevoflurane
NO
what exactly does MAC measure
minimal alveolar concentration required to prevent responses to surgical incision in 50% of cases
Stage 1 of anesthesia
analgesia from conventional to drowsy, count to 10 if you can (propofol is so fast that ususally skip this phase now)
Stage 2 of anesthesia
excitement: delirium and possible combative behavior, increased irregular BP and respiration rate. Propofol reduces/eliminates this stage
Stage 3
surgical anesthesia: loss of muscular tone and reflexes due to further CNS depression. breathing is regular and skeletal muscles relaxed. Need careful monitoring to ensure CNS is not depressed further
Stage 4
death if no support
inhaled anesthetics effect on brain
balance b/w decreased metabolic activityand the fact that Volatile anesthetics also cause cerebral vasodilation
inhaled anesthetics effect on heart
halogenated= decreased contractility and MAP
which anesthetics maintain CO as well as reduce preload and afterload?
isoflurane, desflurane, and sevoflurane
inhaled anesthetics effect on lungs
rapid shallow breathing and respiratory depressants
inhaled anesthetics effect uterus
halogenated= potent uterine muscle relaxants
What are 3 compartments
blood, brain and viscera, and muscle/fat
bevocaine and cocaine is what class and subclass
local anesthetic, ester, surface action
procaine is what class and subclass
ester, short acting,
tetracaine is what class and subclass
ester , long acting
lidocaine is what class and subclass
amide, medium acting
bupivocaine is what class and subclass
amide , long acting
local anesthetics are weak acids/ bases
weak bases
increased K levels increase/decrease efficacy of local anesthetics
increase
increased Ca levels increase/decrease efficacy of local anesthetics
decrease
how are esterLA metabolized
pseudocholinesterases
how are amide LA metabolzed
liver, p450
procaine half lfie
1-2 mintues
lidocain half life
1.5 hours
LA mechanism
block voltage dependent Na channels
is ionized/ non-ionized form better at interactin w/ receptor
non ionized
LA work better on narrower or thickier nerve fibers?
narrower
LA work better on heavily myelinated fibers or non/lighlty myelinated
heavily
LA work better on rapidly or slow firing nerves
rapid
LA work better on peripheral nerves or nerve bundle
peripheral
toxicity of LA
- CNS tox can cause convulsion which are treated w/ BZDs or barbs
- Cardiovascular depression which are treated w/ lipid rescue therapy
Isoflurane mechanism
potentites GABA and opens k channels
Isoflurane blood: gas partition coefficient
1.4
isoflurane MaC
1.4%
sevoflurane blood:gas partition coeffiecit
0.69
sevoflurane MAC
2%
NO blood:gas partition coefficient
0.47
Ketolorac only used less than 5 days because..
GI toxicity
propofol mechanism
potentiates GABAa receptor activity
major propofol inteteraction
allergies- eggs
Etomidate pahrm calss
IV general anesthetic and adjunct to general; hypnotic w/ no analgesic
Bupivacaine interactions
MAO-Is, ergot alkaloids w/ epinephrine
